Lipids, CHOs, proteins: can all macronutrients put a 'brake' on eating?

The gastrointestinal (GI) tract and specifically the most distal part of the small intestine, the ileum, has become a renewed focus of interest for mechanisms targeting appetite suppression. The 'ileal brake' is stimulated when energy-containing nutrients are delivered beyond the duodenum and jejunum and into the ileum, and is named for the feedback loop which slows or 'brakes' gastric emptying and duodeno-jejunal motility. More recently it has been hypothesized that the ileal brake also promotes secretion of satiety-enhancing GI peptides and suppresses hunger, placing a 'brake' on food intake. Postprandial delivery of macronutrients to the ileum, other than unavailable carbohydrates (CHO) which bypass absorption in the small intestine en route to fermentation in the large bowel, is an uncommon event and hence this brake mechanism is rarely activated following a meal. However the ability to place a 'brake' on food intake through delivery of protected nutrients to the ileum is both intriguing and challenging. This review summarizes the current clinical and experimental evidence for activation of the ileal brake by the three food macronutrients, with emphasis on eating behavior and satiety as well as GI function. While clinical studies have shown that exposure of the ileum to lipids, CHOs and proteins may activate GI components of the ileal brake, such as decreased gut motility, gastric emptying and secretion of GI peptides, there is less evidence as yet to support a causal relationship between activation of the GI brake by these macronutrients and the suppression of food intake. The predominance of evidence for an ileal brake on eating comes from lipid studies, where direct lipid infusion into the ileum suppresses both hunger and food intake. Outcomes from oral feeding studies are less conclusive with no evidence that 'protected' lipids have been successfully delivered into the ileum in order to trigger the brake. Whether CHO or protein may induce the ileal brake and suppress food intake has to date been little investigated, although both clearly have GI mediated effects. This review provides an overview of the mechanisms and mediators of activation of the ileal brake and assesses whether it may play an important role in appetite suppression.

Meningitis associated with strongyloidiasis in an area endemic for strongyloidiasis and human T-lymphotropic virus-1: a single-center experience in Japan between 1990 and 2010.

Meningitis caused by enteric flora is a known complication of strongyloidiasis, and human T-lymphotropic virus-1 (HTLV-1) predisposes individuals to severe strongyloidiasis. We reviewed the clinical features of bacterial meningitis associated with strongyloidiasis seen at a single center in subtropical Japan, in an area endemic for both strongyloidiasis and HTLV-1. We found 33 episodes in 21 patients between 1990 and 2010. The results were remarkable for the high incidence of meningitis due to Gram-positive cocci (27.3 %), especially Streptococcus bovis, and culture-negative cases (42.4 %). Given the high incidence of Gram-positive meningitis, a modified approach to corticosteroid use would be advisable in areas where strongyloidiasis is endemic, due to the potentially adverse consequences of glucocorticoid therapy.

The emulsified lipid Fabuless (Olibra) does not decrease food intake but suppresses appetite when consumed with yoghurt but not alone or with solid foods: a food effect study.

The lipid emulsion Fabuless (Olibra) has been shown in some studies to decrease short/medium term energy intake (EI) and prevent weight regain. The purported mechanism is the ileal brake. Whether Fabuless is efficacious under a range of dietary conditions is unknown since studies have administered the emulsion within a fermented, semi-liquid dairy yoghurt, and outcomes have been inconsistent. To determine whether Fabuless suppresses post-ingestive satiety and short-term food intake under a range of dietary conditions and forms we administered the emulsion co-presented with 185 mL water, stirred into a semi-liquid dairy yoghurt, and co-presented with a solid food breakfast muffin. This was a cross-over study in 18 lean men randomised to 6 treatments: (i) lipid emulsion, LE (15 g Fabuless, containing 4.2g lipid, 0.2 MJ)+water, (ii) lipid control, LC (15 g non-emulsified lipid/water, containing 4.2g lipid, 0.2 MJ)+water, (iii) lipid emulsion+yoghurt, LE+Y (1.2 MJ), (iv) lipid control+yoghurt, LC+Y (1.2 MJ), (v) lipid emulsion+muffin, LE+M (1.2 MJ), (vi) lipid control+muffin, LC+M (1.2 MJ), each given as a test breakfast at 8.30 am. Participants rated postprandial appetite sensations using visual analogue scales (VAS), and ad libitum energy intake was measured at a lunch meal 3.5h later. The lipid emulsion increased fullness compared with an energy-matched lipid control but only when administered within the semi-liquid fermented yoghurt (P<0.05). There were no effects on satiety ratings when co-presented with water or with the solid food muffin. Energy and macronutrient intake were not significantly decreased by any of the emulsion treatments. We conclude that effects are small, the format in which lipid emulsions are consumed influences postprandial satiety, and there is no evidence that this emulsion alters eating behaviour at the subsequent meal.

Fatty acid chain length, postprandial satiety and food intake in lean men.

High-fat diets are associated with obesity, and the weak satiety response elicited in response to dietary lipids is likely to play a role. Preliminary evidence from studies of medium (MCT) and long chain triglycerides (LCT) supports greater appetite suppression on high-MCT diets, possibly a consequence of direct portal access, more rapid oxidation and muted lipaemia. No data is as yet available on high-SCT diets which also have direct hepatic access. In this study SCT- (dairy fats), MCT- (coconut oil) and LCT-enriched (beef tallow) test breakfasts (3.3 MJ) containing 52 g lipid (58 en% fat) were investigated in a randomized, cross-over study in 18 lean men. All participants were required to complete the 3 study days in randomised order. Participants rated appetite sensations using visual analogue scales (VAS), and energy intake (EI) was measured by covert weighing of an ad libitum lunch meal 3.5 h postprandially. Blood samples were collected by venous cannulation. There were no detectable differences between breakfasts in perceived pleasantness, visual appearance, smell, taste, aftertaste and palatability (P>0.05). There was no significant effect of fatty acid chain length on ratings of hunger, fullness, satisfaction or current thoughts of food, nor did energy (mean, sem: SCT: 4406, 366 kJ; MCT: 4422, 306 kJ; LCT: 4490, 324 kJ; P>0.05) or macronutrient intake at lunch differ between diets. The maximum difference in EI between diets was less than 2%. Postprandial lipaemia also did not differ significantly. We conclude that there was no evidence that fatty acid chain length has an effect on measures of appetite and food intake when assessed following a single high-fat test meal in lean participants.

No effect of an oleoylethanolamide-related phospholipid on satiety and energy intake: a randomised controlled trial of phosphatidylethanolamine.

BACKGROUND: Phosphatidylethanolamine (PE) is a phospholipid which is biosynthesized into long chain N-acylethanolamines (NAEs) including oleoylethanolamide (OEA), a known inhibitor of food intake. The aim of this study was to investigate whether PE-containing lipids can also inhibit intake. This was a 4 treatment intervention where 18 male participants were given a high-fat test breakfast (2.5 MJ, 53 en% fat) containing (i) high-phospholipid, high-PE lipid (ii) high-phospholipid, medium-PE lipid (iii) no-phospholipid, no-PE control lipid or (iv) water control, in a randomised cross-over. Visual analogue scales (VAS) were used to assess post-ingestive hunger and satiety, and energy intake (EI) was measured at an ad libitum lunch meal after 3.5 hours. RESULTS: When compared with the water control, the 3 lipid treatments resulted in lower levels of hunger and thoughts of food, greater fullness and satisfaction (all, treatment*time interaction, P<0.001), and a lower EI (P<0.05). However, there was no difference in any of the VAS measures when the 2 PE lipid treatments were compared with no-PE control lipid, nor when medium-PE was compared with high-PE. Unexpectedly participants ate significantly more energy at the lunch meal when the 2 PE lipid treatments (medium-PE:5406 kJ, 334 sem; high-PE:5288 kJ, 244 sem) were compared with the no-PE control lipid (5072 kJ, 262 sem, P<0.05), although there was no dose effect between the medium- and high-PE treatments. CONCLUSION: Despite the close relationship of PE with OEA, there was no evidence from this acute study that dietary phospholipids containing PE can favourably modify eating behaviour.

The effect of the dietary supplement, Chitosan, on body weight: a randomised controlled trial in 250 overweight and obese adults.

CONTEXT: Chitosan, a deacetylated chitin, is a widely available dietary supplement purported to decrease body weight and serum lipids through gastrointestinal fat binding. Although evaluated in a number of trials, its efficacy remains in dispute. OBJECTIVE: To evaluate the efficacy of chitosan for weight loss in overweight and obese adults. DESIGN AND SETTING: A 24-week randomised, double-blind, placebo-controlled trial, conducted at the University of Auckland between November 2001 and December 2002. PARTICIPANTS: A total of 250 participants (82% women; mean (s.d.) body mass index, 35.5 (5.1) kg/m(2); mean age, 48 (12) y) INTERVENTIONS: Participants were randomly assigned to receive 3 g chitosan/day (n=125) or placebo (n=125). All participants received standardised dietary and lifestyle advice for weight loss. Adherence was monitored by capsule counts. MAIN OUTCOME MEASURES: The primary outcome measure was change in body weight. Secondary outcomes included changes in body mass index, waist circumference, body fat percentage, blood pressure, serum lipids, plasma glucose, fat-soluble vitamins, faecal fat, and health-related quality of life. RESULTS: In an intention-to-treat analysis with the last observation carried forward, the chitosan group lost more body weight than the placebo group (mean (s.e.), -0.4 (0.2) kg (0.4% loss) vs +0.2 (0.2) kg (0.2% gain), P=0.03) during the 24-week intervention, but effects were small. Similar small changes occurred in circulating total and LDL cholesterol, and glucose (P<0.01). There were no significant differences between groups for any of the other measured outcomes. CONCLUSION: In this 24-week trial, chitosan treatment did not result in a clinically significant loss of body weight compared with placebo.