By Trevor G. Marshall, PhD and Liz (F.E.) Marshall, RPh

This is a simplified overview of the full paper "Remission in Sarcoidosis". Always refer to the full paper to resolve any points of confusion.

Sarcoidosis is one of the remaining "mystery diseases" of modern medicine. First discovered in 1877 by Jonathan Hutchinson, it was the work of Guy Scadding in the late 1940's and early 50's that really defined today's view of this disorder as being characterized as "non-caseating granuloma".

'Granuloma' are a special type of inflammation. They are an aggregation of lymphocytes, monocytes, macrophages and epithelioid giant cells. They form in soft tissues throughout the body. Although they are often found in the liver, kidney and brain, most commonly they are found in the interstitial tissue of the lungs. Since the lungs use the interstitial tissue to transfer air and other gasses to and from the bloodstream, the granuloma stop the lungs from functioning properly.

The word "non-caseating" means that the granuloma remain healthy, even while they are creating the inflammatory biochemicals (cytokines) that are designed to help our immune systems attack and kill 'invading', 'foreign', tissue and organisms (viruses, bacteria and fungi).

Earlier this year, a group of Swedish scientists published pictures of bacteria from a tick-borne disease that were living and replicating in the granuloma of 30 Sarcoidosis patients. The organisms were from the genus "Rickettsia". In the USA, these organisms give rise to "Rocky Mountains spotted fever," while in Asia they cause "scrub typhus".

Using an electron microscope, (with a magnification of 84,000X), they photographed two Rickettsia cells which were in the process of replicating by dividing into two. The granuloma are supposed to kill such bacteria, yet here was evidence that bacteria can live and replicate within those granuloma. Other scientists have since found other types of bacteria, which also seem to be involved in sarcoid inflammation.

But granulomatous inflammation does not form in everybody. It seems as though there is a genetic pre-disposition, a tendency running within families that causes this special reaction to the bacteria by forming granuloma.

Some scientists recently summarized sarcoidosis in the following sentence: "One or more microbes behaving in a non-infectious fashion in a genetically predisposed individual, trigger the sarcoidosis granulomatous response".

So now we know why somebody gets sarcoidosis, but why do some get better and some do not? Why does the sarcoidosis attack different organs in different patients?

Actually, now that we know that sarcoidosis is caused by bacteria, it becomes fairly easy to see why some patients become more ill than others.

If somebody is attacked by 'microbes' they typically suffer from fever and intense pain, usually for several weeks. The actual sarcoid inflammation is usually not discovered until years afterwards. During the initial attack, the fever is treated with antibiotics.

When the fever subsides it is then assumed that the body's immune system has rejected the microbe, and the patient has been 'cured'.

Unfortunately, in that fraction of the population with the genetic pre-disposition to form sarcoid granuloma, the bacteria continue to live in the granuloma, and the body's immune system continues to try and reject them. Sometimes the immune system is successful, and the patient goes into "remission". But sometimes the inflammation continues for the remainder of the patient's lifetime.

Unless an antibiotic is used that is capable of attacking the bacteria which are living in the soft tissue and granuloma, the microbes might never be killed. Penicillin just doesn't do the job. The antibiotics that have been most successful against this type of bacteria are the Tetracyclines, and Minocycline has been proven effective in sarcoidosis. The low-dose Minocin treatment which Dr. Mercola developed for his rheumatoid arthritis patients is a good way to treat the bacteria of sarcoidosis.

There is a hormone which allows the sarcoid granuloma to flourish. It is called 1,25-dihydroxyvitamin D. It is formed in the kidneys from 25-hydroxyvitamin D, the metabolite formed when our bodies take in Vitamin D from sunlight or from food. Although the 1,25 D hormone is normally manufactured in the kidneys, it is also manufactured in the granulomatous inflammation of sarcoidosis.

Consequently, the concentration of this hormone in the blood of sarcoid patients can rise to quite high levels, and cause them to suffer from the symptoms of "Hypervitaminosis D". These include fatigue, pins and needles, numbness, muscle pain, muscle cramps, dizzyness, loss of balance and even facial palsy.

Your doctor can measure the levels of the 1,25 D hormone and also of 25-hydroxyvitamin D, its precursor. When the D-Ratio is calculated from this blood work, it gives a measure of the amount of granulomatous inflammation which is present in a sarcoid patient's body. This D-Ratio can be tracked to ascertain the effectiveness of the Minocin therapy.

One way to stop high levels of this 1,25 D hormone from forming is to reduce the amount of Vitamin D that our bodies are taking in. This has to be done carefully, as our bodies need some Vitamin D to function properly. Nevertheless, the granuloma of sarcoidosis manufacture this hormone very vigorously, and so sarcoid patients are especially sensitive to sunlight and dietary Vitamin D.

The symptoms of fatigue, numbness, pain and cramping all go away after the level of the 1,25 D hormone has been brought back down to normal levels. Your doctor needs to measure the level of the 1,25 D hormone and make sure it doesn't fall too low.

"Especially sensitive to sunlight" means stay indoors. Even a little bit of sunlight will feed the inflammation and make the fatigue worse. Sunshades may even have to be worn in brightly lit indoor environments, and very, very, dark sunshades are needed if you have to venture outside during the daylight hours. You should also cover all exposed skin with thick clothing, and wear leather gloves while driving.

The effects of an exposure to the sun are not immediate, indeed, pleasure is the first response, and discomfort takes 4 to 8 hours to develop. During the following 2-4 days, however, is when the symptoms are at their worst. Since most people tend to live on a daily cycle, they are rarely out of the sun for 2-4 days at a time.

Consequently they might never correlate their symptoms with the sun exposure until after they read about it.

In addition, Vitamin D is stored in the body's fat. Sometimes it may take several months until the blood work shows that the 25 D level has fallen, and the reserves in body fat have been used up. Although the fatigue usually eases fairly quickly, numbness and muscle pain only ease after the fat storages have been significantly depleted.

Your doctor may suggest that you take an angiotensin receptor blocker, such as Benicar. It turns out that Angiotensin II is not only important to cardiac health and blood pressure, but it's also an important part of the inflammatory cycle in the granuloma. ARBs are a relatively safe family of drugs that can dramatically ease any discomfort that remains once a sarcoid patient has gotten their Vitamin D under control.