|Image 1: Pomegranate - I loved to eat them even before I realized that their seeds are the #1 dietary source (83%) of punic acid.|
CLnA - Conjugated Linolenic Acid is not a typo ;-)
Within the last couple of years even the medical establishment has come to realize that the chronic omega-6 (n6: linolic acid) overload in our diet is killing us. The "heart-healthy" PUFAs have now become the more and less heart-healthy PUFAs with the totally healthy *rofl* omega-3s and the not just as healthy omega-6s - both, of course, still totally "essential" and WAY better than saturated fats,... (attention: the afore statements are full or irony! Saturated fats are of course NOT the bad guys. Sorry, David if that lead to confusion)... but I am getting derailed, here. So let's get to the point. What every reasonable person appears to agree on, these days, is that we have to lower the ratio of n6:n3 fatty acids in our diets. Now, I am asking you: Has it ever occured to you that CLA essentially is an omega-6 fatty acid? I mean its conjugated linoleic acid - "linoleic" as in omega 6 = linoleic acid! Probably not, right? The reason for that is yet (hopefully ;-) not that you are dump, but simply that the existence of an omega-3 "variety of CLA", namely conjugated linolenic acid, or short, CLnA, is something about which you will only hear, when you read blogs (such as the SuppVersity ;-), which do not stick to copying, pasting and commenting the stuff the authors have read on one of the major news-portals.
|Table 1: CLnA isomer content in natural sources (data adapted from Hennesey. 2011)|
Adiposity, hyperlipidemia, cancer - CLnAs could help with all!
Hennesey. 2011). In a 2002 article that was published in the Journal of Applied Biochemistry and Biotechnology, Nishimura et al. report that CLnA isomers exert apoptotic effects on mouse preadipocyte 3T3-L1 cell - or, in plain English, incubation with CLnA did not only hinder the "pubertal" fat cells from becoming mature adipocytes, it actually killed them. In vivo studies with rodents, such as Arao et al. (2004), where the administration of a diet that was enriched with 1% pomegrenate seed oil lead to a 27% reductin in omental white adipose tissue, were able to confirm the "rodent-real world signficance" of these test-tube results.
Other studies showed a normalization of hyperlipidemia in rodent models of the metabolic syndrome and a hand full of studies have explored the usage of CLnA isomers as cytotoxins in the treatment of cancer. In their concise review of the literature, Hennesey, et al. thusly rightly conclude that with their "potent inflammatory and immune modulating properties", their ability to "reduce the risk of obesity, improve cardiovascular health, and mediate strong anti-carcinogenic activity", the use of CLnA isomers or dietary enrichments could offer treatment strategies for pathologies, which "represent some of the greatest mortality risks to humans in the Western world and have been inextricably linked with diet" (Hennesey. 2011).
Adding diabetes to the list of potential targets for CLnA
For today, we are however going to focus on the most recent result from the research front: The effects of CLnAs on diabetes, or, to be precise, the increases in blood glucose, and decreases in anti-oxidant capacity that go hand in hand with the latter. In a recently published study (Saha. 2011), Siddhartha S. Saha and Mahua Ghosh from the Department of Chemical Technology at the University College of Science and Technology of the University of Calcutta (I don't have to tell you that this is in India, do I?) injected male albino lab rats with 60mg/kg streptozotocin (STZ) - this is a common and well-established method to induce a metabolic state that serves as a model of type II diabetes - and fed them diets that contained either no, or 0.5% of the total fat in the form of alpha-eleostearic acid (from bitter gourd, cf. table 1) or punic acid (which was in this case taken from snake gourd oil, but could as well have been extracted from the eponymous pomegrenate, cf. table 1).
|Figure 1: Relative blood glucose levels vs. non-STZ injected control in streptozotocin injected rats over the course of the dietary intervention (data calculated based on Saha. 2011)|
|Figure 2: Relative level of lipid peroxidation (left) and total antioxidant capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)|
|Figure 3: Relative expression of inflammatory cytokines, TNF-alpha and interleukin 6 in plasma capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)|