My last post—part 1 of Diet and Inflammation—left off with my conclusion that the answer to the widespread prevalence of chronic inflammation was a nutritional imbalance incurred by the typical Western diet, specifically deficiencies or imbalances in 3 key nutrients: omega-3 (v. omega 6) fatty acids, salicylic acid and glycine (v. methionine).
What exactly happens in inflammation? Inflammation is the basic action of the innate immune system to destroy potentially pathogenic microbes that get into the internal body tissues. It is a non-specific aggressive action by amoeba-like cells called macrophages (derived from the Greek and meaning “big eaters”), the immune system’s first responders, which can literally gobble up bacteria and other microbes. Several types of these cells—called granulocytes—have long been recognized as circulating in the blood as a type of white blood cell. More recently, macrophages have been recognized as populating all sorts of organs and tissues.
But all these diverse types of macrophages are immune system cells, and all of them originate in the bone marrow. If there is tissue injury, injured cells and cell debris will be gobbled up by these macrophages. But if there is infection—the recognition of the generic signature of bacteria, for example—these macrophages get activated, producing toxins such as hydrogen peroxide in order to kill the bacteria. In order to amplify the reaction, these macrophages release chemical signals called prostaglandins to recruit and activate other macrophages, the purpose being to destroy the infecting microbes before they can destroy the host. Of course, like other first responders, the macrophages will put down the infection just like the firemen will put out the fire, but they will also do lots of damage to normal tissues.
Unfortunately, there is still lots of confusion out there about the role of inflammation and innate immunity; most medical authorities believing that inflammation is part of the healing response and a normal response to tissue injury. Why? Because it always seems to happen with tissue injury. You sprain your ankle, and it gets swollen and painful and immobilized; i.e., inflamed. But why should this happen if there is no route of infection? There are no microbes to kill. And we all know that, contrary to healing, the inflammation inhibits healing, which is why we have to put ice on the injury, to suppress inflammation. So why does your body do it?
Here’s where nutrition comes in. The activation of macrophages is affected by an electrochemical switch mechanism on the cell surface membrane. When these cells are at rest, they are, so to speak, switched off, there is a resting voltage between the outside and the inside of the cell (positive outside; negative inside). Just like a light switch on your wall, when it is off, there is a resting voltage (120 volts in the US) between the hot wire attached to the switch and the light fixture. When the light is switched on, the voltage drops as the energetic electrons flow through the switch and activate the fixture. The electrochemical switches in cells are channels in the membrane which allow positively charged ions (calcium or sodium ions) to flow across the membrane. The voltage drops when these channels open up momentarily, activating the cell. That’s how nerve impulses (called action potentials) activate muscles, for example. But it’s also how macrophages get activated.
However, the cell surface membrane is a very dynamic envelope, like a constantly moving, constantly changing, highly sophisticated soap bubble. In the course of ordinary activity, lots of leakage of ions occurs, and there are specialized channels in the membrane that let negatively charged chloride ions in to maintain the resting voltage of 0.07 volts. A substantial proportion of these chloride channels are operated—i.e., maintained in an open position—by the amino acid glycine. Glycine is ordinarily present in body fluids at high concentrations. But if they are not high enough, the glycine-gated chloride channels (aka glycine receptors) are not open enough to allow adequate chloride entry. Thus, the voltage between the outside and inside of the cell deteriorates and the cell is too easily activated, like when there is tissue injury but no infection. Once a macrophage is activated, the extent to which it recruits and activates other macrophages to the site of inflammation is related to the levels of the two other key nutrients: salicylic acid and omega-3 v. omega-6 fatty acids.
How the balance—or imbalance—in the intake of these types of polyunsaturated fatty acids (PUFAs) will be the subject of Part 3 in this series.
About the Author
Joel Brind, Ph.D. has been a Professor of Biology and Endocrinology at Baruch College of the City University of New York for 28 years and a medical research biochemist since 1981. Long specializing in steroid biosynthesis and metabolism and endocrine-related cancers, he has specialized in amino acid metabolism in recent years, particularly in relation to glycine and one-carbon metabolism. In 2010 he founded Natural Food Science, LLC to make and market glycine supplement products via http://sweetamine.com , which includes his own blog HERE.