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Vol. 2 - No. 2 - June 1998 - Polyunsaturated Fatty Acids in Nutrition and Disease Prevention Editorial
A diet that is based on processed foods with high fat content is characteristic of the industrial societies. Yet even those most devoted to it can be educated to change their ways, whether they are customers of potato chip vendors in Edinburgh or consumers of buttered steaks in Finnish logging camps. An example is provided in our first report from the ISSFAL third annual meeting, held this year in Lyons, France. Professor Rudolph Riemersma of Edinburgh University reminded his audience at a notable symposium on LCPUFA and triglycerides of the importance of a correct diet. Research has shown, for example, that persuading heart patients to eat more fish and fish oil can lead to a reduction in death rates fully comparable to what can be achieved by the lipid-lowering statins. Prof. Riemersma reported that, by giving intensive dietary counselling, he and his colleagues were able to get patients to eat more fruit, wholemeal bread, cut down on potato chips, and drink less fatty milk. Thus, even though the Scots remained unpersuaded in regard to the benefits of fresh vegetables, they made enough changes in their diet to bring about a much improved picture overall concerning their fatty acids. Considerations of this kind are important when the physician is dealing with elevated triglycerides. There is already consid-erable evidence, both epidemiological and experimental, that triglycerides are likely to be an important risk factor in CHD. Fish oils are powerful antihyperglyceridaemic agents, and in concluding the symposium Professor William Connor recommended that they be considered the agents of choice in normal situations. This is particularly the case in view of their safety in use. But there are also significant lifestyle aspects, and he pointed out that any such treatment should also include advice to the patient on improvement in diet, and more physical exercise. In this context, it is useful to mention that we also publish in this issue a report by a research group in India of a recent randomized controlled clinical trial concerning the cardiac benefits of fish oil and mustard oil. Cardiac mortality in patients taking fish oil was half the rate seen with placebo, and patients who received either fish oil or mustard oil experienced fewer cardiac events than the placebo group. Meanwhile, in the area of
infant growth and development, there is a growing body of scientific data,
and also criticism, in regard to the low levels of LCPUFA in formulas.
Docosahexaenoic acid (DHA), and perhaps also arachidonic acid (AA) are
important to ensure proper growth. This issue includes a review of a paper
by Michael Crawford and colleagues in which they draw attention to the
risk of nutritional deficiencies in preterm babies because of the inadequacies
of the feeds now available. The question has also been raised whether we
should not in any case put more emphasis on maternal LCPUFA supplementation
during pregnancy, since we cannot know in advance which infant is going
to be born prematurely. It is time to open these issues to wider, action-oriented
debate.
CONFERENCE REPORT
Role of Omega-3 LCPUFA in Lowering Triglycerides ISSFAL , the International Society for the Study of Fatty Acids and Lipids, meets about every two years; its third meeting was held in Lyons, France, from 2-5 June. Here we summarize the main points of the symposium on triglycerides, for which Professor Rudolph Riemersma (University of Edinburgh, UK) and Professor William Harris (University of Kansas,USA) were co-chairmen. Triglycerides as a risk factor - epidemiology A link between elevated triglyceride levels and ischaemic heart disease has been known since the 1950s, Professor Michael Miller of the University of Maryland, USA, pointed out, but until 1980 the effect was attributed to cholesterol. The Framingham study showed that triglyceride levels per se were strongly correlated with coronary heart disease (CHD) risk, especially in women. These effects were often reduced after adjusting for other co-variables, but recent studies confirm that triglycerides are a risk factor in their own right. Hokanson & Austin 1996 showed that for each mmol/L rise in triglycerides, CHD risk rose by 14% in men and 37% in women. These figures are confirmed by Austin of Seattle's 1996 meta-analysis of major trials, comprising 14000 individuals, evaluating fasting triglyceride levels. The Copenhagen study of 3000 healthy males, published in Circulation earlier this year, gave similar indications. Triglycerides also predict which patients will show disease on arteriography. Recent studies have also shown a correlation between triglyceride levels and carotid ischaemia. As doubling triglyceride levels raises risk by 50% in men and doubles it in women, this begs the question of what the recommended safe upper limit should be. A consensus panel of the US National Institutes of Health (NIH) in 1993 put it at 200 mg/dL, but Miller argued that it should be halved to 100. The NIH- recommended upper limits for triglycerides and cholesterol are both set at 200 mg/dL. Yet the average US cholesterol level is around 200, twice the mean triglyceride level of around 100 (112 in men, 88 in women). Long-term follow-up of a group of cardiac patients in Baltimore showed that those in the lowest triglyceride group had the fewest cardiac events, even when all other factors were adjusted for, which adds further support to the argument for a lower cutoff point. The next step should be to design an intervention study that will show the effect on CHD incidence of lowering triglycerides. Triglycerides as a risk factor - clinical view Professor Peter Schwandt
of the University of Munich, Germany, pointed out that high plasma triglycerides
not only double the CHD risk, but are a component of four other serious
lipid disorders:
How should these disorders be treated? Prof. Schwandt suggested that the first clinical objective should be to lower serum triglycerides to under 200 mg/dL, except for diabetics, where the target should be to get below 150 mg/dL. Weight reduction lowers LDL cholesterol, but, unfortunately, less so in diabetics than in controls. Advice to patients would include a better life-style, diet and exercise, reduced alcohol intake, and stopping smoking. Fish oil treatment may be included, particularly since it poses no risk to diabetic patients. Drug treatment, however, should be reserved for severe cases. Cardiovascular disease incidence. Diet and lipids It is generally believed that a good diet, which may include fish oil, can reduce the risk of coronary heart disease, said Dr Riemersma, University of Edinburgh. However, it is often difficult to persuade the public to take dietary advice. Nevertheless, the effort is well worth while. The Dart Trial found that the advice to CHD patients to eat more fatty fish reduced the death rate over two years. This and the results of another dietary intervention study, the Lyons Heart Trial, are better than those obtained by drugs; simvastatin reduced serum cholesterol by 25% and CHD mortality by 32%. However, the evidence of the dietary intervention trials failed to make the same impact in the clinical treatment of patients as the drug trial, perhaps because diet trials are seen to be deficient in certain important aspects, including design and size. Can the Scots be persuaded to change their diet ? Riemersma's research in Edinburg showed that all CHD patients showed a willingness to eat more fruit and wholemeal bread, and to cut down on potato chips. A group giving intensive dietary counselling (up to four hours per patient), including provision of recipes and free margarine, also changed the fatty acid composition of their diet, which was documented by objective tests. However, they baulked at eating more vegetables or drinking less fatty milk. Thus a total dietary change may perhaps be unrealistic. But it should be possible to conduct a large secondary prevention study, using a specially formulated margarine/oil or fatty acid supplements, and that would meet some of the criticisms of earlier trials. Effect of Omega-3 LCPUFA on triglycerides in postprandial states Triglyceride levels rise after meals, and the Physicians' Health Study showed that the amount of this rise was proportional to the amount of atherosclerosis present, and its progression. Dr Helen Roche, Trinity College, Dublin, Ireland, pointed out that the postprandial surge is worse in men than in nonmenopausal women, increases with age, and in women becomes rapidly worse after the menopause. If the surge is plotted on a graph, the area under the curve is a direct predictor of coronary artery disease (CAD). Since it takes 4-6 hours to digest fats, and most people eat three or more meals a day, this means that lipids may be in an almost constant postprandial state. However, the triglyceride surge could be reduced by even quite modest amounts of fish oil, Dr Roche noted. The beneficial effect is dose-related; as the intake of the long-chain polyunsaturated fatty acids (LCPUFA) goes up, the level of postprandial triglyceridaemia goes down. She and Gibney gave 0.54 g eicosapentaenoic acid (EPA) and 0.36 g docosahexaenoic acid (DHA) daily, or placebo, for 16 weeks to two groups, matched for several parameters including fasting triglycer-ide levels. The result was a 20% reduction in fasting triglyceridaemia and a total 30% reduction in the area under the curve. Studies by other workers used different doses and duration of treatment, but all show comparable reductions in fasting triglyceride levels. Even at low doses there can be a reduction of 20-30%. Effects of EPA and DHA on plasma triglycerides Most studies of the effects of LCPUFA have been done using fish oil, where DHA and EPA are of necessity given together; Dr Peter Weber, F.Hoffmann-La Roche, took the discussion a stage further by considering EPA versus DHA. Controlled clinical trials comparing purified EPA with purified DHA have shown that both PUFAs were consistently effective, both during fasting and postprandially. Three studies using purified EPA, 2.7-4.0 g/day, lowered triglycerides by 16 to 33%. DHA, 1.25-6 g/day, gives comparable results, lowering triglycerides by 17 to 26%. The various studies show that there is also a beneficial effect on lipid fractions. DHA may increase high-density lipoprotein (HDL), and EPA is associated with a slight lowering of low-density lipoprotein (LDL). Metabolism of lipoproteins and effects of LCPUFA Professor William Harris, University of Missouri Medical Centre, Kansas City, USA, reviewed the effects of fish oil on human serum lipids and lipoproteins, as shown in well-designed, placebo-controlled, crossover or parallel studies. A recent and under-reported Indian study directly compared fish oil and mustard oil containing alpha-linolenic acid (ALA) against placebo. The two groups received roughly the same amounts of LCPUFA, but much higher volume was needed for mustard oil. However, it was nearly as good as fish oil in reducing angina and arrhythmias, heart failure, and total coronary events. "This is the best study we've got to show that fish oils really do reduce coronary disease," Prof. Harris commented. Summary : Safety aspects and recommendations Professor William Connor, Oregon Health Sciences University, Portland, USA, closed the session with a review of safety aspects. He reminded the audience that many indigenous peoples, including the Chinese living on the banks of the Yangtse River, as well as the Eskimos and Indians living in northwestern coastal areas, have consumed large amounts of fish oil for thousands of years, in quantities as high as 50 g/day. That they have survived and flourished is testimony to the safety of the much smaller doses now given to patients. Nevertheless, there are theoretical risks, none of which have been confirmed despite numerous clinical trials involving thousands of patients. These are born out of some concerns. Eskimos have a high incidence of stroke, but patients in clinical trials do not show any excess incidence. Studies have failed to confirm fears regarding increased peroxide formation, possible worsening of glycaemic control in diabetics, or carcinogenesis: the LCPUFA in fact may slow the development of many cancers. During the decades when cod
liver oil was given to children to prevent rickets, no harm was ever shown.
The tea-spoonful dose contains about 1.25 g of LCPUFA, "almost a therapeutic
level", and fish oil capsules also have vitamin E, which prevents increased
oxidation. Large doses of fish oil reduce the platelet count but not the
total platelet volume, and there is no increased bleeding when patients
given fish oil supplements undergo vascular surgery.
It is therefore logical and
practical to recommend fish oil and its constituent LCPUFAs, EPA and DHA,
said Prof. Connor. It is especially logical to use purified preparations,
which contain 50% or more EPA and DHA, and therefore bring the required
dose down from 6 g/day or more to 1-2 g/day.
GROWTH & DEVELOPMENT
Preterm Feeds Are Deficient in PUFAs Premature and full-term babies have different nutritional needs. The feeds designed for them take these differences into account - with one important exception: although the content of proteins, energy and minerals in the formulas for preterm babies mimics that of the placental blood that otherwise would have nourished them, that of essential polyunsaturated fatty acids (PUFAs) does not. In particular, unlike preterm baby feeds - or even full-term breast milk - placental blood is rich in arachidonic acid (AA) and docosahexaenoic acid (DHA). Since both AA and DHA are essential for proper growth, and for the healthy structure and function of all cell membranes - and in the preterm baby's brain they comprise 10-25% of the fatty acids in the membrane polar phosphoglycerides - a nutritional deficiency of these two PUFAs could have serious consequences. The complications of prematurity include bronchopulmonary dysplasia, intraventricular haemorrhage, retinopathy of prematurity and necrotising enterocolitis. All these conditions could result from the same cause: peroxidative membrane damage. Premature babies are particularly vulnerable to peroxidative injury for several reasons: first, they are exposed to oxygen levels higher than those to which a foetus would be exposed; second, they have low activities of the protective superoxide dismutase enzymes; third, they have low levels of AA and DHA in both brain and endothelium and this makes the membranes especially prone to leakage. The leaky membranes release AA which, because of the deficit in anti-oxidant activity, is peroxidised, setting a vicious cycle of inflammation, ischaemia and cell death. In addition, it has been suggested that the ischaemia would allow the accumulation of nitric oxide and, once blood flow is restored and oxygen levels return to normal, the production of its highly toxic peroxidation product, peroxynitrite. The combination of inadequate anti-oxidant activity and low levels of omega-3 PUFAs causes brain haemorrhages in animal models and these are similar to those seen in preterm babies. Other experiments have shown that the peroxidation products of AA can potentiate platelet aggregation in the presence of only tiny amounts of the free acid. In a recent paper, M.A. Crawford* and colleagues, from the Institute of Brain Chemistry and Human Nutrition, London, UK, suggest that these same mechanisms could be responsible for many of the complications of prematurity. The low AA and DHA content of preterm feeds, by failing to remedy the premature baby's deficiency in these PUFAs, is likely to increase rather than diminish the risks of these complications, they report. * M.A. Crawford et al.
The inadequacy of the essential fatty acid content of present preterm feeds.
Eur J Pediatr (1998); Vol 157 (Suppl1): S23-S27. (492)
Letters to the Editor Conversion of ALA to EPA and DHA In reference to correspondence in the last issue in regard to lipid
composition in infant formula, may I add a comment? A diet including 2
- 3 portions of fatty fish per week, which corresponds to the intake of
1.25 g EPA (20:5n-3) + DHA (22:6n-3) per day, has been officially recommended
on the basis of epidemiological findings showing a beneficial role
of these omega-3 long-chain PUFA in the prevention of cardiovascular and
inflammatory diseases. The parent fatty acid ALA (18:3n-3), found in vegetable
oils such as flaxseed or rapeseed oil, is used by the human organism partly
as a source of energy, partly as a precursor of the metabolites, but the
degree of conversion appears to be unreliable and restricted. More specifically,
most studies in humans have shown that whereas a certain, though limited,
conversion of high doses of ALA to EPA occurs, conversion to DHA is severely
restricted. The use of ALA labelled with radioisotopes suggested that with
a background diet high in saturated fat conversion to long-chain metabolites
is 6% for EPA and 3.8% for DHA. With a diet rich in omega-6 PUFA, conversion
is reduced by 40 to 50%. It is thus reasonable to observe an omega-6/omega-3
PUFA ratio not exceeding 4-6.
Helga Gerster,MA
References: 1. H.Gerster.
Conversion of ALA to EPA and DHA. Internat J Vit Nutr Res 68 (1998) 159-173.
Membrane Lipid Levels As Formula Touchstone What is the optimal content of arachidonic (AA) and docosahexaenoic (DHA) acids in formulas for premature babies? The brain of the human foetus in the last trimester of pregnancy needs large amounts of long-chain polyunsat-urated essential fatty acids (LCPUFAs): per week it accumulates over 40 mg of omega-6 fatty acids, predominantly AA, and over 20 mg of omega-3 fatty acids, mainly DHA. What has not been clear, however, is the optimal level of these LCPUFAs needed in formulas designed for premature babies. A recent study has now provided data in this regard. The 91 premature babies who completed the study were fed for their first six weeks on either their mothers' breast milk or one of four formula feeds. The nutrient composition of the formulas was similar but they contained increasing levels of AA (0-1.1%) and DHA (0-0.76%). The ratio of AA to DHA was constant throughout and based on that of human milk. Although all the formula-fed babies grew faster than the breast-fed ones, no differences in growth rate were seen between the four formula-fed groups. However, there were differences in the membrane phospholipid content of their red blood cells. In the babies fed formula without the added LCPUFAs, as compared to those who were breast-fed or fed supplemented formulas, levels of AA and DHA were lower in the phosphatidylcholine and phosphatidylethanolamine fractions, respectively. There was also a clear dose-response, with the babies receiving the formula with highest levels of AA and DHA also showing the highest levels in their red blood cell membrane phospholipids. These were significantly higher than those of the breast-fed babies. The authors of this report, M.T. Clandinin* and colleagues, from the University of Alberta, Edmonton, Canada, and Wyeth Nutritionals International, Philadelphia, USA, conclude that the group of formula-fed babies whose red blood cell membrane fatty acid composition most closely resembled that of a similar group of babies fed breast milk were receiving "sufficient and perhaps optimum levels" of AA and DHA. The formulas contained about 0.6% and 0.4%, respectively, of these LCPUFAs. *M.T. Clandinin et al. Assessment of the efficacious dose of arachidonic and docosahexaenoic acids in preterm infant formulas: fatty acid composition of erythrocyte membrane lipids. Pediatric Research (1997); Vol 42: 819-825.1 Dietary Fish Oil Increases PUFA in Breast Milk It is now generally recognized that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) play a key role in infant nutrition. With this recognition comes renewed interest in whether a breast-feeding woman's diet can influence the proportion of these PUFAs in her milk. The results of recent investig-ations suggest that it can, both in the short- and the long- term. In one recent study, 14 healthy breast-feeding women consumed six different test fats on six different occasions over 10 weeks with a two-week washout between each test. The fats selected and the fatty acids studied were: menhaden oil ( for EPA and DHA); herring oil (for cetoleic acid); safflower oil (linoleic acid); canola oil (linolenic acid); coconut oil (lauric acid); cocoa butter (palmitic and stearic acids). The women were asked to avoid fats containing the particular fatty acid under study for one week before and after they had consumed it. They were also asked not to change their energy intake and physical activity levels so as not to gain or lose weight and thus to keep constant the contribution of fatty acids synthesized by liver and breast tissue or mobilised from endogenous stores. They collected samples of their breast milk at varying intervals after each test fat meal and the milk samples were then analysed for their fatty acid content. The results showed that the levels of most of the fatty acids studied had increased by six hours after the test meal, peaked between 10 and 24 hours and remained significantly raised for 1-3 days. After consuming 20 g menhaden oil, for example, the level of EPA increased from 0.1% to a peak of 0.8% at 24 hour and remained significantly raised at 0.2% until three days after the test meal (P < 0.05). DHA increased significantly from 0.2% to 1.0% at 14 hours, 1.1% at 24 hours and 0.5% at two days (P < 0.05). After ingestion of 7 g herring oil, cetoleic acid increased from 0% to 0.4% at 14 and 24 hours (P < 0.05), and EPA from 0.06% to 0.12% at 14 hours (P < 0.05). DHA increased signif-icantly over time but not at any of the time points studied. Ingestion of 40 g safflower oil signific-antly increased linoleic acid and signific-ant increases in linolenic acid were observed after the canola oil meal, and in lauric acid and capric acid after the coconut oil meal. A significant increase in stearic acid but not in palmitic acid was seen after the meal of cocoa butter. The investigators, C.A. Francois* and associates from Oregon Health Sciences University, Portland, USA, observe that earlier studies, both theirs and others, have shown dose-dependent increases in EPA and DHA in breast milk in women taking fish-oil supplements for 1-4 weeks. The current study shows that even a single meal of a particular fat may significantly affect breast milk fatty acid composition for 1-3 days, with a maximum increase probably in the first 24 hours. The investigators point out, however, that regularity of intake is also important. If a lactating woman consumes fish regularly, her milk will contain greater amounts of the long-chain polyunsaturated fatty acids EPA and DHA for a longer period of time than will the milk of a woman who consumes fish only occasionally. Thus, for the long-term health of her baby, a woman needs to maintain a high dietary intake of PUFAs for as long as she continues to breast-feed. *C.A. Francois et al. Acute effects
of dietary fatty acids on the fatty acids of human milk. Am J Clin Nutr
(1998); Vol 67: 301-8. 1
CARDIOVASCULAR DISEASE
Cardiac Benefits of Fish Oil and Mustard Oil Numerous epidemiological studies now show that eating a diet rich in fish, fruit and vegetables reduces mortality from coronary artery disease. However, the impact among patients with suspected acute myocardial infarction is less well understood, although a growing body of experimental studies suggests that the LCPUFA may be beneficial. These studies show that unlike saturated fatty acids, LCPUFA can red-uce the risk of thrombosis and arrhythmia, and particularly ischaemia-induced ventricular fibrillation. Moreover, experimental studies suggest that fish oil supplements atten-uate myocardial dysfunction and tissue damage following ischaemia and reperfusion. Fish oil may also reduce the size of an acute myocardial infarction. This suggests that fish oil may protect against restenosis and remodelling as well as lowering total mortality and reducing the cardiac event rate after acute myocardial infarction (AMI). Nevertheless, this has yet to be confirmed clinically. A recent randomized placebo-controlled trial* compared a year's treatment in 122 patients with EPA 1.08 g daily with 120 patients who received mustard oil (alpha-linolenic acid, 2.9 g per day) and 118 patients who received placebo. Treatment started within 18 hours of the suspected AMI. After a year, patients who received fish oil and mustard oil compared experienced fewer cardiac events than the placebo group. A total of 24.5 per cent in the fish oil group experienced a cardiac event, compared to 28 per cent of those receiving mustard oil and 34.7 per cent in the placebo arm. Moreover, patients taking fish oil were less likely to suffer a nonfatal myocardial infarction. Thirteen per cent of the fish oil group experienced a nonfatal myocardial infarction compared to 15.0 per cent in the mustard oil group and 25.4 per cent among those receiving placebo. Nevertheless, mustard oil did not influence the likelihood of cardiac death. On the other hand, only 11 per cent of people taking fish oil died compared to 22 per cent in the placebo arm. Moreover, patients taking fish oil and mustard oil also suffered fewer cardiac arrhythmias, left ventricular enlargement and angina pectoris compared to those receiving placebo. While blood lipoproteins fell only modestly in the fish and mustard oil group, levels of diene conjugates, a measure of free radical status, significantly fell in both arms. The authors speculate that this may indic-ate a reduction in oxidative stress They conclude that this study suggests that both fish oil and mustard oil rapidly protect against reperfusion injury in patients suffering an acute myocardial infarction. On the other hand, a large study is necessary to confirm this. *Singh RB, Niaz MA, Sharma JP et
al Randomised, double-blind, placebo-controlled trial of fish oil and mustard
oil in patients with suspected acute myocardial infarction: the Indian
experiment of infarct survival - 4 Cardiovasc Drug Ther 1997;11:458-91
INFLAMMATION
Essential Fatty Acids and Diet in Crohn's Disease There is experimental evidence to suggest that omega-3 fatty acid supplements could maintain remission among people with Crohn's disease. Firstly, for example, the LCPUFA reduce production of certain inflammatory leukotrienes and cytokines that seem to be pathogenic in Crohn's disease. Secondly, in rat models of colitis, EPA seems to be protective. Finally, patients with ulcerative colitis, which may share some inflammatory pathways with Crohn's disease, seem to benefit from taking omega-3 supplements. However, in a long-term prospective controlled multi-centre German study*, omega-3 fatty acids failed to prolong such remission. The study enrolled 204 patients who suffered an acute relapse of Crohn's disease, which resolved following up to three months' treatment with steroids. Of these, 70 patients took omega-3 fatty acid supplements three times a day (5 g daily of fish oil containing 55 per cent EPA and 30 per cent DHA), while 65 patients took corn oil placebos. Another 69 patients ate an unmatched low carbohydrate diet (84 g daily). Epidemiological studies link carbo-hydrate-rich diets with an increased risk of relapse among Crohn 's disease sufferers. On the other hand, intervent-ional studies, which aim to reduce consumption of refined carbohydrates, have produced mixed results. All patients received low-dose prednisol-one (8 mg) for the first seven weeks, with the dose tapered over the eighth week. The authors assessed compli-ance over the year-long study using serum triglyceride levels, which fall during omega-3 treatment, and diary records of carbohydrate consumption. Not surprisingly, many patients found sticking to the rigorous low carbo-hydrate diet difficult. Overall, five patients failed to comply with supplementation, ten with placebo and 18 with dietary modification. Indeed, only 11 patients claimed that they complied with the low carbohydrate diet for the year. Even among these the study monitor doubted the validity of three claims, reservations that were supported by the diaries. Overall, patients consumed a median of 108 g of carbohydrate daily. Nevertheless, patients showed a 53 per cent reduction in relapse risk while they complied with the diet. However, an intention-to-treat analysis did not show any difference in relapse rates over the year between the dietary group and those taking corn oil placebo - 43 per cent and 30 per cent respectively. Thirty per cent of patients in both the placebo and omega-3 groups relapsed during the year, according to the intent-ion-to-treat analysis. Even among patients who complied, 29 per cent in the omega-3 arm relapsed compared to 28 per cent in the placebo group. In contrast to the diet group, compliance with omega-3 fatty acids seemed good, with serum triglyceride levels relatively and consistently lower. While a subgroup analysis suggested that people with large bowel involvement only may benefit to a greater extent than those with inflammation localized elsewhere along the gastrointestinal tract, the study was inadequately powered to determine whether this regional effect reached statistical signif-icance. The authors conclude that it is not clear whether patients stopped comply-ing with the low carbohydrate diet because they sensed a recurrence, although the inflammation scores did not seem to increase before patients stopped following the diet. Alternately, the inflammation could have worsened when the low carbohydrate diet was stopped. Clearly, further studies are needed to finally clarify the role of carbo-hydrates in the pathology and treatment of Crohn's disease. On the other hand, despite experiment-al evidence that some LCPUFAs may be beneficial in inflammatory bowel diseases, in this study remission was not maintained among patients with Crohn's disease. *Lorenz-Meyer H, Bauer P, Nicolay
C et al. Omega-3 fatty acids and low carbohydrate diet for maintenance
of remission in Crohn's disease. A randomised controlled multicenter trial.
Scand J Gastroenterol 1996;31:778-85
EVOLUTION & DEVELOPMENT
Fishbones in the Rift Valley Paleodiet Did the brain of Homo sapiens evolve because our ancestors ate a diet rich in LCPUFA? Or did our ancestors evolve first of all in a way that allowed them to develop tools and fish more effectively? In a recent review, C. Leigh Broadhurst and colleagues* have assessed data to support the hypothesis that long-chain PUFA were essential for human intellectual evolution. They also warn as a corollary that modern diets may impair our future development. The first identifiable human ancest-ors emerged approximately four million years ago, when the number of land mammals almost tripled. However, the marked and characteristic enlargement of the human cerebral cortex only took place over the last one to two million years. Over this time, the genus Australopithecus died out, while Homo species expanded. Moreover, tool manufacture became more sophisticated, organized hunting became more widespread and culture and speech developed over what would be in evolutionary terms a relatively short period of time. The research group suggests that these important steps in our development may reflect a 'unique' nutritional base in the Rift Valley in East Africa, which contain numerous freshwater lakes, stocked with fish and shellfish rich in long-chain PUFA. Indeed, the ratios are closer to the lipid compos-ition of human brain than any other food source. Early hominids began eating high-quality foods by scavenging meat and fish around two million years ago. This could have allowed increased and sustained cerebral cortical growth without increasing body mass. However, early hominids scav-enged fish opportunistically. For example, a statistical analysis of bone scatter suggests that large numbers of fish were stranded in pools of water, where they could be caught easily by H habilis, A boisei and H erectus as well as carnivores. Nevertheless, opportunistic con-sumption increased intelligence, which allowed our ancestors to fish more often and more successfully. This, in turn, increased omega-3 consumption, which further boost-ed intelligence and led to early man favouring PUFA-rich fish. Even today, traditional fishers value fat rich fish, such as catfish. Then, between 100,000 and 200,000 years ago, H sapiens evolv-ed in East African areas rich in trop-ical freshwater fish and shellfish. It seems that the new human species migrated out of Africa into the rest of the world, rather than evolve independently. Some older species - H erectus and H neanderthalenis - left Africa, which required the intelligence to adapt to diverse environments. However, H sapiens was better prepared for new and possibly hostile environments than his predecessors. For example, H neanderthalenis - which first evolved some 300 thousand years ago - never developed the same range of tools as H sapiens, which included harpoon-type spears, fish hooks and stone tools. While consumption of the PUFA-rich diet in the Rift Valley seems a prerequisite for this migration, genetic environmental and climatic changes also played a role. The paper also offers lessons for today's nutritionists. For example, a relatively modest intake of fish and shellfish, accounting for between 6 and 12 per cent of total dietary energy, provides more arachidonic acid (AA) and DHA than most modern diets. The authors conclude that brain-specific nutrition may still affect our future evolution. They point to the growing body of evidence showing that a lack of AA and DHA in utero can impair a modern child's intelligence and visual acuity as well as contributing to depression and attention deficit disorder. The authors suggest that our present agricultural, processed-food diet may not be able to provide indefinitely for continued intellectual development. *Broadhurst CL, Cunnane SC and Crawford MA Rift Valley lake fish and shell fish provided brain-specific nutrition for early Homo Br J Nut 1998;79:3-21 |
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