The Cause for Heart Disease and Strokes
Pages 122-126
Fred A. Kummerow

DOI: http://dx.doi.org/10.6000/1929-5634.2013.02.02.7
Published: 30 August 2013

Abstract: There has been no solution to heart disease to date. I obtained discarded veins from bypass (CABG) surgeries and subjected them to phospholipid analysis. We also obtained arterial cells from human umbilical cords and cultured them with a decreasing concentration of either cholesterol or oxidized cholesterol. Patients undergoing CABG surgery and aging swine had significantly higher levels of sphingomyelin in their arterial cells than arterial cells from human umbilical cords. Oxidized low-density lipoprotein (OxLDL) and oxysterols further contribute to atherosclerosis by increasing the synthesis of thromboxane in platelets, a clotting factor. When we incubated arterial cells with cholesterol that had not been oxidized, even at twelve times the concentration of the oxidized cholesterols we used, there was no effect on sphingomyelin content, this shows that cholesterol itself is not the reason for heart disease, and has to be oxidized in order to cause harm. My study indicated that atherosclerosis is due to a diet that contains a high level of oxysterols. Normal levels of oxysterols in the plasma will not increase sphingomyelin levels. Removing oxidized fat from the diet should be considered as a therapeutic measure for atherosclerosis. Ancel Keys, who some consider the father of the cholesterol-heart disease hypothesis said in 1997: "There's no connection whatsoever between the cholesterol in food and cholesterol in the blood."

Dissociation of C-Reactive Protein Levels from Long-Chain Omega-3 Fatty Acid Status and Antidepressant Response in Adolescents with Major Depressive Disorder: An Open-Label Dose-Ranging Trial
Pages 235-243
Robert K. McNamara, Mary Perry and Barry Sears

DOI: http://dx.doi.org/10.6000/1929-5634.2013.02.04.8

Published: 30 December 2013

Abstract: Major depressive disorder (MDD) is associated with long-chain omega-3 (LCn-3) fatty acid deficits and indices of chronic sustained inflammation including elevated C-reactive protein (CRP) levels. The present study combined a case-control analysis and a prospective 10-week open-label fish oil (FO) supplementation trial to investigate the relationships among plasma phospholipid LCn-3 fatty acid levels, plasma CRP concentrations, and depressive symptoms in adolescent MDD patients. Compared with healthy controls (n=20), MDD patients (n=20) exhibited significantly lower EPA+DHA levels (-62%, p£0.0001) and a higher ratio of arachidonic acid (AA) to EPA+DHA (+78%, p=0.0002). CRP concentrations did not differ between controls and MDD patients (0.16 vs. 0.17 mg/dL, p=0.96), and were positively correlated with depression symptom severity scores in MDD patients (r = +0.55, p=0.01). CRP concentrations were positively correlated with BMI in MDD patients (r = +0.63, p=0.005) and controls (r = +0.69, p=0.002). Low-dose (2.4 g/d) and high-dose (15 g/d) FO supplementation significantly increased EPA+DHA levels in MDD patients, but did not significantly alter CRP concentrations. Baseline and baseline-endpoint change in CRP levels were not correlated with baseline-endpoint reductions in depression severity. Together, these data demonstrate that the lower plasma phospholipid LCn-3 fatty acid composition exhibited by adolescent MDD patients is not associated with higher CRP levels, and that increasing LCn-3 fatty acid status reduces depression symptom severity independent of changes in CRP concentrations. Collectively, these data suggest that CRP concentrations are dissociable from LCn-3 fatty acid status and antidepressant response in adolescent MDD patients.