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Breath methane has been measured in 1016 people from four populations resident in Southern Africa which experience widely different risks of bowel cancer and other colonic diseases. Highly significant differences in the proportion of subjects with detectable methane in breath were found; % producers--rural black 84, urban black 72, white 52, Indian 41 (chi 2 121 p less than 0.001 3 df). There was a slight preponderance of female producers over male (female producers 63%, males 57%) and an age trend with fewer producers in the older age groups in the urban blacks and Indians, these comparisons being significant when tested by stepwise logistic regression analysis. Bowel cancer risk, determined from a variety of sources, was lowest in rural blacks, greatest in whites, with intermediate rates for urban blacks and Indians. Methane production in the human colon shows significant interethnic differences but which bear no relation to bowel cancer risk in these populations.

The amount and form of nitrogen lost from the human small intestine and the dietary factors which influence it have been studied in six ileostomists. Over a six day period the subjects were fed a series of diets including low nitrogen (LND) 0.17 g N/day, LND + soya beans (5.87 g N/day) and a high fibre diet (HFD) (10.6 g N/day). The soya beans were fed either whole or pureed to test the effect of physical form of food. Total N, protein, amino acids, urea, and ammonia were measured in ileostomy effluent which was collected throughout the study. Total N excretion was LND 0.91 (0.04) (SE) g/day; LND + whole soya beans (WSB) 2.26 (0.15) g/day; LND + pureed soya beans (PSB) 1.42 (0.12) g/day (WSB v PSB, p less than 0.001); and HFD 2.17 (0.11) g/day (HFD v PSB, p less than 0.001, HFD v WSB, NS). N losses as urea, ammonia, and free amino acids were less than 10-15% of total N, the remainder being protein (48-51%) and (by difference) peptides (20-30%). Eighty to 85% of effluent N was in the insoluble (pellet) fraction except on the low N diet where it was 66%. The physical form of food clearly influenced N digestibility in the soya beans whilst changes in dietary fibre seem not to have a significant effect.

A new electronic aggregometer has been described which measures platelet aggregation by monitoring the changes in electrical impedance that occur when a platelet aggregate forms between two electrodes (Cardinal and Flower, 1980). To validate the instrument, the protein content of the platelet aggregate was estimated by the Lowry method (Lowry et al., 1951). Aggregating agents used were ADP (doses (mu mol), 1.0, 0.1, 0.01, 0.005, 0.0025 and 0.001), Thrombin (doses (units) 0.25, 0.20, 0.15, 0.10 and 0.05) and Collagen (doses (micrograms) 20.0, 15.0, 10.0, 5.0, 1.0 and 0.5). The quantity of protein was correlated with the dose of aggregating agent and with 6 characteristics of the aggregation curve. Linear correlation coefficients of the former were 0.92 (Log dose ADP), 0.91 (Thrombin dose) and 0.86 (Collagen dose). Correlation coefficients (Electrode Protein against curve characteristics), were greater than 0.87 for all aggregating agents and the extent of aggregation (ohms), percent of maximum aggregation, percent of maximum aggregation at 6 minutes, and maximum rate of aggregation (ohms/s). Linear correlation coefficients for the curve characteristics, time to maximum aggregation(s) and time to 50% of maximum aggregation(s), for ADP and Collagen were greater than 0.70. However, correlation coefficients of the above two characteristics to Thrombin were 0.32. We have concluded that the maximum extent of aggregation is the best method of assessing platelet aggregation with the electronic aggregometer.

Seven women spent an average of 127 days in hospital and were extensively investigated, including a laparotomy, before their complaints of abdominal pain, diarrhoea, and weight loss were shown to be due to excessive taking of laxatives. All denied taking laxatives and in none were the characteristic features of the effects of cathartics on the colon seen on sigmoidoscopy or radiological examination.Hypokalaemia and other electrolyte abnormalities were common and were thought to be due to a combination of severe diarrhoea and vomiting. The rectal mucosa was seen to be abnormal on biopsy only in the three patients who had taken senna preparations. The diagnosis was not easy and was finally established either by analysis of the urine and stools or by searching the patient's ward locker.

The effect of linoleic acid and of aspirin on platelet aggregation has been measured in six healthy volunteers with a new platelet aggregometer (Wellcome) designed to be used with whole blood. The subjects were given a controlled diet for 6 weeks during which their platelet aggregation, platelet fatty acid composition, dilute blood clot lysis time, bleeding time and serum cholesterol and triglycerides were measured. A basal diet typical of that normally eaten in the UK was fed for 3 weeks, then for a further 2 weeks 60 ml/d of safflower seed oil was added to the diet. Finally there was a further week on the basal diet and on the last day the subjects each took 900 mg of aspirin. The effects of the safflower seed oil was to increase platelet linoleic acid (C18:2 omega 6) content from 5.53 +/- 0.52 micrograms to 10.1 +/- 0.92 micrograms/100 micrograms total fatty acids (P less than 0.001), to decrease platelet aggregation to ADP, and to decreased serum cholesterol. Fibrinolysis and bleeding times were unaltered. Aspirin decreased platelet aggregation, prolonged bleeding time and increased platelet arachidonic acid (C20:4 omega 6) from 24.7 +/- 0.38 micrograms to 25.8 +/- 0.61 micrograms/100 micrograms total fatty acids (P less than 0.01). The Wellcome whole blood aggregometer is a sensitive test of platelet function and using it linoleic acid has been shown to reduce aggregation in conjunction with an increase in polyunsaturated fatty acid content of the platelet membrane.

There is now substantial evidence that some dietary polysaccharides, notably dietary fiber, escape absorption in the small bowel and are then broken down in the large intestine of man. The main end products of this colonic digestive process, which is anerobic, are short chain fatty acids (SCFA), and acetic, propionic, and butyric acids. Although these acids are known to be absorbed from the colon, their subsequent fate and significance is unknown. We have measured venous blood SCFA levels in healthy subjects after a 16-h fast, and then following oral doses of either 50 mmol SCFA, 5, 10, or 20 g doses of the fermentable carbohydrate lactulose, or 20 g of pectin. Fasting venous blood acetate was 53.8 +/- 4.4 mumol/liter (SEM) (n = 14). Fasting arterial blood acetate, taken simultaneously with venous blood in six subjects, was higher; 125.6 +/- 13.5 mumol/liter (arterial) vs. 61.1 +/- 6.9 mumol/liter (venous). Significant levels of propionate or butyrate were not detected in any blood samples. Following an oral dose of 50 mmol mixed SCFA, venous blood acetate reached a peak of 194.1 +/- 57.9 mumol/liter at 45 min and returned to fasting levels at 2 h. Blood acetate also rose in response to lactulose, peak levels occurring 2-4 h after the dose: 5 g, 98.6 +/- 23.1 mumol/liter; 10 g, 127.3 +/- 18.2 mumol/liter; and 20 g, 181.3 +/- 23.9 mumol/liter. Pectin fermentation was much slower, with blood acetate levels starting to rise after 6 h and remaining elevated at about twice fasting levels for the subsequent 18 h. However, areas under the blood acetate curves were closely related (r = 0.97; n = 5), whatever the source of acetate. These studies show that the large intestine makes an important contribution to blood acetate levels in man and that fermentation may influence metabolic processes well beyond the wall of this organ.

An investigation was made of the effect of changing mean transit time (MTT) by administration of drugs which affect colonic motility on faecal microbial mass in man. Senokot was used to accelerate and codeine and/or loperamide to prolong transit in subjects maintained on a constant high fibre diet. Doses of Senokot or codeine/loperamide were adjusted to halve or double transit time measured during a three week control period on diet alone. Stools were collected throughout and analysed for bacterial mass by a gravimetric procedure. Transit was measured by a continuous marker method. Senokot decreased mean transit time from 63.9 to 25.0 hours (n = 6), with increased stool weight from 148 to 285 g/day. Bacterial mass increased in all subjects from a mean of 16.5 to 20.3 g/day (dry weight) (p less than 0.025). Codeine/loperamide increased mean transit time from 47.1 to 87.6 hours (n = 5), with decreased stool weight from 182 to 119 g/day. Bacterial mass decreased in all but one subject from a mean of 18.9 to 16.1 g/day (NS). There was a significant correlation between transit time and bacterial mass in all three periods (r = 0.77, p less than 0.001). Changes in transit time are shown to alter microbial growth in the human colon and result in altered stool output, on a constant diet. Factors which affect transit may be as important as diet in determining large bowel function and hence susceptibility to disease.

The human large intestine absorbs Na+, Cl- and water from its lumen and secretes HCO-3 and some K+. The primary event in absorption is thought to be the active transport of Na+ ions out of the cell and across the baso-lateral cell membrane, by the energy requiring Na+-K+ ATPase. This leads in turn to Na+ entry into the cell via its luminal border and the creation of a potential across the mucosa which drives the transport of other ions. Cl- is coupled to HCO-3 secretion through a common carrier and K+ enters the intestinal lumen partly through an active secretory pathway. Most ions probably cross the epithelium by both transcellular and paracellular (shunt) pathways, water moving in response to solute transport. However the colon is not normally perfused by a saline-bicarbonate solution. It contains an active microflora which ferment 30 g or more of carbohydrate daily, derived from diet and intestinal secretions, with the production of at least 300 mmol of short chain fatty acids (acetic, propionic and butyric acids). About 6 g of urea is also degraded to NH3. These metabolic processes result in the generation of solutes which are then transported across the mucosa and which alter the pattern of water and electrolyte transport significantly. Short chain fatty acids are rapidly absorbed by passive diffusion as the undissociated acids, although anion transport, possibly through a paracellular route, is also feasible. Their absorption leads to the accumulation in the lumen of HCO3, a rise in pH, fall in pCO2 and stimulation of Na+ and water transport. The effect on Na+ transport is thought to indicate the presence of a Na+/H+ exchange in the cell membrane. The amounts of these organic solutes produced in the colon each day are probably greater than the total numbers of inorganic ions such as Na+, K+, Cl- and HCO-3 and as such must be taken into account in any understanding of overall transport processes in the large intestinal epithelium.

A mixed culture of human fecal bacteria was grown for 120 days in a three-stage continuous culture system. To reproduce some of the nutritional and pH characteristics of the large gut, each vessel had a different operating volume (0.3, 0.5, and 0.8 liter) and pH (6.0, 6.5, and 7.0). A mixture of polysaccharides and proteins was used as carbon and nitrogen sources. Measurements of H2, CH4, S2-, sulfate reduction rates, sulfate-reducing bacteria (SRB), and volatile fatty acids were made throughout the experiment. After 48 days of running, porcine gastric mucin (5.8 g/day) was independently fed to vessel 1 of the multichamber system. The mucin was extensively degraded as evidenced by the stimulation of volatile fatty acid production. In the absence of mucin, sulfate-reducing activity was comparatively insignificant and methanogenesis was the major route for the disposal of electrons. The reverse occurred upon the addition of mucin; sulfate reduction predominated and methanogenesis was completely inhibited. This was attributed to release of sulfate from the mucin which enabled SRB to outcompete methanogenic bacteria for H2. SRB stimulated by mucin were acetate-utilizing Desulfobacter spp., lactate- and H2-utilizing Desulfovibrio spp., and propionate-utilizing Desulfobulbus spp. When the mucin pump was switched off, the multichamber system reverted to a state close to its original equilibrium. These data provide further evidence that sulfated polysaccharides such as mucin may be a source of sulfate for SRB in the human large gut.

Protease activities in human ileal effluent were approximately 20-fold greater than in normal faeces. Comparative studies with faeces from a person who did not have a pancreas suggested that a substantial proportion of the proteolytic activity in normal faeces was of bacterial origin. Thimerosal, iodoacetate, EDTA and cysteine significantly inhibited proteolysis in faeces, but not in small intestinal contents, showing that cysteine and metalloproteases were produced by bacteria in the large gut. These results, together with results from studies using p-nitroanilide substrates, demonstrated that faecal proteolysis was both qualitatively and quantitatively different from that in the small intestine. Studies with pure cultures of proteolytic gut bacteria indicated that the cell-bound proteases of Bacteroides fragilis-type organisms were likely to contribute significantly towards proteolytic activity associated with the washed cell fraction and washed particulate fraction of faeces. Extracellular proteases were formed by Streptococcus faecalis ST6, Propionibacterium acnes P6, Clostridium perfringens C16, Cl. bifermentans C21 and Cl. sporogenes C25. Inhibition results suggested that these bacteria, and similar organisms, may be partly responsible for the extracellular proteolytic activity found in the cell-free supernatant fraction of faeces.

The effect on the faecal flora of adding wheat fibre to a controlled diet in four healthy volunteers for a 3-week period has been observed. No change in the concentration of the bacteria in the bacterial groups counted was found, although there was a slight increase in total output associated with increased faecal weight. The predominant organisms in all subjects were non-sporing anaerobes, but the dominant species in each subject was different and was unaffected by changing the diet. Similarly, the concentration of faecal beta-glucuronidase detected in two subjects was unaltered and the concentration of clostridia able to dehydrogenate the steroid nucleus found in one subject was unaltered. It is suggested that the faecal microflora is not primarily controlled by the presence of undigested food residues in the large bowel.

1. At the present time there is no method whereby the completeness of 24 h urine collections can be accurately assessed when clinical studies are undertaken. The suitability of 4-aminobenzoic acid (PAB) given with meals as a marker for completeness of urine collections was therefore investigated. 2. When a single dose of 80 mg of PAB was given to four volunteers 93% was recovered in the urine in 5 h. 3. Eight volunteers living in a calorimeter, where complete urine collection could be guaranteed, were given various doses of PAB divided up throughout the day. 88 +/- 5% was excreted in the urine over a 24 h period. Urine excretion and oral dose were directly related. 4. Thirty-three reliable free-living volunteers eating their normal diet took 80 mg of PAB with meals (240 mg/day). Mean urine recovery over the 24 h period was 223 +/- 9 mg, or 93 +/- 4% of the administered dose. The range in individual recovery from maximum to minimum was 15%, compared with 75% for creatinine excretion per kg fat-free mass. 5. PAB is a safe marker of the completeness of 24 h urine collections. Any collection containing less than 205 out of 240 mg (85%) of PAB, given as 80 mg with each of three meals, is probably incomplete.

A method has been developed, based on techniques used for isolating bacteria from the rumen, that enables human faeces to be fractionated into three major components. The method requires repeated, vigorous agitation of a suspension of faecal solids with detergent, the use of a stomacher, and high-speed centrifugation. By this means the faecal microflora are separated from faecal dietary-fibre residues. These two components, with water-soluble material in the stool, comprise 98.3 +/- 0.9% of faecal solids. The purity of the microbial fraction was demonstrated by Gram and plant stains and by scanning electron microscopy. Microscopic counts of the bacteria in each fraction of the stool showed that the microbial fraction contained 95% of the total bacteria. Chemical analysis of the component sugars indicated 6-7% possible contamination by non-bacterial polysaccharides. The bacterial pellet was 6% nitrogen, and accounted for 60% of the total faecal nitrogen. When faeces from nine healthy subjects on a metabolically controlled British-type diet were studied, bacteria comprised 54.7 +/- 1.7% of the total solids, fibre 16.7 +/- 0.8% and soluble material 24.0 +/- 1.3%. Bacteria therefore represent a much larger proportion of the faecal mass than was previously thought.

1. The effect of dietary fibre digestion in the human gut on its ability to alter bowel habit and impair mineral absorption has been investigated using the technique of metablic balance. 2. Five healthy male students were studied for 9 weeks under controlled dietary conditions and during the last 6 weeks they took 36 g pectin/d. Bowel habit, transit through the gut, faecal fibre excretion, calcium balance and faecal composition were measured. 3. During the control period only 15% of the dietary fibre ingested was excreted in the stools and when pectin was added to the diet there was no increase in fibre excretion. Stool frequency and mean transit time were unchanged by pectin but stool wet weight increased by 33% and faecal excretion increased (%) for fatty acids 80, nitrogen 47, total dry matter 28 and bile acids 35. Ca balance remained unchanged. 4. It may be concluded from these results that dietary fibre is largely metabolized in the human gut and dietary pectin completely so. This could explain its lack of effect on bowel habit and Ca balance. Other changes in the faeces may be related to an increase in bacterial mass.

A method is described that allows rapid estimation of total, soluble, and insoluble dietary fiber as the non-starch polysaccharides (NSP) in plant foods. It is a modification of an earlier, more complex procedure. Starch is completely removed enzymatically, and NSP is measured as the sum of its constituent sugars released by acid hydrolysis. The sugars may, in turn, be measured by gas chromatography (GC), giving values for individual monosaccharides, or more rapidly by colorimetry. Both GC and colorimetry are suitable for routine measurement of total, soluble, and insoluble dietary fiber in cereals, fruits, and vegetables. Values obtained are not affected by food processing so the dietary fiber content of various processed foods and mixed diets can be calculated simply from knowing the amount in the raw materials. The additional information obtained by GC analysis is valuable in the interpretation of physiological studies and in epidemiology where disease is related to type and amount of dietary fiber.

36 G of wheat fibre, pectin, or guar gum was given over 2-week periods to healthy volunteers taking normal diet. Mean serum-cholesterol levels fell significantly while the volunteers were taking guar and pectin by 36-3 and 29-2 mg, per 100. respectively, but rose slightly after wheat fibre by 6-7, mg per 100., Attention should be focused on fruit and vegetable gels rather than wheat fibre in the search of natural hypocholesterolaemic agents.

1. The dietary intakes of sixty-three adults, randomly-selected from the electoral role of a large village near Cambridge, have been measured using the weighed-intake technique for 7 d. 2. Mean (+/- SD) daily intakes (g) for men and women respectively were: energy (MJ) 10.0 +/0 2.4, 8.2 +/- 2.1; fat 104 +/- 27, 90 +/- 27; protein 77 +/- 20, 67 +/- 16; carbohydrate 285 +/- 81, 229 +/- 74; sucrose 91 +/- 47, 57 +/- 33. 3. When interviewed at the end of the study 40% of subjects said they were watching their weight. 4. Women ate less food over all than men, and proportionately less potato and bread, and used only one-third as much sugar in drinks, probably in an attempt to control their weight. Men took considerably more alcohol than the women. In the age-group 20-39 years alcohol provided 9% (1.0 MJ/d) of the total energy intake in the men. 5. Wide variation in the intake of nutrients was observed amongst the individuals. For vitamin C and fibre intake this was partly partly explained by seasonal variation but for most nutrients total energy intake and food choice were the main determinants. The range of intakes of nutrients such as fat was similar in these individuals to that seen amongst countries internationally. It is suggested that if differences in nutrient intake amongst the various populations of the world can be associated with disease risk, then the same interpretation should be possible in individuals.

Epidemiological observations and animal experiments suggest that large bowel cancer is related to serveral factors. Among them, high dietary intakes of animal fat, the presence in the colon of relatively high levels of bile acids, specific patterns of intestinal microflora, slow transit through the gut, and low stool weights. Under metabolic conditions we have observed the effect on these variables of dietes containing 62 or 152 g/day of fat mainly of animal origin in six healthy young men over 4-wk periods. No change attributable to the diet was observed in the subjects' bowel habit, fecal weight, mean transit time through the gut, or in the excretion of dry matter. Total fecal bile acid excretion was significantly higher on the high fat diet (320 +/- 120 mg/day) than on the low fat diet (139.7) +/- 63 mg/day) t test = 7.78 P less than 0.001 as also was the total fecal fatty acid excretion, 3.1+/-0.71 and 1.14+/-0.35 g/day, respectively t test = 11.4 P less than 0.001). The fecal microflora including the nuclear dehydrogenating clostridia were unaltered by the dietary changes as was fecal beta-glucuronidase activity. Dietary changes which increase animal fat intake clearly influence fecal bile acid excretion in a way that would favor the development of large bowel cancer if current theories prove to be true. Dietary fat however has no effect on overall colonic function so other components of the diet must be responsible for the observed associations of bowel cancer with slow transit and reduced fecal bulk.

Nonstarch polysaccharide (NSP) intake was measured in representative samples of 30 men aged 50-59 in 2 urban and 2 rural Scandinavian populations that exhibited a 3-4 fold difference in incidence of large bowel cancer. Intake was measured by chemical analysis of complete duplicate portions of all food eaten over one day by each individual. NSP intakes showed a rural-urban gradient, with 18.4 +/- 7.8 g/day in rural Finland and 18.0 +/- 6.4 g/day in rural Denmark versus 14.5 +/- 5.4 g/day in urban Finland and 13.2 +/- 4.8 g/day in urban Denmark. NSP intakes were also calculated (using food tables) from weighed food records kept over 4 days, one of which was the day on which the duplicate collection was made. Intakes were 2-2.5 g/day higher with this method than with direct chemical analysis, mainly because published tables of values have become outdated and inaccurate as a result of improved methods for measuring NSP in food. Individual variation from day to day in NSP intake was considerable. Average NSP intake and intake of some of its component sugars were inversely related to colon cancer incidence in this geographical comparison. To show a relationship at the individual level between diet and cancer risk in a prospective study would require detailed and accurate methods for the assessment of NSP consumption.

Digestion and absorption from the small intestine of starch and nonstarch polysaccharides (NSP) (dietary fiber) from potato cooked and treated in various ways have been studied in ileostomy subjects. Test meals (300 g) of potato were fed following 24 h on a plant polysaccharide-free diet. Regardless of the treatment the potato had received, greater than 90% of NSP was recovered in ileostomy effluent. Starch from freshly cooked potato was well digested, only 3% being recovered; however, 12% from cooked and cooled potato escaped digestion in the small intestine. Digestibility of starch made resistant to alpha-amylase by cooling improved on reheating. Overall, 9, 18, and 14% of total carbohydrate fed was recovered from freshly cooked, cooled, and reheated potato, respectively. Digestibility of cooled potato was identical when eaten as large lumps or as finely sieved potato. In vitro studies with pancreatin also demonstrated incomplete digestion of cooled potato.

Hydrolytic enzymes were measured in gut contents from four sudden death victims. Pancreatic amylase and total protease activities decreased distally from the small bowel to the sigmoid/rectum region of the large intestine, showing that considerable breakdown or inactivation of the enzymes occurred during gut transit. To determine whether pancreatic enzymes were substrates for the gut microflora, mixed populations of bacteria were grown in a 3-stage continuous culture system on a medium that contained pancreatic extract as the sole nitrogen source. The multichamber system (MCS) was designed to reproduce in vitro, the low pH, high nutrient, fast growth conditions of the caecum and right colon and the neutral pH, low nutrient, slow growth conditions of the left colon. Results showed that pancreatic amylase was resistant to breakdown by intestinal bacteria compared with the peptide hydrolases in pancreatic secretions. Leucine aminopeptidase, trypsin and to a lesser degree, chymotrypsin, were easily degraded by gut bacteria, but pancreatic elastase was comparatively resistant to breakdown. Protein degradation in the MCS, as determined by enzyme activities, protein concentration and ammonia and phenol production, increased concomitantly with system retention time over the range 24-69 h. These results suggest that intestinal bacteria play an important role in the breakdown of hydrolytic enzymes secreted by the pancreas and that this process and protein fermentation in general, is likely to occur maximally in individuals with extended colonic retention times.

Diet, especially the amount of starch and dietary fibre which escape digestion in the small intestine, are major determinants of colon function in man. These carbohydrates are the principal substrates for fermentation by the large bowel flora. Carbohydrate fermentation results in lowered caecal pH and the production of short chain fatty acids of which butyric acid may protect the colon epithelium from dysplastic change. Protein digestion and amino acid fermentation also occur in the large bowel but the nature of its endproducts varies in relation to the amount of carbohydrate available. During active carbohydrate breakdown amino acid fermentation endproducts such as ammonia are used by the bacteria for protein synthesis during microbial growth, but in carbon-limited fermentation amines, ammonia, phenols and indoles, etc, accumulate. Fermentation also results in changes in colon pH which alters the metabolism of bile acids, nitrate, sulphate and other substances. Fermentation is thus controlled to a great extent by substrate availability, especially of carbohydrates which are derived from the diet. The potential to induce mutagenic change in colon epithelial cells and promote tumour growth may readily be influenced by diet.

The absorption of short chain fatty acids by the human rectum in the absence of chloride has been studied using a dialysis bag technique. Absorption rates of sodium, water, and short chain fatty acids were unchanged on replacing chloride with sulphate. Final concentrations of bicarbonate were 35.4 +/- 3.4 mmol/l in the presence of chloride and 37.1 +/- 5.2 mmol/l in the absence of chloride. The rates of movement of bicarbonate into the dialysates were similar. If bicarbonate is secreted in exchange for chloride then it also appears to be secreted in exchange for absorbed short chain fatty acids.

1. Dietary fibre has a moderating impact on glucose metabolism. To test the hypothesis that this effect of fibre may be mediated by its breakdown product acetate, oral glucose tolerance tests were carried out in healthy volunteers with and without acetate. 2. Five subjects received 50 g of glucose orally while taking either acetate (15 mmol every 15 min) by mouth or chloride as control. Oral acetate made no detectable difference to glucose tolerance or to levels of free fatty acids, 3-hydroxybutyrate, lactate, insulin, glucagon and gastric inhibitory polypeptide. 3. The 50 g dose of glucose temporarily depressed acetate levels in blood. This was probably due to an interaction between glucose and acetate in the gastrointestinal lumen as the same effect was seen with 50 g of xylose in three subjects. 4. Plasma acetate concentrations were unaffected by 50 g of oral glucose in one subject when acetate was instilled into the sigmoid colon. 5. It is unlikely that the improvement of glucose tolerance by dietary fibre is mediated by acetate.

The hypothesis that dietary fibre might protect against the development of ischaemic heart disease through an effect on platelet aggregation and blood clotting has been tested in eleven healthy volunteers. In two separate studies the effect of pectin and wheat bran has been measured in subjects living on controlled diets in a metabolic suite. In the pectin study volunteers consumed a basal diet, typical of that normally eaten in the UK, for 6 weeks but for one 3-week period took an additional 36 g/d pectin (Bulmers Firmagel--high methoxy pectin). Although serum cholesterol concentrations were significantly lowered (5.73 +/- 0.36 mmol/l control; 5.18 +/- 0.35 mmol/l + pectin, P less than 0.025), platelet aggregation, platelet fatty acid composition, dilute blood clot lysis time and bleeding times were unaltered. In a similar study in which the volunteers took white bread for 3 weeks and brown and wholemeal breads for a further 3 weeks each, no change was seen in platelet function or in haemostasis. It is concluded that if dietary fibre does protect against heart disease it is probably not through an effect on platelet aggregation or haemostasis.

When dietary fiber intakes are increased by supplementing diets with bran and whole wheat products, then fecal fat, nitrogen, energy, and mineral excretion rise. These changes suggest that fiber may be altering normal digestive and absorptive function. Recent studies have confirmed this and have also shown that fiber of different composition and from contrasting sources produces different physiological effects. The gel-forming polysaccharides such as guar gum and pectin alter the pattern of glucose absorption and are hypocholesterolemic; fiber from cereals is not hypocholesterolemic but exerts a pronounced effect on the large gut. Dietary fiber is largely digested in the colon by the microflora and so influences colonic function, fecal weight, and composition. The significance of the changes in fat, nitrogen, and energy output remains to be evaluated, but the impairment of mineral absorption--particularly of calcium, zinc, and iron--by fiber gives cause for concern. Fiber must now be considered with other dietary constituents in all nutritional studies.

Sulphate-reducing bacteria (SRB) were enumerated in 40 faecal samples obtained from two different human populations in the United Kingdom and rural South Africa. Species able to metabolize acetate, lactate, propionate, butyrate, H2/CO2, succinate, pyruvate, valerate, ethanol and a glutamate/serine/alanine mixture were found in faeces from both populations. Although a variety of nutritionally and morphologically distinct species of SRB belonging to the genera Desulfotomaculum, Desulfobacter, Desulfomonas and Desulfobulbus were identified, Desulfovibrio types always predominated. Significant numbers of SRB were present only in faecal samples from subjects whose breath methane excretion was low or undetectable. Reduced or absent methanogenesis in the presence of SRB was confirmed in fermentation studies with faecal slurries. Fourteen of 20 (70%) British faecal samples contained SRB and the remainder produced methane. The reverse was the case with 20 rural black South Africans, where only three (15%) of the samples had significant levels of SRB; the remaining 85% produced methane. These results suggest that to a large extent, dissimilatory sulphate reduction and methanogenesis are mutually exclusive in the human large gut.

Sulphate-reducing activity in human faecal slurries was followed by measuring sulphide production. Sulphate-reducing bacteria (SRB) were found to outcompete methanogenic bacteria (MB) for the mutual substrate hydrogen in faecal slurries from methane- and non-methane-producing individuals mixed together. When molybdate (20 mmol/l) was added to these slurries, sulphate reduction was inhibited and methanogenesis became the major route of electron disposal. Sulphide production was stimulated by the addition of 20 mmol/l sulphate in non-methanogenic but not in methanogenic slurries. In methanogenic slurries that contained the methanogen inhibitor 2-bromoethanesulphonic acid (BES), hydrogen accumulated whilst sulphide levels were unaffected, confirming the absence of SRB in methanogenic faeces. The addition of nitrate (10 mmol/l) to faecal slurries completely inhibited methanogenesis but only slightly reduced sulphate reduction. The sulphated mucopolysaccharides, chondroitin sulphate and mucin, strongly stimulated sulphide production in non-methanogenic faecal slurries only, suggesting that these substances may be a potential source of sulphate in the large gut.