It has been more than 10 years since conjugated linoleic acid (CLA) was first commercialised on a measurable scale. Since its advent, both the ingredient — which is a ?cocktail? of fatty acids rather than a unimolecular constituent, as its name suggests — and the body of scientific evidence have undergone an evolution. The entry of multinational fine chemicals manufacturers and marketers has further catapulted the maturation of this lipid. One of CLA?s confounding issues is whether the triglyceride (TG) or free fatty acid (FFA) form yields better results.
Studies in the 1990s, conducted on rodents and, to a lesser extent, on pigs, were led primarily by the research group that has assembled a robust patent estate around CLA (University of Wisconsin, US). They first suggested that CLA supplementation (semi-synthetically produced) to humans could elicit dramatic shifts in body composition compartments, specifically reduction of fat and/or augmentation of lean mass.1
A less than rigorously controlled clinical study (form not disclosed), conducted in Norway in the 1990s with 20 subjects, was used to support the initial surge of excitement over its promise as a fat loss/weight loss natural bioactive.2 We and others, using North American populations, were unable to confirm the body composition-modifying efficacy of CLA-FFA over placebo, within intervention periods of one to six months among a variety of subjects.3,4
Two 2005 studies with different CLA preparations have also yielded discordant results. Supplementation with CLA-FFA (and with two different ratios of the predominant isomers of CLA) failed to effect a significantly greater immune response compared to a high linoleic acid placebo,5 while use of CLA-TG did indeed elicit a significant immunomodulatory-anti-inflammatory effect relative to a high oleic acid placebo.6 This appears to be the first human study to describe such an effect.
The difficulty of discerning consistent results with CLA of any form is highlighted in results of an extended duration clinical trial comparing the TG and FFA forms to an olive oil placebo.7,8 In the placebo-controlled study, a population of 180 mostly overweight (nonobese) Norwegian men and women (149 women) were assigned to receive 3.4g CLA (FFA or TG) or placebo daily, and not implement any diet or exercise changes over a period of 12 months.7 In the FFA group, body weight did not differ from placebo after 12 months, but total body fat and lean mass did change favourably and significantly relative to placebo. In the TG group, body weight and total body fat did change favourably and significantly compared to placebo, but lean mass did not.
In the open label (unblinded) continuation of this study (still free living), CLA-TG was used for all 134 of the remaining subjects from the 12-month blinded phase.9 Those switching from placebo to CLA displayed a significant drop in body weight and fatness, but not lean mass, over the latter 12-month phase. Those in the CLA-TG did not regain fat mass but their significant gain in lean mass noted at 12 months did not persist after 24 months.
These findings are contrasted to a one-year CLA-FFA (3.4g/day) study conducted among 101 overweight-obese Danish men and women (57) who were first subjected to an eight-week low-calorie diet to induce weight/fat loss.10 After losing 10kg body weight and 7kg fat mass, one year of CLA supplementation failed to prevent fat and weight regain relative to olive oil placebo.
Collectively, the data on CLA, from all sources and forms, remains equivocal regarding favourable shifts in body composition. Additionally, the mechanism(s) of action of CLA continue to elude confirmation.
What may be the next vista is more rigorous exploration of pure isomer compositions, as evidence indicates that one isomer (trans 10, cis 12) may both promote insulin resistance in select populations,10 and also mediate the anti-inflammatory effects.11
Anthony Almada, MSc, is president and chief scientific officer of IMAGINutrition Inc. Respond: [email protected]
1. Larsen TM, et al. Efficacy and safety of dietary supplements containing CLA for the treatment of obesity: evidence from animal and human studies. J Lipid Res 2003; 44:2234-41.
2. Thom E, et al. Conjugated linoleic acid reduces body fat in healthy exercising humans. J Int Med Res 2001; 29:392-6.
3. Kreider RB, et al. Effects of conjugated linoleic acid supplementation during resistance training on body composition, bone density, strength and selected hematological markers. J Strength Cond Res 2002; 16:325-34.
4. Atkinson R. Conjugated linoleic acid for altering body composition and treating obesity. In: Advances in Conjugated Linoleic Acid Research. Volume I, Yurawecz MP, et al. Champaign, Illinois, USA: AOCS Press, 1999, p348-53.
5. Nugent AP, et al. The effects of conjugated linoleic acid supplementation on immune function in healthy volunteers. Eur J Clin Nutr 2005;59:742-50.
6. Song H-J, et al. Effect of CLA supplementation on immune function in young healthy volunteers. Eur J Clin Nutr 2005; 59:508-17.
7. Gaullier J-M, et al. Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans. Am J Clin Nutr 2004; 79:1118-25.
8. Gaullier J-M, et al. Supplementation with conjugated linoleic acid for 24 months is well tolerated by and reduces body fat mass in healthy, overweight humans. J Nutr 2005; 135:778-84.
9. Toubro S, et al. One year CLA supplement does not prevent weight or fat loss regain. Int J Obes 2004; 28:S149.
10. Ris?rus U, et al. Supplementation with trans10cis12-conjugated linoleic acid induces hyperproinsulinaemia in obese men: close association with impaired insulin sensitivity. Diabetologia 2004; 47:1016-9.
11. Li G, et al. 10t, 12c-conjugated linoleic acid inhibits lipopolysaccharide-induced cyclooxygenase expression in vitro and in vivo. J Lipid Res doi:10.1194/jlr.M500064-JLR200.