Protein-enriched meal replacements do not adversely affect liver, kidney or bone density: an outpatient randomized controlled trial

<p>Abstract</p> <p>Background</p> <p>There is concern that recommending protein-enriched meal replacements as part of a weight management program could lead to changes in biomarkers of liver or renal function and reductions in bone density. This study was designed as a placebo-controlled clinical trial utilizing two isocaloric meal plans utilizing either a high protein-enriched (HP) or a standard protein (SP) meal replacement in an outpatient weight loss program.</p> <p>Subjects/methods</p> <p>100 obese men and women over 30 years of age with a body mass index (BMI) between 27 to 40 kg/m²were randomized to one of two isocaloric weight loss meal plans 1). HP group: providing 2.2 g protein/kg of lean body mass (LBM)/day or 2). SP group: providing 1.1 g protein/kg LBM/day. Meal replacement (MR) was used twice daily (one meal, one snack) for 3 months and then once a day for 9 months. Body weight, lipid profiles, liver function, renal function and bone density were measured at baseline and 12 months.</p> <p>Results</p> <p>Seventy subjects completed the study. Both groups lost weight (HP -4.29 ± 5.90 kg vs. SP -4.66 ± 6.91 kg, p < 0.01) and there was no difference in weight loss observed between the groups at one year. There was no significant change noted in liver function [AST (HP -2.07 ± 10.32 U/L, p = 0.28; SP 0.27 ± 6.67 U/L, p = 0.820), ALT (HP -1.03 ± 10.08 U/L, p = 0.34; SP -2.6 ± 12.51 U/L, p = 0.24), bilirubin (HP 0.007 ± 0.33, U/L, p = 0.91; SP 0.07 ± 0.24 U/L, p = 0.120), alkaline phosphatase (HP 2.00 ± 9.07 U/L, p = 0.240; SP -2.12 ± 11.01 U/L, p = 0.280)], renal function [serum creatinine (HP 0.31 ± 1.89 mg/dL, p = 0.380; SP -0.05 ± 0.15 mg/dL, p = 0.060), urea nitrogen (HP 1.33 ± 4.68 mg/dL, p = 0.130; SP -0.24 ± 3.03 mg/dL, p = 0.650), 24 hour urine creatinine clearance (HP -0.02 ± 0.16 mL/min, p = 0.480; SP 1.18 ± 7.53 mL/min, p = 0.400), and calcium excretion (HP -0.41 ± 9.48 mg/24 hours, p = 0.830; SP -0.007 ± 6.76 mg/24 hours, p = 0.990)] or in bone mineral density by DEXA (HP 0.04 ± 0.19 g/cm², p = 0.210; SP -0.03 ± 0.17 g/cm², p = 0.320) in either group over one year.</p> <p>Conclusions</p> <p>These studies demonstrate that protein-enriched meals replacements as compared to standard meal replacements recommended for weight management do not have adverse effects on routine measures of liver function, renal function or bone density at one year. Clinicaltrial.gov: NCT01030354.</p

Food Use and Health Effects of Soybean and Sunflower Oils

This review provides a scientific assessment of current knowledge of health effects of soybean oil (SBO) and sunflower oil (SFO). SBO and SFO both contain high levels of polyunsaturated fatty acids (PUFA) (60.8 and 69%, respectively), with a PUFA:saturated fat ratio of 4.0 for SBO and 6.4 for SFO. SFO contains 69% C18:2n-6 and less than 0.1% C18:3n-3, while SBO contains 54% C18:2n-6 and 7.2% C18:3n-3. Thus, SFO and SBO each provide adequate amounts of C18:2n-6, but of the two, SBO provides C18:3n-3 with a C18:2n-6:C18:3n-3 ratio of 7.1. Epidemiological evidence has suggested an inverse relationship between the consumption of diets high in vegetable fat and blood pressure, although clinical findings have been inconclusive. Recent dietary guidelines suggest the desirability of decreasing consumption of total and saturated fat and cholesterol, an objective that can be achieved by substituting such oils as SFO and SBO for animal fats. Such changes have consistently resulted in decreased total and low-density-lipoprotein cholesterol, which is thought to be favorable with respect to decreasing risk of cardiovascular disease. Also, decreases in high-density-lipoprotein cholesterol have raised some concern. Use of vegetable oils such as SFO and SBO increases C18:2n-6, decreases C20:4n-6, and slightly elevated C20:5n-3 and C22:6n-3 in platelets, changes that slightly inhibit platelet generation of thromboxane and ex vivo aggregation. Whether chronic use of these oils will effectively block thrombosis at sites of vascular injury, inhibit pathologic platelet vascular interactions associated with atherosclerosis, or reduce the incidence of acute vascular occlusion in the coronary or cerebral circulation is uncertain. Linoleic acid is needed for normal immune response, and essential fatty acid (EFA) deficiency impairs B and T cell-mediated responses. SBO and SFO can provide adequate linoleic acid for maintenance of the immune response. Excess linoleic acid has supported tumor growth in animals, an effect not verified by data from diverse human studies of risk, incidence, or progression of cancers of the breast and colon. Areas yet to be investigated include the differential effects of n-6- and n-3-containing oil on tumor development in humans and whether shorter-chain n-3 PUFA of plant origin such as found in SBO will modulate these actions of linoleic acid, as has been shown for the longer-chain n-3 PUFA of marine oil