Friday, February 03, 2006

Deadly Inflammation from Diet

Okay, I have to admit it, when Dr. Barry Sears and I were discussing obesity in terms of it being benign or malignant, with one being a non-issue and the other deadly, my eyes started to glaze over with all the scientific-mumbo-jumbo coming my way.

Not that I wasn't interested in what we were discussing - it was just that much was way over my head and too abstract to really grasp. But, that's what often happens when you talk to a doctor or scientist and aren't one yourself. He graciously did explain much of what he was saying in terms I understood when I asked him to and that helped a lot but still did not allow my brain to fully take it all in at that moment.

Sometimes you just need some time to let it all sink in, do some additional reading to grasp what you've been given for knowledge and ask questions of those who do understand what was said. Now, with a couple of weeks since that conversation, with my brain mulling over much of what he had to say about the role of inflammation in the process of making obesity "malignant" - I'm now convinced he's onto something. He might not have it all right, but he's definitely onto something important in our understanding of how obesity can turn deadly when the environment is right.

In the last two weeks I've done some intensive reading and researching along with asking dozens of questions to various people in medicine and areas of research. Believe me, what he was saying was compelling, but still a bit "out there" from my base of understanding. Which is why I spent some time seeking out more information to be able to discuss his ideas from a grounding in the evidence rather than from the perspective of 'well, Dr. Sears says so...'

Today, the opportunity to do so was provided with three separate articles - one from Diabetes Care, A Single Factor Underlies the Metabolic Syndrome, another from the Journal of Endocrinology, Detrimental actions of metabolic syndrome risk factor, homocysteine, on pancreatic b-cell glucose metabolism and insulin secretion (full-text PDF), and lastly a study detailed in this article, Omega-6 Fatty Acids Cause Prostate Tumors to Grow Twice as Fast.

As is often the situation, disparate organizations and researchers don't communicate with each other, and therefore it is difficult to 'connect the dots' to find plausible answers to some of our scientific questions and find agreement about underlying mechanisms in the metabolism that trigger disease. The three articles about are fascinating and thought provoking and connect to what Dr. Sears and I were discussing.

Specifically, inflammation.

Something you, my readers know I talk about a lot in my articles.

From the Journal of Endocinology we find that researchers have taken a close look at the role of homocysteine on beta-cell function. Why is this important? For one it hasn't been investigated much in the past and beta-cell function is part of the problem in the body of those with Metabolic Syndrome and Diabetes. What the researchers found in their investigation is very interesting - "These data indicate that homocysteine impairs insulin secretion through alterations in beta-cell glucose metabolism and generation of key stimulus-secretion coupling factors. The participation of homocysteine in possible beta-cell demise merits further investigation."

Basically, what this tells us is that homocysteine (an inflammatory marker) impairs the body's ability to secrete insulin, thus it impairs glucose (sugar) metabolism. Not only that, but it also slowly kills beta-cells, which over-time is seriously damaging the pancreas. Can you say "diabetes?"

In the second article from Diabetes Care we find that researchers have taken the time to finally explore the possibility that Metabolic Syndrome has a "single factor" that triggers the cluster of features to develop and progress. "These analyses support the current clinical definition of the metabolic syndrome, as well as the existence of a single factor that links all of the core components. "

What a concept!

The researchers do not speculate about what that single factor may be however, and acknowledged that they did not explore the role of inflammation, "Second, inflammatory and procoagulant variables, such as C-reactive protein, plasminogen activator inhibitor-1, and fibrinogen, which have also been proposed as components of the metabolic syndrome, were not measured in the current study."

They should have - if Dr. Sears is correct, it is an inflammatory response in the body that triggers what he terms "malignant obesity," where the body weight goes from a benign state to a deadly contributor in the disease process as inflammation in the body increases with more and more arachidonic acid (AA) building in the body. AA is the precursor molecule for the prostaglandins, many of which are direct mediators of inflammation!

That last article reviews a study that specifically investigated the role of omega-6 fatty acids in tumor growth. The findings were compelling, especially when we consider the amount of omega-6 rich oils we consume in the United States and our poor intake of omega-3's. In this study, researchers found that the omega-6 fatty acid, arachidonic acid, stimulated tumor growth because it "turned on" a dozen inflammatory genes!

"Investigating the reasons for this rapid growth, we discovered that the omega-6 was turning on a dozen inflammatory genes that are known to be important in cancer. We then asked what was turning on those genes, and found that omega-6 fatty acids actually turn on a signal pathway called PI3-kinase that is known to be a key player in cancer," said lead researcher Hughes-Fulford.

When Dr. Sears and I were discussing obesity as a "protective" measure triggered in the body to survive an assault, I was thinking "yeah right, what about those excess calories?" But now, I'm sitting here thinking about this from the perspective of the foremost primal survival of the body - that is exactly what the body strives for - survival - without "thinking" about it. Its function is survival and reproduction, and it has a host of mechanisms to do this through optimal, sub-optimal and even dangerous conditions.

While we "think," the body just continues to function at its primal level no matter how logical we think our lifestyle choices are or how good we think our environment is. Some of the very things we do are contrary to the function of our primal metabolism and our body's desire to maintain homeostasis (balance) within.

If Dr. Sears is correct, the solution lies in understanding what is triggering the inflammation and resolving that issue, not masking it with medications that alleviate symptoms of the problem without actually resolving the underlying problem. If the above research starts to open the door to our understanding, the main assault upon our body today is our diet - too many glucose producing sugars/carbohydrates that increase insulin coupled with too many omega-6 fatty acids, leading to an unbalanced state in the body.

Yes, these are only three studies - but I'm fairly certain that a review of the literature will begin to reveal a real trend of findings that supports the idea that our diet, and our current dietary recommendations, are slowly killing by creating an environment of low-level, chronic inflammation in our bodies.


  1. A recent study found that a low carb (Atkins style) diet increased inflammation in the body after just a week! So the trick for low carb dieters who also want to avoid the consequences of inflammation (aging skin, increased risk of heart disease, and so on) is to choose foods that are not only low in carbs but also anti-inflammatory. You can find out about ways to do this at

  2. Do you have a link to the study?

  3. Regina, this link takes you to the Virginia Polytechnic Institute, where the research was done by Mary Whitlock and Janet Rankin...its the second study described in the round-up. The authors are preparing the findings for journal publication.


  4. Hi Monica,

    Thanks for the interesting read!

    I'd like to point out longer-term research findings and the imprecise nature of short-term, one-week conclusions.

    First, longer-term findings (not an exhaustive list, just a few I have handy on my hard drive):

    Seshadri et al (Am J Med. 2004 Sep 15;117(6):398-405) findings from a six month trial found CRP decreased in both diets included in their study (low-carb vs. conventional low-fat) and noted that patients with a high-risk baseline CRP level (greater than 3mg/dL, n=48) experienced a greater decrease in CRP on a low-carb diet (difference = -2.0mg/dL, p=0.005) independent of weight loss.

    Sharman & Volek (Clin Sci (Lond). 2004 Oct;107(4):365-9) concluded, after measuring a number of inflammatory risk markers including CRP, that energy-restricted low-fat and very-low-carbohydrate diets both significantly decreased several biomarkers of inflammation. These data suggest that, in the short-term, weight loss is primarily the driving force underlying the reductions in most of the inflammatory biomarkers.

    Noakes et al (Nutr Metab (Lond). 2006 Jan 11;3(1):7) found that a very-low-carb diet (VLCARB) that was high in saturated fat lowered fasting insulin 33% compared to a 19% fall on a diet high in unsaturated fats (HUF), and no change on a very low-fat diet(VLF) (P<0.001). The VLCARB meal also provoked significantly lower post prandial glucose and insulin responses than the VLF and HUF meals. All diets decreased fasting glucose, blood pressure and CRP (P<0.05).

    Due et al (Diabetes Obes Metab. 2005 May;7(3):223-9) only compared to low-fat diets with varying carbohydrate/protein ratios and concluded that dietary carbohydrate/protein ratio has no effect on inflammatory markers, but the study confirmed that body fatness is positively associated with levels of serum CRP.

    Brinkworth et al (Int J Obes Relat Metab Disord. 2004 May;28(5):661-70) compared a high-carb diet with a low-carb/high-protein diet and found that both diets significantly increased HDL cholesterol concentrations (P<0.001) and decreased fasting insulin, insulin resistance, sICAM-1 and CRP levels (P<0.05).

    That said, I have to point out that short-term changes in various markers are not predictive of long-term changes. Any researcher worth their salt knows this and is clear of the need for longer-term data and replication of findings from short and long-term studies.

    Also it is difficult to judge data and suggested findings without publication of the data after a peer-review process. Without access to the data, it's hard to judge the comparison diets, foods included and such to determine if the dietary "rules" imposed by either diet were accurately representing the dietary requirements of the plans or if they were influenced to reach a particular finding?

    Anyway, I do look forward to seeing the data when it is published. Do you know which journal the manuscript has been submitted to?