Arthritis-ameliorating cheese, anyone? Asthma-moderating yogurt? How about a scoop of lupus-fighting ice cream? Although such foods don't yet exist, they might one day. Data from a new study finds that an unusual fatty acid, a type of dairy fat, can modulate the injurious, runaway inflammation that underlies these and many other diseases.
The agent is a variant of the essential nutrient linoleic acid. It's one of a pair of agents, known as conjugated linoleic acids (CLAs), that occur as trace constituents of animal fats. Both possess novel—although different— pharmacologic attributes. However, their concentrations in milk and other dairy goods are too low to make a recognizable difference.
At elevated doses, such as those delivered by over-the-counter food supplements available in health-food stores, each CLA appears to have potential for fighting disease in people and other animals.
For instance, a few years back, Mark E. Cook and his colleagues at the University of Wisconsin–Madison found that administering a mix of the two linoleic acid variants could prevent a common wasting syndrome in farm and laboratory animals that traced to uncontrolled inflammation. Moreover, the CLA supplementation dampened the injurious inflammation—an inappropriate immune attack—without impairing the animals' ability to produce antibodies or launch a healthy immune response to infection.
The unusual fats ratcheted down the body's production of an enzyme—COX-2—that serves as an inflammation trigger. COX-2 has been indicted as a player in many chronic diseases, from cancer and autoimmune disease to arthritis. Indeed, several drugs that target COX-2 were developed to treat the pain associated with inflamed joints.
In their new study, Cook, Guangming Li, and their colleagues traced the COX-2 effect, in mice, to just one of the two CLAs. Moreover, the new study indicates that this particular CLA fights inflammation in several ways at once. The new evidence proves, says Cook, that the dietary ingredient "is pretty amazing."
A good trans fat
Linoleic acid is a molecule with a backbone of 18 carbon atoms, most of them linked by single bonds. At two sites, those carbons are linked by more-rigid double bonds. If chemical reactions shift those double bonds so that they are separated by only one single bond, the molecule is described as having conjugated double bonds. And that's what CLAs are—a linoleic molecule whose double bonds are now conjugated.
Fats will bend at the site of a double bond. Ordinarily, linoleic's two double bonds are both in what chemists refer to as a cis configuration. This means that the carbon backbone takes on somewhat of a U-shape around each bond. In CLAs, however, one of the double bonds instead sports a trans configuration, meaning that the bond induces a slight zigzag in the backbone (SN: 11/10/01, p. 300: Available to subscribers at Trans Fats).
The existence of that trans bond means that CLAs are a type of trans fat. The trans bond in their structure imparts an unusual physical property: It keeps the trans fats hard at room temperature. It's a feature in other trans fats the food industry has capitalized on—transforming vegetable oils into surrogates for butter, lard, and other products rich in saturated fats. Unfortunately, most trans fats also pose the same artery-clogging risks that saturated fats do (see Stronger Proof That Trans Fats Are Bad).
CLAs, however, don't seem to harm people's arteries. To date, the one known as cis-9, trans-11 (c9,t11) has gotten the most attention for its potential to not only prevent certain cancers and atherosclerosis, but also to limit the accumulation of body fat (see The Good Trans Fat).
Cook's team is now focusing on a different CLA—trans-10, cis-12 (t10,c12). It's this fat that the researchers have found is most responsible for ratcheting down inappropriate inflammation. Although c9,t11 also showed some weak anti-inflammatory action in the team's test-tube studies, it failed to curb inflammation in animals.
The fact that both of these CLAs have demonstrated health benefits in a host of studies over the past 2 decades has won them an exemption from recent government rules requiring that food labels list concentrations of heart-threatening trans fats (see No Hiding Most Trans Fats).
Cox suppression and more
In their new studies, Cook and his colleagues probed how the t10,c12 CLA worked. They found that it modulated the activity of a molecule, NF-kappa-B, that controls parts of the immune response. Ordinarily, NF-kappa-B rests quietly in the liquid part of certain immune system cells. When the immune system is stimulated by any of a range of agents, however, NF-kappa-B races to the cells' nuclei and there activates genes that turn on the production of all sorts of inflammatory agents, among them COX-2.
The more of the CLA administered to animals or immune cells, the more resistant those animals and cells were to producing COX-2 and other inflammatory agents.
Not only did the CLA's impact on NF-kappa-B activity reduce the production of the COX-2 enzyme, but it also dampened the activity of any COX-2 that was made. "This is baffling," Cook told Science News Online, and suggests that CLA has at least two independent roles in tempering COX-2's overstimulation of inflammation.
Studies by other researchers have shown that a cow's diet can greatly influence her milk's CLA concentrations (see Why Grass Makes For Better Milk). Grass-fed cows tend to produce far more of the c9,t11 form, Cook notes, than do grain-fed animals. In contrast, grain feeding spurs more production of t10,c12 CLA. He now plans to work with animal scientists to investigate how much they can boost the t10,c12 in cow's milk. The goal would be dairy products—from cheese to yogurt—naturally endowed with extra inflammation-fighting attributes. For instance, they might limit inflammatory pain without the side effects of aspirin or other drugs.
It's also possible, Cook notes, to simply fortify foods with extra t10,c12 CLA or pop dietary supplements, already on the market, that include both of the beneficial CLAs.
The Wisconsin team calculates that it might even be possible to get pharmacologically active doses of t10,c12 CLA naturally from a dairy-rich diet today. Doing so assumes, he says, that the CLA's immunological responses will be as potent in people as they have been in lab animals. It would also require eating lots of milk-based foods. How much? Cook's team estimates that based on current CLA concentrations typical of milk, people would have to derive roughly half of their daily fat allotment—perhaps 100 grams—from dairy products. And they can't be skim-milk products, he notes, since the t10,c12 CLA is a fat.
Mark E. Cook and Guangming Li
University of Wisconsin, Madison
Department of Animal Science
Animal Science Building 1064
1675 Observatory Drive
Madison, WI 53706
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