The Carb-Sane Asylum

This post contains sufficient updates from the original (dated 5/11/11) that I consider it more of a fully updated version vs. a bump.   This began with my intent to link to this post in an upcoming discussion of triglycerides, when I noticed that Dr. Ronald Krauss was amongst the authors.   This study originally caught my eye because of    Marc Hellerstein 's name, he of  DNL not a major pathway in humans fame , that I've  blogged on  previously. Now I have excerpted copiously from the discussion because the authors make several points relevant to the discussion of what comprises a healthy lipid profile.  As part of updating, I am breaking those excerpts up a bit more and adding some/more emphasis and additional commentary.

Palmitic acid is 16 carbons long, fully saturated, and commonly found in palm oil and animal products, including beef, eggs, milk, poultry, and seafood.  Palmitic acid has long been implicated in CVD, as it tends to raise LDL cholesterol.  Among the saturated fats, it would appear palmitic acid does pose the greatest likelihood of increasing LDL cholesterol.  However, palmitic acid has also recently been shown to be vital both to forming new memories and accessing long-held memories.  As we shall see when we investigate how our diet has changed, a Paleo diet supplies an adequate amount of palmitic acid for optimum cognitive function while limiting the intake to levels that are not harmful to the cardiovascular system.  It is also important to note that excessive carbohydrate intake leads to palmitic acid production.  If you recall from the insulin chapter, when liver glycogen is full, additional carbohydrate is converted to palmitic acid.  This pro...

Comparative toxicity of fatty acids on a macrophage cell line (J774) In the present study, the cytotoxicity of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on a macrophage cell line (J774) was investigated. The induction of toxicity was investigated by changes in cell size, granularity, membrane integrity, DNA fragmentation and phosphatidylserine externalization by using flow cytometry. Fluorescence microscopy was used to determine the type of cell death (Acridine Orange/ethidium bromide assay). The possible mechanisms involved were examined by measuring mitochondrial depolarization, lipid accumulation and PPARγ (peroxisome-proliferator-activated receptor γ ) activation. The results demonstrate that fatty acids induce apoptosis and necrosis of J774 cells. At high concentrations, fatty acids cause macrophage death mainly by necrosis. The cytotoxicity of the fatty acids was not strictly related ...

Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans We previously demonstrated in the rat that long term exposure to fatty acids inhibits B-cell function in vivo and in vitro. To further assess the clinical significance of these findings, we tested in human islets the effects of fatty acids on glucose-induced insulin release and biosynthesis and on pyruvate dehydrogenase (PDH) activity. PDH is the enzyme thought to control the entry of acetyl CoA from glycolysis into the Kreb's / TCA /Citric Acid Cycle. These authors did an in vitro  study with human cells to see if the results compared with those seen both in vitro and in vivo  in rats.  While in vitro  observations don't always correlate with what we see in whole organisms, this did correlate for the rat.  Therefore it is reasonable to believe that the results of this experiment are applicable to human metabolism. Human islets were obtained...