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Dairy Farmers of Canada
Address reprint requests to: Helen B. MacDonald, Dairy Farmers of Canada, 1801 McGili College Avenue, Suite 1000, Montreal, Quebec, H3A 2N4, CANADA.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONBACKGROUNDCONCLUSIONS AND FUTURE...REFERENCES |
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There is, however, insufficient evidence from human epidemiological data, and very few of the animal studies have shown a dose-response relationship with the quantity of CLA feed and the extent of tumor growth. Further research with tumor models is needed to test the efficacy and utility of CLA in cancer and other disease prevention and form the basis of evaluating its effect in humans by observational studies and clinical trials.
Key words: conjugated linoleic acid, CLA, cancer, heart disease, antioxidant, fatty acids
Key teaching points:
• CLA may inhibit the development of tumors through its effect on antioxidants.
• It may also have a role in preventing atherosclerosis and modulate certain aspects of immune system.
• The evidence is primarily based on in vitro and animal studies.
• Further research with tumor models and human epidemiological data is warranted.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONBACKGROUNDCONCLUSIONS AND FUTURE...REFERENCES |
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BACKGROUND |
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TOPABSTRACTINTRODUCTIONBACKGROUNDCONCLUSIONS AND FUTURE...REFERENCES |
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CH—CHCH—(CH2)7—COOH 9c,11t-18:2 trans cis
Where Is CLA Found?
Nine different positional and geometric isomers of CLA have been reported as minor components of a variety of products [12]. CLA may have products common to furans in their overall oxidative scheme [13]. Interestingly, food lipids originating from ruminant animals (beef, lamb and dairy) contain much higher levels of CLA than lipids from non-ruminants. CLA concentrations in dairy products typically range from 2.9 to 8.92 mg/g fat, of which the 9-cis, 11-trans isomer makes up to 73% to 93% of the total CLA. Beef also contains CLA in a similar range with the 9-cis, 11-trans isomer contributing 57% to 85% of total CLA [14–16]. Vegetable oils and margarines contain little CLA. CLA concentrations in fats from non-ruminants and vegetable oils typically range from 0.6 to 0.9 mg/g fat [16]. CLA is sold in health food stores as a muscle builder and is made by hydrogenation of oils, the process being somewhat difficult, as some of the CLA isomers are very unstable. Some typical values of CLA from various foods are given in Table 1. Values on margarines and spreads were not available.
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Factors Affecting CLA Levels.
In ruminant tissue and milk, the levels as well as the isomer distribution of CLA are likely to be modulated by the microbial population in the rumen, which in turn, is influenced by the quantity of animal feed and its dietary oils content (linoleic acid and/or linolenic acid) [20]. Milk from cows grazing pasture had a higher content of CLA than cows fed conserved diets containing 50:50 forage and grain housed indoors [21]. Supplementing feeds with a full-fat rapeseed or soybean concentrate increases milk fat CLA. CLA levels also vary with season: the highest levels were observed between May and September, the lowest in March [22]. The individual cow to cow variation in CLA levels may range from 1.6 to 16.0 mg/g milk fat, partly due to the number of lactations the cows have undergone [22]. The CLA content of dairy foods is influenced by processing conditions [12, 14, 23]. In general, aged cheeses have lower amounts of CLA than cheeses with a shorter ripening period [16]. In processed cheeses, a higher temperature, the addition of sodium caseinate, hydrogen donors (butylated hydroxytoluene, propyl gallate or ascorbic acid), whey powder, nonfat dry milk or iron increase the content of CLA [14, 23]. No changes however, were observed when storing or processing dairy products such as lowfat yogurt, regular-fat yogurt, lowfat and regular-fat ice cream, sour cream or cheeses at low temperatures [24].
Ha et al. [12] suggested that grilling beef may increase CLA content by about four-fold. This was surprising in view of the literature that suggests that grilling beef at high temperatures produces mutagens and carcinogens which belong to polynuclear aromatic hydrocarbons or heterocyclic amines such as IQ (2-amino-3methylimidazol[4,5-f] quinoline). Earlier studies by Pariza et al. [25] have however shown that ground beef contained a factor which exhibited a selective antimutgenic action and that the inhibitory activity was also present in raw ground beef. While Shantha et al. [15] did not suggest an increase in CLA content due to cooking, they did demonstrate that CLA is stable and not destroyed by cooking or storage.
CLA in Human Tissue.
Low concentrations of CLA are found in human blood and tissues [26,27]. Its presence may be accounted for via two possible pathways [26]. First CLA may be produced in vivo from free radical-mediated oxidation of LA. Hydrogen abstraction by a free radical species and subsequent diene conjugation produces an LA lipid radical with conjugated diene structure. In the presence of protein, the LA radical may react with protein instead of molecular oxygen, giving rise to a CLA molecule and a protein radical. Second, CLA in human tissues may be derived from dietary sources, such as fried ground beef and dairy products. Blood CLA levels have been increased in human subjects by feeding CLA-rich diets. In a study by Huang et al. [28] on nine men, plasma CLA increased 19% to 27% following a four weeks feeding of cheddar cheese, but no appreciable changes in linoleic and arachidonic acids, cholesterol or phospholipid levels were observed. This finding may be of importance in changing the levels of CLA in biological fluids by altering specific dietary foods and fatty acids as sources of CLA and, thereby, protecting against cancer.
CLA and Carcinogenesis
There is a large and growing body of evidence indicating that free radicals and radical-mediated oxidation processes play a role in many pathological conditions, including cancer and atherosclerosis [29]. Although the mechanism of action is not well understood, CLA has been found to be an effective antioxidant in vitro and in animals.
In Vitro Studies.
Shultz et al. [30,31] incubated human malignant melanoma (M21-HPB), colorectal cancer cells (HT-29), as well as human breast cancer cells (MCF-7) for 12 days in a culture medium supplemented with various concentrations (1.78–7.14 x 10(-5) M) of linoleic acid or CLA. Linoleic acid initially stimulated MCF-7 cell growth with an optimal effect at concentrations of 3.57–7.14 x 10(-5) M, but was inhibitory at similar concentrations after eight and 12 day of incubation. In contrast, CLA was inhibitory to cancer cell growth at all concentrations and times tested. Cell growth inhibition by CLA was dose- and time-dependent. Growth retardation at the prescribed LA and CLA concentrations ranged, respectively, from 4% to 33% and from 54% to 100% following eight to 12 days of treatment. At similar LA and CLA concentrations, cytostatic and cytotoxic effects of CLA were more pronounced (8% to 81%) than LA. These in vitro results suggest that CLA is cytotoxic to MCF-7 cells. CLA also inhibited the proliferation of human malignant melanoma and colorectal cancer cells. Furthermore, CLA was more effective than beta-carotene. Schonberg and Krokan [32] observed that CLA exerted a dose-dependent reduction in proliferation of the lung adenocarcinoma cell lines, possibly due to increased production of cytotoxic lipid peroxidation products, such as malondialdehyde.
Animal Studies.
Pariza and Hargraves [33] first reported that topical applications of a partially purified extract from grilled ground beef (enriched with mutagenesis modulator) five minutes prior to DMBA (7,12-dimethylbenz[a]anthracene) treatment reduced the number of papillomas per mouse as well as the number of mice with papillomas. The anticarcinogenic factor was then isolated and identified as a mixture of dienoic derivatives of linoleic acid. Since then, synthetic CLA has been shown to be anticarcinogenic in several animal models.
Role in Initiation of Cancer.
CLA has inhibited the development of mouse epidermal tumors [34], mouse forestomach cancer [35] and rat mammary cancer [29, 36, 37]. Feeding mice [35] and rats [36] a mixture of CLA isomers resulted in the preferential incorporation of the 9-cis, 11-trans isomer into membrane phospholipids, suggesting that the 9-cis, 11-trans CLA is the biologically active isomer. Ha et al. [34] initially examined chemically prepared CLA for anti-initiation activity in the two-stage mouse epidermal carcinogenesis model. CLA was topically applied at seven days (at a dose pf 20 mg/mouse), three days (20 mg) and five minutes (10 mg) before DMBA treatment. Control mice were painted with linoleic acid before DMBA administration. All mice were given 12-O-tetradecanoylphorbol-13-acetate for tumor promotion. It was found that CLA reduced the number of papillomas by half, compared with that in the linoleic-acid treated control subjects. In a second study performed by the same investigators [35], the synthetic CLA mixture decreased benzo(a)pyrene-induced forestomach tumors in mice by 50%. A dose of 0.1 mL of CLA was administered by gavage in this experiment at four and two days before treatment with benzo(a)pyrene during first week, and this sequence was repeated for four consecutive weeks. Short-term CLA feeding for five weeks, from weaning to the time of carcinogen administration at 50 days of age, also offered significant protection against subsequent mammary tumor occurrence. This period corresponds to maturation of the mammary gland to the adult stage in the rat. The inhibitory response to short-term CLA exposure was observed with the use of two different carcinogens: 7,12-dimethylbenz(a)anthracene and methylnitrosourea. The fact that CLA was protective in the methylnitrosourea model suggests that it may have a direct modulating effect on susceptibility of the target organ to neoplastic transformation. The proliferative activity of the mammary epithelium was assessed by the incorporation of bromodeoxyuridine. Immunohistochemical staining results showed that CLA reduced the labeling index of the lobuloalveolar compartment, but not that of the ductal compartment of the mammary tree. Since the lobuloalveolar structures are derived from the terminal end buds which are the sites of carcinogenic transformation, the above finding is consistent with the bioassay data of tumor inhibition. Thus, changes in gland development and morphogenesis may be a locus of action of CLA in modulating mammary carcinogenesis. Its implication for mammary gland development among humans may be important, considering that developmental changes in the mammary gland during the period of adolescence and pregnancy determine the risk of breast cancer: early onset of puberty increases, but early pregnancy decreases the risk in women.
Zu and Schut [38] examined the effect of CLA on carcinogen activation and detoxification by studying IQ-DNA adduct formation in CDF1 mice. The heterocyclic amine, IQ, is capable of inducing tumors in certain organs of mice (e.g. liver, forestomach and lung), but the site of the neoplasm depends on the gender. CLA pre-treatment was found to inhibit IQ-DNA adduct in both target organs (liver in male and lung in female) and non-target organs (large intestines and kidney). The inhibitory response was however, not seen in the stomach (a target organ) and the small intestines (a non-target organ). Liew et al. [39] fed CLA to a group of male F344 rats who were subsequently given IQ as a carcinogen. Rats were killed 6 hours after the final carcinogen dose in order to quantify IQ-NA adducts or after week 16 to score colonic aberrant crypt foci (ACF). CLA had no effect on the size of foci but inhibited significantly the number of ACF/colon as well as lower IQ-DNA adducts in the colon. Mechanism studies indicated that CLA and other fatty acids interact with certain heterocyclic amines in a manner consistent with substrate-ligand binding. The possibility that CLA may suppress IQ-induced tumors requires further investigation.
Level and Type of Fat.
Ip et al. [36] reported that 1% CLA in the diet suppressed mammary carcinogenesis in rats given a high dose (10 mg) of 7,12-dimethylbenz(a)anthracene, the effect being independent of the level or type of fat in the diet [29]. The fat was present at 10%, 13.3%, 16.7%, or 20% by weight in the rat diet, representing the range of fat intake of the US diet. For the fat composition experiment, a 20% (w/w) fat diet containing either corn oil or lard was used; the two fat sources differ considerably in linoleate content. These results suggested that CLA does not necessarily compromise eicosanoid production from linoleic acid.
In a recent study, Visonneau et al. [40] examined the effect of dietary CLA on the growth of human breast adenocarcinoma cells in severe combined immunodeficient (SCID) mice. Mice were fed 1% CLA for two weeks prior to subcutaneous inoculation of 10(7) MDA-MB468 cells and throughout the study. Dietary CLA inhibited local tumor growth by 73% and 30% at nine and 14 weeks post-inoculation, respectively. Moreover, CLA completely abrogated the spread of breast cancer cells to lungs, peripheral blood and bone marrow. These results indicate the ability of dietary CLA to block both the local growth and systemic spread of human breast cancer via mechanisms independent of the host immune system.
CLA and Atherosclerosis
Unlike linoleic acid, there is a paucity of information regarding the effect of dietary conjugated linoleic acid on plasma lipoproteins and aortic atherosclerosis. Lee et al. [41] first tested whether CLA might affect the initiation and progression of atherosclerotic lesions in rabbits through its effect on lipid peroxidation. They reported that rabbits fed an atherogenic diet and supplemented with 0.5g CLA per day for 22 weeks had significantly less plasma triglyceride, plasma LDL-cholesterol (LDL-C) and LDL-C/HDL-C ratio than control animals. CLA feeding also resulted in fewer aortic fatty lesions. Subsequently, Nicolosi and Laitinen [42] reported that hamsters fed CLA collectively had significantly reduced levels of plasma total cholesterol, non-high-density lipoprotein cholesterol, (combined very-low- and low-density lipoprotein) and triglycerides with no effect on high-density lipoprotein cholesterol, as compared to controls. They also developed 45% fewer aortic fatty streaks than control animals. However, the intact linoleic acid and CLA derived from linolenic acid (C18:3) did not have any effect on fatty streak formation, although they did affect the blood lipoproteins, suggesting that blood lipoproteins do not play an important role in CLA’s mechanism of action. Compared to the control group, plasma tocopherol/total cholesterol ratios determined from plasma pools for the low, medium and high conjugated linoleic acid and linoleic acid groups were increased by 48%, 48%, 86% and 29%, respectively, suggesting a tocopherol-sparing effect, at least for the conjugated linoleic acid treatment. In a recent study by Sugano et al. [43], CLA fed to rats at 2.3 energy % level did not show a cholesterol lowering effect on serum and liver, in contrast to the hypocholesterolemic observation in rabbits. CLA decreased linoleic acid in liver cardiolipin. The decrease in linoleic acid in cardiolipin of heart mitochondrial membrane diminished heart cytochrome C oxidase activity that required cardiolipin as an activator. The results of Sugano et al. [43] suggest that modified fatty acid composition in liver cardiolipin might affect mitochondrial respiratory function in liver.
CLA and the Immune System
Since the immune system is central to defense against cancer, it is possible that the anticancer activity of CLA may be mediated through enhanced immune function. The physiological role of CLA in normal and immune-stimulated animals was studied by Cook and Pariza in the early 1990s. Cook conducted studies to determine how nutritional methods could prevent growth suppression that is usually observed with immune stimulation in animals, e.g. vaccination [44]. Cook and Pariza investigated the ability of CLA to influence growth in baby chicks following immune stimulation with bacterial lipopolysaccharide (LPS, otherwise known as endotoxin). Typically chicks lose body weight for 24 hours after being injected with LPS, a loss as a result of cytokines released by immune cells. These cytokines (primarily interleukin-1 and tumour necrosis factor, TNF) induce skeletal muscle catabolism [45]. CLA was found to be protective against the growth suppression associated with immune stimulation [46].
Miller et al. [47] also examined the ability of conjugated linoleic acid to prevent endotoxin-induced growth suppression. Mice fed a basal diet or diet with 0.5% fish oil lost twice as much body weight after endotoxin injection than mice fed conjugated linoleic acid. By 72 hours post injection, mice fed conjugated linoleic acid had body weights similar to vehicle injected controls; however, body weights of basal and fish-oil fed mice injected with endotoxin were reduced. Conjugated linoleic acid prevented anorexia from endotoxin injection. Splenocyte blastogenesis was increased by conjugated linoleic acid. Based on the observation that CLA feeding decreased tissue arachidonic acid content, the authors concluded that CLA may be preventing the catabolism of tissue by removing eicosanoid precursors [46, 47].
Wong et al. [48] studied the effects of conjugated linoleic acid on lymphocyte function and growth of a transplantable murine mammary tumor. In Experiment 1, eight-week-old female Balb/c mice (n = 8/group) were fed 0.1%, 0.3% or 0.9% CLA for three or six weeks. Lymphocyte proliferation, interleukin-2 production and lymphocyte cytotoxicity were assessed using splenic lymphocytes. Plasma CLA concentrations increased in a dose-dependent manner with CLA feeding. Lymphocyte proliferation in mice fed 0.3% and 0.9% CLA was enhanced in phytohemagglutinin-induced but not in concanavalin A- or lipopolysaccharide-stimulated cultures. Production of IL-2 also was stimulated by CLA. In contrast, CLA had no effect on lymphocyte cytotoxicity. In Experiment 2, mice (n = 20/treatment) were fed the same diets for two weeks before being infused with 1 x 10(6) WAZ-2T metastatic mammary tumor cells into the right inguinal mammary gland. Tumor volume and latency were recorded for 45 days. Dietary CLA did not affect mammary tumor growth. Tumor latency, tumor incidence and tumor lipid peroxidation activity also were unaffected by CLA. Body weight and feed intake were similar among treatments. Therefore, dietary CLA modulated certain aspects of the immune defense but had no obvious effect on the growth of an established, aggressive mammary tumor.
CLA’s Effects on Fat Partitioning and Metabolism
Effect on Body Weight and Body Fat.
A surprising finding during these experiments was that CLA fed animals ate less food, contrary to the belief that CLA was a growth promoter [19]. After several studies it was concluded by Chin et al. [49] that CLA improved feed efficiency. Although improved growth on less food appeared paradoxical, body composition studies revealed that CLA significantly reduced whole body fat by over 50% and increased body protein in rats, mice and chicks.
Work from Pariza et al. [50] suggests that CLA plays a key role in regulating body weight as well as body fat distribution. Studies in rats fed diets supplemented with 0.5% CLA from three to eight weeks of age revealed that, in the rats fed CLA, body weights were significantly higher than in controls, even though the food intake was not affected [49]. Preliminary work from Pariza et al. [50] showed that CLA feeding was associated with a reduction in body fat mass and a slightly pronounced increase in lean body mass depending on the animal. Mice, rats and chickens fed 0.5% CLA supplemented diet (5.5% corn oil or 5% corn oil + 0.5% CLA) for four to eight weeks had body fat reductions of 57% to 70%, 23% and 22% respectively, while lean body mass or carcass water was significantly increased by 5% to 14%, 3% and 4% respectively. These findings may have implications in the use of CLA as a feed additive to produce leaner animals and perhaps for weight loss in humans. CLA has a direct effect on adipocytes: it decreases the lipoprotein lipase activity. CLA also affects norepinephrine response. Park et al. [51] also reported studies suggesting that the effects of CLA on the body composition of mice appear to be due in part to reduced fat deposition and increased lipolysis in adipocytes, possibly coupled with enhanced fatty acid oxidation in both muscle cells and adipocytes. Mice fed a CLA-supplemented diet exhibited 57% (males) and 60% (females) lower body fat and 5% (males) and 14% (females) increased lean body mass relative to controls, but no differences were found in body weight.
The data on humans is scarce. In the only human trial known, Atkinson et al. (personal communication) conducted a double blind placebo-control study with 20 healthy volunteers, ages 27 and 28, lean to modestly obese. CLA dose given was 3.6 g/day (60% of active CLA isomers). In the three month period of study, the CLA group experienced a 1.6 lbs. body weight loss and a 20% reduction of body fat while the control group gained 1.4 lbs body weight. The study was limited by a small sample size and inaccuracies in body fat measurements.
CLA and Bone Health
Most studies show an increase in percent of ash when CLA is fed to chicks. This effect is presumed to be due to protection conferred by CLA on bone loss. An increase in cytokines increases bone loss and CLA appears to counter the effect of cytokines. Rodents fed butter had a greater trabecular bone formation (most important to prevent osteoporosis) than animals fed vegetable oil.
CLA and Epidemiology
There are no known published studies on the effect of CLA and health from population studies, but studies on milk and milk fat could be used as surrogates for the effect of CLA, since CLA is highly correlated with these. High intakes of milk and milk fat were found to be associated with a low risk of breast cancer in some studies [52]. Garland et al. (unpublished) in a cohort of 2000 women, followed for 8 to 10 years, showed that coronary heart disease incidence decreases with higher intakes of whole milk and CLA. No protection was seen with skim milk.
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CONCLUSIONS AND FUTURE DIRECTIONS |
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TOPABSTRACTINTRODUCTIONBACKGROUNDCONCLUSIONS AND FUTURE...REFERENCES |
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Although it is possible that CLA concentrations could be increased by manipulation of the nutritional regimes of the animals, by food processing technology or by changing food habits, certain limitations of the available evidence must be recognised before any recommendations can be made. Foods high in CLA are also high in fat. Not only is there insufficient evidence based on human epidemiological data, it would be difficult to evaluate from such data the impact of CLA alone because of its high correlation with fat intake. There is also a need to compile an extensive CLA database in cooked and uncooked foods. The complexity of interpretation of epidemiological data is evident from the fact that, while case-control studies implicate a high fat diet as a risk factor for breast cancer, cohort studies often show a negative association. In addition to this lack of data from human studies, the evidence from animal studies is based on too few in vivo reports. Most of the studies have arisen from the same laboratories over the last decade, raising the possibility of some inherent systematic bias. Very few studies have shown a dose-response relationship with the quantity of CLA feed and the extent of tumor growth or other possible markers such as phosphilipid CLA. The kinetics of CLA incorporation in the phospholipids and its turnover rate is little understood. Questions such as the effect of age at exposure to CLA and the maturation of the mammary gland at exposure, other nutrients in the diet, immune status and so on also need to be addressed.
Again, as mentioned earlier, not all the individual isomers of CLA are absorbed to a similar extent and not only the magnitude of deposition but also the composition of CLA differs depending on the tissue. Thus it is difficult to predict which isomer(s) is the putative candidate, although 9c,11t-isomer is postulated as the most biologically active form of CLA. The esterification step in isomer analysis may also sometimes contribute to unreliable results. In addition, since most experiments have used a feed mix, sometimes of unspecified composition, it makes it difficult to point out the active isomer.
Despite these concerns, if the potential benefits of CLA can be characterised further, given that dairy foods are a rich source of CLA, it can result in increased demand for consumption of dairy foods and a boost to the dairy industry. Findings of plant foods as sources of naturally occurring substances that may improve people’s health and attenuate diseases, especially diseases of aging, have already set the trend for seeking other such natural foods. Further research with tumor models is needed to test the efficacy and utility of CLA in cancer and other disease prevention and to form the basis of evaluating its effect in humans by observational studies and clinical trials.
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