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While IL6 holds an important role in immune function, starting the inflammation response when bacteria are detected in the bloodstream and supporting the fever response, it is central to many, many other functions in the body. Bodybuilders and athletes don’t care about leukocytes, but they do care about muscle and fat. Now (over 300 words later) the article becomes interesting. The relationship between IL6 and obesity or conditions that might increase or decrease fat storage has been a confusing tale of conflicting science. Initially, IL6 was believed to be a pro-obesity factor, as it is increased in obese people and has been shown to increase insulin resistance in animal studies as well as lab studies using human tissue from certain organs.2-5 Yet, other studies have shown that IL6 increases the metabolism and fat burning.6-9 The whole issue is still so unresolved, as to have the leading experts in the field still debating on whether IL6 is a factor that aids or impairs aspects relating to weight management and metabolic health.10,11 Fortunately, as new information is released and scientists’ knowledge and experience expand, the role of IL6 in humans is becoming clearer. Unfortunately, only a few scientists are looking at the topic broadly enough to understand the effects of IL6 under a variety of human conditions. Rodents are often used as the experimental subjects in many studies because they are expendable, cheap, have short life spans and a physiology that resembles humans. Unfortunately, with the exception of attorneys and career politicians, rats and humans are different enough to make it difficult to compare the findings in one species to the other.10 Further, the conditions humans live in are extremely varied and often quite extreme. It is important to understand the impact of the subjects when trying to interpret the results of IL6 clinical studies. Lastly, it is important to realize that because IL6 is involved in so many different systems in the body, that changes unrelated to fat loss/fat gain may affect IL6 levels.
Early on, it was believed that IL6 promoted fat gain and supported the condition of obesity, because IL6 levels are higher in obese people compared to lean people.12 Obesity has been found to cause a condition of chronic (persistent or long-lasting) inflammation. Remember, IL6 plays a central role in inflammation, so it is not surprising to see that IL6 is increased during an inflammatory state (obesity). The inflammation exists in the intra-abdominal fat, especially the visceral fat that surrounds the intestines and other internal organs.13 High levels of visceral fat are closely associated with a number of poor health conditions, such as diabetes, cardiovascular disease and the Metabolic Syndrome. At first, this bit of evidence seems damning, suggesting IL6 is a pro-obesity factor. However, looking more closely at the role of IL6 in inflammation and later data finds this may be (and likely is) misleading. IL6 co-exists with another cytokine called tumor necrosis factor-alpha or TNF. TNF is released in high concentration by visceral fat cells (inside the abdomen) and reaches the liver in very high amounts. TNF is thought to be a causative factor in a number of negative cellular and metabolic effects, such as insulin resistance, type 2 diabetes and cardiovascular disease. TNF also stimulates the production of IL6.
Often, when a hormone stimulates the production of another hormone, it is doing so to generate a second signal or carry the effect of the first hormone into other cells. However, sometimes a second hormone is produced to regulate the first hormone in order to prevent an excess of the original signal. Yep, that was confusing. Think of testosterone, which actually reduces the release of LH (the pituitary hormone that stimulates testosterone production). This is called negative feedback. In humans, IL6 suppresses (reduces) TNF, an anti-inflammatory effect. Thus, it is clear that conditions that create high levels of TNF would also create high levels of IL6, which attempts to protect against the overproduction of TNF. Without understanding the relationship between these two cytokines, one would tend to blame the effects caused by TNF on IL6 as well, sort of a molecular guilt-by-association.
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Research and Review 
