Kyllä, CLA valmisteissa ON eroja. Tuon vahvuuden sijaan suosittelisin tarkkailemaan (myös) mitä CLA-isomeerejä juuri kyseinen tuote sisältää. Pääasiassa erot muodostuvat siis kahden pääisomeerin, cis-9, trans-11-18:2 sekä trans-10, cis-12-18:2 osalta ja näiden keskinäisistä suhteista. On vaikea kuitenkaan sanoa, mikä komponenteista(mahdollisesti joku muu?) pahoinvointisi aiheuttaa.. Itse en ainakaan ole törmännyt dataan CLA'n olevan yleisesti käytettyinä määrinä kovinkaan vatsaepäystävällinen (kunhan ei käytetä useita grammoja päivässä, joka onkin sitten jo eri asia ja riski kasvaa).
Pääsääntöisesti olisi suositeltavaa käyttää tuotteita, joissa painopiste olisi yllä mainituissa kahdessa pääisomeerissä.
"However, the suspected presence of both impurities and particular isomers might induce undesirable side effects. Despite this potential health risk, only a few CLA preparations have been tested under rigorous conditions for clinical efficacy and safety. Based on the limited results available, it is possible to suggest that preparations enriched in c9,t11 and t10,c12 isomers are preferable for human consumption compared to preparations containing four isomers, in terms both of safety and efficacy."
Lipids. 2002 Nov;37(11):1019-25.
Clinical trial results support a preference for using CLA preparations enriched with two isomers rather than four isomers in human studies.
Gaullier JM, Berven G, Blankson H, Gudmundsen O.
CLA-komponentti eri isomeereineen itsessään ja markkinoilla olevat CLA-tuotteet ovat tietysti sitten kaksi eria asiaa.
"Because research on CLA has been almost exclusively in animals and the mechanism(s) by which CLA exerts its effects remain largely unknown, scientists are extremely cautious about making definitive statements about CLA."
Conjugated linoleic acid: health implications and effects on body composition.
Journal of the American Dietetic Association, Volume 104, Issue 6, Pages 963-968
L. Rainer, C. Heiss
Sitten hieman laajamittaisempaa arvioita alla. Koska alla oleva osuus CLA'n turvallisuusarviosta löytyy eräästä erinomaisesta kokonaisartikkelista, copypastean sen nyt tähän kokonaisuudessaan, koska kaikilla asiasta kiinnostuneilla ei varmasti ole käyttöoikeuksia American Journal of Clinical Nutrition-julkaisuun..(?) So, here it goes;
"
CONJUGATED LINOLEIC ACID SAFETY
Safety is the paramount consideration. A substance that is not safe when used as intended should not be sold as a food ingredient or dietary supplement, irrespective of whether it is physiologically effective. Animal tests are typically used in preclinical evaluations of the safety of new food ingredients. CLA safety has been evaluated in several well-conducted animal toxicologic studies.
Scimeca (35) conducted a 36-wk feeding trial in which Fischer 344 rats were fed either control diet or diet supplemented with 1.5% CLA, a level 30 times greater than humans would ingest at 3 g CLA/d. Food disappearance, body weights, cageside examinations, and hematologic and histopathologic analyses of 15 major organs were conducted. No adverse effects were observed.
O’Hagan and Menzel (36) conducted a subchronic 90-d oral rat toxicity study, accompanied by a battery of in vitro genotoxicity studies that are typical for assessment of food ingredient safety, on a commercial preparation of CLA that consisted of equal amounts of the c9,t11- and t10,c12-CLA isomers in the form of glycerides (rather than free fatty acids). They concluded that the no observed adverse effect levels for male and female rats were 2433 and 2728 mg • kg body wt–1 • d–1, respectively.
In addition to these peer-reviewed published studies, there are 2 abstracts of note that relate to CLA safety assessment in animal models. Schulte et al (37) and Pfeiffer et al (38) conducted comprehensive toxicologic evaluations of CLA methyl esters in dogs and pigs, using standard toxicologic protocols approved by European Organisation for Economic Co-operation and Development Guidelines. They concluded that CLA methyl esters did not produce adverse effects in these species even when fed at 5% of the diet. These findings should, of course, be considered preliminary until the full-length manuscripts are available for review.
A number of human clinical trials that relate to safety and efficacy were also conducted. In designing human trials, CLA quality is a topmost issue. The most successful clinical studies were conducted with high-quality CLA preparations that consist almost entirely (ie, >90%) of the 2 biologically active isomers (Figure 1) in approximately equal amounts (ie, about 45% each), as reviewed by Gaullier et al (32). It should also be noted that such high-quality CLA, when consumed at 3–6 g/d, does not appear to induce adverse effects in humans (7, 11, 33, 34).
Despite these conclusions some researchers have recently raised concerns about the potential safety of CLA for humans (39-41). The concerns include the induction of fatty liver, insulin resistance, and lipodystrophy in mice fed CLA-supplemented diets and in some human trials enhanced C-reactive protein, lipid peroxidation, unfavorable changes in serum lipids, and reduced milk fat. I consider these concerns in order, in light of the overall scientific literature database on CLA.
Fatty liver is induced in mice fed CLA-supplemented diets [reviewed in Pariza et al (4)]. However, this finding appears limited to mice in that it has not been reported for other species. Hamsters fed CLA and female rats fed diet supplemented with 15% CLA also exhibit enlarged livers, but this result is due to hypertrophy, not fat accumulation (36). It should be noted that neither fatty liver nor liver hypertrophy is considered by toxicologists to be a toxic effect (42). O’Hagan and Menzel (36) reported that the liver hypertrophy observed in female rats fed diet supplemented with 15% CLA was completely reversible when the animals were switched to a diet free of CLA.
The induction of mild insulin-resistance in mice was studied extensively and appears to be related to experimental conditions. For example, the effect is observed in mice fed diet supplemented with 1% CLA for 39 d (43) but not in mice fed diet supplemented with 0.5% CLA for 4 or 49 d (26) (0.5% CLA is sufficient to maximally induce body fat reduction in this species). Additionally, diabetic C57BLKS-Leprdb/leprdb(db/db) mice fed a diet supplemented with 1.2% CLA for 23 wk exhibited significant reductions in blood glucose and improved insulin sensitivity even in the face of an oral glucose challenge (44, 45). One could speculate that this transient insulin resistance results from CLA-induced changes in adipocyte dynamics, ie, older less responsive cells being replaced by younger more metabolically active cells. It should also be noted that in the Zucker fatty rat dietary CLA restores sensitivity and reduces symptoms of diabetes (5, 6).
A related effect, lipodystrophy, was reported in mice fed a diet supplemented with CLA. Like fatty liver, lipodystrophy has not been reported to occur in other species, and it is possible that lipodystrophy is seen in mice because mice are so sensitive to CLA-induced body fat reduction. Increasing the amount of fat in CLA-supplemented diet substantially reduces the lipodystrophy effect (46).
With regard to these seemingly negative effects, it should be noted that dietary CLA significantly extended the life span of NZB/WF1 mice, which are prone to developing lupus erythematosus (47, 48). This finding is consistent with the conclusion that CLA does not induce toxic effects and is important because mice appear to be the most sensitive and responsive known species to the effects of CLA on lipid metabolism (30).
Concern about elevations in oxidative stress and unfavorable changes in blood lipids has arisen from studies by Riserus et al (41) who investigated the effects of CLA in men with metabolic syndrome. They compared a typical high-quality CLA preparation consisting of equal amounts of c9,t11- and t10,c12-CLA with a supplement that is not commercially available, enriched for t10,c12-CLA but containing very little c9,t11-CLA. Riserus et al (41) observed evidence of enhanced lipid peroxidation (measured as urinary isoprostane), enhanced C-reactive protein in serum, and elevated VLDL coupled with reduced HDL. These negative effects were significant relative to placebo for the patients taking the t10,c12-CLA supplement but were reduced (in some cases below statistical significance) for patients taking the typical commercially available CLA supplement relative to placebo. Interestingly, the apparent t10,c12-CLA-induced oxidative stress did not result in reduced blood antioxidants but rather was correlated with increased blood vitamin E.
Riserus et al (41) concluded that these findings indicate that CLA could enhance inflammation and cardiovascular disease risk. However, other groups that have studied this issue have concluded that CLA reduces inflammation. For example, pigs fed a commercial mixture of CLA isomers displayed reduced inflammation (17), and dietary CLA not only reduced atherosclerosis in animal models (9, 49) but also reduced preestablished atherosclerotic lesions in rabbits (9) and mice (50). Additionally, the researchers of a comprehensive clinical study of the effects on serum lipids of a high-quality CLA preparation consisting of c9,t11- and t10,c12-CLA in approximately equal amounts concluded, "The study confirms that some of the cardioprotective effects of CLA that were shown in animal studies are relevant to man" (7).
Riserus et al (41) also reported that the men in their study who were given the t10,c12-CLA supplement exhibited enhanced insulin resistance. Again, there was no significant difference in this condition between the placebo group and the group receiving the typical commercially available high-quality CLA isomer mixture, a finding that is also consistent with a previous report from Riserus’s group (51). Evidence of enhanced insulin resistance has not been observed in other CLA clinical trials either (7, 32, 33).
It is well documented that t10,c12-CLA reduces milk fat. This effect has been most thoroughly studied in cows (52) but is also observed in lactating women who consume CLA supplements (53). The researchers of the latter study (53) concluded that the reduction of milk fat might lead to less energy availability for the nursing infant. However, in a study with rats (54) it was found that the pups nursing dams fed CLA-supplemented diet actually grew to a larger body size. Because very little t10,c12-CLA carries over to milk, whereas the c9,t11-CLA isomer is concentrated in milk, it could be concluded that c9,t11-CLA could be a growth factor for young rats, as it appears to be for young mice (4). Similar findings were obtained in a study with pigs in which the researchers concluded, "Irrespective of the dietary fat supplied in the starter period, piglets reared on the CLA sows had greater final body and warm carcass weights (P <0.01), and greater feed intake (P = 0.02) than piglets reared on the [control] sows" (55). It seems likely that in these studies (54, 55) nursing animals compensated for reduced calories because of milk fat reduction by consuming more milk. "
http://www.ajcn.org/cgi/content/full/79/6/1132S
