Is CLA good for our health?
- 06-17-2007, 06:54 PM
Is CLA good for our health?
Efficacy and safety of dietary supplements contain...[J Lipid Res. 2003] - PubMed Result
Dietary supplements containing conjugated linoleic acid ( ) are widely promoted as weight loss agents available over the counter and via the Internet. In this review, we evaluate the efficacy and safety of supplementation based on peer-reviewed published results from randomized, placebo-controlled, human intervention trials lasting more than 4 weeks. We also review findings from experimental studies in animals and studies performed in vitro. CLA appears to produce loss of fat mass and increase of lean tissue mass in rodents, but the results from 13 randomized, controlled, short-term (<6 months) trials in humans find little evidence to support that CLA reduces body weight or promotes repartitioning of body fat and fat-free mass in man. However, there is increasing evidence from mice and human studies that the CLA isomer trans-10, cis-12 may produce liver hypertrophy and insulin resistance via a redistribution of fat deposition that resembles lipodystrophy. CLA also decreases the fat content of both human and bovine milk. In conclusion, although CLA appears to attenuate increases in body weight and body fat in several animal models, CLA isomers sold as dietary supplements are not effective as weight loss agents in humans and may actually have adverse effects on human health.Life is a terminal condition.
- 06-17-2007, 07:03 PM
Isn't CLA also technically a Trans-Fat?. I never thought it was a good idea to supplement with CLA. I tried some only once. There is a difference between the CLA produced by supplement manufacturers and CLA found in food. Cla is found in dairy products. It also in red meat I believe.
06-17-2007, 08:23 PM
Efficacy of conjugated linoleic acid for reducing fat mass: a meta-analysis in humans
Leah D Whigham, Abigail C Watras and Dale A Schoeller
1 From the Department of Obstetrics and Gynecology, University of Wisconsin School of Medicine and Public Health, Madison, WI (LDW), and the Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, WI (ACW and DAS)
Background:Conjugated linoleic acid (CLA) has been shown to be an effective supplement for reducing fat mass in animals, whereas results in humans have been inconsistent.
Objective:This is a meta-analysis of human studies in which CLA was provided as a dietary supplement to test its efficacy in reducing fat mass.
Design:We searched the PubMed database (National Library of Medicine, Bethesda, MD) and references from the resulting search to identify studies in which CLA was provided to humans in randomized, double-blinded, placebo-controlled trials and in which body composition was assessed by using a validated technique.
Results:We identified 18 eligible studies. Of these, 3 were single-isomer studies, and results comparing CLA isomers were inconclusive. We compared the length of treatment by using studies in which a mixture of purified isomers were used and those in which purified trans-10,cis-12 isomers were used. This comparison indicated that the effect of CLA was linear for up to 6 mo and then slowly approached an asymptote at 2 y. An analysis of the dose effect indicated that fat loss compared with placebo was –0.024 kg · g CLA–1 · wk–1 (P = 0.03). After adjustment to the median dose of 3.2 g CLA/d, CLA was effective and produced a reduction in fat mass for the CLA group alone (0.05 ± 0.05 kg/wk; P < 0.001) and for the CLA group compared with placebo (0.09 ± 0.08 kg/wk; P < 0.001)
Conclusion:Given at a dose of 3.2 g/d, CLA produces a modest loss in body fat in humans.
Key Words: Body composition • obesity • weight loss • conjugated linoleic acid
06-17-2007, 08:40 PM
There are plenty of studies that show CLA does not work - but at too low of a dose.
If one analyzed only those studies (maybe they didn't use enough data for their meta analysis) - then yeah, CLA doesn't work.
As far as the side effects - you'd have to say how much of that was animal and how much was human. I don't place a whole lot of stock in animal studies - they don't always translate.
But - that does sound bad if true in humans. I'd have to see how much of that isomer is present in the various CLA products.
06-17-2007, 08:59 PM
Life is a terminal condition.
06-17-2007, 09:31 PM
Good suggestion B!
I was going to buy the 50:50 blend of NP caps - but I'll hold off on the 70:30 blend.
06-17-2007, 09:45 PM
But it seems to me that the increased fat loss ratio of 70:30/t10,c12:c9,t11 is the same one that increased insulin resistance. No?However, there is increasing evidence from mice and human studies that the CLA isomer trans-10, cis-12 may produce liver hypertrophy and insulin resistance via a redistribution of fat deposition that resembles lipodystrophy.
Life is a terminal condition.
06-17-2007, 09:51 PM
06-17-2007, 09:59 PM
very interesting discussions going on here.
06-17-2007, 10:06 PM
06-17-2007, 10:08 PM
I would say one might consider something like Cinnulin PF when on a CLA run. That helps modulate insulin response.
Or Na-R-ALA maybe. Or AP.
Just a thought. Maybe this becomes a necessity like biotin with R-ALA...
06-17-2007, 10:15 PM
This one is the one that references my opening post PebMed* Insulin resistance - Proponents of CLA often quote studies in which it improves insulin sensitivity in rat models of diabetes [1-2, 4]. Additionally, CLA favorably alters metabolic parameters in humans with type II diabetes . Unfortunately the opposite effect is seen in nondiabetic individuals. Induction of insulin resistance, or markers thereof, has been noted in pigs, mice, hamsters, and rats fed CLA despite fat loss [1-2, 4]. Even in a study in pigs in which there were no changes in body composition, fasting insulin rose by 37% . Additionally, 3.4 g daily of t10,c12 CLA for 12 weeks increased insulin resistance (by 19%) and C-reactive protein (a marker of inflammation and predictor of cardiovascular risk) in obese men [1, 13]. This effect may be related with increased levels of TNF-alpha . It can be concluded that although CLA is beneficial to those with diabetes, it may increase insulin resistance in normoglycemic individuals.So, my thinking is that the 50:50 would be less 'toxic' and would be better suited with substantial amounts of Fish Oil (epa/dha) which increases insulin sensitivity, and uber amounts sesathin.* Other effects - There are a variety of other effects of CLA. On the positive side, CLA reduces bone inflammation  and has a positive role in bone formation in rats . CLA also appears to improve immune response in healthy men  and protects against end-stage symptoms of lupus erythematosis, although it accelerates the onset of this condition . Multiple studies have found CLA to increase markers of lipid peroxidation and oxidative stress in both healthy and obese humans, an effect which is not reduced by vitamin E [1-2, 16-17]. Additionally, CLA causes liver steatosis (fat accumulation) in mice and chicken and liver and kidney enlargement in hamsters despite a decrease in body weight, and this effect has been attributed to the t10,c12 isomer [1-2, 18].
Dosage and administration
For fat loss, the t10,c12 isomer is the important one, and the amount of this isomer present in studies in which significant fat loss was seen ranges from .5-2.5 g for 4-12 weeks (note that this is equivalent to about 2.5-12.5 g of CLA powder or 1.5-7.5 g of 30% t10,c12 CLA oil). More significant fat loss would be seen if the dosage was closer to that used in animal studies (which would be equivalent to upwards of 25 g of CLA oil daily ), but the risk of liver enlargement and insulin resistance will be proportionally increased, so this quantity is not recommended (nor is it economically feasible for most). It would be wiser to use a lower dose of CLA in conjunction with other fat loss agents, and monitor glucose and insulin levels and liver parameters if possible. Side effects reported in clinical trials include gastrointestinal discomfort and fatigue .
Oh, yes, and AP and maybe ALA, NAC and maybe other anti-o's as well.
Life is a terminal condition.
06-18-2007, 12:00 AM
06-18-2007, 12:04 AM
06-18-2007, 07:19 AM
I was thinking about this, and I'm curious about the insulin sensitivity effects. Could this really be a bad thing? Capsaicin causes insulin resistance, and it's being used researched as a possibly cure/remedy for Type II diabetes for this effect.
I'm just wondering if the insulin resistance might play a role in CLA's nutrient reparitioning effects.
06-18-2007, 08:17 AM
The truth of the matter is that the studies don't all give an isomer break down. Some do. So they seem to contradict. The ones with increased insulin resistance do not indicate isomer breakdown. This first one does indicate that the insulin sensitivity is attributed to the c9,t11-CLA isomer. This does further suggest to me that the higher quality or greater t10,c12:c9,t11 ratio may indead be better for fat loss but be responsible for insulin rsistance as well.Antidiabetic effects of cis-9, trans-11-conjugated...[Diabetes. 2007] - PubMed Result
Antidiabetic effects of cis-9, trans-11-conjugated linoleic acid may be mediated via anti-inflammatory effects in white adipose tissue.
Moloney F, Toomey S, Noone E, Nugent A, Allan B, Loscher CE, Roche HM.
Nutrigenomics Research Group, Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin, St. James's Hospital, Dublin 8, Ireland.
Adipose tissue may be the source of insulin desensitizing proinflammatory molecules that predispose to insulin resistance. This study investigated whether dietary fatty acids could attenuate the proinflammatory insulin-resistant state in obese adipose tissue. The potential antidiabetic effect of cis-9, trans-11-conjugated linoleic acid (c9,t11-CLA) was determined, focusing on the molecular markers of insulin sensitivity and inflammation in adipose tissue of ob/ob C57BL-6 mice. Feeding a c9,t11-CLA-enriched diet reduced fasting glucose (P < 0.05), insulin (P < 0.05), and triacylglycerol concentrations (P < 0.01) and increased adipose tissue plasma membrane GLUT4 (P < 0.05) and insulin receptor (P < 0.05) expression compared with the control linoleic acid-enriched diet. Interestingly, after the c9,t11-CLA diet, adipose tissue macrophage infiltration was less, with marked downregulation of several inflammatory markers in adipose tissue, including reduced tumor necrosis factor-alpha and CD68 mRNA (P < 0.05), nuclear factor-kappaB (NF-kappaB) p65 expression (P < 0.01), NF-kappaB DNA binding (P < 0.01), and NF-kappaB p65, p50, c-Rel, p52, and RelB transcriptional activity (P < 0.01). To define whether these observations were direct effects of the nutrient intervention, complimentary cell culture studies showed that c9,t11-CLA inhibited tumor necrosis factor-alpha-induced downregulation of insulin receptor substrate 1 and GLUT4 mRNA expression and promoted insulin-stimulated glucose transport in 3T3-L1 adipocytes compared with linoleic acid. This study suggests that altering fatty acid composition may attenuate the proinflammatory state in adipose tissue that predisposes to obesity-induced insulin resistance.
PMID: 17327424 [PubMed - indexed for MEDLINE]Dietary conjugated linoleic acid preserves pancrea...[Metabolism. 2007] - PubMed Result
Dietary conjugated linoleic acid preserves pancreatic function and reduces inflammatory markers in obese, insulin-resistant rats.
Noto A, Zahradka P, Ryz NR, Yurkova N, Xie X, Taylor CG.
Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB, Canada R3T 2N2.
Pancreatic preservation is an important part of diabetes management that may occur with improved peripheral insulin sensitivity and attenuated low-grade adipose tissue inflammation. The objective of the current study was to determine the response of obese, insulin-resistant fa/fa Zucker rats vs lean controls to dietary conjugated linoleic acid (CLA) supplementation with respect to pancreatic islet size, insulin resistance, and markers of inflammation and adipose glucose uptake. Six-week-old fa/fa and lean Zucker rats (n = 20 per genotype) were fed either a 1.5% CLA mixture or control diet for 8 weeks. Oral glucose tolerance testing was conducted at 7.5 weeks. Fasting serum haptoglobin, insulin, and C-peptide were assayed, and select messenger RNA (mRNA) and protein markers of inflammation and glucose metabolism were measured in adipose and liver tissues. CLA-fed fa/fa Zucker rats had smaller islet cell size, improved oral glucose tolerance and insulinemia, and attenuated serum haptoglobin levels compared with control-fed fa/fa Zucker rats, despite no differences in body weight and a slightly higher visceral adipose mass. CLA did not alter insulin sensitivity or islet size in lean Zucker rats. The CLA-fed fa/fa rats also had greater adipose glucose transporter-4 mRNA and less adipose tumor necrosis factor alpha mRNA and protein compared with control-fed fa/fa rats. In contrast, other markers of inflammation and glucose metabolism including adipose macrophage inflammatory factor, macrophage inflammatory protein-2, and liver pyruvate carboxylase and pyruvate dehydrogenase kinase 4 were not significantly changed. These results suggest that CLA supplementation preserved pancreatic function in conjunction with improved peripheral glucose use and reduced inflammation in fa/fa Zucker rats.
PMID: 17161237 [PubMed - indexed for MEDLINE][Effects of conjugated linoleic acid on expression...[Zhonghua Yu Fang Yi Xue Za Zhi. 2007] - PubMed Result
[Effects of conjugated linoleic acid on expression of GLUT4 protein in skeletal muscle of insulin resistant rat]
[Article in Chinese]
Sun CH, Zhou XR, Wen Y, Liu YM.
Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin 150001, China.
OBJECTIVE: To study the effects of conjugated linoleic acid (CLA) on expression of glucose transporter 4 (GLUT4) protein in skeletal muscle of insulin resistant rat, and explore the mechanism of resisting diabetes by CLA. METHODS: Male Wistar rats were randomly separated into control group, high-fat group and high fat plus CLA group (0.75 g%, 1.50 g%, 3.00 g% by deit weight), and the effects of CLA on blood glucose and insulin levels of insulin resistant rat were observed , by using Western blot technique to measure the expression level of GLUT4 protein in skeletal muscle of insulin resistant rat. RESULTS: The serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) microU/ml, and (5.09 +/- 0.66) mmol/L, the supplement of CLA might decrease the hyperinsulinemia and hyperglycemia, and in CLA groups (0.75 g%, 1.50 g%, 3.00 g% by deit weight) the serum insulin was (6.99 +/- 1.77) microU/ml, (7.36 +/- 1.48) microU/ml and (7.85 +/- 1.60) microU/ml (P < 0.05), and the glucose levels were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L (P < 0.05), (4.06 +/- 0.63) mmol/L (P < 0.05) respectively. The expression of GLUT4 protein in skeletal muscle of rat fed with high fat diet were decreased as compared with those fed with basic deit, and CLA might increase the expression of GLUT4 protein in skeletal muscle fed with high fat diet. CONCLUSIONS: CLA improve the insulin resistance of obese rat, possibly acting through increasing the expression of GLUT4 protein in skeletal muscle of rat fed with high fat diet.
PMID: 17484206 [PubMed - in process]Conjugated linoleic acid inhibits glucose metaboli...[Mol Cell Endocrinol. 2007] - PubMed Result
Conjugated linoleic acid inhibits glucose metabolism, leptin and adiponectin secretion in primary cultured rat adipocytes.
Pérez-Matute P, Marti A, Martínez JA, Fernández-Otero MP, Stanhope KL, Havel PJ, Moreno-Aliaga MJ.
Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain.
Conjugated linoleic acid (CLA) supplementation has been reported to induce insulin resistance in animals and humans, however, the underlying mechanisms remain unclear. The aim of this study was to examine the direct effects of CLA on leptin and adiponectin secretion, two hormones with actions known to influence insulin sensitivity. Isolated rat adipocytes were incubated with CLA (1-200microM) in the absence and presence of insulin (1.6nM). CLA inhibited both basal and insulin-stimulated leptin gene expression and secretion (-30 to -40%, P<0.05-0.01). CLA also inhibited basal adiponectin production (-20 to -40%, P<0.05-0.01), but not in the presence of insulin. CLA (50-200muM) decreased basal glucose uptake (P<0.05-0.01) and significantly increased the proportion of glucose metabolized to lactate (P<0.01). Insulin treatment partially prevented the inhibitory effects of CLA on glucose uptake and induced a significant increase (P<0.05-0.01) in the percentage of glucose metabolized to lactate. A strong inverse relationship was observed between the increase in the anaerobic utilization of glucose and the decreases of both leptin and adiponectin secretion. In addition, lipolysis and the expression of the adipogenic transcription factor PPARgamma were decreased by CLA. These results indicate that CLA inhibits leptin and adiponectin secretion and suggest that increased anaerobic metabolism of glucose may be involved in these effects. The inhibition of PPARgamma could also mediate the inhibition of adiponectin induced by CLA. Furthermore, the inhibition of leptin and adiponectin production induced by CLA may contribute to insulin resistance observed in CLA-treated animals and humans.
PMID: 17321040 [PubMed - indexed for MEDLINE]
Life is a terminal condition.
06-18-2007, 10:59 AM
Treatment With Dietary trans10cis12 Conjugated Linoleic Acid Causes Isomer-Specific Insulin Resistance in Obese Men With the Metabolic Syndrome -- Risérus et al. 25 (9): 1516 -- Diabetes Care
Effects of cis-9,trans-11 conjugated linoleic acid...[Am J Clin Nutr. 2004] - PubMed Result
Conjugated Linoleic Acid Impairs Endothelial Function -- Taylor et al. 26 (2): 307 -- Arteriosclerosis, Thrombosis, and Vascular Biology
I'm beginning to think the use of CLA is not a good idea regardless of isomer ratio.
Life is a terminal condition.
06-18-2007, 11:06 AM
I believe there was a great discussion over at M&M regarding CLA, and how inhibiting Lipogenisis is not exactly a great thing, I will try and dig up the link.
06-18-2007, 11:08 AM
The site is down, but you are right there was. virtualcyber was the thread starter I believe.
Life is a terminal condition.
06-18-2007, 11:10 AM
04-22-2009, 04:11 PM
Just wanted to add some new info to this old but informative thread:
Conjugated linoleic acid-induced toxic hepatitis: first case report.
Dig Dis Sci. 2009 May;54(5):1141-3. Epub 2008 Aug 23.
Ramos R, Mascarenhas J, Duarte P, Vicente C, Casteleiro C.
Gastroenterology Department, Covilhã University Hospital, Quinta do Alvito, 6000-251 Covilhã, Portugal.
A 46-year-old female patient was referred to our department with presenting symptoms of asthenia, jaundice, and pruritus. There was no medical history or clinical evidence of viral hepatitis, autoimmune hepatitis, hemochromatosis, or Wilson's disease. The patient revealed that 14 days prior to admission she had begun self-medicating with conjugated linoleic acid (CLA) to reduce body fat, leading to the suspicion of CLA hepatotoxicity, which was subsequently confirmed by a liver biopsy. After the patient ceased to ingest CLA, liver enzymes levels normalized. To the best of our knowledge, this is the first report of hepatotoxicity due to CLA ingestion.
Unfortunately the full text does not reveal what dose the woman was taking. I'd like to avoid taking any products with liver toxicity, but I am tempted to use CLA for cutting.
The evidence for CLA's effectiveness in this regard is not looking good, however.
04-22-2009, 04:19 PM
The research reviews with non-vested interests in CLA are rather scathing lol. It seems to benefit obese individuals with insulin sensitivity issues .
04-22-2009, 09:49 PM
wow i don't think i'm taking cla anymore i been feeling pains in my side right where my liver is for the past couple days and i've been taking cla for like the last 5 months str8 everyday at 4 a day dose after i finish this little bit i have left i'm done with it and i was just about to order like 4 more bags
04-22-2009, 10:35 PM
Yeah I've decided to return the bottle I just bought. I think I've abused my liver enough, I don't need to take a substance with questionable benefits and numerous concerns. This liver toxicity and the insulin resistance issues are enough to dissuade me, especially without any good study demonstrating fat loss effectiveness or basically anything good. I really should have read more about it before I clicked "add to cart".
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