Primary open-angle glaucoma (POAG) is a complex chronic neurological disease that can result in blindness. The goal of understanding the aetiology of POAG is to be able to target effective treatment to individuals who will eventually go blind without it. Epidemiological studies of POAG have not specifically addressed the possibility that nutrition may play a role in the development of POAG. A handful of papers have considered that nutrition may have an impact on POAG patients. POAG is not believed to be a ‘vitamin-deficiency disease’. The concept of ‘vitamin-deficiency diseases’ and the recommended daily allowances have not kept pace with the growing understanding of the cellular and molecular functions of vitamins and other micronutrients. The aetiology of POAG remains a mystery. Discoveries in cell physiology can be assimilated from the literature and applied to known homeostatic mechanisms of the eye. In this way the possible roles of nutritional components involved in the aetiology of POAG can be described. The mechanisms may be subject to many influences in ways that have yet to be defined. Two distinct changes in the trabecular meshwork can be identified: trabecular meshwork changes that cause intra-ocular pressure to increase and trabecular meshwork changes that are directly correlated to optic nerve atrophy. Compelling evidence suggests that collagen trabecular meshwork extracellular matrix (ECM) remodelling is correlated to increased intraocular pressure in POAG. Elastin trabecular meshwork ECM remodelling is correlated to POAG optic nerve atrophy. There appear to be two different pathways of ECM remodelling and apoptosis induction in POAG. The pathway for collagen remodelling and apoptosis induction seems to be exogenously influenced by water-soluble antioxidants, for example, glutathione. The pathway for elastin remodelling and apoptosis induction seems to be influenced by endogenous lipid-soluble antioxidants, for example, vitamin E. Roles can be defined for antioxidants in the two different pathways of ECM remodelling and apoptosis induction. This suggests that antioxidants are important in maintaining cellular homeostasis relevant to the aetiology of POAG.

Consumption of fruits and vegetables has been associated with cancer prevention; flavonoids are widely distributed in plant foods and considered to be the active ingredients. Quercetin and kaempferol are two of the most commonly found dietary flavonols, and have been reported to prevent cancer. We have previously reported that the isoflavone genistein and the flavone baicalein exert differential actions on the oestrogen receptor (OR) α in HepG2 cells. Because of the structural resemblance to both isoflavone and flavone, we examined the effects of these dietary flavonols on ORα– and ORβ–specific transactivations and their subsequent involvement in inducing MCF-7 cell death. In the present study, both quercetin and kaempferol were able to compete for OR binding in a cell-free system and were agonistic to ORα and -β expressed in HepG2 cells, while some additive effect was observed in the oestrogen response element (ORE)-driven transcription when 17β-oestradiol was co-administered. Since the bcl-2 promoter contained two ORE, and ORE-driven transcriptional activity and Bcl-2 mRNA expression were increased by treatment with 10 μm-quercetin or kaempferol, it is possible that quercetin and kaempferol might up-regulate Bcl-2 expression through OR transactivation in MCF-7 cells. Cell death ELISA assay performed on MCF-7 cells indicated that an increase of apoptosis occurred at 25 μm-, but not 10 μm-, quercetin or kaempferol. Indirectly the results suggest that OR activation is not sufficient to induce apoptosis and that apoptosis is induced despite an increase in Bcl-2 expression.

Quercetin is an important dietary flavonoid with putative beneficial effects in the prevention of cancer and CVD. The in vivo bioactivity of quercetin depends on its bioavailability, which varies widely between foods. We used an in situ rat intestinal perfusion model to study whether differential small intestinal hydrolysis of the sugar moiety of five naturally occurring quercetin glycosides determines the small intestinal uptake and subsequent biliary excretion of quercetin. After 30 min perfusion, a decrease of intact quercetin glycoside in perfusate was observed for quercetin-3-O-ß-glucoside (20·9 (sem 1·4) μmol/l) and quercetin-4′-O-ß-glucoside (23·5 (sem 1·6) μmol/l), but not of quercetin-3-O-ß-galactoside, quercetin-3-O-ß-rhamnoside and quercetin-3-O-α-arabinopyranoside. Appearance of free quercetin in perfusate and conjugated quercetin metabolites (quercetin, isorhamnetin, and tamarixetin) in portal and peripheral plasma and bile were also significantly greater after treatment with quercetin-3-O-ß-glucoside or quercetin-4′-O-ß-glucoside compared with any of the other glycosides. Thus, the type of sugar moiety is a major determinant of the small intestinal absorption of quercetin glycosides, but the position (3 or 4′) of the glucose moiety does not further influence absorption. The poor bioavailability of important dietary quercetin glycosides has implications for their in vivo bioactivities.

Recent experimental data point to an interaction of dietary flavonol monoglucosides with the intestinal Na-dependent glucose transporter 1 (SGLT1). To investigate this interaction in more detail, we performed experiments with SGLT1-containing brush-border-membrane vesicles (BBMV) from pig jejunum. The flavonol quercetin-3-O-glucoside (Q3G) concentration-dependently inhibited Na-dependent uptake of radioactively labelled d-glucose into BBMV. Uptake of l-leucine was not inhibited by Q3G, indicating a specific interaction of the glucoside with SGLT1. Whereas the maximal transport rate of concentration-dependent initial glucose uptake was not altered in the presence of Q3G, the constant for half-maximal glucose uptake was increased, suggesting a competitive type of inhibition of glucose uptake by Q3G. Trans-stimulation experiments suggested the transport of Q3G via SGLT1. In addition, Q3G decreased the Na-independent diffusive uptake of glucose into BBMV. Other flavonoids were also tested for their inhibitory effect on d-glucose uptake. Among the tested quercetin glycosides, only the 4′-O-glucoside (Q4G) also inhibited Na-dependent glucose uptake into BBMV, whereas the 3-O-galactoside, the 3-O-glucorhamnoside and the aglycone quercetin itself were ineffective. Glucosides of some other flavonoid classes such as naringenin-7-O-glucoside, genistein-7-O-glucoside and cyanidin-3,5-O-diglucoside were ineffective as well. Thus, dietary quercetin monoglucosides, for example, Q3G and Q4G, have an impact on intestinal nutrient transporters such as SGLT1 and related systems.

The objectives of the present study were to evaluate the effects of a methionine-supplemented diet on systolic blood pressure (BP) and vasomotor functions in Sprague–Dawley (SD) and deoxycorticosterone acetate (DOCA)–salt hypertensive rats. SD and DOCA rats were fed a normal or a methionine (8 g/kg)-supplemented diet for 10 weeks. Systolic BP was monitored and plasma homocysteine, methionine and cysteine levels were determined at the end of the experiment. Vasoconstriction and vasodilatation of aortic rings were measured. The methionine-supplemented diet induced a greater increase in homocysteinaemia concentration in DOCA rats than in SD rats and an increase in plasma cysteine concentration in DOCA rats. This diet was associated with an increase in systolic BP in SD rats and with a lesser development of DOCA–salt hypertension. An enhanced aortic constriction and a decreased responsiveness to acetylcholine, bradykinin and sodium nitroprusside in the SD rats fed the methionine-rich diet were consistent with the elevated systolic BP. In DOCA rats the increased responsiveness to bradykinin was in accordance with the systolic BP-lowering effect. In conclusion, the methionine-enriched diet cannot simply be considered as model of hyperhomocysteinaemia, since other metabolites and mechanisms seemed to be implicated in these complex interactions. The differential vasopressive effect of the methionine supplementation in SD and DOCA rats, and in particular the lowering of systolic BP obtained with a greater degree of hyperhomocysteinaemia in DOCA rats, suggest that more complex interactions exist between hyperhomocysteinaemia and BP than the simple positive association described previously.

We measured the coefficients of viscosity, shear rates and shear stresses of chicken small intestinal and caecal contents, including solid particles, using a tube-flow viscometer. The coefficients of viscosity of chicken small intestinal and caecal contents were correlated negatively with their shear rates, a characteristic typical of non-Newtonian fluids. The coefficient of viscosity of the small intestinal contents was lower than that of the caecal contents at a shear rate of 1 s−1. Chicken caecal contents were more viscous than pig caecal contents. The exponential relationship between shear stress and shear rate showed that chicken small intestinal and caecal contents had an apparent Herschel–Bulkley fluid nature. These results indicate that solid particles, including uric acid crystals, are mainly responsible for the viscosity of the digesta in the chicken.

Canned and bottled tea drinks contain not only green tea epicatechins (GTE), namely (−)-epigallocatechin gallate (EGCG), (−)-epicatechin gallate (ECG), (−)-epigallocatechin (EGC) and (−)-epicatechin (EC), but also four GTE epimers, namely (−)-gallocatechin gallate (GCG), (−)-catechin gallate (CG), (−)-gallocatechin (GC) and (−)-catechin (C). In the present study we examined the antioxidant activity and bioavailability of these epimers compared with their corresponding precursors. The epimerisation reaction was induced by autoclaving GTE extract derived from longjing green tea at 120°C for 20 min. Isolation and purification of each GTE and epimer were accomplished by various column chromatographic and semi-preparative HPLC techniques. The antioxidant activity of each epimer with its corresponding GTE precursor was conducted in the three in vitro systems, namely human LDL oxidation, ferric reducing–antioxidant power (FRAP), and anti-2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical assays. The results of all three assays demonstrated that CG had similar antioxidant activity with its precursor ECG, while GC was less potent as an antioxidant than its precursor EGC. Regarding EGCG and GCG, the antioxidant potency was similar for both LDL oxidation and DPPH free radical assays, but GCG was statistically less effective than EGCG in the FRAP assay. For EC and C, the latter had less anti-free radical activity in the DPPH assay, but in LDL oxidation and FRAP assays the antioxidant activity was similar. Oral and intravenous dosing of GTE–epimer mixture led to increase in total plasma antioxidant capacity in rats. In general, both epicatechins and epimers had low bioavailability (0·08–0·31) and most of the observed differences between epicatechins and their corresponding epimers were small, even if they were statistically significant in some cases. It was concluded that the epimerisation reaction occurring in manufacturing canned and bottled tea drinks would not significantly affect antioxidant activity and bioavailability of total tea polyphenols.

The effects of dietary lipids on the abundance of dendritic cells in adipose tissue in anatomically defined relationships to chronically inflamed lymph nodes were investigated in mature male rats fed plain chow or chow plus 20 % sunflower-seed or fish oil. The popliteal lymph nodes were stimulated by local subcutaneous injection of 20 μg lipopolysaccharide to both hindlegs three times/week for 2 weeks. The masses of the major adipose depots and the numbers of dendritic cells emerging from perinodal adipose tissue and samples 5 and 10 mm from the popliteal lymph nodes were measured, and those from omental and mesenteric adipose tissue around and remote from lymphoid tissue, and mesenteric and popliteal lymph nodes. Dendritic cells were most numerous in the perinodal adipose tissue, with the corresponding ‘remote’ samples containing 25–50 % fewer such cells under all conditions studied. Dietary sunflower-seed oil increased the numbers of dendritic cells by about 17 % in all adipose samples and fish oil reduced the numbers in perinodal tissue by about 5 %. The fish-oil diet diminished responses of the intra-abdominal adipose depots to local stimulation of the popliteal node. Correlations in dendritic cell numbers were stronger between perinodal samples from different depots than between remote and perinodal samples from the same depot and after the sunflower-seed-oil diet compared with fish oil. These data show that dietary lipids modulate the number of dendritic cells in lymphoid tissue-containing adipose depots and support the hypothesis that perinodal adipose tissue interacts locally with lymphoid cells.

To determine the effects of EPA, stearidonic acid (STA) or γ-linolenic acid (GLA) on immune outcomes, healthy male subjects consumed one of seven oil blends for 12 weeks. EPA consumption increased the EPA content of peripheral blood mononuclear cells (PBMC). Consumption of GLA (2·0 g/d) in the absence of STA or EPA increased di-homo-GLA content in PBMC. Neither STA nor its derivative 20:4n-3 appeared in PBMC when STA (<1·0 g/d) was consumed. However, STA (1·0 g/d), in combination with GLA (0·9 g/d), increased the proportion of EPA in PBMC. None of the treatments altered neutrophil or monocyte phagocytosis or respiratory burst, production of inflammatory cytokines by monocytes, T lymphocyte proliferation or the delayed-type hypersensitivity response. Production of cytokines by T lymphocytes increased in all groups, with no differences among them. The proportion of lymphocytes that were natural killer cells decreased significantly in subjects receiving 2·0 g EPA or GLA/d. There were no other effects on lymphocyte sub-populations. Plasma IgE concentration decreased in most groups, but not in the control group. Plasma IgG2 concentration increased in the EPA group. Thus, EPA or GLA at a dose of 2·0 g/d have little effect on key functions of neutrophils, monocytes and T lymphocytes, although at this dose these fatty acids decrease the number of natural killer cells. At this dose EPA increases IgG2 concentrations. STA can increase immune cell EPA status, but at 1·0 g/d does not affect human immune function.

The effects of various dietary fibres on gut health have been studied extensively but their combined effects are scarcely documented. In the present study the effects of 2 % (w/w) polydextrose (PDX), 2 % (w/w) disaccharide lactitol, or 2 % (w/w) PDX+2 % (w/w) lactitol on gut microflora, microbial metabolism and gut immune responses were investigated in rats. Both PDX and lactitol alone had an effect on many of the studied parameters, but their combination had stronger than additive effects in some parameters. The PDX+lactitol combination altered the microbial community structure as seen by a culture-independent method, percentage guanine+cytosine (%G+C) profiling, increasing the areas of %G+C 35–39 (P<0·0001) and %G+C 45–49 (P=0·0002), and decreasing %G+C 65–74 (P<0·0003). These changes were also reflected in the microbial metabolism so that the production of biogenic amines and branched volatile fatty acids was significantly reduced, by 12 (P=0·03) and 50 % (P=0·002), respectively, indicating a shift from putrefactive towards saccharolytic metabolism. PDX increased the secretion of IgA in the caecum (P=0·007). Secretion of IgA increased even more, almost ten-fold, with the combination of PDX+lactitol (P<0·0001) when compared with the control group. Lactitol increased the production of butyrate by caecal microbes by two- to three-fold when compared with the PDX or control group (P<0·0001). Butyrate is a preferred energy source for mucosal cells; thus a boost in the availability of energy for immune cells may have still added to the synergistic effects of PDX and lactitol on immune cells. It is noteworthy that improvement in the IgA secretion occurred without signs of mucosal inflammation.

Acetate is normally regarded as an endproduct of anaerobic fermentation, but butyrate-producing bacteria found in the human colon can be net utilisers of acetate. The butyrate formed provides a fuel for epithelial cells of the large intestine and influences colonic health. [1-13C]Acetate was used to investigate the contribution of exogenous acetate to butyrate formation. Faecalibacterium prausnitzii and Roseburia spp. grown in the presence of 60 mm-acetate and 10 mm-glucose derived 85–90 % butyrate-C from external acetate. This was due to rapid interchange between extracellular acetate and intracellular acetyl-CoA, plus net acetate uptake. In contrast, a Coprococcus-related strain that is a net acetate producer derived only 28 % butyrate-C from external acetate. Different carbohydrate-derived energy sources affected butyrate formation by mixed human faecal bacteria growing in continuous or batch cultures. The ranking order of butyrate production rates was amylopectin > oat xylan > shredded wheat > inulin > pectin (continuous cultures), and inulin > amylopectin > oat xylan > shredded wheat > pectin (batch cultures). The contribution of external acetate to butyrate formation in these experiments ranged from 56 (pectin) to 90 % (xylan) in continuous cultures, and from 72 to 91 % in the batch cultures. This is consistent with a major role for bacteria related to F. prausnitzii and Roseburia spp. in butyrate formation from a range of substrates that are fermented in the large intestine. Variations in the dominant metabolic type of butyrate producer between individuals or with variations in diet are not ruled out, however, and could influence butyrate supply in the large intestine.

Probiotics reduce the risk of colon cancer by inhibiting carcinogen-induced DNA damage in animals, but there are no analogous data in human subjects. To enhance knowledge of the effects of probiotics in human subjects, we have investigated the genotoxicity of faecal water after dietary intervention with standard yoghurt or with probiotic yoghurt, which included the strains Lactobacillus acidophilus 145 and Bifidobacterium longum 913. Faeces were collected from nine healthy volunteers after intervention with probiotic yoghurt or standard yoghurt. Faecal water was isolated and incubated with human colon tumour cells HT29clone19A. DNA strand breaks, oxidised DNA bases and damage after challenge with H2O2 were determined by micro-gel-electrophoresis. Faecal water was genotoxic in comparison with NaCl, but protected against H2O2-induced DNA strand breaks. The intervention with probiotic yoghurt significantly lowered faecal water genotoxicity compared with standard yoghurt. However, probiotic intervention also increased oxidative damage; this either reflected prooxidative activity or stimulation of endogenous defence systems. Altogether, the balance of effects favoured protection, since faecal water from the probiotic group reduced overall genetic damage. Thus, there was a reduction of strand break-inducing compounds in human faeces after dietary intervention with probiotic bacteria. This protection reflected results from previous studies in carcinogen-exposed animals where probiotics reduced DNA damage in colon cells.

In the present study we investigated the metabolic conversion of cyanidin glycosides in human subjects using solid-phase extraction, HPLC–diode array detector, MS, GC, and enzymic techniques. Volunteers consumed approximately 20 g chokeberry extract containing 1·3 g cyanidin 3-glycosides (899 mg cyanidin 3-galactoside, 321 mg cyanidin 3-arabinoside, 51 mg cyanidin 3-xyloside and 50 mg cyanidin 3-glucoside). Blood samples were drawn at 0, 0·5, 1, and 2 h post-consumption of the extract. Urine samples were also collected at 0, 4–5, and 22–24 h. We have confirmed that human subjects have the capacity to metabolise cyanidin 3-glycosides, as we observed at least ten individual anthocyanin metabolites in the urine and serum. Average concentrations of anthocyanins and anthocyanin metabolites in the urine reached levels of 17·9 (range 14·9–20·9) μmol/l within 5 h post-consumption and persisted in 24 h urine samples at levels of 12·1 (range 11·1–13·0) nmol/l. In addition, average total levels of anthocyanins and anthocyanin metabolites detected in the serum were observed at 591·7 (range 197·3–986·1) nmol/l within 2 h post-consumption. Cyanidin 3-galactoside accounted for 55·4 % (9·9 (range 7·2–12·6) μmol/l) and 66·0 % (390·6 (range 119·4–661·9) nmol/l) of the detected anthocyanins in the urine and serum samples, respectively. The metabolites were identified as glucuronide conjugates, as well as methylated and oxidised derivatives of cyanidin 3-galactoside and cyanidin glucuronide. Conjugation probably affects the biological activity of anthocyanins and these metabolic products are likely in part responsible for the reported health benefits associated with the consumption of anthocyanins.

The elderly population undergoes a series of physiological and sociological changes common to old age with a high probability of suffering degenerative illness and malnutrition. A dessert rich in phenolic compounds has been designed by using concentrated juices of grape, cherry, blackberry, blackcurrant and raspberry with the aim of it being used as a complementary food in adulthood. In the present study, we investigated the effect of the intake of this dessert (a jar of 200 g daily for a period of 2 weeks), with an antioxidant activity equivalent to ten servings of fruits and vegetables, on several markers of oxidative and antioxidant status in DNA and plasma in a group of elderly individuals. Non-smoking institutionalised elderly subjects were recruited from a pool of volunteers in an old-age home in Murcia (Spain). Twenty-two subjects (six men and sixteen women) participated in the study. The study was designed as a randomised intervention trial with a period of 2 weeks. At days 1 and 15, blood samples were collected to analyse total antioxidant capacity, biochemical parameters, antioxidant vitamins, LDL peroxidation, and DNA damage in peripheral blood lymphocytes. The conclusion of the present study is that a 2-week intervention with our dessert enriched with natural polyphenol compounds in elderly individuals does not give enough time to find changes in the antioxidant and oxidative status. Also, the view that the marked antioxidant ability of polyphenols in vitro does not translate to analogous effects in vivo was confirmed. Moreover, a highly oxidative stress status during ageing was confirmed, together with the need to perform follow-up nutritional studies to improve this situation.

Hydration status and the effects of hypohydration have been the topic of much public and scientific debate in recent years. While many physiological responses to hypohydration have been studied extensively, the subjective responses to hypohydration have largely been ignored. The present investigation was designed to investigate the physiological responses and subjective feelings resulting from 13, 24 and 37 h of fluid restriction (FR) and to compare these with a euhydration (EU) trial of the same duration in fifteen healthy volunteers. The volunteers were nine men and six women of mean age 30 (SD 12) years and body mass 71·5 (SD 13·4) kg. Urine and blood samples were collected and subjective feelings recorded on a 100 mm verbally anchored questionnaire at intervals throughout the investigation. In the EU trial the subjects maintained their normal diet. Body mass decreased by 2·7 (SD 0·6) % at 37 h in the FR trial and did not change significantly in the EU trial. Food intake in the FR trial (n 10) provided an estimated water intake of 487 (SD 335) ml and urinary losses (n 15) amounted to 1·37 (SD 0·39) litres. This is in comparison with an estimated water intake of 3168 (SD 1167) ml and a urinary loss of 2·76 (SD 1·11) litres in the EU trial. Plasma osmolality and angiotensin II concentrations increased from 0–37 h with FR. Plasma volume decreased linearly throughout the FR trial amounting to a 6·2 (SD 5·1) % reduction by 37 h. Thirst increased from 0–13 h of FR then did not increase further (P>0·05). The subjects reported feelings of headache during the FR trial and also that their ability to concentrate and their alertness were reduced.

Hypercholesterolaemia is a common finding in patients with anorexia nervosa (AN). To investigate the type, frequency and pathophysiological mechanisms of changes in lipoprotein metabolism in AN we performed a cross-sectional study in fifty-eight female patients (mean age 24·2 years, BMI 15·3 (SD 1·5) kg/m2) and fifty-eight healthy age-matched controls (CO; BMI 22·2 (SD 1·7) kg/m2). Total cholesterol and LDL-cholesterol were higher in AN (5·5 (SD 1·3) v. 5·0 (SD 0·8) mmol/l, P=0·023; 3·6 (SD 1·1) v. 3·2 (SD 0·7) mmol/l, P=0·025 respectively). LDL particles were significantly more enriched in cholesterol and triacylglycerol in AN. In multiple regression analysis with LDL-cholesterol as the dependent and BMI, total body fat ( %), lathosterol:cholesterol ratio (endogenous cholesterol synthesis), 7α-hydroxy-4-cholesten-3-one (bile acid synthesis), non-esterified glycerol, free triiodothyronine and free thyroxine as independent variables, BMI was the only significant predictor in CO (R2 0·36, overall P=0·001). In AN the variability of LDL-cholesterol was significantly predicted by total body fat, free thyroxine, BMI, free triiodothyronine and non-esterified glycerol (R2 0·55, overall P<0·001). Subgroup analysis between restricting (AN-R) and binge-eating–purging patients (AN-B) indicated that in AN-R changes in lipoproteins, BMI and total body fat were more pronounced. AN-R patients had lower bile acid synthesis than AN-B (P=0·02). We conclude that elevated cholesterol concentrations in AN are generally due to an increase in LDL-cholesterol, which is mostly determined by the severe loss of body fat and the resulting changes in thyroid hormones, increased lipolysis and decreased endogenous cholesterol synthesis with resulting decrease in LDL removal. The clinical subtype of AN plays a major role in the mechanisms leading to hypercholesterolaemia.

Integrating information about the glycaemic index (GI) of foods into the Caribbean diet is limited by the lack of data. Therefore, we determined the GI of eight staple foods eaten in the Caribbean and the effect on GI of crushing selected tubers. Groups of eight to ten healthy volunteers participated in three studies at two sites. GI was determined using a standard method with white bread and adjusted relative to glucose. The mean area under the glucose response curve elicited by white bread was similar for the different groups of subjects. In study 1, the GI of cassava (Manihot esculenta; 94 (SEM 11)) was significantly higher than those of breadfruit (Artocarpus altilis; 60 (SEM 9)), cooking ‘green’ banana (Musa spp.; 65 (SEM 11)) and sadha roti (65 (SEM 9)) (P=0·018). There was no significant difference in the GI of the foods in study 2: dasheen (Colocasia esculenta var. esculenta; 77 (SEM 10)), eddoes (Colocasia esculenta var. antiquorum; 61 (SEM 10)), Irish potato (Solanum tuberosum; 71 (SEM 8)), tannia (Xanthosoma sagittifolium; 60 (SEM 5)) and white yam (Dioscorea alata; 62 (SEM 6)), and, in study 3, crushing did not significantly affect the GI of dasheen, tannia or Irish potato. However, when the results from studies 2 and 3 were pooled, the GI of dasheen (76 (SEM 7)) was significantly greater than that of tannia (55 (SEM 5); P=0·015) with potato being intermediate (69 (SEM 6)). We conclude that dasheen and cassava are high-GI foods, whereas the other tubers studied and sadha roti are intermediate-GI foods. Given the regular usage of cassava and dasheen in Caribbean diets we speculate that these diets would tend to be high GI, although this could be reduced by foods such as sadha roti and white yam. The range of GI between the staples is sufficiently large that health benefits may be accrued by replacing high-GI staples with intermediate-GI staples in the Caribbean diet.