Friday, March 2, 2007

Nothing Nice About Chronic Swell

When I go to parties, I sometimes tell people I'm a landscaper. It guarantees nobody will ask me questions like they do when I say I'm a trainer. But it's not the questions that are hard, it's the answers. Most people don't like them, few people listen to them and many spend the rest of the night telling me in painstaking detail the multitude of reasons they can't follow any of my advice. Besides, it's the wrong angle to take because if I could explain foods impact beyond the tedium of spare tires it would light sparks. If instead I could get everyone to educate themselves about inflammation, without sounding like Cassandra of course, diets would change, waistlines would shrink and doctors would have enough time to frequent parties where they could field questions about random medical research posed by landscapers.

When I say inflammation, I'm not talking about a reaction to blunt force trauma - it makes for more compelling party chatter but it's not relevant to any of the guests other than those in the room who tend towards tipsy. I'm talking about chronic inflammation in reaction to food, in response to imbalanced polyunsaturated fats and as a byproduct of stress.

Systemic inflammation in it's most obvious form, contributes to heart disease. At it's most diabolical, however, it manifests itself as insulin resistance. It's a sneaky hemorrhaging of health and vitality and nobody seems to be talking about it at social gatherings.

In matters of the heart, cholesterol's role continues to be misunderstood while C-reactive protein (CPR), an acute phase protein that increases during systemic inflammation, remains a greater mystery to most in spite of the fact that it's a far better marker of cardiovascular disease risk. According to 'Inflammation, Heart Disease and Stroke: The Role of C-Reactive Protein' from the American Heart Assoc., "The American Association and the Centers for Disease Control and Prevention recently published a joint scientific statement about using inflammatory markers in clinical and public health practice. This statement was developed after systematically reviewing the evidence of association between inflammatory markers (mainly CRP) and coronary heart disease and stroke." Though this is obviously known well enough to be discussed in mainstream arenas, doctors still don't appear to be incorporating regular testing.

Notably not a topic for a casual chat with strangers especially over communal Hors d'Ĺ“uvres, infectious disease may also be a contributor. Also mentioned by the American Heart Assoc., "Possible infectious bacteria include Chlamydia pneumoniae and Helicobacter pylori. Possible viral agents include herpes simplex virus and cytomegalovirus. Thus, it may be that antimicrobial or antiviral therapies will someday join other therapies used to prevent heart attacks." Fabulous - talk of chlamydia and herpes - a guarantee that by the end of your dinner party repartee you won't contract either one of them.

Talk of antimicrobials should have been an a-ha moment for those of you who regularly read my blog. I've talked about the antimicrobial properties of saturated fats and enzymes in raw dairy. I feel the vibe of all my regular folks, leaning out of their seats and thrusting hands in the air. "Ooh, ooh, I know this one. . . ."

For me, the link between insulin resistance and inflammation is far more compelling. If hipster jeans did anything other than make the dressing room experience even more horrifying, they exposed the telltale Syndrome-X bellies of the walking wounded. So many of us are suffering from mild symptoms of a snowballing problem that could and should be addressed now. The cruel part is that even the stress of growing bellies could be growing your belly since stress has proven to be a big part of the equation.

This link is discussed in research done by the Department of Microbiology, Boston University School of Medicine. "Evidence is presented that the liver, the endothelium, and fat cell depots are the primary sources of cytokines, particularly IL-6, and that IL-6 and the acute phase protein (APP), C-reactive protein (CRP), are strongly associated with, and likely play a dominant role in, the development of this inflammatory process which leads to insulin resistance, non-insulin dependent diabetes mellitus type II, and Metabolic syndrome X. The possible role of psychological stress and the major stress-related hormones as etiologic factors in the pathogenesis of these metabolic diseases, as well as atherosclerosis, is discussed. The fact that stress can activate an APR, which is part of the innate immune inflammatory response, is evidence that the inflammatory response is contained within the stress response or that stress can induce an inflammatory response. The evidence that the stress, inflammatory, and immune systems all evolved from a single cell, the phagocyte, is further evidence for their intimate relationship which almost certainly was maintained throughout evolution."

And while we're on the subject, what is WAT and what does it have to do with anything? I'll let the research explain it:

It now appears that, in most obese patients, obesity is associated with a low-grade inflammation of white adipose tissue (WAT) resulting from chronic activation of the innate immune system and which can subsequently lead to insulin resistance, impaired glucose tolerance and even diabetes. WAT is the physiological site of energy storage as lipids. In addition, it has been more recently recognized as an active participant in numerous physiological and pathophysiological processes. In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. Recent data indicate that obese WAT is infiltrated by macrophages, which may be a major source of locally-produced pro-inflammatory cytokines. Interestingly, weight loss is associated with a reduction in the macrophage infiltration of WAT and an improvement of the inflammatory profile of gene expression.

Several factors derived not only from adipocytes but also from infiltrated macrophages probably contribute to the pathogenesis of insulin resistance. Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. Leptin could modulate TNF-alpha production and macrophage activation. TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. However, its actual involvement in glucose metabolism disorders in humans remains controversial. IL-6 production by human adipose tissue increases during obesity. It may induce hepatic CRP synthesis and may promote the onset of cardiovascular complications. Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway.

In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. Adiponectin inhibits liver neoglucogenesis and promotes fatty acid oxidation in skeletal muscle. In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems.

Scary, yes? So next time, can we talk about your job?