The Low-Cost, Moderate-Cost, and Liberal Food Plans, 2007

The Low-Cost, Moderate-Cost, and Liberal Food Plans, three fundamental parts of the U.S. food guidance system, have been revised by USDA’s Center for Nutrition Policy and Promotion, with assistance from USDA’s Food and Nutrition Service, Economic Research Service, and Agricultural Research Service. The plans provide representative healthful market baskets at three different cost levels. This revision maintains the same inflation-adjusted costs as those of the previous three food plans, last revised in 2003. In line with previous food plans, an assumption used to develop these plans was that all purchased food is consumed at home. The newly revised (2007) Low-Cost, Moderate-Cost, and Liberal Food Plans differ from, and improve upon, the previous versions in a number of ways: • The Plans are based on the most current dietary standards: the 2005 Dietary Guidelines for Americans as well as the 2005 MyPyramid Food Guidance System. • The Plans use the latest data on food consumption, nutrient content, and food prices: the 2001-2002 National Health and Nutrition Examination Survey and the 2001- 2002 Food Price Database. • The Plans offer a more realistic reflection of the time available for home food preparation; hence, each plan incorporates more prepared foods within the recipes and requires fewer preparations from scratch.USDA Food Plans, Low-Cost Food Plan, Moderate-Cost Food Plan, Liberal Food Plan, Diet Quality, Cost of Food, Agricultural and Food Policy, Consumer/Household Economics, Food Consumption/Nutrition/Food Safety, Health Economics and Policy,

The Low-Cost, Moderate-Cost, and Liberal Food Plans, 2007

The Low-Cost, Moderate-Cost, and Liberal Food Plans, three fundamental parts of the U.S. food guidance system, have been revised by USDA’s Center for Nutrition Policy and Promotion, with assistance from USDA’s Food and Nutrition Service, Economic Research Service, and Agricultural Research Service. The plans provide representative healthful market baskets at three different cost levels. This revision maintains the same inflation-adjusted costs as those of the previous three food plans, last revised in 2003. In line with previous food plans, an assumption used to develop these plans was that all purchased food is consumed at home. The newly revised (2007) Low-Cost, Moderate-Cost, and Liberal Food Plans differ from, and improve upon, the previous versions in a number of ways: • The Plans are based on the most current dietary standards: the 2005 Dietary Guidelines for Americans as well as the 2005 MyPyramid Food Guidance System. • The Plans use the latest data on food consumption, nutrient content, and food prices: the 2001-2002 National Health and Nutrition Examination Survey and the 2001- 2002 Food Price Database. • The Plans offer a more realistic reflection of the time available for home food preparation; hence, each plan incorporates more prepared foods within the recipes and requires fewer preparations from scratch

USDA's Low-Cost, Moderate-Cost, and Liberal Food Plans: Development and Expenditure Shares

The Low-Cost, Moderate-Cost, and Liberal Food Plans represent nutritious diets at various costs. This revision of the market baskets of each food plan using a mathematical optimization model reflects recent changes in dietary guidance and incorporates updated information on food composition, consumption patterns, and food prices at the same inflation-adjusted cost of the previous food plans. This analysis shows how food expenditures need to change to obtain a healthful diet. The analysis is particularly significant because average food expenses exceed the cost of the Low-Cost Food Plan. Hence, Americans could achieve a healthful diet at less the cost than they are currently paying

Eating a Healthy Diet: Is Cost a Major Factor?

We examine the association between food expenditure and overall diet quality using a model where we assumed dietary quality is a function of health conditions, life style choices, total food expenditures, and socio-economic status. We use cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) 2001-02 and the U.S. Department of Agriculture (USDA)’s Center for Nutrition Policy and Promotion Food Prices Database. Diet quality is measured using the USDA Healthy Eating Index-2005. Our findings suggest that there is no statistically significant association between total diet quality and diet cost for men, but a small association for women. Compared with diet cost, health conditions, life style choices, and socio-economic status play an important role in determining diet quality

Cluster Differentiating 36 (CD36) Deficiency Attenuates Obesity-Associated Oxidative Stress in the Heart

<div><p>Rationale</p><p>Obesity is often associated with a state of oxidative stress and increased lipid deposition in the heart. More importantly, obesity increases lipid influx into the heart and induces excessive production of reactive oxygen species (ROS) leading to cell toxicity and metabolic dysfunction. Cluster differentiating 36 (CD36) protein is highly expressed in the heart and regulates lipid utilization but its role in obesity-associated oxidative stress is still not clear.</p><p>Objective</p><p>The aim of this study was to determine the impact of CD36 deficiency on cardiac steatosis, oxidative stress and lipotoxicity associated with obesity.</p><p>Methods and Results</p><p>Studies were conducted in control (Lean), obese leptin-deficient (Lep^ob/ob) and leptin-CD36 double null (Lep^ob/obCD36^-/-) mice. Compared to lean mice, cardiac steatosis, and fatty acid (FA) uptake and oxidation were increased in Lep^ob/ob mice, while glucose uptake and oxidation was reduced. Moreover, insulin resistance, oxidative stress markers and NADPH oxidase-dependent ROS production were markedly enhanced. This was associated with the induction of NADPH oxidase expression, and increased membrane-associated p47^phox, p67^phox and protein kinase C. Silencing CD36 in Lep^ob/ob mice prevented cardiac steatosis, increased insulin sensitivity and glucose utilization, but reduced FA uptake and oxidation. Moreover, CD36 deficiency reduced NADPH oxidase activity and decreased NADPH oxidase-dependent ROS production. In isolated cardiomyocytes, CD36 deficiency reduced palmitate-induced ROS production and normalized NADPH oxidase activity.</p><p>Conclusions</p><p>CD36 deficiency prevented obesity-associated cardiac steatosis and insulin resistance, and reduced NADPH oxidase-dependent ROS production. The study demonstrates that CD36 regulates NADPH oxidase activity and mediates FA-induced oxidative stress.</p></div

Effects of CD36 deficiency on cardiac lipid contents, fatty uptake and incorporation in lipids.

<p>Cardiac lipid contents (A) were determined enzymatically after lipid extraction as described in the Methods. Fatty acid uptake in indicated organs (B) was assessed using ¹²⁵I-BMIPP. Mice were injected with 5 μCi of ¹²⁵I-BMIPP into the tail vein and tissues were removed 2 h later. Incorporation of BMIPP in heart lipids (C) was examined after extraction and TLC separation. Polar lipids include phospholipids and monoacylglycerides. Results are presented as mean ± SEM (n = 6–7 per group). Differences between Lep^ob/ob and Lean mice are indicated with asterisks ** p < 0.01, and * p < 0.05. Differences between Lep^ob/ob CD36^-/- and Lep^ob/ob mice are indicated with alphabetic letters with ^a p < 0.01 and ^b p < 0.05.</p

Effects of CD36 deficiency on glucose metabolism parameters.

<p>A) Glucose tolerance test (GTT) in overnight fasted control lean (Lean), leptin null (Lep^ob/ob) and leptin and CD36 double null (Lep^ob/obCD36^-/-) mice. B) Insulin tolerance test (ITT) in 4-h fasted mice. C) Uptake of ¹⁸F-2-FDG in organs of overnight fasted mice. Mice were injected with 5 μCi of ¹⁸F-2-FDG in a lateral tail vein and glucose uptake in indicated organ was determined as described in the Methods. Results are presented as mean ± SEM (n = 5–7 per group). For GTT and ITT, statistical differences between initial time (0 min) and subsequent time points (after glucose and insulin injection) were performed by repeated measurement ANOVA test. Differences between groups Tukey’s and student t tests. Statistical significance between Lep^ob/ob and Lean mice are indicated with asterisks ** p < 0.01, and * p < 0.05. Significance between Lep^ob/ob CD36^-/- and Lep^ob/ob mice are indicated with alphabetic letters with ^a p < 0.001, ^b p < 0.01 and ^b p < 0.05. Statistical significance between Lep^ob/ob CD36^-/- and Lean mice are indicated with a capital alphabetic letter ^A p < 0.01.</p

Effects of CD36 deficiency on protein expression.

<p>Representative blots (A) and mRNA abundance (B) of CD36, FATP1, H-FABP, PPARα in hearts of mice (n = 6 per group). Protein levels were examined by Western blotting and mRNA abundance was investigated with qPCR as described in the Methods. Differences between Lep^ob/ob and Lean mice are indicated with an asterisk * p < 0.05, and differences between Lep^ob/ob CD36^-/- and Lep^ob/ob mice are indicated with an alphabetic letter ^a p <0.05.</p

Effects of CD36 deficiency on insulin signaling.

<p>A) Representative blots and B) ratio of phosphorylated (p) to total (t) Akt and IRS1 in hearts 10 minutes after insulin injection. Results are presented as mean ± SEM (n = 5 per group). Statistical differences between Lep^ob/ob and Lean mice are indicated with an asterisk * p < 0.01, and differences between Lep^ob/ob CD36^-/- and Lep^ob/ob mice are indicated with an alphabetic letter with ^a p <0.05.</p