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Dynamic Chiropractic – November 18, 2009, Vol. 27, Issue 24

The Anti-Inflammatory Diet, Part 3

An Interview With Dr. David Seaman

By G. Douglas Andersen, DC, DACBSP, CCN

Editor's note: Part 1 of this article appeared in the Sept. 23 issue; part 2 appeared in the Oct. 21 issue.

To conclude this series on inflammation, David Seaman, MS, DC, DACBN, has been kind enough to advise us on ways to "deflame" the typical diet and comment on the science of diet and inflammation. For those of you who don't know, Dr. Seaman has always been well ahead of the curve on how different foods can up- or down-regulate the metabolic reactions that promote or suppress inflammation.

Q: It's been over 10 years since you wrote your landmark book, Clinical Nutrition for Pain, Inflammation and Tissue Healing. Regarding systemic up-regulation of pro-inflammatory states induced by food choices, what has science told us since you wrote the book?

A: Fortunately, I was lucky to get interested in an area of research related to nutrition that has been very consistent over the years. In other words, the contents and suggestions in the book are consistent with the emerging research. The difference is that we now know more about the dietary up-regulation of systemic inflammation. Some of this involves more confusing biochemistry such as cytokines, growth factors, and cell signaling molecules like nuclear factor kappa-B. And some is very basic, such that we should view basic biochemical problems from the view of chronic inflammation.

For example, we have known for many years that overeating sugar and fat leads to postprandial hyperglycemia and hyperlipemia; however, we now know that the degree of hyperglycemia and hyperlipemia is associated with increasing levels of systemic inflammation. Additionally, we have always known that being "overfat" can be associated with diabetes and heart disease. We now know that excess body fat functions as a factory that produces inflammatory mediators.

Q: In my last article, I promised the readers advice on easy ways to transition toward a so-called anti-inflammatory way of eating. I guess the first step in the process would be determining areas to address regarding what they currently eat. Do you have any thoughts on how the average DC can identify the major problems a patient has with regard to inflammation?

A: There are some very basic and accurate things we can do. For example, visual inspection is helpful. Anyone who is overweight is moving toward a state of chronic inflammation. We add excess pounds by eating pro-inflammatory foods such as sugar, refined flours, and too many fat calories. So, [in general] an overweight person should be viewed as one who eats too few vegetables, fruit, and lean meat and fish.

If a patient is regularly taking NSAIDs or Tylenol, this tells us to look at diet. Linoleic acid from seed/legume oils (corn, safflower, sunflower, cottonseed, peanut, and soybean) converts into arachidonic acid, which we find in obese meat from domesticated animals. The arachidonic acid is converted into prostaglandin E2 by the now-famous COX enzymes, which are inhibited by NSAIDs and Tylenol.

A diet history for 3-7 days is also helpful. It becomes readily apparent that patients do not eat enough vegetation, lean meat, and fish. They can also use the "deflaming" guidelines I have on my Web site,, which contains an inflammation checklist and dietary/supplement recommendations.

Q: How can we help patients "deflame" (to coin your phrase) without selling them a trunkload of pills and powders?

A: The key to deflaming is really diet, not supplements. The lion's share of calories should come from vegetation, lean meat, fish, sweet potatoes, raw nuts, and seeds such as hemp, chia and flax. A bare-bones supplement approach to support the deflaming process includes magnesium, fish oil and vitamin D. I think adding a multivitamin and a probiotic are also good choices if the patient can afford it.

Q: Making a nutrition plan too costly, too strict or too extreme is a recipe for failure in all but the highly motivated or borderline obsessive. How can the average person eat a diet that is anti-inflammatory and still live within the norm (meaning they can still have a slice of pizza after their kid's ballgame or hit a drive-thru on occasion)?

A: People can easily deflame by shopping at Super Walmart or other large stores. Lean meat, chicken breast and fish are affordable. Five-pound bags of frozen vegetables are inexpensive, as are family-size bags of frozen fruit. Sweet potatoes are also very inexpensive, and so are regular potatoes. And when a modest potato portion is consumed with protein, the glycemic response [from the potato] is blunted. If people eat this way for 80-90% of their calories, then the remaining percentage can be used for pizza, drive thru's and dessert.

Q: Any thoughts on the emerging concept that just being overweight is inflammatory?

A: As you know, we are learning that our genes can be protective against disease or promoters of disease. So, I think the overweight issue is dependent on our unique genetic makeup, which we can get an idea about by looking at some basic blood tests. For example, high-sensitivity C-reactive protein (hsCRP) should be below 1 mg/dL. Fasting glucose should be below 100. When these rise, we should be thinking that an overweight patient is inflamed. And we should be more concerned if elevated hsCRP and glucose are coupled with substantially elevated cholesterol and triglycerides.

An even more basic marker is blood pressure. We know that elevated blood pressure reflects chronic systemic inflammation. Some individuals are able to handle more weight and keep these markers within normal limits; it is a mixed bag and should be considered on an individual basis. However, in general, excess body fat is considered to be a reservoir of inflammatory mediators. In fact, macrophages are attracted to excess adipose tissue, where they can become activated and overproduce inflammatory mediators. Adipose tissue itself produces mediators called adipokines - some are pro-inflammatory and some are anti-inflammatory. With excess adipose tissue, we produce excessive pro-inflammatory mediators like resistin and leptin, and less anti-inflammatory adiponectin.

Q: How about the fact that foods which drive inflammation also seem to stimulate appetite?

A: The gut-brain appetite connection is complex, as is the effect of diet on the endocrine system. The inflammation connection is more palpable and understandable for me. I cannot tell if inflammatory foods actually stimulate appetite or if anti-inflammatory foods function to suppress appetite. Lean protein and fiber tend to make us feel satiated, so we eat less.

Additionally, I am not sure to what degree the emotional attachment to inflammatory foods plays a role. I do know that people have variable negative visceral responses when they are told to eat less sugar and flour, and to eat more anti-inflammatory foods. I wonder if there is an actual subtle addiction mechanism at work here that propels people to overeat. In this regard, the movie "Super Size Me" should make us all pause and think about our eating behaviors.

Dr. Seaman, thank you for advising and updating us on this fascinating aspect of nutrition.

Dr. David Seaman is also a columnist for DC, writing on "Essentials of Nutrition." For a complete bio and a link to previous articles, visit his columnist page:

Click here for previous articles by G. Douglas Andersen, DC, DACBSP, CCN.

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