Friday, March 5, 2010

Ancient Bacteria

It's generally agreed that low-grade chronic inflammation is related to metabolic syndrome, cardiovascular disease, and type 2 diabetes. But no one knows what causes this generalized inflammation.

Acute, localized inflammation is a good thing. It's what walls off an infection, "eats" the offending organism, and then digests it with the help of heavy-duty oxidants. Then, when things are working right, the body repairs the damage, and the cells that have been doing all this leave the scene.

Chronic inflammation, on the other hand, is not a good thing, and the more scientists can find out about it, the better.

Hence I was intrigued by a recent paper in Nature that proposed a totally new idea and confirmed an old idea. You can read a popularized description here, or a link to the original paper here.

When we are invaded by pathogens, the body mounts what is called the innate immune response. This is a nonspecific response triggered by certain chemicals on the surface of many organisms that are unique to them and are not found on our own cells. The body sends out cells called macrophages to engulf the offending organisms and sends chemical signals to recruit other cell types to help rid the body of the organisms and then repair any damage that occurred.

This response is more primitive than the adaptive immune response that uses antibodies and is more specific than the innate immune response.

Usually, the cause of the response is clear, as bacteria or viruses or other pathogens can be found in the blood. But sometimes people seem to have such a response when no pathogens can be found. This puzzled scientists for a long time.

But Carl Hauser and colleagues, the authors of the Nature paper, came up with a fascinating hypothesis. It is generally accepted that mitochondria, known as the "powerhouses of the cell" because they are where most of the cell's energy is produced, were originally bacteria that invaded the cells of other organisms and adapted to the benefit of both.

Mitochondria have their own DNA, which comes only from the mother.

Hauser and colleagues wondered if perhaps trauma that destroys cells could release mitochondria from the damaged cells into the bloodstream. Then, because the mitochondria are descended from bacteria, they might have surface molecules that our bodies would interpret as foreign, so we would mount an innate immune response, just as we do to other bacteria.

His researched suggested that this does indeed happen.

It explains why severe trauma patients sometimes get reactions that look like severe infections when no signs of infecting organisms can be found.

And I wonder if less severe chronic trauma could cause just enough of an innate immune response to trigger chronic disease. For example, we know that chronic gum disease can increase blood glucose levels, along with various signs if inflammation. Could this be because the gum disease is causing gum cells to break down and release mitochondria?

Could other hidden infections be doing the same? By reducing various chronic infections, could we reduce people's chance of getting type 2 diabetes?

I find this research exciting, not because it offers an immediate chance for a cure of type 2 diabetes, but because it's a new idea and I find new paradigm-shifting ideas much more fascinating than huge studies of drugs that rely on statistics to prove anything. Even then, although the statistics can show that the drug worked on average, it can never show whether or not it will help you in particular, as I discussed here.

Creative new ideas can suggest new research paths that may some day lead to real cures.



  1. Certainly seems to lend support for following an anti-inflammation diet.

  2. If such a diet does significantly reduce inflammation.

  3. Hi Gretchen.

    Completely off-topic, but I can't find your blog post where you compared an oral fat load with an oral carb load on your blood glucose & TGs during the day. Can you point me in the right direction?



  5. I came here from that post. That post doesn't contain details of how many grams of fat you ate in the high-fat breakfast. I could have sworn that we discussed that here on this blog. Was I hallucinating?

  6. Nigel, you're not hallucinating. I remember looking up and typing up exactly what I ate on that experiment. But I can't remember where I posted it. I thought it was on the Davis blog, but apparently not. I didn't weigh the fat foods, but I estimated it was about 50 grams, a heck of a lot.

    The second peak is from some salmon, and it is more reasonable, more like what I usually eat.

    If anyone comes across where I posted that, please let me know. One of my problems is that once I've written something down, I clear the memory banks about that item.

    A long time ago a woman came up to me during a concert intermission and was going on and on about some funny newspaper piece she'd read. I finally said, "I'm afraid I never read that."

    She looked very annoyed and said, "You wrote it."

    Another time I found an old short story I'd read and was racing through it to find out how it ended. I hadn't a clue.

  7. Found it! It's in Saturated Fat and Heart Disease. My memory isn't what it used to be and I keep forgetting conversations I've had on various blogs.

  8. Thanks Nigel. I'm glad I'm not the only one with a less-than-perfect memory. I searched that blog for the fat content but apparently didn't search the comments.

    Anyway, we found it. Thanks.

    Apparently when you search a blog for a term (I searched for 50 and fifty), it doesn't search the comments.

  9. Bacteria, as asexual organisms, inherit identical copies of their parent's genes (i.e., they are clonal). However, all bacteria can evolve by selection on changes to their genetic material DNA caused by genetic recombination or mutations. Mutations come from errors made during the replication of DNA or from exposure to mutagens. Mutation rates vary widely among different species of bacteria and even among different clones of a single species of bacteria.Genetic changes in bacterial genomes come from either random mutation during replication or "stress-directed mutation", where genes involved in a particular growth-limiting process have an increased mutation rate.

  10. Different, true. But I'm not sure what this has to do with this topic.