Part 2. The Inflammation Bucket

In my previous post I listed everything in our lives contributing to ill health (directly or indirectly) by increasing inflammation. I often think of it as a bucket, a vessel filling up more and more for every added factor fueling inflammatory processes. Due to differences in genetics some of us have large buckets, some of us have small. When the bucket flows over, we end up with symptoms.

Inflammation always appears for a reason

I will try to simplify the vastly complex phenomenon of inflammation. Inflammation is a consequence of the body defending itself against pathogens, toxins, allergens and cell damage and is characterised by pain, redness and swelling. The purpose of inflammation is to remove damaging elements and substances and promote healing. When immune cells detect some kind of damage or harmful substance in the body, they signal to other immune cells to re-locate to the spot and perform their designated tasks. So, it’s important to keep in mind that while inflammation can be damaging, it is an essential part of the healing process and always appears for a reason.

Inflammation can be acute or chronic, where the first sometimes turn into the second. This happens when the immune system hasn’t been able to fully neutralize the harmful element. A kind of trench warfare ensues, which can go on for all eternity unless one of two things happen: the immune system is strengthened enough to win the battle, or the damaging substance is eliminated by other means.

Part of the immune system’s work is producing antibodies, also called immunoglobulins. A type of immune cell called B-cell marks pathogens or proteins with such antibodies as a signal to other immune cells to eliminate them.

When the bucket flows over

At a certain level of inflammation the figurative bucket flows over, causing among other things autoimmunity. When the inflammation level gets beyond a certain point, the safety mechanism supposed to curb the accidental formation of antibodies towards the body’s own proteins (endogenous proteins) fails – it is too busy and simply cannot keep up. Immune cells then start attacking the body’s own tissue, called friendly fire.

A phenomenon called molecular mimicry is often involved. It happens when a protein or part of a protein from a pathogen or food gets into the body, past a barrier typically keeping them out (such as the intestinal wall). This triggers a response where immune cells recognise the intruding molecule as foreign and tries to destroy it. Unfortunately these proteins can sometimes be similar to the body’s own, and therefore autoantibodies are often formed towards endogenous proteins by this process. If the ”bucket” is overflowing and the system in place to stop this has ceased to work or is unable to keep up the process is allowed to continue: the body’s own proteins who happen to look like intruders are marked for destruction and get broken down. That is autoimmunity.

Someone having autoantibodies in their blood doesn’t necessarily mean they have symptoms. Many people who feel quite healthy do carry detectable amounts of them – it’s only when the level crosses a certain threshold that it becomes a problem. Interestingly, it’s possible to carry autoantibodies towards a certain protein many years before developing any clinical manifestations. This can be used to predict who might develop a particular autoimmune disease further on.

General inflammation is driven by inflammatory mediators

While these autoantibodies are forming the level of pro-inflammatory proteins such as cytokines, chemokines, vasoactive amines etc is elevated. These molecules are needed to battle a threat such as an infection, and signal to cells that they need to mobilise. Cytokines can cause hormone resistance and collateral damage to organs, and they are often measured in blood or tissue as biomarkers of inflammation. Sometimes they work locally and sometimes they spread through the body and contribute to the vicious circle of systemic inflammation, also by triggering or suppressing the expression of an enormous amount of genes whose corresponding proteins are either directly involved in inflammation or have other functions such as altering metabolism or physiology.

Cytokines begets immune cell activation begets cytokines; this cycle is preferably interrupted by removing the original sources of inflammation. The safety mechanisms can then start working again and the production of antibodies drops. It is commonly believed that systemic inflammation is entirely capable of driving itself and to continue for all eternity even when the source of inflammation is long gone, but this does not make biological sense and I do not believe it to be true.

The most common approach is to target the molecules that mediated  inflammation or by activating anti-inflammatory receptors rather than targeting its source, using drugs like corticosteroids, NSAIDs and TNF alpha inhibitors. Sometimes this approach is successful, sometimes it comes with a broad range of more or less dangerous side effects – but never ever does it remove the underlying causes of the overflooded bucket.

Treating the inflammation sources will reduce symptoms

The standard view is that when your body has learnt how to produce antibodies (for example towards an endogenous protein) it will keep doing it forever. It’s true that the body cannot unlearn this ability. And a certain type of antibody (IgG) can remain for months or years after an infection has passed. But a passed infection is not likely to be such a large source of general inflammation (cytokines etc) that a person should be severely and progressively ill for decades. Something must be keeing their systems from returning to homeostasis. Thus, should the original source indeed be long gone, something else must be ramping up the immune system, in which case those additional sources of inflammation should be targeted.

Countless examples from real life demonstrates that it is possible to reduce autoantibody production dramatically (and often quickly) by reducing overall inflammation and dealing with the root causes. Hypothetically, this happens because the safety mechanisms start working again. B cells produce many different antibodies that attach to different protein sequences in a pathogen, and perhaps the body can finally identify the self-reacting ones and eliminate the cells that produce them, while keeping the others. However, while many types of infections tend to pass it’s not unusual that untreated infections turn chronic, in particular vector-borne and periodontal infections. They could then become very powerful sources of inflammation.

The core message here it that by treating the underlying causes you can get your body to 1) produce minimal amounts of autoantibodies and cytokines 2) reverse your disease or perhaps even become entirely symptom free.

Part 3. Do you have an inflammatory condition (without knowing it)?

Further reading

Origin and physiological roles of inflammation

Mechanisms of human autoimmunity

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