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Articles by Penny M. Kris-Etherton
Total Records ( 5 ) for Penny M. Kris-Etherton
  Yumei Cao , David T. Mauger , Christine L. Pelkman , Guixiang Zhao , Stacie M. Townsend and Penny M. Kris-Etherton
 

Background

Dyslipidemia increases coronary heart disease (CHD) risk and often presents in diabetes, which amplifies risk of CHD. Lower fat (LF) diets increase triglyceride (TG) and decrease high-density lipoprotein cholesterol (HDL-C); moderate fat (MF) diets decrease TG and lower HDL-C less.

Objective

To quantify the magnitude of lipid and lipoprotein responses to MF versus LF cholesterol-lowering weight maintenance diets in subjects with and without diabetes.

Methods

A meta-analysis of 30 controlled-feeding studies (n = 1213 subjects) was conducted to evaluate LF versus MF diets on lipids and lipoproteins in subjects with and without diabetes.

Results

In all subjects, MF and LF diets decreased low-density lipoprotein cholesterol (LDL-C) similarly. MF diets decreased HDL-C less versus LF diets. The estimated increase in HDL-C after MF diets versus LF diets was 2.28 mg/dL (95% confidence interval 1.66 to 2.90 mg/dL, P < .0001). MF diets decreased TG, whereas LF diets increased TG. The decrease in TG was −9.36 mg/dL (−12.16 to −6.08 mg/dL, P < .00001) for MF versus LF diets. In subjects with diabetes, there was a similar increase in HDL-C (2.28 mg/dL) versus subjects without diabetes; however, there was a greater reduction in TG (−24.79 mg/dL, P < .05) on the MF diet. Subjects with diabetes had greater reductions in the total cholesterol (TC) to HDL-C ratio (TC:HDL-C) (-0.62, P < .0001) and non-HDL-C (−5.39 %, P < .06) after MF versus LF diets.

Conclusions

Both men and women had greater estimated reductions (6.37% and 9.34%, respectively) in predicted CHD risk after MF diets compared to LF diets. Moreover, based on greater reductions in TG, the TC:HDL-C ratio and non-HDL-C in subjects with diabetes, the CHD risk reduction would be greater for a MF versus a LF weight maintenance, cholesterol-lowering diet.

  Rodney A. Velliquette , Peter J. Gillies , Penny M. Kris-Etherton , John W. Green , Guixiang Zhao and John P. Vanden Heuvel
 

Background

Polyunsaturated fatty acids lower serum triglycerides by a mechanism that may involve the inhibition of stearoyl-CoA desaturase (SCD).

Objective

We sought to evaluate the effects of serum fatty acids on 1) the SCD index in a controlled clinical setting, and 2) SCD regulation in Hep G2 cells.

Methods

The SCD index was determined in 23 subjects randomly sequenced through 3 diets for 6 weeks in a crossover study. Diets were variably enriched with n-3 and n-6 polyunsaturated fatty acids; notably, monounsaturated fatty acids were held constant. Effects of linoleic acid (LA), α-linolenic acid (ALA), and eicosapentaenoic acid (EPA) on mRNA levels of SCD, fatty acid elongases 5 and 6 (Elovl5 and Elovl6), fatty acid synthase, carnitine palmitoyltransferase-1, and sterol response element binding protein-1c were investigated in Hep G2 cells after 24-hour incubations.

Results

The SCD indexes C18:1/18:0 and C16:1/C16:0 were significantly (P < .0001) correlated with serum TG with R2 values of 0.71 and 0.58. The correlation was negatively associated with LA and positively associated with ALA. LA and EPA decreased SCD mRNA (EC50 of 0.50 and 1.67 μM), whereas ALA did not. Likewise, LA and EPA decreased sterol response element binding protein-1c mRNA (EC50 of 0.78 and 1.78 μM), but ALA did not. Similar results were observed for Elovl6. GW9662, a peroxisome proliferation activator receptor antagonist, did not obviate the effects of LA and EPA on SCD mRNA.

Conclusions

Diets enriched in LA, ALA, and by metabolic inference EPA, can regulate SCD activity at the level of transcription, a nutritional intervention that may be useful in the management of increased levels of serum triglycerides in cardiometabolic disorders.

  Seth J. Baum , Penny M. Kris-Etherton , Walter C. Willett , Alice H. Lichtenstein , Lawrence L. Rudel , Kevin C. Maki , Jay Whelan , Christopher E. Ramsden and Robert C. Block
  Research dating back to the 1950s reported an association between the consumption of saturated fatty acids (SFAs) and risk of coronary heart disease. Recent epidemiological evidence, however, challenges these findings. It is well accepted that the consumption of SFAs increases low-density lipoprotein cholesterol (LDL-C), whereas carbohydrates, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) do not. High-density lipoprotein (HDL)-C increases with SFA intake. Among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C; compared with a low-fat diet, a moderate-fat diet will lower triglycerides and increase HDL-C. Now, there is some new evidence that is questioning the health benefits of even MUFAs and PUFAs. In addition, in a few recent studies investigators have also failed to demonstrate expected cardiovascular benefits of marine-derived omega-3 fatty acids. To clarify the clinical pros and cons of dietary fats, the National Lipid Association held a fatty acid symposium at the 2011 National Lipid Association Scientific Sessions. During these sessions, the science regarding the effects of different fatty acid classes on coronary heart disease risk was reviewed.
  Harold E. Bays , Peter P. Toth , Penny M. Kris-Etherton , Nicola Abate , Louis J. Aronne , W. Virgil Brown , J. Michael Gonzalez-Campoy , Steven R. Jones , Rekha Kumar , Ralph La Forge and Varman T. Samuel
  The term “fat” may refer to lipids as well as the cells and tissue that store lipid (ie, adipocytes and adipose tissue). “Lipid” is derived from “lipos,” which refers to animal fat or vegetable oil. Adiposity refers to body fat and is derived from “adipo,” referring to fat. Adipocytes and adipose tissue store the greatest amount of body lipids, including triglycerides and free cholesterol. Adipocytes and adipose tissue are active from an endocrine and immune standpoint. Adipocyte hypertrophy and excessive adipose tissue accumulation can promote pathogenic adipocyte and adipose tissue effects (adiposopathy), resulting in abnormal levels of circulating lipids, with dyslipidemia being a major atherosclerotic coronary heart disease risk factor. It is therefore incumbent upon lipidologists to be among the most knowledgeable in the understanding of the relationship between excessive body fat and dyslipidemia. On September 16, 2012, the National Lipid Association held a Consensus Conference with the goal of better defining the effect of adiposity on lipoproteins, how the pathos of excessive body fat (adiposopathy) contributes to dyslipidemia, and how therapies such as appropriate nutrition, increased physical activity, weight-management drugs, and bariatric surgery might be expected to impact dyslipidemia. It is hoped that the information derived from these proceedings will promote a greater appreciation among clinicians of the impact of excess adiposity and its treatment on dyslipidemia and prompt more research on the effects of interventions for improving dyslipidemia and reducing cardiovascular disease risk in overweight and obese patients.
  Jerome D. Cohen , Karen E. Aspry , Alan S. Brown , JoAnne M. Foody , Roy Furman , Terry A. Jacobson , Dean G. Karalis , Penny M. Kris-Etherton and Ralph LaForge
  The workshop discussions focused on how low-density lipoprotein cholesterol (LDL-C) goal attainment can be enhanced with the use of health information technology (HIT) in different clinical settings. A gap is acknowledged in LDL-C goal attainment, but because of the passage of the American Recovery & Reinvestment Act and the Health Information Technology for Economic and Clinical Health Acts there is now reason for optimism that this gap can be narrowed. For HIT to be effectively used to achieve treatment goals, it must be implemented in a setting in which the health care team is fully committed to achieving these goals. Implementation of HIT alone has not resulted in reducing the gap. It is critical to build an effective management strategy into the HIT platform without increasing the overall work/time burden on staff. By enhancing communication between the health care team and the patient, more timely adjustments to treatment plans can be made with greater opportunity for LDL-C goal attainment and improved efficiency in the long run. Patients would be encouraged to take a more active role. Support tools are available. The National Lipid Association has developed a toolkit designed to improve patient compliance and could be modified for use in an HIT system. The importance of a collaborative approach between nongovernmental organizations such as the National Lipid Association, National Quality Forum, HIT partners, and other members of the health care industry offers the best opportunity for long-term success and the real possibility that such efforts could be applied to other chronic conditions, for example, diabetes and hypertension.
 
 
 
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