Omega-6 and Omega-3 Balance References

Summary and conclusion
Direct enhancement of insulin secretion by n-3 PUFAs is indicated by the results of some studies, mostly in vitro. The in vivo data and human studies have inconsistent outcomes, indicating that the species of n-3 PUFAs, length of fatty acid treatment, how they are provided, and the specific physiological state are important for the effect of n-3 PUFAs on insulin secretion and β cell function. n-3 PUFAs may be able to modulate insulin secretion from pancreatic β-cells directly by altering lipid raft structure and function, and binding to receptors including PPAR, GPR40, and GPR120, and indirectly by promoting adipokine production and inhibiting the expression of pro-inflammatory mediators in adipose tissue (Fig. 3). However, these hypotheses have not been stringently tested. n-3 PUFAs may have value as supplements to prevent or slow down the impairment of insulin secretion in diabetes, and to decrease the use of anti-diabetic drugs, which warrants more comprehensive studies.

Abstract
n-3 polyunsaturated fatty acids (PUFAs) are a subgroup of fatty acids with broad health benefits, such as lowering blood triglycerides and decreasing the risk of some types of cancer. A beneficial effect of n-3 PUFAs in diabetes is indicated by results from some studies. Defective insulin secretion is a fundamental pathophysiological change in both types 1 and 2 diabetes. Emerging studies have provided evidence of a connection between n-3 PUFAs and improved insulin secretion from pancreatic β-cells. This review summarizes the recent findings in this regard and discusses the potential mechanisms by which n-3 PUFAs influence insulin secretion from pancreatic β-cells.

Wang X1, Chan CB2.
Author information
1Department of AgriculturalFood and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3.
2Department of AgriculturalFood and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3 cbchan@ualberta.ca.
J Endocrinol. 2015 Mar;224(3):R97-106. doi: 10.1530/JOE-14-0581. Epub 2014 Dec 8.

Christopher E. Ramsden, MD Keturah R. Faurot, PA, MPH Pedro Carrera-Bastos, BA Loren Cordain, PhD Michel De Lorgeril, MD, PhD Laurence S. Sperling, MD
Department of Physical Medicine and Rehabilitation, Program on Integrative Medicine, University of North Carolina–Chapel Hill School of Medicine
Current Treatment Options in Cardiovascular Medicine 2009, 11:289–301 Current Medicine Group LLC ISSN 1092-8464

The totality of worldwide medical and scientific evidence indicates that wide ranges of total fat intakes are compatible with a healthy diet and that fat quality, rather than total fat quantity, plays a central role in determining CHD risk. Integrating evolutionary, historical, and global perspectives with modern experimental evidence provides a broader framework for identifying key elements of optimal diets for CHD prevention. This approach also may be less likely to cause harm. As demonstrated, convergence of numerous lines of evidence leads to the following conclusions:

− n-3 PUFAs, especially long-chain n-3 PUFAs, reduce CHD risk.
Increasing intake is unlikely to cause harm.

− Industrially produced TFAs increase CHD risk. Restricting or eliminating TFA intake is unlikely to cause harm.

− MUFAs possibly reduce CHD risk. Substituting MUFAs for TFAs or SFAs, especially palmitate, is unlikely to cause harm.

− High consumption of palmitate may increase CHD risk. The relationship of stearate, laurate, and myristate to CHD is less clear. Partial substitution of MUFAs for palmitate, and perhaps other SFAs, may reduce CHD risk and is unlikely to cause harm.

− Optimal n-6 LA intake for CHD prevention is a matter of controversy. US health promotion agencies recommend high LA consumption despite the fact that 1) modern Western LA intake is unnaturally high by evolutionary, historical, and global standards, and 2) populations with very low CHD risk have uniformly low LA intakes. CHD risk declined markedly in the sole long-term randomized trial in which LA was lowered as part of a Mediterranean diet, indicating that high LA intake is not a requirement for CHD risk reduction. Controlled trials and observational studies comparing high with very high LA intakes are insufficient for drawing conclusions regarding optimal LA intake. In light of current guidelines urging high LA intake, the CHD impact of lowering LA to preindustrial levels is an issue of major public health importance. For now, the replacement of LA-rich oils with MUFA-rich oils (eg, olive oil) may provide considerable cardiometabolic benefits and is unlikely to do harm.