Metabolic diseases

The overarching cause is energy imbalance The health and wellbeing of Australia's children and adolescents, now and in the future, is under threat. In 2002–2003, the most prevalent child health issues affecting children are preventable: obesity, dental disease, emotional and behavioural problems, bullying and learning delays. These problems often present as comorbidities. Overweight and obesity affect about 23% of Australian children and adolescents, with 6% being obese.1 These are conservative estimates, as there has been no systematic monitoring of the prevalence of overweight and obesity in Australian children and adolescents since 1995. However, over the previous decade, the prevalence of overweight children almost doubled, and the prevalence of obese children more than tripled.1,2 There is no reason to believe that the rapid rise in prevalence rates has not continued. Studies of historical datasets have also revealed that the prevalence of overweight and obesity in children and adolescents doubled over the period 1985–1997, a far greater rate of increase than in the preceding 16 years.3 Health inequalities related to overweight and obesity are evident. There is a higher incidence of overweight and obesity in children of parents of particular backgrounds,3 and maternal education is the strongest social determinant of overweight and obesity in childhood.4 Although there are limited national data, and combined New South Wales, Victorian and National Nutrition datasets1 failed to find a rural/urban difference, Victorian epidemiological data show a statistically significant, higher proportion of overweight and obese boys in metropolitan areas, but this difference was not found for girls (Ms K Hesketh, NHMRC PhD Scholar, Centre for Community Child Health, Melbourne, VIC, personal communication). The health consequences of overweight and obesity are substantial, although Australian data remain unclear in certain areas.5 At least in the United States, obesity carries more stigma in children than any physical disability, and this is evident across all socioeconomic and ethnic groups.6 Issues of social acceptance, athletic competence and physical appearance are well known to obese children and affect their sense of social and psychological wellbeing. Obese children with decreasing self-esteem are more likely to smoke and drink alcohol compared with those whose self-esteem increases or remains the same.7 Obese children and adolescents may also have a range of medical conditions including hypertension, dyslipidaemia, and even type 2 diabetes. Other problems, such as musculoskeletal discomfort, obstructive sleep apnoea, heat intolerance, asthma and shortness of breath, greatly affect their lifestyle.8 Implications for the future can be gathered from longitudinal studies. Combined cohort studies indicate that relative body weight is sustained from childhood to adulthood, and, once children or adolescents are overweight or obese, their weight is unlikely to track backwards.5 If this is not sufficient reason for concern, reflect that these studies (of the long-term consequences of child and adolescent obesity) were all performed before the worldwide obesity epidemic developed. What, then, will be the outcome, in 10 or 20 years' time, of large numbers of children and adolescents entering adulthood, already with abdominal obesity and well established risk factors for cardiovascular disease and type 2 diabetes? Focusing on children highlights their contribution to contemporary society and future populations. Addressing the determinants of health and wellbeing for children and adolescents will improve population health and wellbeing overall. The overarching cause of the obesity epidemic is energy imbalance — a relative increase in energy intake (food intake) together with a decrease in energy expenditure (decreased physical activity and increased sedentary behaviour). Identifying the most important predictive determin-ants of each of these behaviours, as well as the most effective and sustainable remedial strategies, is complex and involves parental education and employment; housing environments; play, recreation and physical activity; food and nutrition; accessible active transport; and child-friendly physical and social environments.9 Some simple trends suggest relatively amenable remedies. Children's fruit and vegetable consumption has decreased over the past 20 years. Their physically active time has also decreased, while time spent in sedentary activities such as television watching and computer games has increased. Finally, consumption of energy-dense foods (including sweet soft-drinks and snack bars with a high sugar content) has increased. Possible remedies include: parental education strategies regarding healthy food choices, activity options, obesity trends, as well as supportive behavioural change strategies; supportive policies and environments in the places children and families spend their time (child care, school, workplaces, home, local neighbourhoods); and prioritisation of free time for physical activities. Evidence from controlled trials (although these trials are heterogeneous as regards the age groups and settings studied) highlights the potential for school-based programs that promote physical activity, modify dietary intake and reduce sedentary behaviours. However, recent qualitative research indicates that differences in outcomes will only be achieved if sustainable changes involve all generations, tackle the widely held beliefs regarding eating and activity,10 involve population-wide health promotion messages, and dispel myths such as children's overweight being just "puppy fat". Further, there are environmental aspects that are well beyond an individual family's ability to modify, including: regulation of marketing of unhealthy food choices for children; provision of safe, cheap and accessible public transport; and urban planning initiatives that give priority to child-friendly and pedestrian-friendly environments. The latter options are more controversial, and vested interests may seek to cloud the community's perceptions of factors driving the overweight epidemic. We need to actively involve industry in partnerships for environmental change. Health practitioners working in the community, child and family nurses and general practitioners are crucial in any comprehensive strategies, as they provide a widely available service to families and can tailor specific strategies for individual families.11,12

Elizabeth B Waters MPH, DPhil · Louise A Baur PhD, FRACP

Objective: To measure the prevalence of obesity in Australian adults and to examine the associations of obesity with socioeconomic and lifestyle factors.Design: AusDiab, a cross-sectional study conducted between May 1999 and December 2000, involved participants from 42 randomly selected districts throughout Australia.Participants: Of 20 347 eligible people aged > 25 years who completed a household interview, 11 247 attended the physical examination at local survey sites (response rate, 55%).Main outcome measures: Overweight and obesity defined by body mass index (BMI; kg/m2) and waist circumference (cm); sociodemographic factors (including smoking, physical activity and television viewing time).Results: The prevalence of overweight and obesity (BMI > 25.0 kg/m2; waist circumference > 80.0 cm [women] or > 94.0 cm [men]) in both sexes was almost 60%, defined by either BMI or waist circumference. The prevalence of obesity was 2.5 times higher than in 1980. Using waist circumference, the prevalence of obesity was higher in women than men (34.1% v 26.8%; P < 0.01). Lower educational status, higher television viewing time and lower physical activity time were each strongly associated with obesity, with television viewing time showing a stronger relationship than physical activity time.Conclusions: The prevalence of obesity in Australia has more than doubled in the past 20 years. Strong positive associations between obesity and each of television viewing time and lower physical activity time confirm the influence of sedentary lifestyles on obesity, and underline the potential benefits of reducing sedentary behaviour, as well as increasing physical activity, to curb the obesity epidemic.

Adrian J Cameron MPH · Paul Z Zimmet MD, FRACP, FAFPHM · David W Dunstan PhD · Marita Dalton GradDipEpidemiol · Jonathan E Shaw MD, MRCP · Timothy A Welborn MB BS, PhD · Neville Owen PhD · Jo Salmon PhD · Damien Jolley MSc

Comment: Nutritional rickets is highly prevalent in countries such as Mongolia, Tibet and China1 where winter sunlight is reduced and there is no universal vitamin D supplementation. Paradoxically, rickets is also prevalent in developing countries in the tropics and subtropics where sunlight is unlikely to be a limiting factor. Low calcium intakes (including vegetarian diets), prolonged breast feeding, and covering of the skin may all contribute.2,3 Published reports and clinical experience in Sydney suggest an increase in prevalence of rickets, especially in infants and mothers in immigrant populations2,4-7 Other Western countries have reported similar findings. The vitamin D deficiency described by Johnson and Willis in an infant in Perth highlights a high-risk group — infants of mothers who are veiled. Treatment of associated nutritional deficiencies, especially iron deficiency,4,5 and giving a minimum of 300 000 IU of vitamin D over 6–8 weeks, should resolve the rickets. Data on the epidemiology of vitamin D deficiency in these high-risk groups in Australia and other Western societies are lacking and should be the subject of future research. The major source of vitamin D and its circulating form, 25-hydroxyvitamin D3 (25OHD3), in children and adults is the skin. It is estimated that exposure to sunlight for 15 minutes three times per week normalises 25OHD3 levels.8 Dark skin, increasing age, sun protection agents, and the angle of the sun in winter will attenuate this increase in 25OHD3.8 Neonates acquire their vitamin D3 stores from their mothers via the placenta, with only a small amount transferred in breast milk.9 By screening high-risk pregnant women, specifically veiled women and those with dark skin,10,11 prevention of most cases of infant rickets is possible. Levels of 25OHD3 should be measured and, if low, the mother should receive 4000 IU of vitamin D daily until 25OHD3 levels are normal. There is currently no recommendation for routine supplementation of vitamin D in infants, and most cereals and foods are not fortified with vitamin D. However, infant formulas are supplemented with 200 IU of vitamin D per litre. It is estimated that sufficient vitamin D levels to prevent rickets could be achieved if 400 IU of vitamin D were provided daily as part of a multivitamin supplement to high-risk infants.

Christopher T Cowell

To the Editor: In the abstract of his article on asthma prevention with dietary manipulation,1 Mellis states that "we know" that the major modifiable dietary environmental risk factors for childhood asthma are not having been breastfed and low intake of omega-3 fatty acids. In his discussion of the evidence, Mellis suggests that breastfeeding may be protective and, importantly, acknowledges the controversy. He further states (in the abstract) that observational studies have shown a reduction in childhood asthma in children who eat fish regularly (that is, have a high intake of omega-3 fatty acids), similar to those who were exclusively breastfed for three months. However, he provides no references for these observational studies, and nor does he discuss any specific evidence in support of including omega-3 fatty acids for reducing childhood asthma. While there are some suggestions of such an association, the evidence is extremely limited compared with the extensive literature on the potential for the protective effect of breastfeeding. Further, there are substantial methodological issues associated with the few studies that do exist, not the least of which is the measurement of the relevant dietary parameters. Australian studies have suggested a protective influence of at least two fish meals per week on bronchial hyperresponsiveness in 7–11-year olds2 and of eating oily fish3 on the prevalence of childhood asthma. However, neither of these studies had the capacity to measure omega-3 fatty acid nor fish intake in a valid way. These limitations were acknowledged by the authors of the studies, and have been noted by others;4 they need to be included in any discussion of a putative protective effect. It should also be noted that the biological plausibility of such an association has been challenged.4 There are many valid reasons for promoting the consumption of omega-3 fatty acids, but shouldn't we wait for the outcome of the randomised clinical trial currently under way before accepting the statement that "we know" that a low intake of these fatty acids increases the risk of childhood asthma?

Jill L Sherriff

In reply: Sherriff is correct in pointing out that the studies showing protection from bronchial asthma (and bronchial hyperresponsiveness) are based on consumption of fish meals rather than a direct measure of omega-3 fatty acid intake. This protection has been observed consistently in cross-sectional studies of New South Wales primary school children. Thus, the level of evidence is at best Level III, albeit using a proxy for omega-3 fatty acid intake. Results of a randomised-controlled trial of omega-3 fatty acid supplementation currently under way in western Sydney are now in the public arena at 18-month follow-up.1,2 At this early stage, it is uncertain who has genuine asthma rather than other wheezing syndromes. Nevertheless, the group who received omega-3 fatty acid supplementation have differences in rates of wheeze compared with those not supplemented.1,2 For example, the rate of "ever" having had wheeze was 52.6% in the controls versus 42.8% in the supplemented group (absolute risk reduction, 9.8%; number need to treat, about 10). In the table of recommendations in my article,3 I carefully pointed out that supplementing infants with omega-3 fatty acid is something to "consider" rather than strongly recommending it. It should also be noted the level of evidence is low (Level III). Stronger recommendations will depend on the long-term results of randomised trials, such as the western Sydney trial.1,2 In summary, at this stage the only strong dietary recommendations which can be made are: not to use strict elimination diets during pregnancy (Level I evidence); and to consider using lactobacillus probiotic supplements. The evidence for lactobacillus is Level II (from a single randomised controlled trial), although the protection shown is for atopy rather than asthma. Clearly, the children in the lactobacillus study will need further follow-up, and the trial will need to be repeated in other populations. All of this highlights the need for better-quality studies in the area of primary prevention of asthma, based on dietary factors during pregnancy or early infancy.

Craig M Mellis

The main source of vitamin D for Australians is exposure to sunlight. Thus, levels of serum 25-hydroxyvitamin D3, the indicator of vitamin D status, vary according to the season and are lower at the end of winter. In Australia and New Zealand, the prevalence of vitamin D deficiency varies, but is acknowledged to be much higher than previously thought. One study found marginal deficiency in 23% of women, and another frank deficiency in 80% of dark-skinned and veiled women. The groups at greatest risk of vitamin D deficiency in Australia are dark-skinned and veiled women (particularly in pregnancy), their infants, and older persons living in residential care. Only a few foods (eg, fish with a high fat content) contain significant amounts of vitamin D. In Australia, margarine and some milk and milk products are currently fortified with vitamin D. The average estimated dietary intake of vitamin D for men is 2.6–3.0 µg/day and for women is 2.0–2.2 µg/day. The estimated dietary requirement of vitamin D is at least 5.0 µg/day and may be higher for older people. Adequate intake of vitamin D is unlikely to be achieved through dietary means, particularly in the groups at greatest risk, although vitamin D-fortified foods may assist in maintaining vitamin D status in the general population. An appropriate health message for vitamin D needs to balance the need for sunshine against the risk of skin cancer.

Caryl A Nowson PhD, DipNut · Claire Margerison BSc(Hons), MND

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

To the Editor: A number of recently published articles indicate that the prevalence of overweight and obesity in children is increasing at an alarming rate on a national1 and international2 level. Overweight children are more likely to become overweight adults and to experience chronic health problems associated with adult obesity. We report results obtained from a survey of primary schoolchildren on the New South Wales Central Coast which extends the time series from that in the article by Magarey and colleagues (1985 and 1995 data)1 to the year 2000. We undertook a cross-sectional study of children at a Central Coast primary school in November 2000 as part of a community study. This study was approved by the Central Coast Health Ethics Committee. All children in each class were asked to take part. With parental consent, weight and height were measured in children from all class groups (aged 7–11 years) by child health nurses using standardised procedures. Children were classified as overweight or obese using the standard international cutoffs for body mass index.3 They were compared with data obtained during the 1985 Australian Health and Fitness Survey (AHFS85) and the National Nutrition Survey of 1995 (NNS95).1 A total of 268 children (127 girls, 141 boys) were surveyed (average of 25 girls and 28 boys of each age). This represented a 70% response rate. The Table shows that the incidence of overweight and obesity in Australian children has continued to increase, with relative risks for the increase between 1985 and 1995 of 1.37 (95% CI, 1.07–1.75) for boys and 1.82 (95% CI, 1.49–2.22) for girls, and relative risks for the increase between 1995 and 2000 of 1.71 (95% CI, 1.21–1.43) for boys and 1.21 (95% CI, 0.87–1.67) for girls. Our findings indicate a marked increase in proportions for boys in only five years since NNS95. While the increase for girls was not statistically significant, the pattern is consistent. Prevalence of overweight and obesity in children aged 7–11 years for 1985, 1995 and 2000 Sex Year Number Overweight (%) Obese (%) Overweight + obese (%) Boys 19851 2425 9.7 1.5 11.2 19951 457 11.6 3.7 15.3 2000 141 16.3 9.9 26.2 Girls 19851 2443 11.0 1.9 12.9 19951 430 17.2 6.3 23.5 2000 127 21.3 7.1 28.4 Thus, the incidence of overweight and obesity in Australian children is steadily increasing. Importantly, according to the 1996 Census Socio-Economic Indexes for Areas,4 the school we surveyed is situated in an area ranked in the middle quintile for relative socioeconomic disadvantage (state and national average), and is immediately adjacent to one 4th- and several 1st-quintile and 2nd-quintile areas. We believe our findings are representative of the Australian population of children. The challenge to healthcare workers is significant. The National Health and Medical Research Council's Acting on Australia's weight5 identifies goals for preventing further weight gain in adults, and eventually reducing the proportion of the adult population that is overweight or obese, and to ensure the healthy growth of children. Recommended strategies range from national dietary and physical activity guidelines to increasing physical activity through the design of towns, transport systems and public recreational facilities. Effective strategies are urgently needed to alter food intake and physical activity at individual, school, community and population levels.

Susan Goodman · Peter R Lewis MB BS, FAFPHM · Andrew J Dixon · Cheryl A Travers

To the Editor: In a recent editorial, Mason and Diamond state that ergocalciferol (vitamin D2) is bioequivalent to cholecalciferol (vitamin D3) and that 1000 IU/day of ergocalciferol is sufficient for the treatment of vitamin D deficiency.1 Both statements are contentious. Although ergocalciferol (vitamin D2) is the only single prohormonal form of vitamin D available on prescription in Australia, there are three reasons to be cautious about the use and dose equivalence of ergocalciferol (vitamin D2) compared with cholecalciferol (vitamin D3). Cholecalciferol (and not ergocalciferol) has been shown in two randomised trials to reduce fracture rates when administered concomitantly with calcium to elderly patients.2,3 Furthermore, all recently studied agents for treating postmenopausal osteoporosis (alendronate, risedronate, raloxifene and parathyroid hormone 1-34 [the first 34 amino acids of the hormone]) were shown to lower fracture rates, but study participants were routinely given supplementary calcium and vitamin D when deficiency was established. At least two studies specified the use of cholecalciferol. Vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) are probably not bioequivalent.4,5 Ergocalciferol administration to vitamin-D-replete premenopausal women reduced the amount of circulating 25-hydroxyvitamin D3 (25OHD3) while only modestly increasing 25OHD2 levels, with a resultant marginal effect on the total 25OHD level.4 In contrast, the equivalent dose of cholecalciferol increased the circulating level of 25OHD3 significantly.4 Lastly, while radioimmunoassays (RIAs), such as the INCSTAR/DioSorin assay (Stillwater, Minnesota, USA), used in both studies of vitamin D levels published recently in the MJA6,7 are able to measure 25OHD levels, they are incapable of differentiating between 25OHD2 and 25OHD3. Furthermore, neither of the commercially available RIAs (the other one is made by IDS Ltd, Tyne and Wear, UK) is able to measure both vitamin D metabolites with equivalent accuracy. In a study comparing RIAs for the measurement of 25OHD against high performance liquid chromatography (the gold standard method) both assays did not recognise 25OHD2 as well as 25OHD3, with r2 of 0.74 and 0.58, respectively, for 25OHD2.8 Until further research is available, using more patients and a greater number with vitamin D deficiency, caution must be exercised in the interpretation of 25OHD levels measured with RIAs. This applies especially to individuals taking ergocalciferol (vitamin D2) for the treatment of vitamin D deficiency. Thus, it would appear that cholecalciferol (vitamin D3 ) has a role to play in the reduction of osteoporotic fractures, but only when administered with calcium. If administering ergocalciferol (vitamin D2), a far greater dose than 1000 IU/day may be needed, and the use of commercial RIAs to determine the therapeutic response may be misleading.

Paul Glendenning PhD, FRACP · Rebecca S Mason · Terrence H Diamond

In reply: Glendenning raises a number of interesting points, which require some clarification. Are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) biologically equivalent? The statement that ergocalciferol and cholecalciferol are bioequivalent in humans is made by most authoritative textbooks, based mainly on evidence from early studies of the antirachitic efficacy of ergocalciferol and cholecalciferol compounds, and contrasts with reduced efficacy of ergocalciferol in birds and monkeys.1 Recent studies using more precise measurements have raised some doubts as to the absolute equivalency of ergo- and cholecalciferol, but the differences are marginal2 and not universally found.3 There are few recent data on relevant biological endpoints. Serum concentrations of the active hormone, 1,25-dihydroxyvitamin D, were not different after administration of ergo- or cholecalciferol,2 and increases in bone mineral density were greater after ergocalciferol therapy than after cholecalciferol in patients taking anticonvulsants.1 In short, on current evidence, differences in biological activity between ergocalciferol and cholecalciferol are likely to be relatively minor. Are there problems monitoring therapy? 25-Hydroxyvitamin D values may be used for monitoring treatment. The possibilities of impaired detection of the 25-hydroxy metabolite of ergocalciferol by some assays,2 and perhaps a smaller rise in total 25-hydroxyvitamin D concentrations after low doses of ergocalciferol, should be borne in mind when monitoring therapy. What is the current recommendation for vitamin D supplementation? While the availability of larger dose sizes and/or cholecalciferol preparations would be helpful, 800 IU of ergocalciferol and 1 g of calcium for six months was shown to reduce secondary hyperparathyroidism in older patients,1 and 600 IU/day (same for ergo- and cholecalciferol) is the new recommended adequate intake for older patients with limited sun exposure.1

Paul Glendenning

To the Editor: There is much conflicting evidence that increased intake of vitamin C enhances the natural protective mechanisms of the body and decreases both the incidence and severity of the common cold.1 It is regrettable that the study by Audera and colleagues failed to show a significant therapeutic effect of megadose vitamin C in treatment of the common cold.2 The groups compared had, on average, similar composition after randomisation. However, the viral infections that cause the common cold and its progression to ill health, as evidenced by multiple symptoms, are affected by many factors, while symptom severity is well known to vary greatly. Therefore, the study's reliance on respondents' self-diagnosis of symptom severity and onset is a significant weakness in design. Randomisation of participants to the treatment groups may have been insufficient to override this design deficit, thereby significantly biasing the outcome. A better design might have combined patient self-report of symptom severity with physical examination, thus allowing independent and professional assessment of severity. Also, proper assessment of previous history of severity of cold symptoms is crucial for proper randomisation to treatment groups. If Audera and colleagues' study failed to control for this history, then randomisation may have also failed to balance its effect equally between treatment groups, significantly compromising the study's validity to detect any therapeutic benefit of vitamin C. Cold symptoms also vary diurnally, while severity varies with alcohol use and smoking status,3,4 which also affect vitamin C absorption.5,6 No information was provided on study participants' alcohol consumption and smoking status. Finally, the study did not assess stress, which may constitute a further, important uncontrolled bias. A recent cohort study of stress and the common cold concluded that all four dimensions of stress investigated — stressful life events, negative affects, positive affects and perceived stress — were significantly related to occurrence of the common cold.7 Stress may also have significantly affected symptom severity and participants' perception of their symptoms. Certainly, the trend observed in the placebo group of shorter duration of some symptoms and lower mean severity could have been due to less severe symptom history, compounded by a lower degree of overall stress.

Luis Vitetta · Avni Sali · Bill Paspaliaris · Nicola J Reavley

In reply: Precisely because of the temporal variation in symptom severity described by Vitetta and colleagues, we judged that medical professionals are not as well able, in a variably timed interview, to quantify patients' cold symptoms as the patients themselves can do on a continuing basis. Therefore, we consider that our study1 would have been no more valid if the detailed symptom severity cards had been supplemented by one or more physical examinations. In that respect, we are in good company with others who have studied the common cold over many years.2 We agree that double-blind randomisation does not necessarily distribute all relevant variables equally. That is why, in Box 2 of our study report, we presented four variables — age, sex, mean number of colds in the previous year, and mean number of days unwell with colds in the previous year.1 The likelihood that stress, smoking and alcohol status would have been sufficiently maldistributed in this large group to mask a significantly beneficial effect in even one of the three groups which received high-dose vitamin C seems vanishingly small. Nevertheless, we acknowledge that the study would have been stronger if we could have reported the distribution of these three potential confounders. We contest the view of Vitetta and colleagues that the evidence from randomised controlled trials of vitamin C in treating the common cold conflicts significantly (see Box 1 of our article1). The overview finding — that mega-doses of vitamin C for prophylaxis produce a relatively trivial reduction in cold severity but no reduction in incidence3 — was the stimulus for our own study. No community studies of this issue have been flawless, but the mounting collective evidence suggests that we should look elsewhere for a cold panacea.

Carmen Audera · Roger V Patulny · Beate H Sander · Robert M Douglas

Fitness and fads Estimating historical changes in physical activity levels Garry J Egger, Neeltje Vogels and Klaas R Westerterp MJA 2001; 175: 635-636 Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Psychiatry Abstract Objective: To compare activity levels between a simulated "historical" lifestyle and a "modern" lifestyle to try to validate earlier estimates of secular changes in activity. Design: Triaxial accelerometers (TRACMORs) were used to measure activity levels in a "historical" group of seven male actors who were paid to live like early Australian settlers at a theme park north of Sydney (eg, minimising the use of modern technology) for a week. Results were compared with those from a group of seven "modern" sedentary office workers. Results: Activity levels were up to 2.3 times greater in the historical group than the modern group. Calculations based on body weight and energy expenditure suggest the difference is the equivalent of walking up to 16 km per day more in the past than today. Conclusions: These findings accord with two previous estimates of changes in daily activity levels over time and suggest that recent public health guidelines for increasing physical activity may be inadequate. An inactive lifestyle has been linked to a range of diseases, many of which are mediated through obesity.1 Intuitively, it seems apparent that average activity levels have decreased with modern industrial development and have mirrored the worldwide rise in obesity. Proxy measures of inactivity, such as the sale of motor vehicles and television viewing time, show a clear relationship to the development of obesity in the presence of a declining food intake. For this reason, some obesity experts suggest that the modern phase of the obesity epidemic (from 1980 onwards) is probably mediated more by inactivity ("sloth") than overconsumption ("gluttony"). However, the quantitative dimensions of a change in physical activity are difficult to estimate.2 If they could be (even roughly) determined, they might provide valuable information against which to assess modern physical activity guidelines for weight loss and maintenance. A "back of an envelope" calculation suggested an average decline in energy expenditure in the United Kingdom from the years after World War II to 1995 of around 800 kcal/d.3 At an energy cost of around 50 kcal/km for a 70 kg man,4 this suggests a decline in activity levels equivalent to walking about 16 km less per day. More recently, a comparison of activity levels of hunter-gatherer populations with those of individuals in modern Western societies suggested that the average daily difference may be equivalent to walking about 19 km.5 In an attempt to validate these estimates, we recently mocked up a small experiment for a lifestyle television production (Burke's Backyard). Our experiment was designed to compare activity patterns in Australian settlers of 150 years ago with modern-day sedentary office workers. We then attempted to calculate differences in terms of distance walked daily to compare with the previous estimates. Methods Movement levels were monitored in two groups of men by use of a triaxial accelerometer (TRACMOR, Maastricht University, Maastricht, the Netherlands) worn around the waist during waking hours. This has recently been validated against doubly-labelled water,6 and is regarded as one of the most sophisticated modern ambulatory measurement monitors. The device measures movement in activity units on three axes (forwards, sidewards and upwards), and includes even relatively minor movements such as fidgeting and upper-body actions. Seven male actors aged 30-60 years who work at "Old Sydney Town", a historic theme park north of Sydney set around the early 19th century, were selected to represent a historically active group. The men are paid to play the role of early Australian soldiers, convicts and settlers for about eight hours every day. They agreed to wear a TRACMOR during waking hours for one week, and were asked to avoid the use of modern technology as much as possible when they were not working at the park during the week. In an attempt to further authenticate this process, five of the men lived on the premises in convict huts for up to four days and nights. A second group of seven male modern sedentary workers, aged 30-60 years, including accountants, information technology personnel, doctors, a taxi driver and an entertainer, were also given TRACMORs to wear during waking hours, and were asked to continue their normal lifestyle over the course of a week. All records were downloaded into a computer program developed by the developers of the TRACMOR at Maastricht University in the Netherlands for analysis of results. Results The mean activity level (arbitrary units) for the historical group was 88 533 (95% CI, 33 697-143 369; range, 62 204-129 924), compared with 54 920 (95% CI, 32 019-77 821; range, 38 322-70 399). Thus, the historical group were on average 1.6 times more active than the modern group. However, the task was taken more seriously by some in the historical group than others (eg, some still used cars and televisions to some extent during the week). Hence, the two main outliers in the group, who kept rigidly to the experimental requirements, may provide a better reference point for calculations. These two individuals (with activity levels of 129 924 and 125 800 units) were 2.3 times more active than the modern group. Using estimates derived from energy expenditure tables (see Box), it was calculated that the difference in activity levels between the means of the two groups was equivalent to walking about 8 km per day. However, when the two outliers in the historical group were compared with the mean of the modern group, the difference was equivalent to walking about 16 km per day. Discussion A difference in daily activity levels equivalent to walking 8-16 km per day between previous and modern times represents a huge secular change in daily energy expenditure. At the upper level, this coincides roughly with previous estimates.3,5 It probably also accords with the levels of movement required for foraging for survival throughout most of human evolution. Anthropological evidence suggests that early humans, like modern hunter-gathers, may have transported tools, weapons and game over a daily range of about 15 km.8 Given their other daily tasks, this would have added up to a substantial daily energy use which was rarely, if ever, likely to be exceeded by food intake over an extended period, thus reducing the chances of energy imbalance. As a result, human populations, up until the past 2-3 decades, have not been significantly overweight. The growth of time-saving and time-using technologies,9 however, means that these activity levels are unlikely ever to be reached without conscious effort. In the presence of an abundant (and energy-dense) food supply, obesity, at least at the population level, is almost an inevitable consequence of modernisation. More telling are the implications this has for physical activity recommendations for optimal health and weight management. Recent government recommendations suggest an added daily energy requirement of 30 minutes of accumulated mild- to moderate-intensity activity.10,11 However, for a 96 kg sedentary office worker, such as in this study, this would account for perhaps an extra 200 kcal/d, which is 300-800 kcal (the equivalent of walking 5-13 km) short of the 500-1000 kcal difference estimated here. These findings support the suggestion that, if the evolutionary perspective (which has dominated almost all of human existence) is indicative of requirements for optimal health, an increase in activity levels up to three times those recommended in modern guidelines may be necessary.5 Supporting this, data from the United States Weight Control Registry, a database of people who have lost more than 14 kg and maintained this for at least five years, have shown that people who achieve the greatest benefits are consciously active for up to 80 minutes a day.12 This is about three times greater than current recommendations.10,11 These figures are based on people who have been previously obese, and maintenance of weight loss may be more difficult than prevention of weight gain. Nevertheless, it is an awesome task, in the absence of a major environmental change, to expect these activity levels to be met in our society. The figures presented in this study should be interpreted with caution. Although we used a validated modern movement-sensing device,13 the results involve only small numbers under artificial conditions. In their present form, they merely add support to other attempts to calculate human activity levels over time and provide an indication of the activity requirements needed to correct these secular changes. References Powell KE, Blair SN. The public health burdens of sedentary living habits: theoretical but realistic estimates. Med Sci Sports Exerc 1994; 26: 851-856. Prentice A, Jebb S. Obesity in Britain: Gluttony or sloth? BMJ 1995; 311: 437-439. James WPT. A public health approach to the problem of obesity. Int J Obes Relat Metab Disord 1995; 19: S37-S45. Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 2000; 32 (9 Suppl): S498-504. Cordain L, Gotshall RW, Eaton SB. Physical activity, energy expenditure and fitness: an evolutionary perspective. Int J Sports Med 1998; 9: 328-335. Bouton C, Verboeket-van de Venne WP, Westerterp KR. Physical activity assessment: comparison between movement registration and doubly labelled water. J Appl Physiol 1996; 81: 1019-1026. Movahedi A. Simple formula for calculating basal energy expenditure. Nutr Res 1999; 19: 989-995. Gowlett J. Mental abilities of early man: a look at some hard evidence. In Foley R, editor. Hominoid Evolution and Community Ecology. New York: Academic Press, 1984; 167-192. Bowden S, Offer A. Household appliances and the use of time: the United States and Britain since the 1920s. Econ Hist Rev 1994; XLVII: 725-748. United States Surgeon General. Physical activity and health: a report of the Surgeon General. US Department of Health and Human Services. Atlanta: Centers for Disease Control, 1996. Egger G. National physical activity guidelines for Australians: scientific background report. Canberra: Commonwealth Department of Health and Aged Care, 1999. Klem ML, Wing RR, McGuire MT, et al. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr 1997; 66: 239-246. Westerterp K. Pattern and intensity of physical activity. Nature 2001; 410: 539. (Received 25 Sep, accepted 22 Oct, 2001) Authors' details Deakin University, Melbourne, VIC, and GutBusters Pty Ltd, Sydney, NSW. Garry J Egger, MPH, PhD Adjunct Professor of Health Sciences. Masstricht University, The Netherlands. Neeltje Vogels, BBiolSc Student; Klaas R Westerterp, PhD, Professor of Human Energetics, Department of Biological Sciences. Reprints will not be available from the authors. Correspondence: Professor G J Egger, PO Box 313, Balgowlah, NSW 2094. eggergjATozemail.com.au Make a comment Calculation of distance equivalents Activity units measured by the TRACMOR are not readily convertible to energy units (kilocalories). However, an estimate of relative differences in activity levels can be made by assuming a total daily energy expenditure 1.4 times that of resting metabolic rate for the men in our modern group.5 With an average weight of 96 kg and age of 44 years, a mean resting metabolic rate of about 2000 kcal/d can be estimated.7 Therefore, total energy expenditure would be 1.4 x 2000 = 2800 kcal/d, of which 800 kcal represents daily physical activity. As activity counts in our historical group ranged from 1.6 times those of the modern group on average to 2.3 at the extremes, this implies a total daily physical activity level in this group of 1280-1840 kcal/d, or a net difference of about 500-1000 kcal/d between the groups. Using energy values for walking of 0.716 kcal/kg per kilometre (or about 61 kcal/km for a 90 kg man),4 this implies a net difference between the groups equivalent to walking about 8-16 km per day. Back to text

Garry J Egger · Neeltje Vogels · Klaas R Westerterp

Fitness and fads Quick weight loss: sorting fad from fact David C K Roberts MJA 2001; 175: 637-640 Abstract - How to recognise a fad diet - Why fad diets "work" - Our metabolic flexibility has limits - Low carbohydrate diets - High carbohydrate, very low fat diets - Other types of fad diets - How to advise patients - Acknowledgements - References - Authors' details - - More articles on Nutrition Abstract This article reviews popular diets for their ability to produce effective weight loss. Most of the "evidence" for fad diets is based on anecdotal findings, theories and testimonials of short term results. The most prominent elements of fad diets are those of ritual and sacrifice. These diets offer quick and painless weight loss while allowing consumption of favourite or tasty foods, but place severe restrictions on certain other foods or food categories. Fad diets often work in the short term because they are low-kilojoule diets in disguise; that is, energy intake as a result of the diet is lower than the person's requirements. Successful long term weight loss depends on the consumption over a long period of time of less energy than is expended. The ideal approach is to increase physical activity while modifying eating behaviour to achieve a nutritionally balanced intake. As the desire for instant thinness continues to be a feature of our society, so is the appearance of new and not-so-new fad diets. The Journal published an article in 1999 reviewing substances used in weight loss; the authors concluded that most had no evidence to support their action.1 An excellent review of popular weight-loss diets has been published elsewhere by Anderson and co-workers.2 In this article, I review popular diets for their ability to produce effective weight loss, and provide additional information to assist practitioners in distinguishing fad from fact. As a nation, we are fat. According to the latest National Nutrition Survey,3 64% of Australian men and 47% of women are overweight or obese. The situation is getting worse rather than better — the proportion of overweight or obese adults has increased since 19834 by about 52% for men and 34% for women. Personal efforts to address the overweight problem, while common, are apparently not working. One in three Australians claim they are on some type of "diet",3 yet energy intake has increased and physical activity levels have decreased.5 Mathematical modelling suggests that weight loss is a simple matter, with limited inputs and outputs to be controlled.6 Yet most people who successfully lose weight return to their old eating habits, and within two years regain most of the lost weight.7 The methodology and design of reported weight-loss studies have been questioned,8 especially in studies involving long term follow-up. Weight loss can be a treatment effect (weight loss to improve diabetes control) or it can be an outcome of some other treatment (medication used to produce weight loss), making randomised controlled trials difficult to interpret. The lure of rapid weight loss promised by each new popular diet is undoubtedly compelling. A survey in the United States found that more than one in five dieters used fad diets.9 Fad diets feed into the psyche of people who seek to look better and feel better with the minimum of effort. Sensible eating for weight loss often does not appeal to people who feel they are already doing the best they can. However, very simple dietary changes, followed diligently, can often produce effective weight loss at a rate that can be maintained over the longer term.10 Conversely, when weight loss is too fast, changes in body composition, especially the loss of lean body mass, can compound the problem of overweight in the longer term. One large study reported an overall increased risk of major weight gain in the long term (at 6 and 15 years) in those who undertook weight-loss attempts (dieting) at baseline.11 However, these findings do not rule out the potential success and benefit of weight-loss programs which aim to encourage permanent changes in behaviour. How to recognise a fad diet To the aware practitioner, fad diets are relatively easy to spot (Box 1), but they can be quite convincing to the lay person. They offer a quick solution to a long term problem. The author or promoter presents what appear to be scientifically valid explanations or references to support the dieting theory. The promoter may be tertiary educated, although frequently has no formal nutrition or dietetic qualifications.12 The theory behind the weight loss approach is often explained using scientific terminology that simplifies or expands upon the biochemical and physiological facts that provide the evidence to support the claims. However, the validity of the scientific support is often questionable. Most of the "evidence" for fad diets is based on anecdotal findings, theories and testimonials of short term results. The most prominent elements of fad diets are those of ritual and sacrifice. The ritual aspect is to always include, say, grapefruit daily but never add sugar to your beverage (sacrifice). These diets offer quick and painless weight loss while allowing consumption of favourite or tasty foods, but severely restrict certain other foods or food categories. Why fad diets "work" Fad diets often work in the short term because they are low kilojoule diets in disguise (Box 2); that is, energy intake as a result of the diet is lower than the person's requirements. This is the only way to lose weight — to consume less energy than the body needs. No magic ingredients, strange food combinations or pseudoscientific formulas will alter this metabolic fact. The rate of weight loss (which reflects shifts in water equilibrium as well) varies depending on the relative proportions of the three major nutrients in the diet — carbohydrate, fat and protein. The macronutrient composition can also affect appetite: high-protein diets can suppress appetite, as can ketosis, which results from severe carbohydrate restriction.7 Because energy from food comes only from these nutrients (and alcohol), the number of dietary permutations and combinations is limited. Thus, most diets can be categorised into three main types: low carbohydrate with the emphasis on high protein; low carbohydrate with the emphasis on high fat; and high carbohydrate with an emphasis on low fat. To complete the picture, some fad diets promote one food or a very limited range of foods, while others may be based on individual characteristics such as blood type or personality, or on an unproven physiological concept (such as cleansing "toxins" from the body). Fad diets are generally nutritionally unbalanced and lack essential nutrients.13 They have the potential for health risks. A major problem is that the unfounded nutritional theories espoused with these diets undermine sound nutrition education and public awareness of the importance of healthy long term eating combined with regular physical activity. Our metabolic flexibility has limits The primary objective in effective weight loss is to lose fat and not lean body mass (muscle). From a biochemical point of view, this means encouraging the body to use fatty acids for energy with minimal reliance on glucose as an energy source, except for those tissues with an obligate requirement for glucose, such as red blood cells. With limited carbohydrate in the diet, once carbohydrate (glycogen) stores have been used the only source of glucose available to the body is that derived from the carbon skeletons of amino acids. In this situation, and in the absence of sufficient dietary protein, body protein (lean body mass) is catabolised to provide glucose. Muscle mass will therefore decline markedly on a very low carbohydrate, restricted protein diet. The ideal weight-loss diet should provide enough carbohydrate to prevent net protein catabolism, enough good quality protein to meet the normal needs of protein turnover, and enough fat to meet essential fatty acid requirements. Low carbohydrate diets Low carbohydrate diets have a long history. The Greek Olympians are said to have eaten high meat, low vegetable diets to improve athletic performance.7 The modern popularity of low carbohydrate diets has been influenced by the seeming "failure" of low fat diets because of a misunderstanding that energy intake is not important and that you can eat as much low fat food as you like and still lose weight.12 Furthermore, low carbohydrate diets appear to work, as they produce rapid weight loss in the first week.7Because the body's demand for glucose is constant, body glycogen stores are mobilised in the early phases of a low carbohydrate diet, and for each gram of glycogen lost two to four grams of intracellular water are lost (intracellular water maintains isotonicity). Consequently, there is greater water and hence weight loss in the early days of this type of diet. Water equilibrium is re-established in the second and subsequent weeks, so that, in the longer term, weight loss simply reflects the energy deficit. Energy-nitrogen balance studies have demonstrated that the greater weight loss on a low carbohydrate, high fat diet is accounted for by losses in body water.7 If carbohydrate restriction is severe (for example, less than 60 g), ketosis can result, which decreases appetite and causes nausea, but can also cause hyperuricaemia as ketones compete with uric acid for renal tubular excretion.7 Popular low carbohydrate, high protein diets include the Zone Diet,14 the Carbohydrate Addict's Diet,15 and the Sugar Busters! diet.16A popular low carbohydrate, high fat diet that has been around since the 1970s is the Dr Atkins diet.17 Low carbohydrate, high protein diets As with other low carbohydrate diets, high protein diets result in initially rapid weight loss. If continued, they produce weight loss because they are also low kilojoule diets. There is also evidence that higher-protein diets are more satiating. People feel fuller and eat less after a meal with a high protein content (31%-54% energy).18-20 A low fat, higher-protein diet (25% of energy) has also been found to produce a significantly reduced energy intake and greater weight and fat loss over six months compared with a low fat diet with 12% energy from protein.21 However, energy restriction is responsible for the weight loss. An additional problem of high protein diets is the extra solute load placed on the kidneys owing to greater production of nitrogen waste products, particularly in situations of high water loss from perspiration or inadequate fluid intake contributing to dehydration.7 In the long term, very high protein diets may increase the risk of osteoporosis in people with inadequate calcium intake by increasing calcium excretion.7,22 Low carbohydrate, high fat diets Popular for many years, the Dr Atkins diet17 allows protein-rich foods such as meats, fish, chicken and eggs, but also encourages fatty foods like butter, cream, fats, oils and salad dressings in large amounts. The key principle of the diet is to develop ketosis, which is seen as a dieting advantage because loss of ketones in the urine is regarded as wasting "usable" energy. The early stage of the diet restricts carbohydrate to no more than 20 g per day to achieve this. However, the actual energy value of urinary ketone losses is insignificant compared with the energy deficit of around 30 MJ required to lose one kilogram of fat. The daily loss of energy from ketones rarely exceeds 2%-3% of the total energy requirement.23 After ketosis is established, small amounts of carbohydrate (up to 60 g per day) are allowed back into the diet, provided urinary ketone losses are maintained. Common consequences of following this type of diet include dehydration, diarrhoea, weakness, headaches, dizziness and bad breath. Over the longer term, such a diet can increase the risk of atherosclerosis — one study has shown that this diet increases serum cholesterol levels and may increase the risk of coronary heart disease by more than 50% with long term use.2 This type of diet also does not include sufficient fruits and vegetables for good health and promotes the misconception that energy intake is not important. High carbohydrate, very low fat diets High carbohydrate diets for weight loss can be consistent with healthy eating if they recommend high fibre intakes and provide sufficient essential fatty acids and fat-soluble vitamins. However, if lean meat and fish and low fat dairy products are allowed only in tiny amounts (eg, as "condiments" only), there is the risk of inadequate intakes of calcium, iron, zinc and high quality protein. The Pritikin diet,24 for instance, recommends that fat intake be less than 10% of energy intake, which is likely to be unpalatable for many people used to a Western diet and is close to the lower limit of our requirement for essential fatty acids. The Pritikin diet is also quite low in protein in one of its forms (Maximum Wt Loss), so the quality of any protein present becomes important. A US study of popular diets has demonstrated that diet quality (measured by dietary variety and intake of five food groups, fat, saturated fat and sodium) is higher in high carbohydrate diets and lowest in low carbohydrate diets.25 The same study showed body mass index is lower in people following high carbohydrate diets and highest in people on low carbohydrate diets. Other types of fad diets Over the years, an array of "one food" diets have been promoted, such as the rice diet, banana diet, and the grapefruit diet. These types of diet are potentially dangerous, nutritionally unbalanced and unscientific, and encourage poor eating habits and food faddism. Some diets base their theories on unproven information about physiology and metabolism, such as that which suggests that blood type influences the best food pattern for you,26 and diets that suggest excess weight is caused by liver dysfunction and not energy imbalance.27 How to advise patients Successful long term weight loss depends on the consumption over a long period of time of less energy than is expended (Box 3). The ideal approach is to increase physical activity while modifying eating behaviour to achieve a nutritionally balanced intake.10Energy needs for weight loss are best established by determining the energy needs of the person at their desired weight and then providing for a weekly energy deficit of about 30 MJ, or 4.2 MJ (1000 kcals) per day. This usually means a suggested energy intake of around 5 MJ (1200 kcals) per day for a woman and up to 8 MJ (1900 kcals) per day for a man. All foods should be allowed, with an emphasis on fibre-rich carbohydrate foods (cereals, breads, fruit and vegetables), fish and other seafood, lean meat and low fat dairy foods, with small amounts of unsaturated fat as oil or margarine. Behaviour modification to help control impulsive eating is also useful. The eating plan should be based on the principles of the Australian Guide to Healthy Eating.28 Increased and regular physical activity adds substantially to the success of weight loss programs, so regular physical activity should be encouraged.29 Acknowledgements I wish to thank Ms Toni Irwin (APD), Dietitian/Nutritionist, for her help and assistance in the preparation of this article. References Egger G, Cameron-Smith D, Stanton R. The effectiveness of popular, non-prescription weight loss supplements. Med J Aust 1999; 171: 11-12. Anderson JW, Konz EC, Jenkins DJ. Health advantages and disadvantages of weight-reducing diets: a computer analysis and critical review. J Am Coll Nutr 2000; 19: 578-590. Australian Bureau of Statistics and Commonwealth Department of Health and Family Services. National nutrition survey: selected highlights, Australia. Canberra: ABS, 1997. (Catalogue no. 4802.0.) National Heart Foundation of Australia. Risk factor prevalence study No. 2. Canberra: NHF 1983. Armstrong T, Bauman A, Davies J. Physical activity patterns of Australian adults. Results of the 1999 National Physical Activity Survey. Canberra: Australian Institute of Health and Welfare, 2000. (Catalogue no. CVD-10.) Kozusko F. A setpoint based dieting model. Math Comput Model 1999; 29: 1-7. Denke M. Metabolic effects of high-protein, low-carbohydrate diets. Am J Cardiol 2001; 88: 59-61. Lean ME. Is long-term weight loss possible? Br J Nutr 2000; 11 Suppl 1: s103-s111. Jeffery RW, Folsom AR, Luepker RV, et al. Prevalence of overweight and weight loss behavior in a metropolitan adult population: the Minnesota Heart Survey experience. Am J Public Health 1984; 74: 349-352. Goodrick G, Poston WS, Foreyt J. Methods for voluntary weight loss and control: update 1996. Nutrition 1996; 12: 672-676. Korkeila M, Rissanen A, Kaprio J, et al. Weight-loss attempts and risk of major weight gain: a prospective study in Finnish adults. Am J Clin Nutr 1999; 70: 965-975. Stein K. High-protein, low-carbohydrate diets: do they work? J Am Diet Assoc 2000; 100: 760-761. Fisher MC, Lachance PA. Nutrition evaluation of published weight-reducing diets. J Am Diet Assoc 1985; 85: 450-454. Sears B, Lawren B. The Zone — a dietary road map. New York: Harper Collins, 1995. Heller RF, Heller RF. The carbohydrate addict's diet. The lifelong solution to yo-yo dieting. London: Reed International, 1992. Steward HL, Bethea MC, Andrews SS, Balart LA. Sugar Busters! London: Random House, 1998. Atkins R. Dr Atkins' new diet revolution. New York: Avon, 1992. Stubbs RJ. Macronutrient effects on appetite. Int J Obes Relat Metab Disord 1995; 19 Suppl 5: s11-s19. Stubbs RJ, Ritz P, Coward WA, Prentice AM. Covert manipulation of the ratio of dietary fat to carbohydrate and energy density: effect on food intake and energy balance in free-living men eating ad libitum. Am J Clin Nutr 1995; 62: 230-237. Stubbs RJ, Harbron CG, Murgatroyd PR, Prentice AM. Covert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am J Clin Nutr 1995; 62: 316-329. Skov AR, Toubro S, Ronn B, et al. Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int J Obes Relat Metab Disord 1999; 23: 528-536. Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. JAMA 2001; 285: 785-795. Friedman RB, Kindy P Jr., Reinke JA. What to tell patients about weight-loss methods. 1. Diets. Postgrad Med 1982; 72: 73-80. Pritikin N. The Pritikin permanent weight loss manual. New York: Grosset and Dunlap, 1981. Kennedy ET, Bowman SA, Spence JT, et al. Popular diets: correlation to health, nutrition, and obesity. J Am Diet Assoc 2001; 101: 411-420. D'Adamo P. Eat right for your type. London: Century, 1997. Cabot S. The liver cleansing diet. Sydney: Women's Health Advisory Service, 1996. Population Health Division, Commonwealth Department of Health and Aged Care. Australian Guide to Healthy Living. <http://www.health.gov.au/pubhlth/ strateg/food/guide>. Accessed 7 November 2001. Population Health Division, Commonwealth Department of Health and Aged Care. National physical activity guidelines for Australians [brochure]. Available at <http://www.health.gov.au/pubhlth/publicat/document/physguide.pdf>. (Received 4 Oct, accepted 31 Oct, 2001) Authors' details School of Health Sciences, University of Newcastle, Newcastle, NSW. David C K Roberts, BSc, PhD, Foundation Professor of Nutrition and Dietetics Reprints will not be available from the author. Correspondence: Professor D C K Roberts, School of Health Sciences, University of Newcastle, Newcastle, NSW 2308. david.robertsATnewcastle.edu.au Make a comment 1: Common features of fad diets Promises of rapid weight loss Elements of ritual and sacrifice Magical food or food combination Unlimited foods of some type Rigid menus or monotonous food choices Jargon and scientific half-truths Lack of good scientific evidence Lack of acknowledgement of physical activity needs Back to text 2: How to assess weight loss diets — GP checklist Does the diet promote a new fact or newly discovered secret? Does the diet involve purchase of a commercial product? Is there a promise of rapid weight loss? Has the diet been independently tested and results published in a reputable journal? What are the credentials of the author or promoter? Will the diet result in only small quantities of carbohydrate foods being eaten? Does the diet promote adequate intakes of the main food groups: fruit and vegetables, cereal foods, low fat dairy foods, lean meats? Is there an overemphasis on dietary fat or any one food type? Is the energy-balance equation recognised and physical activity promoted as an important part of this? Back to text 3: Features of an appropriate weight-loss diet Considers the individual's current habits, preferences and risk factors. Sets realistic weight loss targets (0.5-1 kg/week). Has a minimum daily intake of 5000 kJ (1200 kcal) for women and 6500 kJ (1500 kcal) for men. Has carbohydrate intake in excess of 150 g per day. Includes foods from each of the food groups. Emphasises dietary fibre. Recommends increased physical activity. Is based on change of life-long eating habits. Back to text

Viewpoint Importance of retaining a national dietary guideline for sugar The Australian Dietary Guidelines are currently being revised and updated. There has been public discussion about the advisability of retaining a guideline for sugar because of insufficient evidence linking sugar consumption to ill health. However, there are concerns about the quality of the self-reported food intake data on which this conclusion is based. In addition, the doubling in diabetes prevalence in Australia in the past 20 years, which is linked to increased obesity from consumption of energy-dense foods, including those with added sugars (sugar-sweetened drinks being particularly important), provides a strong rationale for retaining a dietary guideline for sugar. Kerin O'Dea and J I Mann MJA 2001; 175: 165-166 A Working Group convened by the National Health and Medical Research Council's Health Advisory Committee is currently reviewing the Australian Dietary Guidelines, and reconsideration of the New Zealand dietary guidelines is also likely. Because of insufficient scientific evidence to link sugar consumption with ill health, a case has been made to abandon the guideline referring to sugar, "Eat only a moderate amount of sugar".1 Discussion of this issue is timely as sucrose consumption appears to be increasing. For example, New Zealand national nutrition surveys suggest that, between 1988 and 1997, self-reported sucrose intake increased on average from 42 to 62 g/person per day in males and from 27 to 45 g/person per day in females.2 Even more striking increases were evident in the age group 15-24 years. Dietary studies: Much of the evidence relating diet and disease comes from epidemiological studies, both cross-sectional and prospective. The nutritional and epidemiological methods currently available are insufficiently robust to accurately assess intakes and disentangle the effects of interrelated nutrients. Prospective studies have advantages over cross-sectional surveys, but there are still problems with assessment of dietary intake (which is usually only assessed on one occasion and by methods which are seriously flawed). Much of the evidence on which diet-disease relationships is based is self-reported, and there is substantial under-reporting of foods perceived to be unhealthy (eg, those rich in sugar, fat and alcohol). In particular, people who are obese tend to under-report, and do so selectively.3 Even randomised controlled clinical trials can be difficult to interpret, an excellent example being the CARMEN study.4 In this multicentre trial, 398 moderately obese adults were allocated at random to a seasonal control group (no intervention), a control diet group (dietary intervention typical of the average national intake), or one of two low-fat, high-carbohydrate groups (in which the carbohydrate was derived primarily from "simple" or "complex" carbohydrate). The weight changes on the latter two diets were not significantly different statistically, and the authors therefore concluded that the nature of carbohydrate is a relatively unimportant determinant of body weight. However, closer examination of the data reveals interesting trends: body weight loss on the low fat/high simple carbohydrate diet was 0.9 kg (P < 0.05) and on the high complex carbohydrate diet 1.8 kg (P < 0.001). A similar trend was apparent for change in fat mass. With a larger sample size, these differences might have become significant. Obesity and diabetes: The prevalence of obesity has risen sharply in Australia and New Zealand over the past 20 years. The recently released Diabesity and associated disorders in Australia 20005 draws attention to some of the devastating consequences of overweight and obesity. The association between type 2 diabetes and adiposity is arguably of even greater importance than the previously well described association with cardiovascular risk factors (hypertension and dyslipidaemia). Diabetes prevalence in the Australian adult population has doubled since 1980, the increase occurring in parallel with the rising prevalence of obesity. The estimated number of Australians with diabetes has reached almost one million, of whom less than 500 000 are aware of the diagnosis. The greatly increased risk of coronary heart disease and other vascular diseases, as well as the microvascular complications of diabetes (eg, retinopathy and nephropathy), emphasise the consequences of this disease, which has now reached epidemic proportions. This serious public health issue brings obesity to centre stage. It is caused by a complex interaction between genetic predisposition and environmental trigger factors, but the current epidemic of obesity has to be attributed to the "obesogenic environment"6 — the human genome has not changed in this period! The environmental facilitators of obesity are food intake and energy expenditure. While acknowledging the undoubted contribution of our increasingly sedentary lifestyle to the obesity epidemic, our discussion will focus on diet. Diet: Much of the discourse on the role of diet in the development of obesity highlights the role of fat, due to its high energy density (kJ/g of food or beverage) and its propensity, if consumed in excess, to be deposited as adipose tissue. However, there is now evidence that fat gain is similar with overfeeding of carbohydrate or fat.7 Energy intake is strongly influenced by energy density. Covert manipulation of energy density (ie, providing diets of different energy density without participants' knowledge) results in sustained changes in energy intake.8 The increased use of low-fat products, many of which are energy dense due to their high sugar content, and sugar-containing beverages now contributes significantly to total energy intake and are examples of the means by which sugar may enhance the energy density of the diet. If sugar does contribute to excessive energy consumption and to the problems of overweight and obesity, then clearly retention of a guideline is important. Evidence is accumulating that the form in which the sucrose is consumed is also important. A recent prospective study from Ludwig and colleagues9 showed a clear-cut, graded relation between the consumption of sugar-sweetened drinks and the development of obesity in children. The prevalence of obesity among children in the United States doubled between 1980 and 1994; 11% are now above the 95th reference percentile of body mass index (BMI) for age and sex. The observation that this increase paralleled the increase in sugar-sweetened soft drinks prompted Ludwig et al to enrol 548 ethnically diverse schoolchildren in four Massachusetts communities in a prospective study for 19 months. The difference in measures of obesity was related to change in consumption of sugar-sweetened drinks and other possible determinants of obesity, including physical inactivity and fat intake. For each additional serving of sugar-sweetened drinks both BMI (mean, 0.24 kg/m2) and frequency of obesity (odds ratio, 1.6) increased, after adjustment for anthropometric, demographic, dietary and lifestyle variables. Changes in diet soft drink intake were not related to obesity incidence. Of course, an observational study does not prove causality, but it is of interest that another recently published study in an entirely different group of older individuals produced similar results. Elmslie and coworkers10 compared a group of bipolar (manic depressive) patients and matched controls; the patient group had higher rates of overweight and obesity than the controls. The bipolar patients reported a higher energy intake, the increased energy being derived almost entirely from sucrose in sweetened drinks. Energy from drinks (regardless of whether it is from sugar, fat or alcohol) adds to total energy intake, and does not displace energy from other forms.11 Furthermore, compensation at subsequent meals for energy consumed in the form of liquid (drinks) appears to be less complete than for energy consumed in solid form (food) (ie, people overconsume more easily when excess energy is in the form of energy-containing beverages).12 While these new data suggest an obesity-promoting effect of sugar-containing beverages, it may also be relevant to recall data published some 30 years ago.13 Middle-aged men were asked to replace, as far as possible, sucrose with foods rich in starch to maintain energy balance. Despite regular advice and encouragement from a dietitian they were unable to maintain energy balance and lost weight, presumably because of the greater satiety-promoting qualities of the starchy foods. While not providing direct evidence for sugar as an aetiological factor, these observations do suggest that recommending a reduction in sugar may be a potentially useful public health measure in countries where obesity and its comorbidities have reached epidemic proportions. Implications for Indigenous populations: Our discussion has particular significance for Australian and New Zealand Indigenous populations, who have very high rates of lifestyle-related chronic diseases occurring at much younger ages than the non-Indigenous population.14,15 Indigenous people often have poor-quality diets, high in sugar and fat, and depleted in fruit and vegetables. For example, Lee and coworkers16 analysed the food supply at six remote Aboriginal communities in the Northern Territory using the "store turnover" method, and found a very high consumption of sugar per se and in soft drinks. The diets had high levels of animal fat (mainly from poor-quality meat) and very low levels of fruit and vegetables (ie, energy-dense and nutrient-poor). Most of the sucrose was consumed in liquid form as sugar in tea and in carbonated beverages. Retention of a dietary guideline for sugar: The evidence we have assembled here leads us to strongly advocate the retention of a dietary guideline for sugar in Australia and New Zealand. In fact, given the marked rise in consumption of carbonated beverages in Australia over the past 30 years (47.3-114.4 L/person per year between 1968-69 and 1996-97), we also advocate an addition: "Consume only moderate amounts of sugars and foods and beverages containing added sugar". This is in line with the recently revised US dietary guidelines,17 which include the recommendation "Choose beverages and foods that limit your intake of sugars". There is also a strong population health rationale for mandatory labelling of foods with clear information, including sugar, fat, and total energy content. References Williams P. Sugar: is there a need for a dietary guideline in Australia? Aust J Nutr Diet 2001; 58: 26-31. New Zealand food: New Zealand people. Key results of the 1997 National Nutrition Survey. LINZ Activity and Health Unit, University of Otago for the Ministry of Health. Dunedin, NZ: University of Otago, 1999. Heitmann BL, Lissner L. Dietary underreporting by obese individuals - is it specific or non-specific? BMJ 1995; 311: 986-989. Saris WHM, Astrup A, Prentice AM, et al. Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates on body weight and blood lipids: the CARMEN study. Int J Obesity 2000; 24: 1310-1318. Dunstan D, Zimmet P, Welborn T, et al, on behalf of the AusDiab Steering Group. Diabesity and associated disorders in Australia: the accelerating epidemic. Report of the Australian Diabetes, Obesity and Lifestyle Study. Melbourne: International Diabetes Institute, 2001. Egger G, Swinburn B. An "ecological" approach to the obesity pandemic. BMJ 1997; 315: 477-480. McDevitt RM, Poppitt SD, Murgatroyd PR, Prentice AM. Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose or fat in lean and obese women. Am J Clin Nutr 2000; 72: 369-377. Stubbs RJ, Johnstone AM, O'Reilly LM, et al. The effect of covertly manipulating the energy density of mixed diets on ad libitum food intake in "pseudo free-living" humans. Int J Obesity 1998; 22: 980-987. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective observational analysis. Lancet 2001; 357: 505-508. Elsmlie J, Mann JI, Silverstone JT, et al. Determinants of overweight and obesity in patients with bipolar disorder. J Clin Psychiatry 2001; 62. In press. Poppitt SD, Prentice AM. Energy density and its role in the control of food intake: evidence from metabolic and community studies. Appetite 1996; 26: 153-174. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrates in fluids. Physiol Behav 1996; 59: 179-187. Mann JI, Truswell AS, Hendricks D, Manning EB. Effects on serum lipids in normal men of reducing dietary sucrose or starch for five months. Lancet 1970; 1: 870-872. Daniel M, Rowley KG, McDermott R, et al. Diabetes incidence in an Australian Aboriginal population: eight year follow up study. Diabetes Care 1999; 22: 1993-1998. Simmons D, Harry T, Gatland B. Prevalence of known diabetes in different ethnic groups in inner urban South Auckland. N Z Med J 1999; 112: 316-319. Lee AJ, O'Dea K, Mathews JD. Apparent dietary intake in remote Aboriginal communities. Aust J Public Health 1994; 18: 190-197. Nutrition and your health: dietary guidelines for Americans. 5th edition, 2000. Home and Garden Bulletin No 232. Washington, DC: Department of Agriculture, Department of Health and Human Services; 2000. Authors' details Menzies School of Health Research, Darwin, NT. Kerin O'Dea, PhD, Professor and Director. University of Otago, Dunedin, New Zealand. J I Mann, PhD, DM, FRACP, Professor in Human Nutrition and Medicine. Reprints will not be available from the authors. Correspondence: Professor Kerin O'Dea, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. kerinATmenzies.edu.au Make a comment

Kerin O'Dea · J I Mann