Nutrition Discussion Forum

DOI: 10.1079/BJN2002730 Nutrition Discussion Forum Approaches to health via lowering of postprandial glycaemia A recent issue of the British Journal of Nutrition reflects a marked change in the importance we now attach to the role of dietary carbohydrates in both managing and retarding the development of non-communicable diseases, with four commentaries: Choosing your carbohydrates to prevent diabetes (Mathers, 2002); Low carbohydrate does not mean low glycaemic index! (Wolever, 2002); Diet, satiety and obesity treatment (Tremblay et al. 2002); Handbook of dietary fibre (Cummings, 2002). Among these there are important messages on public health and expressions of hope for the future. However, the commentaries on starchy staples and glycaemic index (GI) have implications beyond diabetes and may be more easily understood in a broader context that aims for low postprandial glycaemia, eventually by more than one approach based on diet together with weight restriction and/or reduction. Certainly one can welcome a possible role for low-GIstarch foods in the prevention of type 2 diabetes mellitus (DM), as suggested by Mathers (2002). The weight of published evidence to date, nevertheless, is in diabetic subjects (not pre-diabetic or glucose-intolerant subjects), is based largely on intervention trials with diets characterised analytically as low-GI-carbohydrate (not necessarily lowerGI-starch as sometimes intended) and measurement of biochemical risk factors (not clinical outcomes, either microvascular or macrovascular). Advice to consume low-GI-starch foods can also elevate intake of sugars (G Livesey, unpublished results), many of which have GI values less than common starch-rich staple foods. Interestingly, there is anecdotal evidence in favour of using low-GI-starch foods in diabetic subjects in a non-western setting, where the likelihood of a spontaneous intake of more sugars would seem less: physicians of ancient India treated DM with barley and Bengal gram (Kapur & Kapur, 2001), which we now know to be amongst the lowest-GI-starch foods available. Efficacy of such treatment on clinical outcome was unreported and now possibly unknown without further study. There is a scarcity of published dietary intervention studies with low-GI foods that examine prevention of clinical disease in subjects at risk, such as those who are glucose intolerant. However, there appears to be improved pancreatic b-cell function with low-GI-carbohydrate diets among some subjects who are glucose intolerant (Wolever & Mehling, 2002). Moreover, in the STOP-NIDDM randomised trial the glycaemic response to diet was reduced by slowing digestion with an a-glucosidase inhibitor (acarbose), and there were both significantly fewer conversions of glucose-intolerant to type 2 DM patients and more reversions to normal (Chiasson et al. 2002). Mathers’ (2002) comments are presumably a call to further arm us with similar knowledge as may be got from more research on diets. Hence, however good the outlook, we do not know yet the level of disease reduction that will come from intervention with low-GI diets (let alone low-GIstarch foods). Nevertheless, the future burden of disease from diabetes (obesity, stroke and heart disease too, which may be greater problems) is expected to overburden government (and private) health budgets. Waiting for conclusive proof on the magnitude of efficacy of low-GI-carbohydrate foods on clinical end points may therefore be unwise, given the suggested absence of risk from reduced postprandial glycaemia (American Diabetes Association, 2001), a positive outlook (c.f. Canadian Diabetes Association, 2000; Buykens et al. 2000, 2001) and prospective evidence from epidemiological studies that low-GI diets (again not uniquely low-GI-starch diets, though inclusive of wholegrain cereals) appear to lower the advent of type 2 DM, CHD and possibly stroke (all disease outcomes rather than biochemical markers of disease) (Salmerón et al. 1997a,b; Liu et al. 2000a,b, 2002). Further, we have to consider whether reduced glycaemia might benefit a majority of the population (Khaw et al. 2001) and not just those believed to be at greatest risk. The last paper (Khaw et al. 2001) indicates glycosylated haemoglobin (HbA1c) is an important prospective marker of macrovascular disease. This, in addition to microvascular diseases seen in diabetics, and the need to control glycaemia more broadly than for diabetes prevention, supports earlier epidemiological work on glycaemic index (or glycaemic load) and CHD. Interpretation of the epidemiological evidence is difficult. It is unclear whether the advent of type 2 DM and CHD is linked to the GI of the carbohydrate ingested or to glycaemic load (i.e. GI £ carbohydrate intake). The latter seems to hold the stronger association with both advent of diseases (Salmerón et al. 1997a,b; Liu et al. 2000a) and C-reactive protein, a marker for CHD risk (Liu et al. 2002). Yet, this might not have been expected: as with low-carbohydrate intake, low glycaemic load could imply higher fat intake, causing damage that obscures the true strength of benefit from low glycaemia. Such obscuring might explain why sometimes (e.g. Meyer et al. 2000) the association between disease and glycaemia does not always manifest itself strongly. Wolever (2002) rightly points out that low GI (as applied to carbohydrate) does not mean the same as low carbohydrate. GI describes carbohydrate quality not quantity, and so low GI cannot imply low-fat intake. Indeed, low GI can imply any level of fat intake, which makes it important to specify that healthy diets are those that are of high intake of low-GI carbohydrates. However, overfocusing on GI limits our scope of vision. We may: (1) Downloaded from https://www.cambridge.org/core. IP address: 54.163.42.124, on 07 Jun 2020 at 20:43:09, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1079/BJN2002730 British Journal of Nutrition (2002), 88, 741–744 q The Author 2002 G. Livesey fail to recognise the importance of low postprandial glycaemia as a real health benefit that can outweigh other health risks; (2) become overcautious in using all forms of carbohydrate (even damaging high-GI starch) to ensure fat as a health risk is displaced from the diet (here meaning total fat because displacement is on an energy basis without discrimination over the type of fat) (c.f. American Diabetes Association, 2002); (3) fail to consider or follow up other dietary approaches to lowering postprandial glycaemia. Thus, Tremblay et al. (2002) rightly point out that postprandial glycaemia can be reduced by methods other than replacing one carbohydrate source with another of lower GI value; their example study was exchange of protein and carbohydrate (Dumesnil et al. 2001). Several possibilities for lowering postprandial glycaemia exist: should absence of benefit be encountered, it might be traced to co-modification of other obscuring risk factors, outlined as follows. Some carbohydrate foods that elicit a high glycaemic response (high GI) in peripheral blood may be replaced by carbohydrate foods that elicit a lower response (low GI). Applied to starch-rich staple foods, this advice also increases the intake of unavailable carbohydrates (dietary fibre), which might also benefit health. Since the total benefit of low-GI carbohydrate is conditional on maintaining a presence of carbohydrate to displace fat from the diet, it makes no sense for low-GI-food recipes to be rich in fat. To make life more interesting and easier, advice to consume more low-GI-carbohydrate foods brings exposure to a wider variety of nutritious foods (Wolever, 1997) and can reduce conflict in families that include a diabetic patient (Gilbertson et al. 2001). For a useful trail of analytical reviews, as opposed to commentaries, see Miller (1994), Wolever (1997), Frost & Dornhorst (2000) and Jenkins et al. (2002). There seems to be little risk from such advice. Some food-ingredient carbohydrates might be partly replaced by alternatives such as lower-energy, low-glycaemic sugars, polyols and non-digestible polysaccharides. These tend to be used as carbohydrate replacers when low-GI starches are not suitable; again, risk to health is unknown and gastrointestinal disturbances are minimal when consumed in realistic amounts. This particularly applies to sugar-free sweets when sweets are desired, and to snack foods and fruit preserves when lower energy, lower glycaemia and lower insulinaemia are desirable. It might be thought that the lower-energy-value foods, due to unavailability of the carbohydrate present, would be compensated by other energy sources at later meals. It is notable, therefore, that intervention studies in free-living subjects indicate unavailable carbohydrate is substantially more effective at reducing body weight, on a weight-forweight basis, than replacing dietary fat with carbohydrate (G Livesey, unpublished results), such benefit being limited by the quantity that can be readily consumed. Both energy restriction and body weight reduction improve prospects of health (Christiansen et al. 2000). Viscous polysaccharides might be used to slow absorption and reduce postprandial glycaemia; again, there is little health risk when foods are adequately formulated. Some high-GI carbohydrate might be replaced by protein (e.g. Tremblay et al. 2002), particularly vegetables or fish, but not meat. In addition to improved atherogenic risk factors after 1 week of treatment, the replacement of starch in bread with protein for 3 months showed improved carbohydrate tolerance and decreased HbA1c in type 2 DM patients (Stilling et al. 1999). Improvement in insulin sensitivity has also been seen in diabetic patients with kidney disease (Gin et al. 2000), though not consistently so (Stefikova et al. 1997). Reduced food intake (energy, glycaemic load and saturated fat) (Dumesnil et al. 2001) may partly explain the improved biochemistry even prior to body-weight reduction (or visa versa or both with possible spiralling improvement). Certain comments may be warranted in regard to high-protein diets: (1) while higher protein intake would be contraindicated by nephropathy, on a population or other group basis, the potential for use in prevention of type 2 DM and prevention and intensive management of CHD and possibly obesity is substantial, and so the approach merits exploration to establish longerterm efficacy and limit the risks, both for high-risk groups and in population samples; (2) the results at present might seem to support the hypothesis of McCarthy (2000) that protein –carbohydrate interactions promote insulin secretion and obesity, although raising the concentration of one putative interactant while lowing the concentration of the other provides no information about the existence or possible importance of the interaction; (3) replacement of high-GI carbohydrate with protein does not automatically mean a McDougall type or similar ketotic diet where carbohydrate is highly restricted. An intake requirement for carbohydrate (which could be low-GI carbohydrate) for the purpose of optimal health nevertheless may be helpful, though setting the value is problematic; (4) knowledge about high-protein diets is limited, and so protein should not for the present replace low-GI carbohydrate as the preferred means to displace high-GI carbohydrates. Eventually, protein might be seen as an energy source to help replace some saturated fat; (5) risks of higher protein (20 – 40 % energy) possibly include adequacy of Ca retention, kidney stone formation due to lower citrate excretion from carbohydrate (Reddy et al. 2002) and possibly higher advent of type 1 DM. Some high-GI carbohydrates could be replaced by monounsaturated fats (Garg, 1998; Luscombe et al. 1999; American Diabetes Association, 2002). However, this might be objectionable when low-GI carbohydrates can be used instead, because the higher energy density might elevate energy intake and body weight (for which there is little evidence for monounsaturated fats) and reduced pancreatic b-cell function among glucose-intolerant (and potentially type 2 diabetic) subjects (Wolever & Mehling, 2002). Monounsaturated fats may have a role to replace saturated fats with advantage as the latter may promote insensitivity to insulin, at high intakes at least (Vessby et al. 2001), and so reduce long-term glycaemic control. Combinations of high-monounsaturated fats (replacing particularly C12, C14 and C16 fats) and low-GI carbohydrate diets (replacing high-GI carbohydrate) for optimal metabolic control and health deserves examination. In some food products, replacement of saturated fats with lowenergy, low-fat alternatives has a place. Downloaded from https://www.cambridge.org/core. IP address: 54.163.42.124, on 07 Jun 2020 at 20:43:09, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1079/BJN2002730 742 It is possible to replace high-GI carbohydrate with saturated fats (but do not do it!), and so reduce glycaemia acutely. This approach would certainly be objectionable for reasons related to body weight, CHD and diabetes control. More specifically, in respect of postprandial glycaemia it would lead to a loss of insulin sensitivity and impairment of b-cell function, so increasing long-term postprandial glycaemia. Restriction of food intake to reduce body weight inevitably increases the chance of lowering carbohydrate intake and so postprandial glycaemia. The risks appear to be minimal other than for possible concern for adequate Ca, Fe, Mg and Zn intakes, and for growth in children. Increased physical activity may also reduce postprandial glycaemia via demand for glucose and improved insulin sensitivity (Ratzmann et al. 1981; Yamanouchi et al. 1995). There is an acute risk of hypoglycaemia in unprepared diabetics. A theoretical improvement in glycaemia might be expected from nibbling. In the free-living situation, this may be obscured by a sedentary social context such as watching television. However, redistribution of food intake throughout the day would neither affect glycaemic index nor glycaemic load from food. Little benefit is seen in type 2 DM on blood glucose concentrations (Arnold et al. 1997), although long-term studies, particularly on HbA1c, are absent. This should not overshadow improvement in the blood lipid profile (Jenkins et al. 1989) and possibly body weight (Kirk, 2000; WesterterpPlantenga et al. 2002). When it is critical to reduce postprandial glycaemia, it can also be achieved partly by inhibitors of carbohydrate digestion, the drug equivalent of simultaneously lowering both carbohydrate GI and availability (Brooks et al. 1998), and by appropriately designed insulin and drug therapy (Kapur & Kapur, 2001; Kelley, 2002). General risks from drug-based approaches (other than inhibitors of digestion) occur when doses exceed need, and include more episodes of hypoglycaemia, body-weight gain and greater cardiovascular risk dependent on the drugs used. The list is not exhaustive and the examples have yet to be fully or adequately researched. Nevertheless, it is clear that reduced postprandial glycaemia can be attempted in a number of different ways, with overall benefit likely to be limited by the associated risks accompanying the method(s) chosen. It does seem that postprandial glycaemic reduction offers greater preventive and therapeutic potential than does reduction of glycaemic index of available carbohydrates alone, but also greater risks when achieved by some approaches. Given the severity of these non-communicable diseases, their prevalence, expected overall rising trend and limited health budgets, we may have to welcome several approaches to dietary therapy with the goal of reduced postprandial glycaemia, allowing each approach and combination of approaches to find appropriate effective niches, from acute treatment to near lifelong exposure. Physical activity, reduced food intake, limitation of the fat content of the diet and raised dietary fibre intake are established preventative and therapeutic strategies in the public domain with broadly adequate (though too limited 743 and inaccurate) food labelling. At present however, the public are not informed about how carbohydrate-containing foods affect postprandial glycaemia, or about ways to limit postprandial glycaemia by choice of foods and food preparation methods. With certain foods (e.g. potatoes, rice; Foster-Powell et al. 2002) this is not easy as there is great variety and preparation methods markedly affect the value. However, these need not be seen as obstacles, rather they are opportunities for improvement of foods and diets. An increasing realisation of the relationship between HbA1c, dietary glycaemic load and non-communicable diseases is truly very remarkable given that just over a decade ago starch in particular (and perhaps available carbohydrate in general) seemed as though it was just a make-weight, health-bland source of energy: good, it seemed, only because it kept fat out of the mouth (Department of Health, 1990). Postprandial glycaemia is now emerging as one of the major risks that the public encounters; meanwhile, consumers are neither empowered via food labelling or local authoritative food tables nor advised to protect themselves. In addressing this problem, we ought not now to lose sight of other possible dietary approaches and we ought to consider a role for lower postprandial glycaemia as contributing to the benefits of both increased physical activity and energy restriction. Geoffrey Livesey Independent Nutrition Logic Pealerswell House Wymondham Norfolk NR18 0QX UK References Arnold L, Mann JI & Ball MJ (1997) Metabolic effects of alterations in meal frequency in type 2 diabetes. Diabetes Care 20, 1651– 1654. American Diabetes Association (2001) Post-prandial blood glucose [a consensus statement]. Diabetes Care 24, 775– 778. 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