What is the purpose of this study? CVD & Diabetes

This was a very well executed and performed study about cytokines in CVD and diabetic women. The researchers went into depth about IL-6, TNF-a, and other chemicals. However, I was not sure as to why this study was performed. It is nothing that researchers have not already determined. It has been well known that these chemicals affect inflammatory responses amongst CVD and diabetes.

The researchers did not seem to state a specific reason for undertaking this study other than support the thesis about cytokines and the inflammatory response. I would have liked to read about why they performed this. Like to help cure these diseases or to help find a medicine to help the side affects.

This study did not answer the “so what?” question for myself. At the end of the paper I was left saying “so what?” Why did they write this paper? I am not sure of that. It almost seems as if this paper was written to obtain a grant or research money. There have been plenty of studies, cited in this paper, that have been performed in the past having the same outcomes. I would have liked to see the researchers focus on a new topic or some sort of treatment.

Possible Causes of Hypoxia and its Relationship with Inflammation.

There is significant data from research that suggests low oxygenation (hypoxia) in the adipose tissue of the obese could be a risk factor for chronic inflammation. For example a study that was conducted showed that the control lean mice had a partial pressure of oxygen of 47.9mm Hg. In the obese mice the partial pressure of oxygen was only 15.2 mm Hg. As you can see this is a substantial difference. This represents a 70% reduction in oxygen. To verify the relationship between obesity and hypoxia the researchers reduced the calorie intake of the mice. Once the mice started to lose weight they saw an improvement not only in oxygenation of the adipose tissue but most importantly there was a reduction in inflammation.

We know that hypoxia leads to chronic inflammation through the expression of inflammatory genes but we still don’t know the exact mechanisms of how hypoxia is generated in the adipose tissue of the obese. One concept presented in the article was (ATBF) adipose tissue blood flow. Researchers speculate that ATBF might be a possibility for the cause of hypoxia. A generator for ATBF is thought to be Insulin sensitivity. I know that there are still other factors that we must consider besides obesity and ATBF. For example VEGF was the only gene that was not increased in the ob/ob mice. VEGF is a vasodilator so this could possibly help with the low oxygenation of adipose tissue. Since VEGF is controlled by the gene HIF-1-alpha (hypoxia inducible factor 1 alpha) more research into this specific gene could prove to be valuable. Studies have shown that hypoxia is a major cause of inflammation so once we understand how to control hypoxia we could then begin to reduce chronic inflammation significantly.

I noticed in Obesity and the Flu (Obioha, MD) that four out of five respiratory complications of influenza are those of imflammation! I did not realize inflammation was such a prominent effect of other illnesses or infections, but now that I know more about what inflammation actually involves and includes, I can see that almost any kind of infection or disease can have an inflammatory response, which in turn causes more compliactions. However, in this same article, I found some completely irrelevant statements, which I was not expecting since the article is so short and attempting to be informative. In the paragraph titled "Obesity and the Overweight Connection," it states that we as American encounter excess weight issues in our "daily lives - physically, emotionally, mentally, and even financially;" and that "those with serious weight issues are at much greater risk for developing life-threatening illnesses." This is confusing to me - what exactly are we talking about now? The article somewhat explains that cortisol is one connection between obesity, inflammatory rseponse, and how it leads to other compliactions, however it does not elaborate on how the emotional, mental, and financial excess weight can contribute to illness, and therefore these things should have never been mentioned.
After reading articles relating to obesity and inflammation, my opinion concerning obese humans is strengthened. Adipose tissue, especially in excessive amounts, is extremely deterimental to one's health, and not just because it's fat. My concern is for our nation: why is it that we push "get skinny quick" products rather than inform society that being overweight is actually extremely unhealthy?? Let's start a "get healthy, not skinny" campaign and inform America of the physiological reality of being obese, not the superficial fantasy of being "skinny."

Popcorn is inflammatory??? : )

http://www.nytimes.com/2007/09/05/us/05popcorn.html

The above article is from the New York Times and might be interesting to all of us (It talks about inflammation and the person was diagnosed at National Jewish Hospital in Denver)!!

Comment: "Hypoxia is a potential risk factor for chronic inflammation..."

Since hyperglycaemia and obesity go seemingly hand-in-hand, I am assuming that it is safe to say that VEGF transcription is inhibited in obese individuals, just as it is in those with a high glucose level. If this is true, then as the adipocytes of an obese patient increase in diameter (without dietary restrictions), the blood vessels cannot adequately supply nutrients to the fatty tissue, thus inducing a hypoxic state. Proinflammatory cytokines are released in this hypoxic state roughly two hours after the hypoxia is detected, and hypoxia response genes are then released about eight hours after the initial detection. Could this vicious cycle be prevented by somehow increasing VEGF expression to adequately perfuse blood (oxygen) to the growing masses of adipose tissue?