Blog from the American Heart Association’s Epidemiology and Cardiovascular Disease Meeting


Beyond Cholesterol: Role of Omega-3 Fatty acids in etiology of Coronary Heart Disease

Lecturer: Daan Kromhout, MD (Wageneengen University, The Netherlands)
Blogger: Hsiao Lai, MD (East Carolina University – Brody School of Medicine)

[Critique this blog]

Reviewed several studies:
“7 Countries Study – n=500”
Observational study comparing CHD mortality in 16 cohorts composed of several regions in Europe, US, Serbia, and Japan.

Found that US and N. Europe had highest 6-9 yr RR vs areas with “Mediterranean” type diets higher in O-3 fatty Acids (OFAs) such as Mediterranean S. Europe and SE Inland Europe. Japan had lowest RR of CHD.

Also found ~ 12% increase in RR of cardiovascular disease with every 20mg/dL increase in serum cholesterol.

Leiden Intervention Trial
Showed positive correlation between TC/HDL and mean coronary artery internal diameter
In addition demonstrated regression of coronary a. atherosclerosis with reduction of TC/HDL

Metaanalysis by Mazzarina & Ramsden et al: Br. J. Nutr 2010
Replacing Saturated FA (SFA) with polyunsaturated FA (PUFA)
The conglomerate of studies were not able to demonstrate an overall improvement in survival, in fact some studies showed a small negative effect
Further subanalysis of the studies showed a difference in the type of PUFA:
n-3 (EPA/DHA +ALA) vs n-6 (linoleic acid)
n-3: increased dietary levels may result in increase percent of RBC cell membrane
n-3 content and beneficial effect on ion channel function,
n-6: may have adverse effects on cardiovascular mortality
Comparison of Inuit (high in fish protein) vs Danish dietary composition
With increasing quartile of fish intake found decreasing adjusted OR of cardiac arrest from OR=1 (0 gm/day) to OR=0.4 at highest quartile of fish intake (460gm/day)
Steepest reduction in OR of cardiovascular death demonstrated when comparing individuals with no fish intake to 30 grams/day.

Zutphen 20-yr Study: NEJM May 1985, v312, n19
0 gm/day -> 1-14 gm/day fish intake ↓RR by 40%
0 gm/day -> 1-2x/week fish intake ↓RR by 50%

Dart Trial & Dart2 Trial
Substituted margarines with different compositions of PUFA in angina patients.
Found no effect of EHA/DHA substitution for margarine on endpoints.

In summary: The Jury is still out on PUFAs. The type of PUFA may determine the effect of SFA replacement with PUFA. More studies are needed in this area. Strong observational data demonstrating that diets high in O3-FA are correlated with lower cardiovascular mortality. In addition increasing fish intake especially from none or very low amounts to low or modest amounts may have a beneficial effect in terms of risk reduction for cardiovascular mortality.


Gastric Bypass as Treatment for Type 2 DM
Lecturer: David Cummings, MD
Blogger: Hsiao Lai, MD (East Carolina University – Brody School of Medicine)

[Critique this blog]

COSMID Trial
30-88% reduction in mortality in MOB following Rou en Y Gastric Bypass (RYGB)
80-85% full remission of T2DM after RYGB at 1-3 years postop

Potential Mechanisms
1. Weight Loss
2. Improved insulin sensitivity in hepatic, muscle or adipose tissue
3. Other

Banding vs RYGB
Response in terms of reduction of HbA1c was more rapid and much more marked with RYGB vs gastric banding despite equivalent weight loss- suggesting an additional mechanism

Thin Asian diabetics (ave BMI 23) also demonstrated benefit with RYGB with improvements in HTN, HLD and diabetic parameters. 80% were off antiglycemic medications at 1 month post bypass and 100% at 3 months, with average HbA1c of 6.1. Average fasting BG at 9mo and 2 yrs off of medications was 89. Some patients however developed delayed episodes of severe refractory hyperinsulinemic hypoglycemia as late as 9 years following RYGB requiring pancreatectomy suggesting Beta cell trophic effect of RYGB.

In obese Caucasian diabetics (BMI 20-35) 88% achieved full remission of T2DM defined as HbA1c <6.5 off medications. 11% demonstrated improved HbA1c. Achieved weight loss in the remission vs improved group were equivalent suggesting that factors aside from just weight loss are at play.

Ghrelin
Peptide hormone produced in stomach and duodenum that causes increased hunger
Moderates other hormones in a prodiabetic manner (incr GH, ACTH, cortisol)
Levels decrease rapidly following eating
24 hr profile is increased following weight loss thus may inhibit long term weight loss
However levels are very low following RYGB and remain low despite significant weight loss

“Lower Intestinal Hypothesis”
Hyperstimulation of GLP1 in distal ileum


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