The New Paleo Diet Study: Paleo-type-style-ish Diets vs. "Paleo"

There's a new Swedish paleo diet study out: A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women.  The title sounds promising, but my first reaction to it, sadly, not so much about the potential findings, but, what exactly is this paleo-TYPE diet??  It would appear to be based loosely on Cordain's original Paleo Diet (I hear that's trademarked).  

This was a small study, 10 women, no control group, lasting only 5 weeks.  There were some benefits including around 10 lbs average weight loss and almost 50% reduction in liver fat.  This shall be for another blog post.  But what diet was tested?  Here's the diet description from the full text:

Participants were given prepared meal portions that were intended to provide an average intake of about 30 energy percentage (E%) protein, 40 E% fat (mostly unsaturated) and 30 E% carbohydrates for breakfast, lunch and dinner, together with 40 g nuts (walnuts and sweet almonds) on a daily basis for 5 weeks.

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Fish & Food Purity Wars

I really like fish -- all kinds.  And fish is one way to get a lot "supplements" -- in whole form, complete with other components that act in synergism with what has been refined out in supplements.  I've been getting more into fish lately as the new Korean-American owned market opened nearby.  They have an amazing seafood department including crystal clean tanks of live fish. (The other Asian market with large tanks is not quite so pristine).  One day they were having a hard time constraining jumpers!  In addition to seafoods you don't usually see elsewhere --  abalone, barrels & tanks of live crabs, octopus -- they have a really nice selection of fish varieties, both common and eccentric.   Even if I'm not in the market for fish I'll still swing by for the Chilean sea bass samples, to die for!

But as protein sources go, fish is pretty danged expensive nowadays.  Even your run-of-the-mill cod While this market is rather more affordable than where we usually go, we recently purchased a trimmed filet mignon for less per pound than most of the filleted fish, especially my beloved salmon and swordfish.   Then you see the sign:  Sale!  $6.99/lb Farmed in Vietnam (or other Asian country).   To buy, or not to buy?  The wild caught (if even available for may varieties) will be in the $12-16/lb range.

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Gestational Diabetes and Pre-Pregnancy Fat Intake

Gestational diabetes -- hyperglycemia during pregnancy -- effects a considerable number of women.  It is also a known risk factor for developing diabetes (T2) later in life.    Some degree of peripheral insulin resistance normally develops during pregnancy.  Why?  Because the fetus' growth and development takes priority in nutrient partitioning so glucose is conserved for the fetus much like it is conserved for the brain in the fasted/starved/glucose-deprived state.  The link of GD to T2 most likely reveals the genetic predisposition towards IR -- in other words, while diet can cause insulin resistance, there is a genetic component in most who eventually develop hyperglycemia as a result.  Most women will compensate for the mild IR state and maintain normal glycemia during pregnancy, while those who are perhaps even mildly IR to begin with will exceed their capacity to compensate during the pregnancy.  In most cases, deliver the baby and the diabetes goes away.  

A prospective study of prepregnancy dietary fat intake and risk of gestational diabetes

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PUFA's, the Primal Blueprint and Low Carb diets

It's sort of a funny thing in low carb circles.  Atkins followers - or those who have fashioned their plans by tweaking Atkins - remain the majority of adherents to this lifestyle, despite the surging popularity of Paleo-styled plans.  

I admit to not knowing or caring a thing about Omega 6 vs. Omega 3 and all that jazz until sometime in 2009 after I'd found the LC web.  Atkins was a big fish oil pusher (if memory serves he had his own line of supplements) and fan of the O3, but he certainly didn't spend much time addressing the dreaded O6 fats.  The root of all evil in the minds of many.

I have his original book, and many recipes contained good old  fashioned industrial mayo made from soybean oil or other veggie oil.  There was no shunning of veggie oils that's for sure, or commercial salad dressings containing them so long as no carbs went along for the ride down the gullet.  Chicken may not have been as highly touted as the more luxurious ribeye, but it certainly had its place.  And when climbing the rungs, nuts were big.  Macadamias preferred, but not because of the O6:O3 ration, but because they happen to be the lowest in carbs.  I just threw out an expired Atkins shake I used to use sometimes in place of cream in my coffee (mocha coffee, yum!) - sunflower oil!  Let's not go into fats in the various "product" around, although many of the newer moose turd look-alike offerings no longer contain these in the name of paleolithic purity.

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Comparative Fatty Acid Toxicity on Macrophages

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 to the number of double bonds in the molecules: palmitic acid>docosahexaenoic acid>stearic acid=eicosapentaenoic acid=arachidonic acid>oleic acid>linoleic acid. The induction of cell death did not involve PPARγ activation. The mechanisms of fatty acids to induce cell death involved changes in mitochondrial transmembrane potential and intracellular neutral lipid accumulation. Fatty acids poorly incorporated into triacylglycerol had the highest toxicity.

 I could C&P the entire introduction to this paper but don't want to do that, so please go read it.  Summary:

• The FFA/NEFA are generally implicated in having toxic effects in non-adipose tissues, aka lipotoxicity
• Saturated fatty acids tend to be more lipotoxic
• Ectopic (non-adipose) triglyceride storage is somewhat protective but this remains under consideration as metabolites/intermediates of triglycerides (ceramides) are implicated in toxicity.
• Cell death contributes to the inflammatory properties of FA's
• PPAR-ɣ increases reduce inflammatory cytokines like IL's and TNF-α

Macrophage infiltration into adipose tissue in obesity is implicated in the inflammatory state associated with obesity.   It should be noted that this study was in vitro (e.g. culture dish) on a non-human (murine to be exact) derived cell line.   But the elevated NEFA associated with insulin resistance and T2 Diabetes would produce a "toxic" state within adipose tissue leading to macrophage death (and adipocyte death?). 

Cell death types:  

• Apoptosis, aka programmed cell death:  When functioning properly, this is the "natural" death of cells for cellular turnover in tissues, etc.  In cancer, apoptosis is short circuited leading to so-called immortal cells.  Some toxic conditions lead to disruption of the normal signals and pre-mature apoptosis.  
• Necrosis:  Premature cell death due to some - always detrimental - external source.  Necrosis initiates a greater immune response as dead cells must be engulfed and removed, and such cells rupture and "spill" more "stuff" into the surroundings than cells undergoing PCD.

Some exerpts:

In the present study, we evaluated whether the induction of cell death could be a mechanism by which FAs modulate macrophage function. Indeed, treatment with different concentrations of FAs was toxic to the macrophage cell line J774, as assessed by loss of membrane integrity and DNA fragmentation.  In most cases, the lowest concentration that caused loss of membrane integrity was the same that induced DNA fragmentation (Table 3), and the percentages were similar. These findings are indicative that necrosis and apoptosis occurred concomitantly.

... high FA concentrations cause macrophage death mainly by necrosis. This effect was also observed by others after treatment of different cell types, such as melanoma, leukaemia cell lines, lung carcinoma and fibroblasts, with high concentrations of FA [49–51].  The results of both loss of membrane integrity and/or DNA fragmentation shown in the present study suggest the following rank of toxicity on J774 cells: PA>DHA>SA=AA=EPA>OA>LA 

... The relationship between lipid accumulation and apoptosis has been demonstrated through a series of experiments with different cell lines [63–65]. Accumulation of excess FAs into the TAGpool has been postulated to divert these molecules from pathways that lead to toxic effects and, thus, lipid bodies may serve as buffers against lipotoxicity [19]. Treatment with all FAs led to an increase of lipid bodies inside J774 cells (Figure 2B).  Cells treated with non-toxic concentrations of the FAs exhibited higher granularity, indicating accumulation of lipid droplets that was observed by fluorescence microscopy. 

A look at Figure 1 indicates a threshold behavior for the toxic effects.

I have not addressed everything in this article and this post is sort-of half book marking, half just putting this out there as I had not seen a discussion of this nature before.