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Is long term CLA use safe. I read an article well over a year ago that said using it for more than 4 months consecutively could do something to your heart. Is this valid? I took it for 3 months last year along with regular cardio and was pleased with results. I just started taking it again (2400 mg a day). Post some info. Thanks.
Gurus drop some knowledge. Ever hear anything bad about CLA?
bump
It is bad for you. Very bad. It actually has plenty of evidence showing that it does exactly opposite of what the bottle claims - like promoting insulin resistance. I don't like diabetes. Don't touch it.
[QUOTE=Dr.Hugenstein;299304371]It is bad for you. Very bad. It actually has plenty of evidence showing that it does exactly opposite of what the bottle claims - like promoting insulin resistance. I don't like diabetes. Don't touch it.[/QUOTE]post research.
First a paper abstract:
1: Przegl Lek. 2007;64(7-8):498-501.Links
[The conjugated linoleic acids in prevention and treatment of obesity]
[Article in Polish]
Swierczynski J, Szolkiewicz M, Rutkowski B.
Katedra i Zakład Biochemii Akademii Medycznej w Gdańsku.
The results of up-to-date performed experimental studies indicated that conjugated linoleic acids (CLA) contained in diet lead to significant both adipose tissue and body mass decrease. It suggests that the CLA-rich diet or CLA-contained medicines can be useful in prevention and treatment of obesity in humans. The CLA-contained medicines are more and more popular, therefore the principle aim of this review is a description of CLA chemical structure, presence in natural products and moreover, their potential influence on adipose tissue mass in humans. Unfortunately, the results of recent trials are disappointing. Most of them indicated that (contrary to experimental studies) CLA were not profitable in adipose tissue mass decrease in humans. Moreover, in a few cases a deterioration of serum lipid profile, glycemia enhancement and decrease of tissue insulin sensitivity were observed. Thus, there is no evidence confirming the positive influence of CLA on adipose tissue mass in humans. However, there are also a few publications, in which the CLA-associated decrease of adipose tissue mass in humans was noted. The results of these studies do not let us totally decline the opinion that CLA are profitable also in humans. This contradictory data definitely needs further studies.
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1: Eur J Clin Nutr. 2008 Sep 3.
Effects of conjugated linoleic acid plus n-3 polyunsaturated fatty acids on insulin secretion and estimated insulin sensitivity in men.
Ahr?n B, Mari A, Fyfe CL, Tsofliou F, Sneddon AA, Wahle KW, Winzell MS, Pacini G, Williams LM.
1Division of Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden.
Background/Objectives:Dietary addition of either conjugated linoleic acid (CLA) or n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) has been shown to alter adiposity and circulating lipids, risk markers of cardiovascular diseases. However, CLA may decrease insulin sensitivity, an effect that may be reversed by n-3 LC-PUFA. Thus, the potential of CLA plus n-3 LC-PUFA to affect insulin secretion and sensitivity in non-diabetic young and old, lean and obese subjects was tested.Subjects/Methods:CLA (3 g daily) plus n-3 LC-PUFA (3 g daily) or control oil (6 g daily) was given to lean (n=12; BMI 20-26 kg/m(2)) or obese (n=10; BMI 29-35 kg/m(2)) young (20-37 years old) or lean (n=16) or obese (n=11) older men (50-65 years) for 12 weeks. The study had a double-blind, placebo-controlled randomized crossover design, and primary end points were insulin secretion and sensitivity during a standardized meal test, evaluated by modeling glucose, insulin and C-peptide data.Results:The combination was well tolerated. There was no significant difference in fasting levels of glucose, insulin or C-peptide after CLA/n-3 LC-PUFA treatment compared with control oil. Neither insulin secretion nor estimated sensitivity was affected by CLA/n-3 LC-PUFA in lean or obese young subjects or in older lean subjects. However, in older obese subjects, estimated insulin sensitivity was reduced with CLA/n-3 LC-PUFA compared with control (P=0.024).Conclusions:The results do not support beneficial effects of CLA/n-3 LC-PUFA for beta-cell dysfunction or insulin resistance in humans but suggest that insulin sensitivity in older obese subjects is reduced.European Journal of Clinical Nutrition advance online publication, 3 September 2008; doi:10.1038/ejcn.2008.45.
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1: Diabetes Res Clin Pract. 2008 Dec;82(3):e23-4.
Effects of trans10cis12CLA-induced insulin resistance on retinol-binding protein 4 concentrations in abdominally obese men.
Ingelsson E, Ris?rus U.
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. [email]erik.ingelsson@ki.se[/email]
In this randomized, placebo-controlled, double-blind study of 57 abdominally obese middle-aged men, conjugated linoleic acid (CLA) did not induce changes in retinol-binding protein 4 concentrations (RBP4), despite marked induced insulin resistance. Further, there were no associations between CLA-induced insulin resistance and changes in RBP4.
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1: J Lipid Res. 2009 Feb;50(2):225-32.
Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated by resveratrol.
Kennedy A, Overman A, Lapoint K, Hopkins R, West T, Chuang CC, Martinez K, Bell D, McIntosh M.
Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402-6170, USA.
Inflammation plays a role in trans-10, cis-12 (10,12)-conjugated linoleic acid (CLA)-mediated delipidation and insulin resistance in adipocytes. Given the anti-inflammatory role of resveratrol (RSV), we hypothesized that RSV would attenuate inflammation and insulin resistance caused by 10,12 CLA in human adipocytes. RSV blocked 10,12 CLA induction of the inflammatory response by preventing activation of extracellular signal-related kinase and induction of inflammatory gene expression (i.e., IL-6, IL-8, IL-1beta) within 12 h. Similarly, RSV suppressed 10,12 CLA-mediated activation of the inflammatory prostaglandin pathway involving phospholipase A(2), cyclooxygenase-2, and PGF(2alpha). In addition, RSV attenuated 10,12 CLA increase of intracellular calcium and reactive oxygen species associated with cellular stress, and activation of stress-related proteins (i.e., activating transcription factor 3, JNK) within 12 h. 10,12 CLA-mediated insulin resistance and suppression of fatty acid uptake and triglyceride content were attenuated by RSV. Finally, 10,12 CLA-mediated decrease of peroxisome proliferator-activated receptor gamma (PPARgamma) protein levels and activation of a peroxisome proliferator response element (PPRE) reporter were prevented by RSV. RSV increased the basal activity of PPRE, suggesting that RSV increases PPARgamma activity. Collectively, these data demonstrate for the first time that RSV prevents 10,12 CLA-mediated insulin resistance and delipidation in human adipocytes by attenuating inflammation and cellular stress and increasing PPARgamma activity.
it cant be bad....CLA is in chicken, steak, etc....
A study that gives me something to think about.. particularly for young obese men, but notice the results in young and older lean and older obese individuals:
1: Obesity (Silver Spring). 2008 May;16(5):1019-24.
Effect of a conjugated linoleic acid and omega-3 fatty acid mixture on body composition and adiponectin.
Sneddon AA, Tsofliou F, Fyfe CL, Matheson I, Jackson DM, Horgan G, Winzell MS, Wahle KW, Ahren B, Williams LM.
Vascular Health Division, Rowett Research Institute, Aberdeen, UK. [email]A.Sneddon@rowett.ac.uk[/email]
This study aimed to determine the effect of supplementation with conjugated linoleic acids (CLAs) plus n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) on body composition, adiposity, and hormone levels in young and older, lean and obese men. Young (31.4+/-3.9 years) lean (BMI, 23.6+/-1.5 kg/m2; n=13) and obese (BMI, 32.4+/-1.9 kg/m2; n=12) and older (56.5+/-4.6 years) lean (BMI, 23.6+/-1.5 kg/m2; n=20) and obese (BMI, 32.0+/-1.6 kg/m2; n=14) men participated in a double-blind placebo-controlled, randomized crossover study. Subjects received either 6 g/day control fat or 3 g/day CLA (50:50 cis-9, trans-11:trans-10, cis-12) and 3 g/day n-3 LC-PUFA for 12 weeks with a 12-week wash-out period between crossovers. Body composition was assessed by dual-energy X-ray absorptiometry. Fasting adiponectin, leptin, glucose, and insulin concentrations were measured and insulin resistance estimated by homeostasis model assessment for insulin resistance (HOMA-IR). In the younger obese subjects, CLA plus n-3 LC-PUFA supplementation compared with control fat did not result in increased abdominal fat and raised both fat-free mass (2.4%) and adiponectin levels (12%). CLA plus n-3 LC-PUFA showed no significant effects on HOMA-IR in any group but did increase fasting glucose in older obese subjects. In summary, supplementation with CLA plus n-3 LC-PUFA prevents increased abdominal fat mass and raises fat-free mass and adiponectin levels in younger obese individuals without deleteriously affecting insulin sensitivity, whereas these parameters in young and older lean and older obese individuals were unaffected, apart from increased fasting glucose in older obese men.
PMID: 18356842 [PubMed - indexed for MEDLINE]
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Even with the concurrent supplementation of an omega-3 fatty acid mixture(which I assume we can all generally agree is good on its own) the results in lean men and older obese men are zilch.
Now there are arguments for both sides of the fence. If you can argue the other side well and back it up, go right ahead, I won't say that you're wrong. Fact is, if even a fifth of the studies out there show the possibility of insulin resistance in humans, I certainly don't want to supplement with it. Why play around with that?
Here's a research summary from scitopics showing both sides of the argument(mainly in favor of though) from sci topics:
Conjugated Linoleic Acid (CLA)
30 July 2008
authors Prof Yeonhwa Park
Category:
Biochemistry, Genetics and Molecular Biology
Cell Biology, Physiology
Lifestyle factors, including diet, influence the development of many types of diseases. In the 1970s, scientists started to search for mutagens/carcinogens from food in hopes of eventually using this knowledge to help prevent cancer. Based on reports that overcooked meat contained mutagens, Dr. Pariza?s group at the University of Wisconsin-Madison investigated the correlation between mutagen formation and cooking temperature and time using ground beef. To their surprise, in addition to mutagens in beef extract they also found a compound that had anti-mutagenic activity (Pariza and Hargraves 1985). This compound was identified and named conjugated linoleic acid (CLA) based on the structural similarity to linoleic acid. In addition to its originally identified anticancer activity, CLA has shown a wide range of biologically beneficial activities; decreased severity of atherosclerosis, reduction of adverse effects of immune stimulation, growth promotion in young rats, and, most interestingly, a reduction of body fat and an increase in lean body mass in several animal species (Pariza 2004; Park and Pariza 2007).
One explanation for the variety of biological activities of this relatively simple structured fatty acid is that CLA is a mixture of isomers. Two main isomers are the cis-9, trans-11 and trans-10, cis-12 isomers. The cis-9, trans-11 CLA isomer is the main isomer of CLA present in food, which originates from biohydrogenation of linoleic acid to stearic acid by rumen bacteria or from Δ 9 desaturation of trans-11 vaccenic acid (Griinari et al., 2000; Kepler et al., 1966). The trans-10,cis-12 isomer is also present in beef or dairy but to a minor extent (Dhiman et al., 2005). It has been proven that both isomers are equally effective with regard to most anticancer activity (Ip et al., 2002). Beyond anticancer effects, these two isomers have shown distinctive activities. The trans-10, cis-12 isomer of CLA is responsible for body compositional changes, inhibition of stearoyl-CoA desaturase activity, protein and/or mRNA, and reduction of apolipoprotein B secretion from cultured human hepatoma cells (Park and Pariza 2007). The cis-9, trans-11 isomer is responsible for growth promotion in rodents, improving lipoprotein profiles, and is more effective in inhibition of tumor necrosis factor-α (TNF-α) than the trans-10, cis-12 isomer (Cook et al., 1993; Valeille et al., 2004; Yang and Cook 2003). There are also instances where the two isomers appear to act in opposition (Song et al., 2004). Hence, the many physiological effects that are reported for CLA appear to be the result of multiple interactions of these two biologically-active CLA isomers (Park and Pariza 2007).
The safety of commercial CLA preparations has also been evaluated in numerous human clinical trials. Commercial CLA preparations intended for human use typically consist almost entirely (i.e. >80-90%) of the two biologically active isomers in approximately equal amounts (i.e. about 40-45% each). There is no evidence to indicate that such high-quality CLA, when consumed at a dose of 3-6 grams per day, will induce adverse effects in healthy humans (Gaullier et al., 2005). Others have expressed concerns over the potential safety of CLA for humans, such as lipodystrophy, fatty liver, glucose intolerance, and oxidative stress. For detailed discussion, please see Pariza's review (2004).
Lifestyle factors, including diet, influence the development of many types of diseases. In the 1970s, scientists started to search for mutagens/carcinogens from food in hopes of eventually using this knowledge to help prevent cancer. Based on reports that overcooked meat contained mutagens, Dr. Pariza?s group at the University of Wisconsin-Madison investigated the correlation between mutagen formation and cooking temperature and time using ground beef. To their surprise, in addition to mutagens in beef extract they also found a compound that had anti-mutagenic activity (Pariza and Hargraves 1985). This compound was identified and named conjugated linoleic acid (CLA) based on the structural similarity to linoleic acid. In addition to its originally identified anticancer activity, CLA has shown a wide range of biologically beneficial activities; decreased severity of atherosclerosis, reduction of adverse effects of immune stimulation, growth promotion in young rats, and, most interestingly, a reduction of body fat and an increase in lean body mass in several animal species (Pariza 2004; Park and Pariza 2007).
One explanation for the variety of biological activities of this relatively simple structured fatty acid is that CLA is a mixture of isomers. Two main isomers are the cis-9, trans-11 and trans-10, cis-12 isomers. The cis-9, trans-11 CLA isomer is the main isomer of CLA present in food, which originates from biohydrogenation of linoleic acid to stearic acid by rumen bacteria or from Δ 9 desaturation of trans-11 vaccenic acid (Griinari et al., 2000; Kepler et al., 1966). The trans-10,cis-12 isomer is also present in beef or dairy but to a minor extent (Dhiman et al., 2005). It has been proven that both isomers are equally effective with regard to most anticancer activity (Ip et al., 2002). Beyond anticancer effects, these two isomers have shown distinctive activities. The trans-10, cis-12 isomer of CLA is responsible for body compositional changes, inhibition of stearoyl-CoA desaturase activity, protein and/or mRNA, and reduction of apolipoprotein B secretion from cultured human hepatoma cells (Park and Pariza 2007). The cis-9, trans-11 isomer is responsible for growth promotion in rodents, improving lipoprotein profiles, and is more effective in inhibition of tumor necrosis factor-α (TNF-α) than the trans-10, cis-12 isomer (Cook et al., 1993; Valeille et al., 2004; Yang and Cook 2003). There are also instances where the two isomers appear to act in opposition (Song et al., 2004). Hence, the many physiological effects that are reported for CLA appear to be the result of multiple interactions of these two biologically-active CLA isomers (Park and Pariza 2007).
The safety of commercial CLA preparations has also been evaluated in numerous human clinical trials. Commercial CLA preparations intended for human use typically consist almost entirely (i.e. >80-90%) of the two biologically active isomers in approximately equal amounts (i.e. about 40-45% each). There is no evidence to indicate that such high-quality CLA, when consumed at a dose of 3-6 grams per day, will induce adverse effects in healthy humans (Gaullier et al., 2005). Others have expressed concerns over the potential safety of CLA for humans, such as lipodystrophy, fatty liver, glucose intolerance, and oxidative stress.
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Further reading
------------------------------
* Cook, M.E., Miller, C.C., Park, Y., Pariza, M., 1993. Immune modulation by altered nutrient metabolism - nutritional control of immune-induced growth depression. Poult. Sci. 72, 1301-1305.
* Dhiman, T.R., Zaman, S., Olson, K.C., Bingham, H.R., Ure, A.L., Pariza, M.W., 2005. Influence of feeding soybean oil on conjugated linoleic acid content in beef. J. Agric. Food Chem. 53, 684-689.
* Gaullier, J.M., Halse, J., Hoye, K., Kristiansen, K., ***ertun, H. , Vik, H., Gudmundsen, O., 2005. Supplementation with conjugated linoleic acid for 24 months is well tolerated by and reduces body fat mass in healthy, overweight humans. J. Nutr. 135, 778- (Link ?)
* Griinari, J.M., Corl, B.A., Lacy, S.H., Chouinard, P.Y., Nurmela, K. V., Bauman, D.E., 2000. Conjugated linoleic acid is synthesized endogenously in lactating dairy cows by delta( 9)-desaturase. J. Nutr. 130, 2285-2291. (Link ?)
* Ip, C., Dong, Y., Ip, M.M., Banni, S., Carta, G., Angioni, E., Murru, E., Spada, S., Melis, M.P., Saebo, A., 2002. Conjugated linoleic acid isomers and mammary cancer prevention. Nutr. Cancer 43, 52-58.
* Kepler, C.R., Hirons, K.P., McNeill, J.J., Tove, S.B., 1966. Intermediates and products of the biohydrogenation of linoleic acid by butyrinvibrio fibrisolvens. J. Biol. Chem. 241, 1350-1354.
* Pariza, M.W., 2004. Perspective on the safety and effectiveness of conjugated linoleic acid. Am. J. Clin. Nutr. 79, 1132S-1136S.
* Pariza, M.W., Hargraves, W.A., 1985. A beef-derived mutagenesis modulator inhibits initiation of mouse epidermal tumors by 7, 12-dimethylbenz[a]anthracene. Carcinogenesis 6, 591-593.
* Park, Y., Pariza, M.W., 2007. Mechanisms of body fat modulation by conjugated linoleic acid ( CLA). Food Res Int 40, 311-323.
* Song, H.J., Sneddon, A.A., Barker, P.A., Bestwick, C., Choe, S.N., McClinton, S., Grant, I., Rotondo, D., Heys, S.D., Wahle, K.W., 2004. Conjugated linoleic acid inhibits proliferation and modulates protein kinase C isoforms in human prostate cancer cells
* Valeille, K., Gripois, D., Blouquit, M.F., Souidi, M., Riottot, M. , Bouthegourd, J.C., Serougne, C., Martin, J.C., 2004. Lipid atherogenic risk markers can be more favourably influenced by the cis- 9,trans-11-octadecadienoate isomer than a conjugated linol
* Yang, M., Cook, M.E., 2003. Dietary conjugated linoleic acid decreased cachexia, macro****e tumor necrosis factor-alpha production, and modifies splenocyte cytokines production. Exp. Biol. Med. (Maywood) 228, 51-58.
[url]http://www.scitopics.com/Conjugated_Linoleic_Acid_CLA.html[/url]
Sources of it may be from beef and chicken, but it's not as potent as taking it as a supplement. Besides, you see the same sort of results from supplementing fish oils as are claimed by proponents of CLA(Which by the way is pushed in the media by dairy companies to sell milk!) without the controversy. I'd prefer to stick with my fish oils.
And yes, I am Expecting a comment on my massive 5 post count.
Dr. H, thanks for the posts. I knew I had heard some negative side to CLA. If I read your initial post correctly it says the risk of getting diabetes was found in older adult males? I am 23, but if I take CLA for a period of 3 months will I be at risk?
I'd like to give you a straight up answer, but I don't know exactly, so I'd be BSing you if I tried.
The fact that it can cause any insulin resistance at all to me is alarming. I would assume that if it increases insulin resistance at all, it would start doing that immediately.
I can't see it just giving you diabetes today, but perhaps sabatoging some of you current and/or future results while slightly increasing your risk later for diabetes?
If you took it before I wouldn't be too afraid of the impending results though, you should be pretty insulin sensitive if you exercise regularly.
My 2 cents: Just avoid it, save your money for something else.
[QUOTE=Dr.Hugenstein;299499261]And yes, I am Expecting a comment on my massive 5 post count.[/QUOTE]
:crickets: !!!
Dont even take it :) [IMG]http://n08q1114fvte161.imageshacknow.info/img/3204/v08w1128rhlb/smile.gif[/IMG]
[IMG]http://n08q1114fvte161.imageshacknow.info/img/3244/v08w1128rhlb/smile.gif[/IMG]
The old school bodybuilders would just put a little Olive Oil in their post-workout shakes.
I hear that this is a good alternative to taking straight CLA.
[QUOTE=Dr.Hugenstein;299489521]A study that gives me something to think about.. particularly for young obese men, but notice the results in young and older lean and older obese individuals:
1: Obesity (Silver Spring). 2008 May;16(5):1019-24.
Effect of a conjugated linoleic acid and omega-3 fatty acid mixture on body composition and adiponectin.
Sneddon AA, Tsofliou F, Fyfe CL, Matheson I, Jackson DM, Horgan G, Winzell MS, Wahle KW, Ahren B, Williams LM.
Vascular Health Division, Rowett Research Institute, Aberdeen, UK. [email]A.Sneddon@rowett.ac.uk[/email]
This study aimed to determine the effect of supplementation with conjugated linoleic acids (CLAs) plus n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) on body composition, adiposity, and hormone levels in young and older, lean and obese men. Young (31.4+/-3.9 years) lean (BMI, 23.6+/-1.5 kg/m2; n=13) and obese (BMI, 32.4+/-1.9 kg/m2; n=12) and older (56.5+/-4.6 years) lean (BMI, 23.6+/-1.5 kg/m2; n=20) and obese (BMI, 32.0+/-1.6 kg/m2; n=14) men participated in a double-blind placebo-controlled, randomized crossover study. Subjects received either 6 g/day control fat or 3 g/day CLA (50:50 cis-9, trans-11:trans-10, cis-12) and 3 g/day n-3 LC-PUFA for 12 weeks with a 12-week wash-out period between crossovers. Body composition was assessed by dual-energy X-ray absorptiometry. Fasting adiponectin, leptin, glucose, and insulin concentrations were measured and insulin resistance estimated by homeostasis model assessment for insulin resistance (HOMA-IR). In the younger obese subjects, CLA plus n-3 LC-PUFA supplementation compared with control fat did not result in increased abdominal fat and raised both fat-free mass (2.4%) and adiponectin levels (12%). CLA plus n-3 LC-PUFA showed no significant effects on HOMA-IR in any group but did increase fasting glucose in older obese subjects. In summary, supplementation with CLA plus n-3 LC-PUFA prevents increased abdominal fat mass and raises fat-free mass and adiponectin levels in younger obese individuals without deleteriously affecting insulin sensitivity, whereas these parameters in young and older lean and older obese individuals were unaffected, apart from increased fasting glucose in older obese men.
PMID: 18356842 [PubMed - indexed for MEDLINE]
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Even with the concurrent supplementation of an omega-3 fatty acid mixture(which I assume we can all generally agree is good on its own) the results in lean men and older obese men are zilch.[/QUOTE]
3g of CLA is on the low end of effective dosing.
I have done a chart some time ago where I compiled almost all available published studies on CLA w/r to effectivity (fat loss) and adverse effects. you would need to search for it at the forum. maybe you should use my old screenname (DRP7) for the search.
Here is a compilation of scientific studies done on CLA and its effects on fat loss:
[B]Overview: controlled clinical trials of CLA effects in humans[/B]
Compiled by me
When judging the effects of a substance it is of highest importance to base one's opinion oh [U]human[/U] trials.
Here I present a small compliation / overview of all studies that I found in Medline by searching after "conjugated linoleic acid" and with the limits: clinical trials and which report effects on body composition parameters.
In sum, CLA appears to have some small effects, especially when higher dosed. not all studies showed "significant" effects, which, IMO is due to the rather small effect size of CLA.
colour code:
------------
blue = positive result (12 studies)
red = negative result (10 studies)
[B]PART I.: Effects on body weight and fat:[/B]
[color=blue][U]1. Steck et al. (2007) [/U][/color]
50:50 ratio of CLA isomers, 3.2 g/d vs. 6.4 g/d vs. placebo group
N = 48 (13 males and 35 females) obese, otherwise healthy subjects
Duration: 12 weeks
Outcome: increase of lean body mass by 0.64 kg in the 6.4g/d CLA-group; significant decreases in serum HDL, sodium haemoglobin and hematocrit; significant increases in alkaline phosphatise, CRP and IL-6
[color=blue][U]2. Gaullier et al., (2007)[/U][/color]
12 g/d CLA vs. placebo
N=118 (BMI: 28-32 kg/m2), healthy overweight/obese subjects
Duration: 6 months
Outcome: reduction of body fat mass at 3.4 % at month 6; mostly located in legts and in women. No effects on bone mineral density.
[color=red][U]3. Nazare et al. (2007) [/U][/color]
3.76 g/d of CLA (50:50) vs placebo
Duration: 98 days
N = 44
Outcome: No effects on body weight, fat mass or free fat mass; increase of basal energy expenditure; increase of PPAR Gamma gene expression; reduction of mRNA of HSL. No effects on UCP-2 and LPL mRNA.
[color=blue][U]4.Colakoglu et al. (2007) [/U][/color]
3.6 g/ CLA with and without exercise vs. placebo
Duration: 6 weeks
Outcome: reduction of fat mass in all experimental groups and body weight reduction in the CLA-only group. Decrease of serum glucose in CLA and CLA+exercise groups and decrease of insulin in CLA +exercise group only.
[color=blue][U]5. Watras et al. (2007) [/U][/color]
3.2 g/d CLA vs. placebo
Duration: 6 months
N = 40, healthy, overweight subjects
Reduced weight gain during holiday seson; after 6 months reduced body fat in CLA vs placebo (1 kg). No effects on restin g metabolic rate, and markers for liver function, inflammation, blood lipids. Significant decrease of markers of endothelial dysfunction.
[color=red][U]6. Tricon et al. (2006) [/U][/color]
0.15 g of cis-9,t-11-CLA (control) vs. 1.42 g of cis-9, t11-CLA (treatment)
N = 32 of middle aged, healthy men
Duration: 6 weeks, 7 weeks wash-out, cross-over
Outcome: no effects on body weight, inflammatory markers, insulin, glucose, trigycerdes, total-, HDL and LDL-cholesterol. However, increased ratio of LDL : HDL.
[color=blue][U]7. Pinkoski et al. (2006) [/U][/color]
CLA 5g/d vs. Placebo
N = 76
Duration: 7 weeks with exercise; 17 subjects crossed over
Outcome: greater increase in lean mass (1.4 kg vs. 0.2 kg), greater loss of fat mass (-0.8 kg vs. +0.4 kg) smallr increase of 3-MH (marker of myofibrillar degradation). Greater increase in bench press.
[color=red][U]8. Larsen et al. (2006) [/U][/color]
CLA 3.4g/d vs. Placebo
Duration: 1 year
N = 101 obese healthy subjects who lost >8% of their initial body weight during a 8-week weight-loss program; during the trial: hypocaloric diet (-1250 kJ/d)
Outcome: no difference in body weight or body fat regain. No index of insulin resistence. Increased leukocyte numbers.
[color=blue][U]9. Gaullier et al. (2005) [/U][/color]
3.4 g/d CLA vs. Placebo
N = 157 (134 during the second 12 months)
Duration: 24 months (during the second 12 months: open study, no control group)
Outcome: during the extended (second 12 months) trial period reduction of body weight in the group that received placebo during the first year. No body weight or fat changes in the group that received CLA during the first year (=stabilisation of weight)
[color=red][U]10. Whigham et al. (2004) [/U][/color]
CLA 6g/d
N = n/a, healthy obese subjects
Duration: 1 year (first part: 13 kcal/kg/d; second part: refeeding with 25-30kcal/kg; third part: open label, all subjects receiving CLA)
Outcome: no difference in body composition between groups.
[color=red][U]11. Riserus et al. (2004) [/U][/color]
c9,t11-CLA 3 g/d vs Placebo
N = 25 of abdominally obese men
Duration : 3 months
Outcome: no difference of body composition between groups; decrease of insulin-sensitivity by 15% in the CLA-group, increase of iso-8-PGF2alpha (by 50%) and 15-keto-dihydro-PGF2alpha (15%).
[color=blue][U]12. Gaullier et al. (2004) [/U][/color]
CLA-FFA, CLA-TG and Placebo (amount?)
N=180 overweight males and females
Duration: 1 year
Outcome: reduced body fat mass in the CLA groups, increased lean body mass in CLA-FFA. Increased LDL, decreased HDL. Increased Lp(a). glycated haemoglobin increased in all groups.
[color=red][U]13. Malpuech-Brugere et al. (2004) [/U][/color]
1.5g/d and 3.0 g/d of c9,t11 vs 1.5/d and 3.0g/d of t10,c12) vs placebo
N=81 overweight healthy men
No significant differences of body fat mass, lean mass between groups
[color=red][U]14. Petridou et al. (2003) [/U][/color]
2.1 g/d CLA
N=16 young non-obese healthy women
duration: 45 days CLA vs 45 days placebo (cross-over design)
outcome: no difference in body-fat, serum-leptin,, TAG, total cholesterol, HDL and ALT.
[color=red][U]15. Kamphuis et al. (2003) [/U][/color]
1.5 g/d vs. 3.6 g/d of CLA vs. Placebo
N = 26 men and 28 women, overweight
Duration: 3 weeks of very low calorie diet; after that 13 weeks intervention period with CLA groups vs. placebo
Outcome: CLA did not have an effect on body weight regain after the diet phase. Favourable effects of CLA on appetite.
[color=blue][U]16. Belury et al. (2003) [/U][/color]
CLA 8g/d vs. Placebo
N= n/a, subjects with diabetes mellitus type II
Duration: 8 weeks
Outcome: Plasma-levels of t10,c12- but not c9,t11-CLA were negatively associated with body weight and serum-leptin
[color=red][U]17. Kreider et al. (2002) [/U][/color]
6g/d CLA vs Placebo
N = 23 healthy, training-experienced subjects
Duration: 28 days during an exercise program
Outcome: no significant effects of CLA on total body mass, fat-free mass, fat-mass, percent body-fat, bone-mass, strength.
[color=blue][U]18.Thom et al. (2001) [/U][/color]
1.8 g/d CLA vs. placebo
N=20 healthy subjects with normal weight and BMI, exercising 3 x per week
Outcome: reduced body fat, no effects on body weight
[color=blue][U]19.Smedman and Vessby (2001) [/U][/color]
4.2 g/d CLA vs. Placebo
N = 53 healthy subjects
Duration: 12 weeks
Outcome: reduction of body fat (3.8%). No effects on bodyweight, BMI, and sagittal abdominal diameter.
[color=blue][U]20. Riserus et al. (2001) [/U][/color]
4.2 g/d CLA vs. Placebo
N=25 abdominally obese men
Duration: 4 weeks
Outcome: reduction of sagittal abdominal diameter.
[color=blue][U]21. Blankson et al. (2000) [/U][/color]
CLA: 1.7 vs. 3.4 vs. 5.1 vs. 6.8 g/d vs. Placebo
N = 60 (47 completed the study), obese subjects
Duration: 12 weeks
Outcome: reduced body fat mass in the CLA groups (3.4 and 6.8 g/d). no effects on lean mass, BMI and blood variables.
[color=red][U] 22. Zambell et al. (2000) [/U] [/color]
3 g/d of CLA vs. Placebo
N = 17 healthy women
Duration: 64 days
Outcome: no effect of CLA on fat mass, fat-free mass and percentage body fat, energy expenditure, fat oxidation and respiratory exchange ratio.
[B]Compilation of human trials on CLA effects
Part II: Potential adverse effects[/B]
similar to the beneficial effects of CLA on fat-loss, the results on unwanted effects are also VERY heterogenous and far from conclusive.
[B] Effects on insulin, blood lipids, immune, inflammatory and vascular markers[/B]
[U]1. Colakoglu et al. (2006)[/U]
decreased serum glucose concentrations (in CLA group) and decreased insulin levels in CLA + exercise
[U]2. Trikon et al. (2006)[/U]
Increased ratio of LDL to HDL in the CLA group
[U]3. Taylor et al. (2006)[/U]
Decreased brachial artery blood flow as a sign of impaired endothelial function in the CLA group
[U]4. Ramakers et al. (2005)[/U]
no increase of CRP in neither c9,t11 nor in t10,c12 supplemented subjects; possibly enhanced immune function
[U]5. Naumann et al. (2006)[/U]
Neither c9,t11 nor t10,c12 had adverse effects on HDL, LDL, triglycerides, glucose and insulin levels in subjects with LDL phenotype B
[U]6. Smedman et al. (2005)[/U]
in healthy subjects, 4.2g/d of CLA significantly raised CRP-levels. TNF-alpha as well as TNF-alpha receptors 1 + 2 were not affected.
[U]7. Nugent et al. (2005)[/U]
A 80:20 (c9,t11 vs t10,c12) CLA-blend increased the PHA-induced lymphocyte proliferation. no effects of CLA on SiCAM-1, IL-4, Leukotriene B4.
[U]8. Song et al. (2005)[/U]
in healthy subjects supplemented with a 50:50 CLA, IgM and IgA levels increased while IgE levels decreased. Decreased the pro-inflammatory TNF-alpha and IL-1b levels and increased the anti-inflammtory IL-10. Decreased the delayed type hyperresponsitivity.
[U]9. Tricon et al. (2004)[/U]
in healthy subjects, CLA caused a dose-dependent decrease of mitogen-induced activation of T-lymphocyte proliferation. no effect on CRP.
[U]10. Moloney et al. (2004)[/U]
In type-II-diabetics, CLA increased HDL(2) levels and significantly reduced LDL-to-HDL ratio. CLA significantly reduced insulin-sensitivity and increased fasting glucose levels.
[U]11. Whigham et al. (2004)[/U]
in healthy obese subjects, CLA had no adverse effects on liver function, glucose, insulin, serum lipids, blood counts, and general chemistry.
[U]12. Tricon et al. (2004)[/U]
in healthy men, no adverse effects of CLA on insulin sensitivity. trans-10,cis-12 CLA increased LDL:HDL cholesterol and total:HDL cholesterol, whereas cis-9,trans-11 CLA decreased them.
[U]13. Riserus et al. (2004)[/U]
in obese men, c9,t11 CLA decreased insulin sensitivity by 15% (P < 0.05) and increased 8-iso-prostaglandin F(2alpha) and 15-keto-dihydro-prostaglandin F(2alpha) excretion by 50% (P < 0.01) and 15% (P < 0.05), respectively (as a sign of increaased lipid peroxidation)
[U]14. Riserus et al. (2004b)[/U]
in obese men, t10c12CLA induced hyperproinsulinaemia that is related to impaired insulin sensitivity, independently of changes in insulin concentrations.
[U]15. Eyjolfson et al. (2004)[/U]
4g/d of 50:50 CLA improved insulin sensitivity in young healthy men.
[U]16. Albers et al. (2003)[/U]
Almost twice as many subjects reached protective antibody levels to hepatitis B when consuming CLA 50:50 fatty acids (1.7g/d). Other aspects of immune function, ie DTH responses, NK cell activity, lymphocyte proliferation and production of TNF-alpha, IL1-beta, IL6, IFN-gamma, IL2, IL4, and PGE(2), were not affected.
[U]17. Riserus et al. (2002)[/U]
in subjects with metabolic syndrome, 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. t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men.
What yous guys think of musclepharm cla core? Any reviews on that? I just started taking it.
[QUOTE=xrichsayzx;851939743]What yous guys think of musclepharm cla core? Any reviews on that? I just started taking it.[/QUOTE]
Read thread. Come to conclusion.
Don't think it is safe without pausing after few months.
Looks like its safe to take. Thanks