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Re: ...that's why I'm asking Larry for articles...

Posted by Larry Hoover on February 7, 2003, at 9:06:48

In reply to ...that's why I'm asking Larry for articles..., posted by IsoM on February 7, 2003, at 1:19:34

> I've never used CLA capsules, so I'm not looking to see what they may have done for me. Instead, I'm looking for genuine sources of organic meat with animals that are fed open range rather than typical feed & grain. I try to get as much as my nutrients from foods rather than pay mega-bucks for supplements that aren't always what they're cracked up to be.

CLA supplements may actually be harmful, as there are many different isomers (28 I think) which would be randomly produced in man-made supplements. You're wise to focus on wholefood sources. If a CLA supplement is *extracted* from whole foods, that would be OK, but I don't know how you'd be able to tell that sort of product from one that is man-made. They could both be labelled "natural source", as the ALA in the man-made product would obviously come from vegetable oil. This is my biggest concern about CLA supplementation, and I admit that I haven't looked into finding a quality product yet.

> CLAs are only found in any amount in the fat of animals that graze on grass.

Actually, CLAs come from ruminants, cud-chewers. It's the lumen bacteria that produce the CLAs from partial hydrogenation of ALA. Beef, dairy cattle, sheep and lamb are the best sources. I believe that grass-feeding is an enhancement, but probably through co-ingestion of "weeds" like dandelion.

>It's not just the brain boosting that interests me but over all health & benefits. I'm glad I never bought into the hype about fats years ago. I've never used margarine or shortening. It was butter or lard if I used anything. My intake of trans-fatty acids has been practically nil - don't like chips, don't eat french fries (maybe once every 2 years), or store-bought baked goods or crackers, etc.

You're exceptional. <grin>

> I'm curious to read what's known about CLAs & figure Larry would probably have the most up-to-date info available.

I appreciate the confidence you place in me. Here's the latest:

**This article links one specific CLA isomer, the trans-10, cis-12 one, to beneficial changes in energy-regulation in type-2 diabetes.

J Nutr 2003 Jan;133(1):257S-260S

The conjugated linoleic acid (CLA) isomer, t10c12-CLA, is inversely associated with changes in body weight and serum leptin in subjects with type 2 diabetes mellitus.

Belury MA, Mahon A, Banni S.

Department of Human Nutrition, The Ohio State University, Columbus, USA. belury.1@osu.edu

Isomers of conjugated linoleic acid (CLA) are found in beef, lamb and dairy products. Diets containing CLA reduce adipose mass in various depots of experimental animals. In addition, CLA delays the onset of diabetes in the ZDF rat model for obesity-linked type 2 diabetes mellitus. We hypothesize that there would be an inverse association of CLA with body weight and serum leptin in subjects with type 2 diabetes mellitus. In this double-blind study, subjects with type 2 diabetes mellitus were randomized into one of two groups receiving either a supplement containing mixed CLA isomers (CLA-mix; 8.0 g daily, 76% pure CLA; n = 12) or a supplement containing safflower oil (placebo; 8.0 g daily safflower oil, n = 9) for 8 wk. The isomers of CLA in the CLA-mix supplement were primarily c9t11-CLA ( approximately 37%) and t10c12-CLA ( approximately 39%) in free fatty acid form. Plasma levels of CLA were inversely associated with body weight (P < 0.05) and serum leptin levels (P < 0.05). When levels of plasma t10c12-CLA isomer were correlated with changes in body weight or serum leptin, t10c12-CLA, but not c9t11-CLA, was inversely associated with body weights (P < 0.05) and serum leptin (P < 0.02). These findings strongly suggest that the t10c12-CLA isomer may be the bioactive isomer of CLA to influence the body weight changes observed in subjects with type 2 diabetes. Future studies are needed to determine a causal relationship, if any, of t10c12-CLA or c9t11-CLA to modulate body weight and composition in subjects with type 2 diabetes. Furthermore, determining the ability of CLA isomers to influence glucose and lipid metabolism as well as markers of insulin sensitivity is imperative to understanding the role of CLA to aid in the management of type 2 diabetes and other related conditions of insulin resistance.


**This one just says nice things about CLAs.

Can J Appl Physiol 2002 Dec;27(6):617-28

Effects of Conjugated Linoleic Acid (CLA) on Immune Responses, Body Composition and Stearoyl-CoA Desaturase.

Ntambi JM, Choi Y, Park Y, Peters JM, Pariza MW.

Department of Biochemistry and Department of Nutritional Sciences, Food Research Institute, University of Wisconsin-Madison, WI.

Conjugated linoleic acid (CLA) has shown a wide range of biologically beneficial effects; reduction of incidence and severity of animal carcinogenesis, reduction of the adverse effects of immune stimulation, reduction of severity of atherosclerosis, growth promotion in young rats, and modulation of stearoyl-CoA desaturase (SCD). One of the most interesting aspects of CLA is its ability to reduce body fat while enhancing lean body mass which is associated with the trans-10,cis-12 isomer of CLA. The effects of CLA are unique characteristics that have not been observed with other polyunsaturated fatty acids. In this review, we will focus on the effects of CLA on immune responses, body compositional changes and stearoyl-CoA desaturase.


**This one shows that CLAs block inflammatory processes both at the enzyme level and at the gene-regulatory level.

Clin Nutr 2002 Dec;21(6):451-9

Colonic anti-inflammatory mechanisms of conjugated linoleic acid.

BASSAGANYA-RIERA J, HONTECILLAS R, BEITZ DC.

Department of Animal Sciences, Iowa State University, Ames, Iowa, USA

Conjugated linoleic acid (CLA) is a mixture of positional (e.g. 7,9; 9,11; 10,12; 11,13) and geometric (cis or trans) isomers of octadecadienoic acid. This compound was first shown to prevent mammary carcinogenesis in murine models. Later investigations uncovered a number of additional health benefits, including decreasing atherosclerosis and inflammation while enhancing immune function. The mechanisms of action underlying these biological properties are not clearly understood. The aim of this review is to highlight recent advances in CLA research related to experimental inflammatory bowel disease. In addition, two possible mechanisms of action (i.e. endoplasmic and nuclear) were discussed in detail in the context of enteric inflammatory disorders. Conjugated linoleic acid was first implicated in down-regulating the generation of inducible eicosanoids (i.e. PGE(2) and LTB(4)) involved in early micro-inflammatory events (endoplasmic). More recently, CLA has been shown to modulate the expression of genes regulated by peroxisome proliferator-activated receptors (PPARs; nuclear). In pigs, prolonged dietary CLA treatment stimulated the expression of PPAR-gamma in the muscle. Thus, evidence supporting both mechanistic theories of CLA acting through eicosanoid synthesis and PPAR activity is available. The further understanding of the anti-inflammatory mechanisms of action of CLA may yield novel nutritional therapies for enteric inflammation.

**This one provides evidence that CLAs are *bad*, with respect to heart disease risk factors and insulin/glucose regulation. (Gotta consider everything.)

Circulation 2002 Oct 8;106(15):1925-9

Supplementation with conjugated linoleic acid causes isomer-dependent oxidative stress and elevated C-reactive protein: a potential link to fatty acid-induced insulin resistance.


Riserus U, Basu S, Jovinge S, Fredrikson GN, Arnlov J, Vessby B.

Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden. ulf.riserus@pubcare.uu.se

BACKGROUND: Conjugated linoleic acids (CLAs), a group of fatty acids shown to have beneficial effects in animals, are also used as weight loss supplements. Recently, we reported that the t10c12 CLA-isomer caused insulin resistance in abdominally obese men via unknown mechanisms. The aim of the present study was to examine whether CLA has isomer-specific effects on oxidative stress or inflammatory biomarkers and to investigate the relationship between these factors and induced insulin resistance. METHODS AND RESULTS: In a double-blind placebo-controlled trial, 60 men with metabolic syndrome were randomized to one of 3 groups receiving t10c12 CLA, a CLA mixture, or placebo for 12 weeks. Insulin sensitivity (euglycemic clamp), serum lipids, in vivo lipid peroxidation (determined as urinary 8-iso-PGF(2alpha) [F2-isoprostanes]), 15-ketodihydro PGF(2alpha), plasma vitamin E, plasma C-reactive protein, tumor necrosis factor-alpha, and interleukin-6 were assessed before and after treatment. Supplementation with t10c12 CLA markedly increased 8-iso-PGF(2alpha) (578%) and C-reactive protein (110%) compared with placebo (P<0.0001 and P<0.01, respectively) and independent of changes in hyperglycemia or dyslipidemia. The increases in 8-iso-PGF(2alpha), but not in C-reactive protein, were significantly and independently related to aggravated insulin resistance. Oxidative stress was related to increased vitamin E levels, suggesting a compensatory mechanism. CONCLUSIONS: t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men. The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance. These unfavorable effects of t10c12 CLA might be of clinical importance with regard to cardiovascular disease, in consideration of the widespread use of dietary supplements containing this fatty acid.


**This one discusses the anti-cancer effects of CLAs.

J Nutr 2002 Oct;132(10):2995-8

Inhibition of carcinogenesis by conjugated linoleic acid: potential mechanisms of action.

Belury MA.

Department of Molecular Medicine, Northwest Hospital, Bothell, WA 98021, USA. Belury@u.washington.edu

Conjugated linoleic acid (CLA) is composed of positional and stereoisomers of octadecadienoate (18:2); it is found in foods derived from ruminants (beef and lamb as well as dairy products from these sources). When a mixture of isomers is fed to experimental animals, chemically induced tumorigenesis of mammary, skin and colon is reduced. Importantly, many isomers of CLA are readily metabolized to desaturated/elongated products as well as beta-oxidized products, suggesting that these metabolites may be important anticancer compounds. Mechanisms of inhibition of carcinogenesis may include reduction of cell proliferation, alterations in the components of the cell cycle and induction of apoptosis. In addition, CLA modulates markers of immunity and eicosanoid formation in numerous species as well as lipid metabolism and gene expression. It is likely that CLA exerts inhibitory properties in carcinogenesis via one or more of these pathways with some tissue specificity. This review will explore recent advances in putative mechanisms of reduction of carcinogenesis by CLA.

 

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Psycho-Babble Medication | Framed

poster:Larry Hoover thread:139853
URL: http://www.dr-bob.org/babble/20030204/msgs/139949.html