Healthy diets with reduced environmental impact? - The greenhouse gas emissions of various diets adhering to the Dutch food based dietary guidelines.

OBJECTIVE: To determine the differences in environmental impact and nutrient content of the current Dutch diet and four healthy diets aimed at lowering greenhouse gas (GHG) emissions. METHODS: GHG emissions (as proxy for environmental impact) and nutrient content of the current Dutch diet and four diets adhering to the Dutch food based dietary guidelines (Wheel of Five), were compared in a scenario study. Scenarios included a healthy diet with or without meat, and the same diets in which only foods with relatively low GHG emissions are chosen. For the current diet, data from the Dutch National Food Consumption Survey 2007-2010 were used. GHG emissions (in kg CO2-equivalents) were based on life cycle assessments. Results are reported for men and women aged 19-30years and 31-50years. RESULTS: The effect on GHG emissions of changing the current Dutch diet to a diet according to the Wheel of Five (corresponding with the current diet as close as possible), ranged from -13% for men aged 31-50years to +5% for women aged 19-30years. Replacing meat in this diet and/or consuming only foods with relatively low GHG emissions resulted in average GHG emission reductions varying from 28-46%. In the scenarios in which only foods with relatively low GHG emissions are consumed, fewer dietary reference intakes (DRIs) were met than in the other healthy diet scenarios. However, in all healthy diet scenarios the number of DRIs being met was equal to or higher than that in the current diet. CONCLUSIONS: Diets adhering to food based dietary guidelines did not substantially reduce GHG emissions compared to the current Dutch diet, when these diets stayed as close to the current diet as possible. Omitting meat from these healthy diets or consuming only foods with relatively low associated GHG emissions both resulted in GHG emission reductions of around a third. These findings may be used to expand food based dietary guidelines with information on how to reduce the environmental impact of healthy diets.

Effect of increased protein intake on renal acid load and renal hemodynamic responses.

Increased protein intake versus maltodextrin intake for 4 weeks lowers blood pressure. Concerns exist that high-protein diets reduce renal function. Effects of acute and 4-week protein intake versus maltodextrin intake on renal acid load, glomerular filtration rate and related parameters were compared in this study. Seventy-nine overweight individuals with untreated elevated blood pressure and normal kidney function were randomized to consume a mix of protein isolates (60 g/day) or maltodextrin (60 g/day) for 4 weeks in energy balance. Twenty-four-hour urinary potential renal acid load (uPRAL) was compared between groups. A subgroup (maltodextrin N = 27, protein mix N = 25) participated in extra test days investigating fasting levels and postprandial effects of meals supplemented with a moderate protein- or maltodextrin-load on glomerular filtration rate, effective renal plasma flow, plasma renin, aldosterone, pH, and bicarbonate. uPRAL was significantly higher in the protein group after 4 weeks (P ≤ 0.001). Postprandial filtration fraction decreased further after the protein-supplemented breakfast than after the maltodextrin-supplemented breakfast after 4 weeks of supplementation (P ≤ 0.001). Fasting and postprandial levels of glomerular filtration rate, effective renal plasma flow, renin, aldosterone, angiotensin-converting enzyme, pH and bicarbonate did not differ between groups. In conclusion, 4 weeks on an increased protein diet (25% of energy intake) increased renal acid load, but did not affect renal function. Postprandial changes, except for filtration fraction, also did not differ between groups. These data suggest that a moderate increase in protein intake by consumption of a protein mix for 4 weeks causes no (undesirable) effects on kidney function in overweight and obese individuals with normal kidney function.

Dietary proteins improve endothelial function under fasting conditions but not in the postprandial state, with no effects on markers of low-grade inflammation.

Endothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3×20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P≤0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P≤0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.

Differential effects of proteins and carbohydrates on postprandial blood pressure-related responses.

Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1) and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and S-nitrosothiols (NO(x)) were measured for 4 h. No differences were observed in TPR responses. Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of meals containing the other two proteins (P≤ 0·01). The ingestion of the pea-protein meal induced the highest NO(x) response (P≤ 0·006). Insulin and glucagon concentrations were lowest after the ingestion of the egg-white-protein meal (P≤ 0·009). Postprandial BP levels were lower after the ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P≤ 0·004), while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than after that of the sucrose and protein mix meals after 1-2 h (P≤ 0·0001). Postprandial NO(x), GLP-1 and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of the protein mix meal (P≤ 0·008). In conclusion, different protein and carbohydrate sources induce different postprandial BP-related responses, which may be important for BP management. Lower postprandial BP levels are not necessarily accompanied by higher NO(x), insulin, glucagon or GLP-1 responses.

Urinary sulfur metabolites associate with a favorable cardiovascular risk profile and survival benefit in renal transplant recipients.

In post-transplant conditions, sulfur may be protective by intermediate conversion to hydrogen sulfide and thiosulfate. However, sulfate, the end product of sulfur-containing amino acids (SAAs), contributes to metabolic acid load and may adversely influence acid-base homeostasis. We investigated the association of urinary sulfur metabolites with cardiometabolic parameters in renal transplant recipients (RTRs) and analyzed their predictive capacity for mortality. We studied urinary sulfate and thiosulfate excretion in 24-hour urine samples from 707 RTRs at a median 5.4 years (interquartile range, 1.9 to 12.2) after transplantation as well as from 110 controls. Diet was assessed for SAA content and various risk factors were measured. Urinary sulfate was similar, whereas thiosulfate was higher in RTRs versus controls. SAA intake was lower in RTRs compared with controls and correlated with sulfate but not thiosulfate excretion. Sulfate beneficially associated with eGFR, net acid excretion, systolic BP, high-sensitivity C-reactive protein, N-terminal probrain natriuretic peptide, and proteinuria (all P≤0.01). Thiosulfate beneficially associated with eGFR, serum acidity, high-sensitivity C-reactive protein, and N-terminal probrain natriuretic peptide (all P≤0.001). During a median 27 months (interquartile range, 22-36) of follow-up, 47 RTRs died. After adjustment for age, sex, and eGFR, hazard ratios for mortality were 0.87 (95% confidence interval, 0.82 to 0.92; P<0.001) for urinary sulfate and 0.60 (95% confidence interval, 0.41 to 0.59; P=0.01) for thiosulfate. Thus, despite the association of urinary sulfate with metabolic acid load, urinary sulfate and thiosulfate beneficially associated with survival in RTRs, possibly by influencing cardiovascular parameters. Intervention studies with exogenous sulfur are warranted to elucidate mechanisms underlying these promising associations in RTRs.

Twenty-four hour urinary urea excretion and 9-year risk of hypertension: the PREVEND study.

OBJECTIVES: It is not yet clear whether dietary protein could help maintaining a healthy blood pressure (BP). We investigated the association between total protein intake, estimated from 24-h urinary urea excretion, and incident hypertension in Dutch men and women. METHODS: We analyzed data of 3997 men and women (aged 28-75 years) who participated in the Prevention of Renal and Vascular Endstage Disease (PREVEND) study, a prospective cohort study. Urea excretion was assessed in two consecutive 24-h urine collections at baseline and approximately 4 years later, from which total protein intake was estimated using the Maroni method. Participants were followed for 9 years for hypertension incidence, defined as BP at least 140/90 mmHg or initiation of antihypertensive medication. Hazard ratios (HR) were obtained in sex-specific quintiles of protein intake using time-dependent Cox regression, adjusted for age, sex, BMI, smoking, alcohol use, and 24-h urinary excretions of sodium and potassium. RESULTS: Baseline BP was on average 119/70 mmHg and 976 participants developed hypertension during follow-up. Mean protein intake (in g/kg ideal body weight) was 1.18 ±â€Š0.26 for men and 1.12 ±â€Š0.25 for women. Estimated protein intake was nonlinearly inversely associated with incident hypertension in the fully adjusted model, with nonsignificant HR of 0.77, 0.75, 0.82, and 0.83 in consecutive quintiles compared with the lowest quintile (P-trend: 0.52). CONCLUSION: Protein intake, as assessed by urinary urea excretion, was not significantly associated with 9-year hypertension incidence in Dutch men and women.

Identification of biomarkers for intake of protein from meat, dairy products and grains: a controlled dietary intervention study.

In the present controlled, randomised, multiple cross-over dietary intervention study, we aimed to identify potential biomarkers for dietary protein from dairy products, meat and grain, which could be useful to estimate intake of these protein types in epidemiological studies. After 9 d run-in, thirty men and seventeen women (22 (SD 4) years) received three high-protein diets (aimed at approximately 18% of energy (en%)) in random order for 1 week each, with approximately 14 en% originating from either meat, dairy products or grain. We used a two-step approach to identify biomarkers in urine and plasma. With principal component discriminant analysis, we identified amino acids (AA) from the plasma or urinary AA profile that were distinctive between diets. Subsequently, after pooling total study data, we applied mixed models to estimate the predictive value of those AA for intake of protein types. A very good prediction could be made for the intake of meat protein by a regression model that included urinary carnosine, 1-methylhistidine and 3-methylhistidine (98% of variation in intake explained). Furthermore, for dietary grain protein, a model that included seven AA (plasma lysine, valine, threonine, α-aminobutyric acid, proline, ornithine and arginine) made a good prediction (75% of variation explained). We could not identify biomarkers for dairy protein intake. In conclusion, specific combinations of urinary and plasma AA may be potentially useful biomarkers for meat and grain protein intake, respectively. These findings need to be cross-validated in other dietary intervention studies.

Blood pressure decreases more after high-carbohydrate meals than after high-protein meals in overweight adults with elevated blood pressure, but there is no difference after 4 weeks of consuming a carbohydrate-rich or protein-rich diet.

The replacement of dietary carbohydrates with proteins can lower blood pressure (BP), but the mechanisms remain unclear. This randomized, double-blind, parallel-group study aimed to compare 12-h postprandial sympathetic and hemodynamic responses after high-protein (HP) meals and high-carbohydrate (HC) meals. Fifty-two men and women with untreated elevated BP were tested on d 1 and after 4 wk of supplementation [3 × 20 g protein (HP) or maltodextrin (HC) per day]. No between-group differences were found in postprandial plasma norepinephrine on d 1 and at wk 4. On d 1, postprandial mean arterial pressure (MAP) decreased more in the HC group than in the HP group (P = 0.002). This difference was not present at 4 wk, because the postprandial decline in MAP tended to become larger in the HP group after 4 wk of supplementation (P = 0.07). On both test days, postprandial total peripheral resistance tended to decrease more in the HC group (P < 0.08). After 4 wk of supplementation, cardiac output tended to increase more in the HC group (P = 0.08). In conclusion, ingestion of an HP diet induced a smaller decrease in BP on d 1 than did ingestion of an HC diet. This difference disappeared after 4 wk due to a more pronounced decrease in BP in the HP group after 4 wk than on d 1. These findings cannot explain the BP-lowering effect ascribed to dietary proteins.

Dietary protein, blood pressure and renal function in renal transplant recipients.

Hypertension is highly prevalent among renal transplant recipients (RTR) and a risk factor for graft failure and cardiovascular events. Protein intake has been claimed to affect blood pressure (BP) in the general population and may affect renal function. We examined the association of dietary protein with BP and renal function in RTR. We included 625 RTR (age 53 (SD 13) years; 57% male). Protein intake was assessed with a FFQ, differentiating between animal and plant protein. BP was measured according to a strict protocol. Creatinine clearance and albuminuria were measured as renal parameters. Protein intake was 83 (SD 12) g/d, of which 63% derived from animal sources. BP was 136 (SD 17) mmHg systolic (SBP) and 83 (SD 11) mmHg diastolic (DBP). Creatinine clearance was 66 (SD 26) ml/min; albuminuria 41 (10-178) mg/24 h. An inverse, though statistically insignificant, association was found between the total protein intake and both SBP (ß = - 2·22 mmHg per SD, P= 0·07) and DBP (ß = - 0·48 mmHg per SD, P= 0·5). Protein intake was not associated with creatinine clearance. Although albuminuria was slightly higher in the highest tertile of animal protein intake compared with the lowest tertile (66 v. 33 mg/d, respectively, P= 0·03), linear regression analyses did not reveal significant associations between dietary protein and albuminuria. Protein intake exceeded the current recommendations. Nevertheless, within the range of protein intake in our RTR population, we found no evidence for an association of dietary protein with BP and renal function. Intervention studies focusing on different protein types are warranted to clarify their effect on BP and renal function in RTR.

Dietary acid load and metabolic acidosis in renal transplant recipients.

BACKGROUND AND OBJECTIVES: Acidosis is prevalent among renal transplant recipients (RTRs) and adversely affects cardiometabolic processes. Factors contributing to acidosis are graft dysfunction and immunosuppressive drugs. Little is known about the potential influence of diet on acidosis in RTRs. This study examined the association of metabolic acid load with acidosis and with cardiovascular risk factors in RTRs and aimed to identify dietary factors associated with acidosis. DESIGN, PARTICIPANTS, SETTING, & MEASUREMENTS: 707 RTRs were included. Metabolic acid load was assessed by measuring 24-hour urinary net acid excretion (NAE; i.e., titratable acid + ammonium - bicarbonate). Acidosis was defined as serum [HCO(3)(-)] < 24 mmol/L. BP and insulin resistance, reflected by hemoglobin A1c, were among cardiovascular risk factors. Diet was assessed with food-frequency questionnaires. Linear regression analysis was applied to investigate association between NAE and acidosis and between dietary factors and acidosis. RESULTS: Mean age ± SD was 53 ± 13 years; 57% of patients were male. Acidosis was present in 31% of RTRs. NAE was associated with acidosis (serum HCO(3)(-): ß=-0.61; serum pH: ß=-0.010; both P<0.001). Patients with high intake of animal protein (i.e., from meat, cheese, and fish) and low intake of fruits and vegetables had significantly lower serum HCO(3)(-) and serum pH. No associations were observed between NAE and cardiovascular risk factors, such as hypertension and insulin resistance. CONCLUSIONS: In addition to conventional factors contributing to acidosis, diet might influence acid-base homeostasis in RTRs. Higher intake of fruits and vegetables and lower animal protein intake is associated with less acidosis in RTRs.

Dietary acid load and risk of hypertension: the Rotterdam Study.

BACKGROUND: Mild metabolic acidosis, which can be caused by diet, may result in elevated blood pressure (BP). DESIGN: The analyses included 2241 participants aged ≥55 y who were free of hypertension at baseline (1990-1993) and who had complete dietary and BP data. Dietary data were obtained from a 170-item food-frequency questionnaire. We used 2 measures to characterize dietary acid load: (1) potential renal acid load (PRAL) by using an algorithm including protein, phosphorus, potassium, calcium, and magnesium, and (2) estimated net endogenous acid production (NEAP) based on protein and potassium. HRs for 6-y incidence of hypertension were obtained in tertiles of PRAL and NEAP with adjustment for age, sex, BMI, smoking, education, and intakes of alcohol, fiber, and total energy. RESULTS: We identified 1113 incident cases of hypertension during 8707 person-years of follow-up. The median dietary acid load ranged from -14.6 to 19.9 mEq/d across categories of PRAL. Hypertension risk was not significantly associated with dietary acid load. The multivariate HRs (95% CIs) in consecutive tertiles of PRAL were 1.00 (reference), 1.01 (0.87, 1.17), and 1.02 (0.88, 1.18) (P trend = 0.83). The median dietary acid loads were 30.4, 36.7, and 43.7 mEq/d, respectively, in consecutive tertiles of NEAP. Corresponding HRs for NEAP were 1.00 (reference), 0.92 (0.80, 1.07), and 0.94 (0.81, 1.10) (P-trend = 0.46). CONCLUSION: The findings from this prospective cohort study provided no evidence of an association between dietary acid load and risk of hypertension in older adults.

Sodium intake and blood pressure in renal transplant recipients.

BACKGROUND: Hypertension is common among renal transplant recipients (RTR) and a risk factor for graft failure and mortality. Sodium intake is a well-established determinant of blood pressure (BP) in the general population. However, data in RTR are limited. International guidelines recommend a maximum daily sodium intake of 70 mmol. We investigated sodium intake in RTR as compared to healthy controls and its association with BP. METHODS: We included 660 RTR (age 53 ± 13 years, 58% male) and 201 healthy controls (age 54 ± 11 years, 46% male). Sodium intake was assessed from 24-h urine collections. The morning after completion of urine collection, BP was measured according to a strict protocol. RESULTS: Urinary sodium excretion was 156 ± 62 mmol/24 h in RTR and 195 ± 75 in controls (difference: P < 0.001), and 95% of RTR had a urinary sodium excretion >70 mmol/24 h. Systolic BP (SBP) and diastolic BP (DBP) were 136 ± 18 and 82 ± 11 mmHg, respectively. Sodium intake was positively associated with SBP (ß = 0.042 mmHg/mmol/24 h, P = 0.002) and DBP (ß = 0.023 mmHg/mmol/24 h, P = 0.007), independent of potential confounders. CONCLUSIONS: Although RTR had a lower sodium intake than healthy controls, their intake still exceeded current guidelines. Reduction of sodium intake to recommended amounts could reduce SBP by 4-5 mmHg. Better control of sodium intake may help to prevent graft failure and mortality due to hypertension among RTR.

Protein supplementation lowers blood pressure in overweight adults: effect of dietary proteins on blood pressure (PROPRES), a randomized trial.

BACKGROUND: Dietary protein intake may help to manage blood pressure (BP) and prevent complications associated with elevated BP. OBJECTIVE: The objective of this study was to determine whether 4 wk of increased protein intake (∼25% compared with ∼15% of energy intake that isoenergetically replaces carbohydrate intake) lowers office and daytime BP compared with increased carbohydrate intake. DESIGN: A randomized, double-blind, parallel study compared consumption of 3 × 20 g protein/d (20% pea, 20% soy, 30% egg, and 30% milk-protein isolate) with 3 × 20 g maltodextrin/d. Protein or maltodextrin were isoenergetically substituted for a sugar-sweetened drink. Primary outcomes were office and daytime BP. A total of 99 men and women [age range: 20-70 y; BMI (in kg/m²): 25-35] with untreated elevated BP (BP ≥130/85 and <160/100 mm Hg) were randomly assigned. Ninety-four completers (51 subjects in the maltodextrin group, 43 subjects in the protein group) were included in the analyses. RESULTS: Office systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 4.9 ± 1.7 mm Hg (P = 0.005) and 2.7 ± 1.3 mm Hg (P = 0.05) lower, respectively, in the protein group. Daytime SBP was 4.6 ± 1.7 mm Hg lower in the protein group (P = 0.006), whereas daytime DBP did not differ between groups (P = 0.37). Urinary sodium excretion was higher in the maltodextrin group (P = 0.004). CONCLUSION: Increased protein intake, at the expense of maltodextrin, lowers BP in overweight adults with upper-range prehypertension and grade 1 hypertension. This trial was registered at www.trialregister.nl as NTR 1362.

Dietary acid load and rapid progression to end-stage renal disease of diabetic nephropathy in Westernized South Asian people.

Diabetic nephropathy is now the most common cause of end-stage renal failure in many countries of the world. Despite increasing implementation of preventive treatment, the chance that an individual diabetic patient will reach end-stage renal failure has been increasing rather than decreasing during recent decades. Current dietary habits in The Netherlands and the rest of the Western world are slowly shifting from relatively alkalinizing (e.g., potatoes and vegetables) toward more acidifying (e.g., rice and meat). Moreover, immigrants who consumed traditional diets in their homelands, usually adapt to Western dietary habits. This phenomenon of diet acculturation could, for instance, be involved in the up to 40 times higher chance of development of end-stage renal failure in association with diabetes in South-Asian immigrants compared with whites, in Western countries. High ingestion of nonvolatile acids with food increases susceptibility for progression to end-stage renal failure. These high dietary acid loads lead to compensatory increases in renal acid excretion and ammoniagenesis. The price paid for maintenance of acid-base homeostasis is renal tubulointerstitial injury, with subsequent decline in renal function and induction of hypertension. The tendency for metabolic acidosis that results from the changing dietary habits could be corrected by a shift toward more alkalinizing food. We hypothesize that promoting such a shift can prevent the epidemic of end-stage renal failure in diabetes.

Dietary protein and blood pressure: a systematic review.

BACKGROUND: Elevated blood pressure (BP), which is a major risk factor for cardiovascular disease, is highly prevalent worldwide. Recently, interest has grown in the role of dietary protein in human BP. We performed a systematic review of all published scientific literature on dietary protein, including protein from various sources, in relation to human BP. METHODOLOGY/PRINCIPAL FINDINGS: We performed a MEDLINE search and a manual search to identify English language studies on the association between protein and blood pressure, published before June 2010. A total of 46 papers met the inclusion criteria. Most observational studies showed no association or an inverse association between total dietary protein and BP or incident hypertension. Results of biomarker studies and randomized controlled trials indicated a beneficial effect of protein on BP. This beneficial effect may be mainly driven by plant protein, according to results in observational studies. Data on protein from specific sources (e.g. from fish, dairy, grain, soy, and nut) were scarce. There was some evidence that BP in people with elevated BP and/or older age could be more sensitive to dietary protein. CONCLUSIONS/SIGNIFICANCE: In conclusion, evidence suggests a small beneficial effect of protein on BP, especially for plant protein. A blood pressure lowering effect of protein may have important public health implications. However, this warrants further investigation in randomized controlled trials. Furthermore, more data are needed on protein from specific sources in relation to BP, and on the protein-BP relation in population subgroups.

Measures of postprandial wellness after single intake of two protein-carbohydrate meals.

The general feeling of wellness after food consumption may play an important role in regulating food intake. This exploratory study aimed at identifying and evaluating measures of such postprandial wellness, tentatively defined as subjective appreciation of life after food intake. The study had a randomized cross-over, double blind design. Twenty-one healthy men with mean age of 33 + or - 14 years received two liquid breakfasts with either high protein/low carbohydrate (HP/LC) or low protein/high carbohydrate (LP/HC) ratio on separate days with a washout period of one week in between. Subjective reports on satiety and postprandial wellness (pleasantness, satisfaction, relaxation, sleepiness, physical energy and mental alertness) were established using visual analogue scales at regular time points after consumption of the breakfasts up to 240 min. Blood concentrations of CCK, ghrelin, glucose, and insulin were determined at the same time points. The HP/LC breakfast induced higher levels of satiety and specific parameters of postprandial wellness (satisfaction, pleasantness and the pleasantness of these feelings) than the LP/HC breakfast at 3 or 4h after consumption. The corresponding higher CCK and lower ghrelin concentrations at these time points supported these subject reported changes. These results indicate that meal composition influences some parameters of postprandial wellness in line with physiological responses. Further research is warranted to confirm the observed relationships. Also the relevance for food intake behaviour remains to be established.

Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men.

BACKGROUND: A high homocysteine concentration is a potential risk factor for cardiovascular disease that can be reduced through betaine supplementation. Choline is the precursor for betaine, but the effects of choline supplementation on plasma total homocysteine (tHcy) concentrations in healthy humans are unknown. OBJECTIVE: The objective was to investigate whether supplementation with phosphatidylcholine, the form in which choline occurs in foods, reduces fasting and postmethionine-loading concentrations of plasma tHcy in healthy men with mildly elevated plasma tHcy concentrations. DESIGN: In a crossover study, 26 men ingested approximately 2.6 g choline/d (as phosphatidylcholine) or a placebo oil mixture for 2 wk in random order. Fatty acid composition and fat content were similar for both treatments. A methionine-loading test was performed on the first and last days of each supplementation period. RESULTS: Phosphatidylcholine supplementation for 2 wk decreased mean fasting plasma tHcy by 18% (-3.0 micromol/L; 95% CI: -3.9, -2.1 micromol/L). On the first day of supplementation, a single dose of phosphatidylcholine containing 1.5 g choline reduced the postmethionine-loading increase in tHcy by 15% (-4.8 micromol/L; 95% CI: -6.8, -2.8 micromol/L). Phosphatidylcholine supplementation for 2 wk reduced the postmethionine-loading increase in tHcy by 29% (-9.2 micromol/L; 95% CI: -11.3, -7.2 micromol/L). All changes were relative to placebo. CONCLUSIONS: A high daily dose of choline, supplemented as phosphatidylcholine, lowers fasting as well as postmethionine-loading plasma tHcy concentrations in healthy men with mildly elevated tHcy concentrations. If high homocysteine concentrations indeed cause cardiovascular disease, choline intake may reduce cardiovascular disease risk in humans.