Posted by larryhoover on December 28, 2012, at 10:44:25
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 28, 2012, at 8:55:02
> I think it is safe to assume that a meal high in saturated fat causes inflammation; that is a well-established fact accepted for at least 15 years.
In mice, yes. In humans, it's a different story. And, in humans, it also depends on how sick their metabolism already is, and what other nutrients are co-ingested.
For example, this study comparing challenge tests of bolus ingestion of fats of differing composition.
http://www.ncbi.nlm.nih.gov/pubmed/21736782
"In addition, ALA and EPA were shown to elicit different effects on the release and mRNA expression levels of inflammatory markers in PBMC cultured ex vivo, with EPA having the most prominent pro-inflammatory potential."The so-called pro-inflammatory PUFA arichadonic acid wasn't pro-inflammatory, but the anti-inflammatory eicosapentaenoic acid was? Hmmmm. In this case PUFAs were inflammatory, but not saturated fat.
Here's a full-text article discussing various fatty acid challenges in people with differing metabolic health. The responses are quite variable across the groups.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402390/Now, as to your references, let's see what they really say.
> Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23.
"The ingestion of fatty meals is associated with a transient, low-grade systemic inflammatory response in human subjects, involving the activation of circulating monocytes and the secretion of pro-inflammatory cytokines."
Note, they do not implicate saturated fats. Moreover, they do not discuss the fact that this is only seen in people simultaneously exposed to both carbs and fat.
The actual study performed was in vitro, which means that the cells were not in a normal matrix, with the normal complex of homeostatic influences. And, having done in vitro work myself, I can assure you that the nutrient broth used is high-carb. Can you say confound?
> Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, Viswanathan P, Chaudhuri A, Dandona P. Differential effects of cream, glucose, and orange juice on inflammation, endotoxin, and the expression of Toll-like receptor-4 and suppressor of cytokine signaling-3. Diabetes Care. 2010 May; 33(5):991-7.
Full-text here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858203/
Interesting opening remark: "We have recently shown that a high-fat high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation."
High-fat HIGH-CARB combination. There it is, plain as day.
From the full-text article's conclusion section: "It would thus appear that the oxidative stress and inflammation-inducing actions of the HFHC meal are due to the combination of saturated fat and the carbohydrate (glucose) at least."
In that conclusion, they are referring to an earlier study they did comparing high-fat high-carb meal to a fruit and fiber meal. They presented no evidence to implicate the saturated fat, however. It's funny how these assumptions persist, without evidence.
This article is quite interesting in one sense, as the only difference in inflammatory response between glucose and cream was with respect to lipopolysaccharides. Glucose itself was extremely inflammatory, and more rapidly than was the cream. I'm going to take a closer look at lipopolysaccharides.
I'll close with a nice summary piece.
http://www.ncbi.nlm.nih.gov/pubmed/19082851
Lipids. 2009 Apr;44(4):297-309. doi: 10.1007/s11745-008-3274-2. Epub 2008 Dec 12.Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet.
Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD.
SourceDepartment of Kinesiology, University of Connecticut, 2095 Hillside Road, Storrs, CT 06269-1110, USA. jeff.volek@uconn.edu
AbstractWe recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.
Lar
poster:larryhoover
thread:1033371
URL: http://www.dr-bob.org/babble/20121217/msgs/1034063.html