Supplement: Essential role of fats throughout the lifecycle

Nutrition is no longer just the science of avoiding deficiencies, but rather is now focused on determining the levels of dietary nutrients that will optimise physiological and health outcomes. Nowhere is this change in the study of nutrition more evident than in the study of dietary fatty acids. In a few short years we have progressed from the simple mantra "saturates are bad, polyunsaturates are good" to a far more sophisticated understanding of the way that individual fatty acids in our foods can manifest physiological change. We now know that not all saturated fatty acids cause a rise in plasma cholesterol levels — some are more atherogenic than others, which explains why some food fats cause a larger rise in plasma cholesterol levels than others. So, foods rich in saturates should still be avoided, but dietary advice can now be more targeted. Equally important is that we have also come to realise that not all polyunsaturated fatty acids (PUFAs) are equal. Nutritionists now differentiate between omega-6 and omega-3 PUFAs, not only because their chemical structures differ, but also because they elicit different effects. Omega-6 PUFAs, for so long a common constituent of a huge variety of spreads, cooking oils and foods, have proven their worth in numerous studies on cholesterol lowering. However, some key studies conducted over the past 10 years have shown the potency of foods containing omega-3 PUFAs. The improved survival of people who had already experienced a cardiac event when they consumed diets rich in omega-3 PUFAs was remarkable. Whether the omega fatty acids were vegetable in origin1 or were marine oils,2 all-cause mortality rates were reduced by 30%–70% and induced comparable large reductions in non-fatal sequelae. These results were equivalent to effects seen in statin trials. In addition, the protective effect of the Mediterranean dietary pattern in the Lyon study1 was maintained up to four years after the first infarction, confirming the previous intermediate analyses and demonstrating the sustainability of this type of diet. Major traditional risk factors, such as high total blood cholesterol level and raised blood pressure, continued to be independent and joint predictors of recurrence, indicating that the diet did not alter, at least qualitatively, the usual relationships between major risk factors and recurrence, but provided additional protection. Given the low risk and low cost of this type of intervention, it seems vital that the usefulness of dietary intervention in secondary prevention be fully realised. There have also been breakthroughs in the use of omega-3 PUFAs in preterm infant nutrition. Because of our limited ability to convert vegetable omega-3 PUFAs to the long-chain PUFA found in marine foods (such as docosahexaenoic acid [DHA]), several clinical trials have tested the effectiveness on short- and long-term development of supplementing formulas with DHA. The results have been consistently positive, highlighting the fact that fats are essential to the normal growth and development of children. Here, the mechanism may seem to be self-evident, as DHA is a major component of brain and retina, and the preterm infant is denied the natural flow of DHA from the mother, which is greatest in late pregnancy. However, the actual role of DHA in these tissues is still being unravelled. Importantly, change has occurred in the market place, and all preterm infant formulas sold in Australia are now supplemented with DHA. There are a number of clinical areas where omega-3 PUFAs in the diet have shown promising results. Benefits have been well documented in down-regulating inflammatory responses in cells and animals, and these results are being translated into an effective treatment for some inflammatory conditions such as rheumatoid arthritis. Some inconsistencies between trial results may be due to the time between disease onset and treatment. Certainly, this disease has a lower incidence in fish-eating cultures, and a higher consumption of omega-3 PUFAs in the national diet may help prevent disease onset. There are a number of challenges for the future. The mechanism of action of many dietary fatty acids is still not fully clear, and their interaction with existing drug therapies needs to be defined. There is no doubt that many effects of fatty acids are mediated by regulation of gene expression. The real challenge for this decade is to quantify the effectiveness of primary prevention programs based on increased omega-3 intakes. After all, this is the area where the most public health benefit is to be gained, keeping people out of hospitals and ensuring the maximum number of healthy years to us all. RecommendationsThe following recommendations are provided to guide medical and allied health professionals working with people at all stages of the lifecycle. Pregnancy and the first year of lifeThe strongest evidence for good developmental outcomes for infants is breastfeeding for at least 6 months. Fish-oil supplementation during pregnancy has been tested in several trials, with small positive effects on length of gestation. There have been no beneficial or harmful effects on cognitive development or growth of infants as a result of fish-oil supplementation in pregnancy. Preterm infants are at the greatest risk of DHA deficiency, and there is evidence for the use of breast milk and DHA-supplemented formulas for positive effects of DHA on visual and cognitive outcomes. Debate continues about the importance of DHA supplementation for term infants. The current consensus is that the benefits of DHA supplementation for term infants are smaller than for preterm infants. Toddlers to preschoolToddlers need to be continually encouraged to try a wide range of foods supplying all types of fats, and with the emphasis on nutrient-dense foods. Reduced-fat products are not appropriate for toddlers when the particular food forms a substantial part of their intake. No sound evidence exists to support the manipulation of dietary fat for the treatment of attention deficit hyperactivity disorder or the prevention or treatment of asthma. Primary schoolFats are essential to the normal growth and development of children. Parents need to understand that the most significant influence on a child's eating patterns are their own eating patterns and preferences. The recommendation of 30% total energy from fat can be achieved by practical changes in eating patterns. This may include limiting high-fat and high-saturated-fat snack foods, like ice cream and potato chips, to occasional or treat items. Adolescence and young adulthoodAdvice supporting regular physical activity, healthy food choices and smoking avoidance is definitely warranted in adolescents. The amount of dietary fat is important in maintaining energy balance and the type of fat is important in reducing the development of heart disease. Low fat foods are suitable, but it is also important to avoid sources of "hidden" saturated fatty acids (biscuits and fast foods) and to include sources of polyunsaturated and monounsaturated fatty acids (oils, margarine, lean meat and poultry and nuts). Adulthood — preventionCardiovascular diseaseTo achieve a more desirable ratio of dietary omega-3 to omega-6 PUFAs, encourage the consumption of fish and omega-3-rich seed oils and spreads, such as canola, soy and flaxseed. A diet that is rich in PUFAs, such as omega-3, and low in saturates, should be encouraged. This type of diet is rich in fish, whole-grain cereals, fruits and vegetables and low-fat dairy foods. Refer to the Box for a sample menu plan. Rheumatoid arthritisThere is evidence for preventive and therapeutic effects of dietary omega-3 fats in rheumatoid arthritis. DiabetesTotal fat intake is not related to the risk of diabetes. However, polyunsaturated fat reduces the risk, monounsaturated fat is neutral, and saturated fat may increase the risk. However, body weight is a more critical predictor than macronutrients in the diet. Putting this into practice for adults A suggested "healthy fats" meal plan for adults is provided in the Box, which aims to: minimise saturated fat intake; incorporate monounsaturated and polyunsaturated fats in moderate quantities from oils, spreads, nuts, seeds and avocado; include sources of omega-3 fats (see Box); be high in fibre; and offer generous amounts of vegetables and fruits, whole grains, and low fat dairy foods. Adulthood — treatmentCholesterol-lowering with plant sterolsMargarines enriched with plant sterols should be considered for patients with increased cardiovascular risk factors, in whom low-density lipoprotein level reduction is desirable. Phytosterol-containing foods are valuable additions to other cholesterol-lowering treatments, including statins. Encourage the consumption of an additional serving of carotenoid-rich fruit or vegetable (eg, rockmelon, mangoes, carrots, pumpkin) to overcome the possible reduction in some carotenoids in plasma. 1: Suggested healthy fats menu plan for adults* Breakfast Wedge of rockmelon or paw-paw Wholegrain or bran cereal or muesli or oats with low-fat milk Soy and linseed toast with canola spread topped with ricotta and tomato slices Lunch Pasta with tomatoes, soy or cannellini beans, capsicum, mushrooms and basil (optional: top with a small can of salmon or tuna) Mixed green salad with flaxseed vinaigrette dressing Dinner Fillet of fish, pan-cooked with a little olive oil, herbs and lemon Baked potato wedges Steamed green beans or zucchini (large serve) with toasted walnuts Between meals Choose from: Vegetable or minestrone soup 2–3 sushi rolls with salmon or tuna or prawn Fresh fruit or fruit salad cup walnuts or pecans Raisin toast with canola spread 2–3 rice cakes with canola spread, sliced banana and honey Carton of low-fat fruit yoghurt avocado Low-fat muesli or breakfast bar *Foods in italics are sources of omega-3 fats.

Robert A Gibson PhD · Maria Makrides BND, PhD · Coral G B Colyer MSc(Nutr

In recent years, it has become clear that fat has a role beyond that of macromolecular energy storage. Indeed, fat participates in intracellular processes as diverse and complex as membrane fluidity, signal transduction and the regulation of gene expression. Furthermore, as specific fats are involved in mediating these effects, the profile of dietary intake assumes vital importance, especially as humans cannot make several of the key lipids themselves. Fatty acids and membrane functionAll cell membranes consist of a bilayer of phospholipids. The membrane is impermeable to charged molecules, so, for communication between cells and compartments to occur, specific protein transporters or receptors have to be embedded in the bilayer. The bilayer is fluid and flexible, allowing free lateral movement of the proteins and the formation of invaginations to permit the processes of endocytosis and exocytosis. Crucially, the length and degree of saturation of the fatty acids in the membrane phospholipids determines the fluidity of the membrane. Long (> 16 carbons) and saturated fatty acyl groups tend to make the membrane less fluid, whereas shorter, unsaturated fatty acids permit greater flexibility and permeability. The functionality of proteins in the membrane is critically dependent on membrane fluidity, especially when the proteins have to collide with other molecules to exert their effects (as in many receptor-mediated pathways) or when the proteins have to be endocytosed (such as the ingestion of low-density lipoproteins [LDLs] after binding to the LDL-receptor). It is vital that a variety of fatty acids be available for membrane phospholipid construction. Many of the fatty acids in membranes are unsaturated and cannot be made by humans de novo. These include alpha-linolenic acid and linoleic acid. Therefore, the mix of fatty acids in the diet can have profound effects on the membrane phospholipid fatty acid composition and on the efficiency of membrane-mediated processes. For example, the ability of insulin to communicate its signal is strongly impaired when animals are fed a diet high in saturated fat and this effect can be overcome with omega-3 poyunsaturated fatty acid intake. This, in turn, is probably related to diet-induced changes in membrane fatty acid profile, as recent studies have shown strong correlations between membrane phospholipid composition and insulin sensitivity in humans.1 Fatty acids and signal transductionSometimes the phospholipids themselves participate in signalling pathways. For example, some activated receptors stimulate phospolipases that cleave phospholipids into the head group and diacylglycerol. Both these moieties can subsequently activate other downstream signalling molecules — either within the membrane itself or in other compartments. For example, the cleavage of the phospholipid glycerolipid phosphatidylinositol (PI) gives rise to inositol tris-phosphate (which can cause the release of calcium into the cytoplasm), and diacylglycerol (which activates the enzyme protein kinase C to stimulate several mitogenic and metabolic signalling cascades).2 As before, the fatty acyl composition of the diacylglyerols involved in the above signalling pathways is strongly influenced by the diet. Other processes involving cleavage of membrane lipids include the production of prostaglandins, prostacyclins, thromboxanes and the precursors of platelet-activating factors. The key point, however, is that all these pathways are dependent on having a suitable pool of membrane fatty acids as substrates, and, although some remodelling of membrane fatty acyl composition can occur,3 the diet is the strongest modulator of intracellular lipid profiles. Indeed, dietary lipid composition can itself affect the activity of the enzymes that control the fatty acid composition of membranes.3 Fatty acids and gene expressionThe expression of genes is regulated by a class of DNA-binding proteins called transcription factors. The latter can be regulated by binding to other proteins, or, as has recently emerged, to fatty acids.4,5 Some of the most-studied lipid-regulated transcription factors are those which regulate adipocyte gene expression and differentiation. For example, the physiological ligands for one of these factors, peroxisomal proliferator-activated receptors (PPARs), are omega-6 and omega-3 fatty acids and related eicosanoid products,6 and this provides a direct link between dietary fatty acid consumption, tissue proliferation and gene expression. In addition, the expression of many lipogenic enzymes is controlled by other transcription factors (eg, sterol regulatory element binding protein [SREBP1]).7 SREBP1 is a membrane-bound protein that is activated after cleavage and release from the membrane — and this is influenced by the fatty acyl composition of the signalling and membrane components. Recently, it has become obvious that these transcription factors are just part of a large superfamily of nuclear receptors which respond to specific fatty acid messengers.8

Gareth S Denyer BA(Oxon), DPhil (Oxon)

The high birthweights and long duration of pregnancies observed in the fish-eating community of the Faroe Islands in the North Atlantic led to the suggestion that fatty acids from marine food could delay spontaneous delivery and increase birthweight.1 Likewise, the low incidence of pre-eclampsia observed in Greenland Inuit2 provided a basis for the first suggestion that fish oil could prevent this condition. The plausibility of these hypotheses was strengthened by the fact that fish oil (omega-3) fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may alter eicosanoid/cytokine balance to modulate vasoconstriction and endothelial damage associated with gestational hypertension, delay the initiation of labour and cervical ripening, and relax the myometrium. Based on this evidence, a number of randomised trials of fish oil supplementation during pregnancy have been undertaken to prevent pre-eclampsia, prevent preterm birth and to increase birthweight. The review of the 10 available trials indicates that fish oil supplementation during pregnancy has a small effect on prolonging gestation, with the effect being greatest in women at high risk of preterm birth, although not apparent in women with twin pregnancies.3,4 There appears to be no benefit of fish oil supplementation on preventing pre-eclampsia or increasing birth weight.3,4 Collectively, these data do not support routine fish-oil supplementation for the primary prevention of pre-eclampsia, preterm birth and low birthweight, but the role of fish-oil treatment in preventing recurrent preterm delivery is worthy of further investigation.3,4 Until 2001, there were no published trials that followed infants beyond the neonatal period to determine if fish-oil supplementation in pregnancy influences the growth or development of the child. The only available study used the Fagan test as an indicator of cognitive function and growth to one year of age. This study shows neither harmful nor beneficial effects of maternal fish oil supplementation on cognitive development or growth.5 All the pregnancy intervention studies supplemented women with high doses of fish oil that had much higher contents of EPA than DHA.3-5 However, it is DHA that has been postulated to be important for the neurobiological development of infants. High levels of DHA are found in the grey matter of the cerebral cortex and in the retina. The fetus and the newborn are dependent on a high supply of DHA from their mothers, either via the placenta or via breast milk. Preterm infantsDHA is most actively accreted into the brain during the last trimester of pregnancy. Preterm infants who are denied this flow of DHA from the placenta are born with reduced fat stores and have a low capacity to synthesise DHA from precursor fatty acids.6 Collectively, this makes them vulnerable to disturbed fatty acid accretion and at risk of deficiency. The focus of research attention has been the effect of dietary DHA on measures of development. Twelve trials designed to test the effect of dietary DHA on the growth or development of preterm infants have been reported. All randomly assigned infants to either a DHA-supplemented or DHA-unsupplemented formula.7 All trials that assessed visual acuity development reported a beneficial effect of DHA supplementation. However, only three trials included more global measures of neurodevelopment. While two of these trials were small and reported little or no effect of diet,7 the remaining, largest trial to date reported, in separate subgroups, eight-point advantages in both Bayley psychomotor development at 12 months corrected age, and language development at 14 months corrected age, to infants fed formulas with DHA compared with controls.8 Although trials involving preterm infants have almost universally shown some improvement in developmental indices of preterm infants supplemented with DHA, some early studies that supplemented infants with fish oil containing both DHA and EPA showed poorer weight and length gain in supplemented versus unsupplemented infants. It was suggested that the poorer growth rates were associated with the reduction in plasma levels of the omega-6 long-chain fatty acid arachidonic acid (AA) caused by these fish oils.7 Subsequent studies have avoided high EPA oils, have added AA and have shown no growth differences between supplemented and unsupplemented infants.7 Based on these findings supplementation of preterm infant formulas with both DHA and AA has been recommended,9,10 and, in Australia, all available preterm formulas are supplemented. Further work is needed to determine the effect of supplementation on long term neurodevelopmental outcomes in children. The breastfed and the formula-fed term infantDHA is never completely absent from breast milk, but its level is largely determined by the mother's diet. For example, vegan women who consume no animal products have the lowest levels of DHA in their breast milk compared with women on omnivorous diets, while women who regularly eat fish have the highest levels of DHA in their milk.3 Developmental outcomes in breastfed infants are consistently reported to be better than formula-fed infants, and it has been hypothesised that one contributing factor may be DHA in breast milk. For this reason, randomised trials of supplementing formula with DHA at levels equivalent to those found in breast milk have been undertaken. These trials have shown either a small statistically significant positive benefit or no effect of DHA supplementation on developmental indices.7 No trials have consistently shown a negative effect on either growth or development.7 That the effect of supplementation is positive or neutral implies that any benefit is likely to be small, and this is no surprise, as term infants have had the benefit of a full in-utero supply of DHA as well as other nutrients. To ensure the best developmental outcomes for their infants, women are encouraged to breastfeed to at least 6 months of age, and preferably longer. If this is not possible, some committees have recommended the use of long-chain polyunsaturated fatty acid (PUFA) supplemented formulas.9,10 These recommendations are, however, not unanimously supported or universally implemented. In Australia, there are a number of formulas supplemented with long-chain PUFAs for term infants. The weaning dietWeaning foods are generally low in fat content and low in DHA content. There have been few studies designed to assess the effect of solid-food interventions on DHA status, growth and development. Because of the low fat content of most weaning foods and the fact that the volume of food consumed is relatively small, it is difficult to increase DHA intake of the weaning infant without specific enrichment. Omega-3-enriched eggs have been shown to substantially increase the DHA intake and status of young children without changing their growth rates.11 Whether there is any influence on developmental outcomes is not known.

Maria Makrides BND, PhD · Robert A Gibson PhD

Dietary fat plays many vital roles for the young child, but, most importantly, its energy density is a bonus for toddlers (1–2-year-olds) and preschoolers (3–4-year-olds), whose needs are high in relation to weight, while their appetites are often small. It is appropriate that fat provides less energy than it does in infancy, but more than that for school-aged children and adolescents. While fat is an important macronutrient, emphasis needs to be placed on foods which contribute not only fat but are nutrient-dense as well, such as dairy products and eggs. Young children display the well-known human preference for high fat and high sugar content foods.1 However, fostering a taste for a variety of nutrient-dense foods is necessary during this time because of high nutrient needs in the face of an often poor appetite and a reluctance to try new foods. Role of fat for developmentIn general, growth during the toddler, and especially the preschool, years is steady and slow compared with infancy. However, the need for nutrients, including energy, is still high relative to weight in order to support the developing body components such as bones, teeth, or muscles. In addition to the energy they supply, dietary fats are also a vital source of essential fatty acids and other bioactive compounds that are crucial requirements for a variety of cells and tissues. The essential fatty acids, linoleic acid (omega-6 family) and alpha-linolenic acid (omega-3 family), continue to be required for skin health (linoleic acid), and as precursors for both the long-chain versions of the omega-3 and omega-6 fatty acids found in the brain (omega-3 and omega-6) and retina (particularly omega-3). What are the fat requirements?Total fat requirements for young children is a contentious subject in that the impact of a low-fat versus a moderate-fat diet in the future development of obesity and atherosclerosis has been vigorously debated since the 1970s.2 Some experts claim that a low-fat diet needs to be encouraged from the age of two years to maximise the likelihood of future healthy dietary habits to reduce the risks of obesity and coronary heart disease, while others are concerned that this approach in toddlers, in particular, may provide insufficient energy for normal growth and development. There are sound arguments on both sides of this public health issue, but each child's case needs to be judged in the context of family eating patterns, as well as his or her growth pattern and family history. In general terms, the toddler is in transition from the high fat diet of infancy to the lower intake required by preschool and older children. Health professionals are likely to see extremes in fat intake, and there will no doubt be specific cases of children who would benefit from moderating their fat intake, and others whose appetites are poor or whose fat intake has been restricted and for whom a higher fat intake is necessary. The 1995 version of the National Health and Medical Research Council's Australian dietary guidelines for children and adolescents3 recommended 35%–40% of energy from fat for 2–5-year-olds, but the more recent draft version of these Guidelines has revised this to 30%.4 It should be noted that the mean percentage energy intake obtained by the 1995 National Nutrition Survey5 was 33% of energy from fat for the 2–3-year-old and 4–7-year-old age groups. No specific guidelines are provided in Australia about the relative contributions from monounsaturated and polyunsaturated fats for this age group, but the draft guidelines recommend no more than 10% of energy from saturated fat for 2–5-year-olds. The limited data from the 1995 National Nutrition Survey for 2–3-year-olds5 suggest that about half the dietary fat is saturated (about 15% of total energy) and relatively little is polyunsaturated. Fat as a source of fat-soluble vitaminsWhile it is apparent that fat-soluble vitamins (A, D, E and K) are located in the fat component of foods, it is not so readily appreciated that their distribution in foods is not uniform. The top sources of vitamin A for the 2–11-years age group are vegetables, milk products, fat spreads and oils.5 Dietary sources of vitamin D are margarine, oily fish and eggs. Regardless of the food source of these compounds, fat needs to be present in the gut for absorption of these fat-soluble compounds. Thus, a diet comprising a moderate amount of fat will ensure that any fat-soluble vitamins consumed can be used. Reduced-fat productsThe 1995 and draft Australian dietary guidelines for children and adolescents recommend that reduced-fat and skim milks should not be used for children aged under two years, because milk is a key fat, and thus a key energy source for this age group.3,4 There are many other reduced-fat products available, and their use for toddlers will largely depend on the choices made for the rest of the family — after all, not many shoppers (or fridges) would cope with providing two versions of all options! As a guide, where products form a major part of the toddler's diet, it is better to use the whole-fat version where possible. Reduced-fat varieties can be encouraged for older children,3,4 and this practice would contribute to the recommended reduction in saturated and total fat intake for 2–5-year-olds. Is there a role for dietary fat modification in managing attention deficit hyperactivity disorder?In most children diagnosed with attention deficit hyperactivity disorder (ADHD) the cause is unknown, but thought to be multifactorial. Some researchers have proposed that one cause involves essential fatty acid metabolism. The limited data available relate to school-aged children rather than pre-schoolers, and indicate some anomalies in blood fatty acid levels of 6–12-year-old boys with ADHD.6 However, the link between this and the expression of behavioural abnormalities has not been established and dietary intervention is not currently warranted. Level of evidence of fats associated with asthmaAsthma is also a heterogeneous, multifactorial condition and is increasing in prevalence among Western children. The idea that dietary fat manipulation may reduce the risk of developing asthma, or the number of episodes of asthma, has been around since the 1980s. Some authors have suggested an increasing linoleic acid intake as a contributing factor to the increasing prevalence,7,8 specifically in relation to the impact of this increase in the ratio of omega-6 to omega-3 fatty acids in our diets. Haby et al studied 3–5-year-olds in regional NSW, but their cross-sectional study used a non-validated short tool to monitor the participants' home use of polyunsaturated fatty acid (PUFA) fat on bread or toast or in roasting and frying for their children's food,8 and did not assess the ratio of omega-6 to omega-3 PUFAs in the children's diets. Similarly, the studies which suggest that fish (a valuable source of long-chain omega-3 fatty acids) is protective9 have not adequately assessed the omega-3 PUFA intake of their participants. Exposure to omega-3 fatty acids in utero or postnatally, or both, may influence immunological development and hence asthma (and allergy) risk; studies involving omega-3 fatty acid supplementation are currently under way around Australia to investigate this possible relationship. In relation to asthma management, the conclusions of a Cochrane review were that there is little evidence to recommend that people with asthma should supplement or modify their dietary intake of marine omega-3 fatty acids to improve their asthma control.10

Jill L Sherriff PhD, APD

"Nutrition is a family affair. . . families need to develop nutrition patterns as a group, as a whole family" (Christina Plaisted, Professor of Human Nutrition, University of North Carolina).1 Increasingly, studies demonstrate the strong influence of family eating on children's food and nutrient intake.2 Fat intake,3 milk intake and children's food choices have been shown to track from preschool or through primary school (ages 5–11 years) and into later years, emphasising the importance of developing healthy eating patterns in early years and through primary school.4 Messages from parents have considerable influence on later eating patterns. Parental restriction may damage the development of a child's self-control in eating, and girls whose mothers are perceived to diet frequently are more likely to diet, while sons of these mothers are more likely to be concerned about weight.5 While younger children's intake is uninfluenced by the amount of food served, children aged over five years are influenced by the serving size offered, and eat more if more is served.6 Current intakes and recommendationsThe National Nutrition Survey of 1995 reports that fat intake among Australian children in the 8–11-years age group provided 33.4% of total energy, with 14.3% from saturated fat, 11.8% from monounsaturated fat and 4.7% from polyunsaturated fat.7 The National Health and Medical Research Council's Dietary guidelines for children and adolescents recommend that dietary fat for children aged 5–15 years should provide 35% of energy, with not more than 10% of total fat as saturated fat.8 This recommendation reduces to 30% of total energy from fat for children 15 years and over. Draft guidelines now under review recommend that children aged 5–14 years include about 30% of total energy as fat, with no more than 10% as saturated fat.9 While total fat intake in 1995 was within that recommended in current guidelines (but several percentage points above that in the proposed revision), saturated fat intake was higher than the recommendation. The largest contributors to saturated fat intake in 1995 were milk products, frozen milk products, cheese and potato products.7 The consumption of fruit and vegetables was well below recommended intake.7 Promoting higher fruit and vegetable intakes may have multiple nutritional benefits, including an impact on fat intake,10 as well as increased fibre, vitamin and antioxidant intakes. Some controversy still surrounds the issue of recommendations for fat intake in children,11 but studies have supported the efficacy and safety for growth and development of limiting fat intake to 30% of energy consumption in this age group.12 Modelling based on Australian eating patterns13 indicates that fat intake providing 30% of total energy can be achieved with practical and acceptable changes. Adequate intakes of other nutrients can be provided. Achieving the suggested level of 10% energy from saturated fat appears to be more difficult to achieve, and requires specific use of appropriate alternative fat sources of monounsaturated fatty acids and polyunsaturated fatty acids. Relationship between fat intake and obesityThe early years of primary school are a period of risk for the onset of obesity, and overweight and obesity is the most significant nutritional problem for children in our community.14 Fat intake is one of a number of nutritional factors that is included in considerations of obesity. Cross-sectional surveys and longitudinal studies have related prevalence of obesity in children to levels of fat consumption. In United States 9–10-year-olds there was a relation between energy intake and adiposity, and also between fat intake and adiposity, with a negative relationship between carbohydrate intake and adiposity after controlling for sex, physical fitness and parental adiposity.15 Children's preferences for high-fat-content foods and their total fat intake have been linked to parental adiposity and eating style.16 Putting recommendations into practiceA family eating pattern based on the "Healthy Diet Pyramid" or the Australian guide to healthy eating,17 with a wide variety of foods, will provide adequate nutrients. Dairy products can include reduced-fat varieties, but skim milk is not necessary. Foods with a high fat content should be replaced with lower-fat choices (eg, sandwiches or rolls instead of pastry, fruit-based frozen desserts instead of ice cream), and quantities of added fats (eg, butter, spreads and fried foods) should be minimised. Spreads and oils used should be from monounsaturated or polyunsaturated sources. Fish is often not a popular item with children, but should be encouraged to assure it a place in a consequent adult eating pattern. Where fat intake is reduced, total energy needs must be met with increased amounts of cereal, fruit and vegetables.13 Some children of lower primary school age with lower appetite (along with any younger children in the family) find achieving adequate energy intake difficult with this bulkier diet, and some discretion must be used within the family about the age at which the lower-fat diet is introduced. For such children, more liberal inclusion of monounsaturated and polyunsaturated fats can be used to restore energy density. For Australian children, food prepared outside the home is somewhat higher in total fat than food prepared at home, whether eaten at home or away from home.7 Where food prepared outside the home is a regular item in the family diet, consideration should be given to the choice of eating places and foods chosen. Snack foods contribute significantly to energy intake over the day,7 and should contribute similarly to nutrient intake. Information from teachers and parents emphasises the prevalence of potato crisps and high fat snack items in the school lunch box.18 Many children have access to a school-based lunch service and the favourite items are often high in fat, such as doughnuts and sausage rolls. Younger children need assistance with ordering better alternatives or limiting access to such high-fat-content foods. After-school snacks should include basic food items (eg, vegetable soup, bread or toast, fruit and milk or yoghurt).

Kay L Gibbons BAppSci (Dietetics), APD

During adolescence and young adulthood dietary fat continues to play important roles as an energy source, a significant cell structural component, a precursor to agents of metabolic function and a potent gene regulator.1 Energy requirements for the final stage of growth can be highly variable, but the increasing prevalence of obesity suggests a problem with energy imbalance. Rather than being the result of excess food intake,2 this has been attributed to reduced physical activity.3 Physical activity levels decline substantially during adolescence and young adulthood.4 Once obese, adolescents are generally even less active than their non-obese counterparts,3 and this is not necessarily accompanied by greater energy or fat intakes.5 Adolescents who are obese are more likely to become obese adults than younger children who are obese.6 As overweight in adolescence is a more powerful predictor of risk of heart disease and atherosclerosis than overweight in adulthood,7 the effect of reduced physical activity at this stage is compelling. Is dietary fat implicated in the development of obesity and heart disease risk at this stage?The impact of dietary fat on obesity needs to be considered in the context of current body composition, physical activity and genetic potential. This is implied in a recent Australian finding that a child's body fatness and parental adiposity were stronger predictors of future and maintained overweight than dietary factors.8 If an adolescent is already overweight, dietary fat may be less well tolerated. Obese and non-obese adolescents appear to consume equivalent amounts of high-fat, low-nutrient-dense foods when adjusted for total energy expenditure,9 and the ability to burn fat after a meal is associated with adiposity in adolescents.10 Type of dietary fat is also significant — in contrast to polyunsaturated fatty acids, saturated fatty acids are less readily mobilised and oxidised, and they are potent gene regulators for fat-cell proliferation.1 The type of dietary fat also has an impact on heart disease risk factors. Longitudinal studies in adolescents and young adults have shown an inverse relationship between total cholesterol and dietary polyunsaturate to saturate (P:S) ratio over time.11 A positive association between dietary saturated fats and total cholesterol level has also been shown in an Australian adolescent population, although dietary factors may be more important in girls, with body composition (possibly exercise related) more important in boys.12 Are low fat foods suitable for adolescents?The draft Australian dietary guidelines for children and adolescents recommend 25% of total energy as fat, with less than 10% of energy from saturated fat for children aged over 15 years.13 The recommendation for 30% of energy as fat should provide the requirements for growth as long as total energy intake is adequate.14 Concern has been expressed that reducing dietary fat in the prepurbertal years may result in inadequate nutrition,15 but a seven-year study has shown the safety and efficacy of low-fat approaches.16 In 1995, the major sources of dietary saturated fat for Australians aged 12–18 years were milk and cereal products (including biscuits, pastries and battered foods). Oils and margarines, and meat and poultry, were major sources of polyunsaturated and monounsaturated fats, respectively.17 Effective strategies for reducing fat intake in children include the use of skim milk and choosing only lean meat, although in one study choosing only lean meat was associated with reduced micronutrient intakes, possibly because of associated lower energy intakes.18 Surveys of Western populations produce fairly consistent views on adolescent eating patterns. Unhealthy behaviours developed in childhood (being sedentary, a high intake of saturated fats, and, later, smoking) persist through adolescence,19 so it is an important time for intervention.

Linda C Tapsell PhD, APD · Marijka J Batterham MSc(Nutr

How much and which kind of fat? This has remained a surprisingly divisive issue. Surprising because the Australian population has gradually reduced fat consumption from over 40% of energy in the middle of the last century to a little over 30% by the end. This has coincided with a substantial reduction in heart attack prevalence. However, the evidence that the quantity of fat is linked to coronary heart disease (CHD) is weak — it is the quality of the dietary fatty acids that matters.1 After all, CHD prevalence remains low in southern Europe, despite high intakes of lipid, mostly as vegetable oils. Prospective cohort studies and intervention trials, both primary and secondary, point that way. The positive link between dietary saturated fat and CHD is strong, as is the evidence that substituting polyunsaturated fatty acids (PUFAs, linoleic acid) for saturates lowers CHD risk. Whereas PUFAs are part of the eating pattern associated with least CHD in prospective trials, the opposite holds for saturates.2,3 The push for even less consumption of fat has abated with recognition that a clear benefit for this is lacking. Atherogenic lipoproteins are reduced and coronary atherosclerosis itself is lessened when mononunsaturates and PUFAs displace saturates.1 On the other hand, diets very low in fat and therefore high in carbohydrates may raise the atherogenic profile of lipoproteins. (The amounts of essential PUFA required for health are relatively small: 1%–2% of energy as linoleate and only 0.5% of energy as linolenate, but the present discussion relates to reducing CHD.) Saturated fatty acids may also have other undesirable, proatherogenic properties, but the evidence for this is equivocal.4 The concerns that PUFAs may predispose to cancer and cause other harm to health have not been substantiated.5 Apart from saturates, and especially dairy fats, for which the association with CHD is possibly the strongest, trans fatty acid consumption has also been linked with excess CHD.1,4 These fatty acids appear to behave like saturates, although they are mostly isomers of oleic acid that are formed from hydrogenation during hardening of oils or by microorganisms in the rumen of cattle. Since trans fatty acids have been largely removed from Australian manufactured spreads, the remaining amounts in dairy and meat fats are of minimal health concern. One interesting isomer of linoleic acid, conjugated linoleic acid, that is also formed in the rumen of cattle may hold possible health benefits for both cardiovascular and non-CHD disorders.6 Omega-6 and omega-3 fatty acidsThere are two major classes of PUFA — linoleic acid, with two double-bonds (so-called omega-6) and the omega-3 (also known as n-3) fatty acids, with up to six double-bonds. The omega-3 fatty acid α-linolenic acid (three double-bonds) is widely present in plants, and the longer omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) are found in fish. Much has been made of the need to balance the omega-6 and omega-3 fatty acids, as each gives rise to different classes of eicosanoids, such as thromboxane, prostaglandins and leukotrienes, that may have opposing effects on inflammation and vascular functions. A balanced dietary mix of omega-6 and omega-3 fatty acids is probably achieved with current intake of linoleic acid (about 6% of energy) and increased consumption of omega-3. This is achievable through eating more fish and α-linolenic-rich oils such as canola. Fish eaters experience fewer CHD events than those who seldom eat fish.7 The strongest epidemiological association between any fatty acid and CHD protection is for the long-chain omega-3 fatty acids of fish. Supplemental fish oil fatty acids tested in a large randomised, placebo-controlled trial (the GISSI trial) achieved significantly reduced cardiovascular mortality, re-infarction and sudden cardiac death.8 The findings refocused attention on the anti-arrhythmic properties of omega-3 fatty acids, clearly established in animal experimentation and also observed in case–control comparisons of sudden deaths.9 The fish oil fatty acids possess other protective characteristics: arterial function (vasodilatation) is improved, thrombogenic and inflammatory processes in the arterial wall are reduced, plasma triglycerides are lowered and HDL raised, and blood pressure may be lowered.10 Similarly strong evidence for the plant omega-3 fatty acid is lacking, although one secondary prevention trial, the Lyon Heart Study,11 provides encouragement for increased consumption of α-linolenic acid from oils such as canola, flax and soy. Several prospective cohort trials also indicate that the consumption of α-linolenic acid is linked to less CHD.1 In humans, the conversion of α-linolenic acid into the long-chain EPA and DHA is not efficient, and the fish oil fatty acids need to be also eaten in larger quantities, probably as two fish meals weekly. Effects on plasma lipidsOils and fats contain mainly triglycerides (three fatty acids on a glycerol backbone), but also fat-soluble vitamins and other fat-soluble substances, so that much of the daily intake of vitamin E derives from eating oils and spreads. Vegetable oils contain no cholesterol, but their fatty acid profile greatly varies. Some, such as palm oil and coconut oil, are rich in saturated fatty acids. Olive oil is rich in the monounsaturated fatty acid oleic; safflower, sunflower and corn oils are rich in linoleic acid, while canola provides the most diversity (very low in saturates, high in oleic acid and containing valuable amounts of linoleic and α-linolenic acids). There is little doubt that most saturated fatty acids raise plasma cholesterol levels, especially low-density lipoprotein (LDL) cholesterol.1,4 The fat profile of dairy fat (butter fat) is the most potent in raising LDL levels. Palm oil (rich in the saturated fatty acid palmitic acid) raises LDL levels, but less so than butterfat. Oleic acid lowers the level of LDL modestly, whereas linoleic acid (omega-6 PUFA) reduces the LDL cholesterol level most. Occasionally, in genetically predisposed people, linoleic acid may lower the high-density lipoprotein (HDL) cholesterol level slightly. In general, saturated fats raise LDL levels most in people who are already hypercholesterolaemic, more in men than in women, and mostly after middle age as capacity for fat clearance diminishes. Although some of the response is genetically linked, this is unlikely to become clinically useful. By contrast, the omega-3 fatty acids, although more unsaturated than linoleic acid, have little cholesterol-lowering effect. α-Linolenic acid has almost no influence on plasma lipids, whereas fish oils lower triglyceride levels potently at intakes of less than 1 g daily, and tend to raise HDL levels.

Paul J Nestel AO, MD, FTSE, FRACP

The bioactive lipids responsible for the signs and symptoms of inflammation belong mainly to the omega-6 family and are represented by prostaglandins and leukotrienes. Antagonism of inflammation by omega-3 fatty acids has been demonstrated in animal models. Studies have shown that omega-3 fatty acids, particularly those in fish oil, can decrease leukocyte production of omega-6 prostaglandins and leukotrienes, as well as cytokines.1 In humans, there is evidence for preventive and therapeutic effects of fish-derived fats. For example, in Japan, a country where levels of fish consumption are considerably higher than in Australia and the United States, the prevalence of rheumatoid arthritis is about 0.4%, compared with about 1% in Australia and the US. This lower disease prevalence in Japan occurs in the context of higher prevalence of a genotype associated with increased susceptibility to rheumatoid arthritis.2 The association of decreased emergence of rheumatoid arthritis with increased fish intake is supported by results of a case–control study of women with the disease. Results indicated that fish consumption was higher in healthy controls than in the women with rheumatoid arthritis. Dietary estimations indicated that being in the top 10% of omega-3 fat intake (> 1.6 g daily) was associated with an approximate 70% decreased probability of having (seropositive) rheumatoid arthritis.3 Ecological and case–control studies provide evidence of associations between dietary fish intake and decreased disease occurrence. Only dietary intervention studies can provide direct evidence of a protective or therapeutic effect of omega-3 fatty acids. Therefore, it is significant that 13 double-blind, placebo-controlled studies with rheumatoid arthritis patients have found benefits from ingestion of fish oil. Not all outcome measures improved in all studies. Tender joint count was the measure which improved in most studies (9 of 11 studies), but other measures to improve were the duration of morning stiffness, grip strength, and time to fatigue.4 Also, there was an indication of an anti-inflammatory drug-sparing effect. It was apparent that 12 weeks was the minimum time at which effects were seen. The finding of a beneficial effect on tender joint count is supported by a meta-analysis.4 An assessment of the value of these results can be made from several viewpoints. When one considers that the median intake of the omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) in these studies was 3.3 g daily, the therapeutic effect may seem modest. On the other hand, the subjects had long-standing disease (mean duration, more than 10 years) and the fish oils were taken in addition to a full range of anti-inflammatory and antirheumatic medication. Overall, it is clear that the effect is genuine and it is possible that the effect size may be larger in more favourable conditions such as early-onset disease, where there is little or no joint damage. When considering whether subjects with rheumatoid arthritis may benefit from fish oil ingestion, an important consideration additional to arthritis therapy is the potential for collateral health benefits. Rheumatoid arthritis has a standardised mortality ratio ≥ 2, which is attributable mainly to increased cardiovascular mortality, and this has led to the conclusion that prevention of cardiovascular disease must be added to one of the aims of rheumatoid arthritis treatment.5 Thus, recommending use of dietary omega-3 fats in rheumatoid arthritis treatment is well justified for preventive effects in cardiovascular disease.

Les G Cleland MD, FRACP · Michael J James PhD

Whether fat has a role in preventing type 2 diabetes has been a vexed question for the past 50 years. There have been two very large prospective studies in women1,2 and one in men.3 The Nurses Health Study showed no relationship between the incidence of type 2 diabetes and intakes of total dietary fat, saturated fat or monounsaturated fat.1 However, polyunsaturated fat was protective and trans fatty acids were harmful, so that replacing 2% of energy from trans fatty acids with polyunsaturated fat lowered the incidence of type 2 diabetes by 40%. In Australia, where trans fatty acids are much less relevant (as they are not present in margarines and hardened fats as they are in the United States), this would translate to replacing 5% of energy from carbohydrates with polyunsaturated fat, resulting in a decrease of 37% in the incidence of diabetes. Similar but weaker findings in relation to vegetable oils came out of the Iowa Women's Study (although trans fatty acids were found to be protective).2 Some smaller studies have found a relationship between total fat intake and incidence of diabetes,4 while other studies have found a relationship between saturated fat intake and fasting glucose levels,5 fasting and postload insulin levels6 or levels of HbA1c.7 Insulin sensitivity may not be altered by fat intake, as the Insulin Resistance and Atherosclerosis Study found no such association,8 confirming the findings of most intervention studies. Only one recent study has shown that substituting saturated fat for monounsaturated fat improved insulin sensitivity in healthy men and women.9

Peter M Clifton MB BS, PhD

Phytosterols, or plant sterols, are present in high concentration in vegetable oils before they are refined. In recent years the low-density lipoprotein (LDL) cholesterol lowering effect of sterols has been rediscovered, having been established and discarded some 30 years ago. The two main sterols that are widely present in plant foods other than oils are sitosterol and campesterol, and most of us eat between 150 mg and 400 mg of phytosterols daily. Consumption by vegetarians is even higher and may account partly for their lower LDL levels. Sterols can be converted to stanols by saturating double-bonds. Plant stanols are found in lower concentration naturally, but, like sterols, stanols have been incorporated into margarines to lower LDL levels. In Australia, only sterols, or more accurately sterol esters, have been introduced into margarines. The evidence for their LDL-level-reducing potential is strong, even better than that for eating less saturated fat! With the appropriate intake of about 1.6–2.4 g of sterols daily, the average LDL cholesterol reduction is more than 10% and, importantly, this occurs in about 90% of individuals. A recent analysis of published controlled, double-blind, randomised trials of sterol or stanol esters reported an 11% mean reduction in LDL level.1 Two studies from Australia with sterol-ester-containing foods, margarine in one2 and a mix of margarine, bread and breakfast cereal in the other,3 resulted in mean falls of 7.7% and 13.6%, respectively. In both trials, this benefit was additional to that achieved with a standard low saturated, low cholesterol, high unsaturated fatty acid diet. Other trials, carried out overseas, have shown that older people benefit most,1 that patients with various types of dyslipidaemia benefit, and that the LDL-level-lowering effect is additive to that of statins.4 The mechanism of action is believed to be through competitive inhibition of cholesterol absorption by phytosterols. Cholesterol requires "solubilisation" within micelles formed in the gut by bile acids and phospholipids; phytosterols may displace cholesterol from the micelle and partly prevent its absorption.4 Cholesterol absorption is roughly halved. This explains the synergistic effect with statins; the combination of the two leads to reductions in both absorption and synthesis of cholesterol. A valid argument can be made for including sterol-ester-containing foods in any cholesterol-lowering therapy. It is essential that patients eat the full dose of sterols daily — the practice of lightly covering a slice of toast with sterol-containing margarine is useless. In addition to inhibiting cholesterol absorption, the absorption of some carotenoids, especially beta-carotene, is also affected. This may result in small but consistent reductions in the concentration of this carotenoid in plasma.5 However, this must be viewed in perspective. The carotenoid concentrations remain within the range of normality and within the degree of variability encountered among individuals. Similar reductions have been noted with high-fibre diets. Importantly, the small fall in beta-carotene can be overcome by eating an extra serve of carotenoid-rich fruit or vegetables daily.2 One unresolved question is whether the absorption of plant sterols into the body, albeit very small, could result in adverse effects over time. The various food regulatory bodies around the world have not considered this a significant issue and the products are generally regarded as safe. In practice, sterol ester margarines (and other products that may emerge in the marketplace) are a useful ancillary dietary measure for moderately lowering the concentration of LDL cholesterol in people with lesser elevations of blood cholesterol and in patients with increased cardiovascular risk. This accounts for a high proportion of middle-aged and elderly Australians who have such disorders as hypertension, diabetes and insulin-resistance syndrome, and for whom cholesterol-lowering measures are appropriate.

Paul J Nestel AO, MD, FTSE, FRACP

Based on the information in this Supplement, the following dietary suggestions for fat consumption are a handy guide for doctors advising their patients on diet and nutrition. These pointers should be communicated within the context of a healthy diet including vegetables, fruit, whole grains, lean meat, fish, chicken and dairy foods. Key points on fat for all patientsFat is an essential nutrient — our bodies need some fat. Reduce the saturated fats which Australians overconsume. Choose fats in the form of monounsaturated and polyunsaturated fats from oils, spreads, avocado, nuts and seeds. Consume some omega-3 fats (see Box 1 and Box 2). Low-fat diets appear adequate and can be introduced after the age of two years for children at high risk of obesity and heart disease. Key points on fat for infants and very young childrenFat is an essential nutrient — babies need fat to fulfil their energy requirements for growth. Women should be encouraged to breastfeed their infants for at least six months and preferably 12 months. A low fat intake is not recommended for children under two years. From the age of six months, fat can come from basic foods like vegetable oils, spreads, eggs, full-fat milk and meat, which provide other key nutrients (see Box 1). Big fat myths — common myths relating to fatThere are many food myths relating to fat and its role in the diet. This is understandable when, for so long, the dietary message has been to reduce fat intake and fat has been cast as the "villain" of the modern, affluent Western diet. Myth: "I don't need to eat any fat"Incorrect: Fat is an essential nutrient required for health and growth, like protein, carbohydrate, vitamins and minerals. Fats supply essential fatty acids such as linoleic acid and alpha-linolenic acid, which our bodies cannot manufacture. Nutritionists suggest that, for adults, about 30% of the kilojoules consumed should be derived from fat. This translates to 50–60 grams of fat daily for a sedentary adult woman consuming 7500 kilojoules (1800 calories) a day. The type of fat is important — no more than 15 grams a day should be saturated fat. This figure will be easier for patients to comprehend when labelling of saturated fat on food products becomes mandatory by the end of 2002. Myth: "Fats don't give us anything except kilojoules (calories)"Incorrect: Fat serves many functions in nutrition. Fat: provides insulation and "cushioning" for internal organs; "spares" protein for its primary role of building; and serves as a "carrier" of fat-soluble vitamins (vitamins A, D, E and K) and fat-soluble antioxidants like beta-carotene and other carotenoids. Myth: "I must eliminate all fat from my diet to lose excess weight"Incorrect: It is not necessary to follow a fat-free diet for weight loss. Energy density of the diet and total kilojoules consumed now appear to be a more critical determinant of weight loss than simply the amount of fat consumed.4,5 However, fat is the most concentrated of all nutrients (see Box 3), so cutting back on fat may be the quickest way to lower energy density for some people. Nevertheless, a balanced weight-loss plan would allow for 30–40 g of fat a day for women, and 40–50 g a day for men. Myth: "Canola is the same as rapeseed"Incorrect: Canola oil is extracted from the seed of the canola plant (Brassica napus or Brassica campestris), a variety of rapeseed that belongs to the Brassica family. While it is derived from the same species of plant, canola oil is distinguished from rapeseed oil by lower levels of erucic acid. By definition, the name "canola" oil can only be used if the level of erucic acid is less than 2%. "Canola" oil was initially a name trademarked by Canadian developers in the 1960s. The original rapeseed is still grown for its oil in some countries, but is only used for non-edible purposes, such as in the production of nylon. Myth: "Canola oil is toxic/contains a poison"Incorrect: This myth has been circulating on the internet with no substantiation. It probably arose from canola's association with its parent, rapeseed, which contains naturally high levels of erucic acid, but this characteristic has been bred out of canola (see above). Myth: "Olive oil is the best oil to use"Incorrect: Olive oil is only one of a number of healthy oils. It is rich in monounsaturates, as are canola oil, peanut oil and macadamia oil. It rose to fame as a key ingredient of the heart-protective Mediterranean diet, but there are many other dietary factors in that diet, such as fish, seafood, garlic, wine and vegetables, that could also contribute. Olive oil has virtually no omega-3 fatty acids. Myth: "Light oils keep your fat intake low"Incorrect: Light or "lite" oils have exactly the same fat and kilojoule content as regular oils. They are simply light in flavour or lighter in colour. 1: How-to tips Reducing saturated fat Limit intake of obvious sources of saturated fat such as butter, butter/oil blends, cream, sour cream, mascarpone, coconut cream/milk, fat selvage on meat, skin on chicken. Limit intake of foods with hidden saturated fats, such as sausages, bacon, devon, salami and other deli meats, meat pies, sausage rolls, potato crisps, corn chips, salty packet snacks, hamburgers, pizza, fried fast foods (hot potato chips, fries, nuggets, potato scallops), gravy, rich sauces, full fat dairy products (milk, cheese, cream cheese and yoghurt), cakes, muffins, pastries, doughnuts, biscuits, chocolate, ice cream. Check labels for saturated fat (note that new regulations to Australian food standards being phased in by the end of 2002 require all food products to list the content of saturated fat per serve and per 100 g). Increase the "healthy" monounsaturated and polyunsaturated fats Use a variety of oils for cooking and salad dressings Swap butter for a soft margarine or spread for bread and toast Consider alternative spreads such as avocado, hummus and peanut butter Snack on unsalted nuts in place of potato crisps, corn chips and similar salty snacks Sprinkle lecithin or wheatgerm over cereals Increase omega-3 polyunsaturated fats Eat fish (canned, frozen or fresh) and seafood (see Box 2) at least twice a week Choose vegetable oils that are good sources of omega-3 fats, such as flaxseed and canola Choose plant sources of omega-3 fats (see Box 2) 2: Sources of omega-3 fats (animal and plant sources listed in decreasing order of magnitude)1,2 Source Examples Animal sources* Oily fresh fish Mullet, Atlantic salmon, smoked salmon, trevally, yellowtail, scad, tailor, tarwhine, mackerel, tuna Canned fish Salmon (especially red salmon), sardines, tuna Eggs Omega-enriched eggs White fresh fish Snapper, perch, gemfish, garfish, flounder, whiting, bream, flathead, John Dory, ling, leatherjacket Seafood Oysters, prawns, mussels, scallops, squid, crab, octopus Plant sources†,‡ Oils Flaxseed, canola, wheatgerm, soybean Spreads Canola-based Seeds Linseeds (flaxseeds), soy and linseed bread Nuts Walnuts, pecans Legumes Soybeans, tofu, soy "milk", other beans and lentils Whole grains Wheatgerm, rye, barley, brans (wheat, oat, barley, rice) Vegetables Most green leafy vegetables * Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). † Alpha-linolenic acid. ‡ Only a small proportion of these short-chain plant sources are converted into the long-chain desirable types by the body. The conversion is enhanced by a diet low in saturated fats and low in omega-6 polyunsaturates. 3: Energy density of selected foods Kilojoules supplied per gram of: Fat 37 Alcohol 29 Protein 17 Carbohydrate 16

Catherine M Saxelby BSc, APD