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Clinical trial affirms palmitoleic acid benefit

Clinical trial affirms palmitoleic acid benefit

Life Extension Update

Tuesday, March 31, 2015. A randomized trial reported in the November-December 2014 issue of the Journal of Clinical Lipidology found lower inflammation, triglycerides and low-density lipoprotein (LDL) cholesterol in men and women given the omega-7 fatty acid palmitoleic acid in comparison with a placebo. "Our objective was to conduct the first randomized controlled trial of purified palmitoleic acid supplementation in humans," write authors Adam M. Bernstein, MD, ScD, and Michael F. Roizen, MD, of the Cleveland Clinic, along with Luis Martinez, MD, MPH, of Xyrion Medical Institute. "We hypothesized that supplementation would improve serum lipids and decrease inflammation."

The trial included 60 adults between the ages of 17 and 70 years who had lipid abnormalities as well as mild systemic inflammation as evidenced by elevated C-reactive protein (CRP) levels. Participants were randomized to receive a capsule containing 220.5 milligrams cis-palmitoleic acid or a placebo for 30 days. Blood samples collected before and after the treatment period were analyzed for high-density lipoprotein (HDL) and LDL cholesterol, triglycerides, CRP and other factors.

Among subjects who received palmitoleic acid, HDL cholesterol increased by 5%, and LDL cholesterol, triglycerides and CRP decreased by 8%, 15% and 44% in comparison with the control group.

"These findings build on a growing body of in vitro, animal, and human studies, demonstrating the importance of palmitoleic acid to regulating metabolism," the authors conclude. "Thus, purified palmitoleic acid may be a therapeutic approach in helping maintain lipid levels within a healthy range as well as improving inflammatory markers in patients with mild dyslipidemia and inflammation."

 
What's Hot
EPA reduces fat cell growth and inflammation in obese mice
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The March 2015 issue of the Journal of Nutrition reported the discovery of a reduction in adipocyte (fat cell) size and inflammation in mice given a high fat diet supplemented with eicosapentaenoic acid (EPA), an omega 3 polyunsaturated fatty acid.

The current study analyzed white adipose tissue from animals utilized in an experiment that compared the effects of a low fat diet, a high fat diet and a high fat diet that contained EPA for eleven weeks, or a high fat diet for six weeks followed by the addition of EPA for five weeks. In comparison with those that received the high fat diet alone, the diet combined with EPA resulted in decreased body weight, body fat, adipocyte size and macrophage infiltration into fat tissue (an indicator of inflammation). While there were no significant differences in body or fat pad weights between mice fed a high fat diet and those given the high fat diet supplemented after six weeks with EPA, the latter group had lower average adipocyte size and macrophage infiltration, indicating that EPA could prevent as well as reverse adipocyte inflammation and hypertrophy resulting from high fat feeding.

In experimentation involving cultured mouse fat cells, the researchers, from Texas Tech University in Lubbock, determined that EPA helped regulate mitochondrial function by increasing oxygen consumption and fatty acid oxidation.

"In this study we showed that both adipocyte size and macrophage infiltration were reduced upon EPA supplementation," the authors conclude. "Future studies will determine the cell signaling and molecular mechanisms mediating these EPA effects."

 
Life Extension Clinical Research Update

Participate in a Clinical Study:
Support Male Sexual Health
South Florida Location

Study Objective:
Assess the effect of a nutritional supplement for male sexual health over the course of 30 days.

To Qualify:

  • You must be between 50 and 70 years of age.
  • Be in a stable sexual relationship for at least 6 or more months.
  • Able to comply with all study procedures and visits.

Your Involvement:

  • You will make 3 visits over 30 days.
  • You will receive the nutritional supplement to be studied, blood pressure evaluations, and blood tests including a male hormone panel.
  • Upon successful completion of the trial, you will be compensated for time and travel up to $100.
Register For This Study

Or call 1-866-517-4536

If you refer someone who enrolls in a study and completes their final visit with closeout procedures, you will be compensated the amount noted for the study.

https://www.lifeextension.com/clinicalresearch/ClinicalTrials.htm


Health Concern

Chronic inflammation

Of the ten leading causes of mortality in the United States, chronic, low-level inflammation contributes to the pathogenesis of at least seven. These include heart disease, cancer, chronic lower respiratory disease, stroke, Alzheimer's disease, diabetes, and nephritis (Centers for Disease Control and Prevention 2011; Bastard et al. 2006; Cao 2011, Jha et al. 2009; Ferrucci et al. 2010; Glorieux et al. 2009; Kundu et al. 2008; Murphy 2012; Singh et al. 2011).

Inflammation has classically been viewed as an acute (short term) response to tissue injury that produces characteristic symptoms and usually resolves spontaneously. More contemporary revelations show chronic inflammation to be a major factor in the development of degenerative disease and loss of youthful functions.

Chronic inflammation can be triggered by cellular stress and dysfunction, such as that caused by excessive calorie consumption, elevated blood sugar levels, and oxidative stress. It is now clear that the destructive capacity of chronic inflammation is unprecedented among physiologic processes (Karin et al. 2006).

The danger of chronic, low-level inflammation is that its silent nature belies its destructive power.

In fact, stress-induced inflammation, once triggered, can persist undetected for years, or even decades, propagating cell death throughout the body. Due to the fact that it contributes so greatly to deterioration associated with the aging process, this silent state of chronic inflammation has been coined "inflammaging".

Read More
 
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