Hi Sydney,

I am finally able to write to you (and others) about why HBOT is the only safe and effective therapy for RSD,

Before I can talk about how HBOT acts on RSD, I need to explain how RSD acts on us, and it isn't nerves affecting other nerves, bone, tissue and microvascular systems (MVS). Only then can we understand why HBO works against this disease.

RSD is an ischemia-reperfusion injury (IRI). This is a well understood disorder that was not discovered until a century after the discovery of RSD. It it is well understood because research into it is light-years ahead of that into the disease we suffer. The research was done because patients who underwent surgery on internal organs had an unacceptably high mortality rate and doctors needed to learn why.

IRI killed these patients because most of our internal organs are essential if we are going to live and because the those organs are made of a different kind of soft tissue than our skin and muscle. The disease killed quickly. We don't die because our skeletal muscle and tissue aren't necessary to sustain life.

IRI begins with a physical trauma. This trauma damages cells and the primary white blood cells (WBCs) of our immune system are programmed to react to cell debris in the same way they react to a pathogen. Attack, destroy and release chemical messengers that activate other WBCs which then begin moving toward the site where the cell debris or pathogen was discovered.

How do these chemicals contain and transmit the information that not only alerts other WBCs but tells them where to go? No one can answer that question, but researchers have demonstrated that it does happen [1].

The reason these WBCs react to cell debris in this way is that many pathogens, and all viruses, do only two things; eat cells and multiply. They are incredibly efficient at both; a virus that enter a cell will become 300 viruses and completely consume the cell interior in about an hour. Once those viruses have eaten the cell, they break through the remaining cell wall and race to find another cell. Do the math and you will see that a single virus can become more than one billion in about six hours. Cell debris could be the leftovers from a meal and the first sign the body has been invaded.

Our WBCs "patrol" the entire circulatory system, but there is only one place they can discover cell debris and be "fairly certain" that other viruses are nearby; the microvascular systems (the arterioles, capillaries and venules that deliver arterial blood to the cells and return "used" blood to the veins. This interface between blood and cells is also the interface between pathogens and WBCs. When a WBC encounters cell debris or a pathogen in an MVS, it is likely that more will be found on the other side of the capillary wall.

In order for the WBCs to get access to the cells on the other side of the capillaries, they must release a destructive "chemical" that creates gaps in the capillary wall large enough for them to pass through. Pathogens and bits of cell debris are much smaller than WBCs and they are able to pass through the capillary wall and into the MVS during the process in which waste is transferred from our body cells to our red blood cells, where it is carried away to be filtered by internal organs.

Once the immune system is satisfied that cell debris from trauma does not mean there are pathogens among the cells, the immune response subsides; except in IRI, something goes wrong and WBCs keep pouring into the area.

The "chemicals" our WBCs release to create gaps in the capillary wall don't destroy the specialized cells that make up that wall, but they do destroy pathogens and cells. I mentioned that viruses and other pathogens invade cells and eat them from the inside; it is necessary to destroy cells in order to destroy the pathogens that may be inside them.

These "chemicals" are also the cause of the inflammation that goes along with an immune response. They cause swelling and generate heat, both of which are critical if the invasion is to be minimized until other WBCs that will destroy every pathogen in the body can be made and released into the blood.

Swelling (edema) causes the sac that holds the cells in place to expand and compress tiny nearby arteries and veins. This compression of veins prevents the pathogens from using them to circulate to other parts of the body. The heat destroys many pathogens, that cannot survive when the temperature around them increases to just two degrees over normal body temperature.

Compressing the tiny arteries prevents all of the WBCs from only reaching the original site where the cell debris or pathogen was discovered. This, too, is critical; it is likely that other pathogens are in nearby cell sacs, and when these WBCs are prevented from reaching their destination because the tiny artery they are in is compressed, they invade other nearby MVS'

They release their chemicals to create gaps in the capillary walls and other WBCs follow behind, enter the cell sacs, and release their chemicals there. This results in the destruction of countless healthy cells in uninfested areas, but our bodies are not programmed the way our justice system is, where 'it is better to let ten guilty men go free rather than wrongly convict one innocent man'; it is better to destroy hundreds of thousands of healthy cells than to allow one pathogen to survive.

As I said earlier, IRI is a disease process that begins when the immune response to cell debris doesn't end as it should. Instead, it spreads over an increasingly widening area as inflammation and edema compress an ever-increasing number of tiny arteries, forcing WBCs to invade cell sacs more and more distant from the site where the original debris was discovered. This is how RSD spreads during the first, or acute (inflammatory) stage of the disease.

But it gets worse. Once our WBCs release their chemicals they literally "morph" into another type of cell; the phagocyte. Their role now is to capture and consume the debris they created earlier. They become adhesive in order to "get a better grip" on the debris as they consume it. After they consume their portion of the debris, they are programmed to die. This program is called apoptosis.

Well, all of those phagocytes don't die in IRI. It may be that there isn't enough debris to go around, and if they can't find any to consume, they just keep looking.

Here is where things really go wrong. I said that our WBCs create gaps in the capillary wall so they can pass through those gaps and enter the sacs containing the cells; blood plasma also passes through those gaps, filling the cell sacs (this serves to increase edema and lengthen the period when veins and arteries are compressed); cell debris, WBCs and adhesive phagocytes float around in the fluid, and some of them drift through the capillary wall and reenter the MVS.

When an adhesive phagocyte enters the MVS, it is carried by the blood from the capillary to the venule. The interior of the venules is smaller than phagocytes or WBCs, and they pass through these venules because the blood pressure pushes them through.

During the immune response, blood pressure in the MVS is lowered as some of the plasma leaks into the cell sacs. A WBC being carried into the venule would have a more difficult time passing through it, and an adhesive phagocyte is not going to make it. It sticks to the venule wall. After a while another phagocyte reenters the MVS and is carried to the venule, where it sticks to the venule wall and to any phagocytes that arrived there before it.

IRI is plugging of the venules of the MVS, If blood can't pass through the venule, fresh arterial blood can't enter the MVS; it is already full.

Without fresh arterial blood, the various products needed to repair the capillary wall can't get to where they are needed. The result of this is called vascular permeability. Oxygen and nutrients can't reach the surviving cells served by that MVS.

Without oxygen and nutrients, our cells have nothing to metabolize (transform matter into energy) and no oxygen that is necessary for metabolism to take place. A cell sac can be served by multiple MVS', and WBC invasion of other MVS' is random; not every MVS in the affected area will suffer the damage to capillary walls or plugging of venules.

Our cells interact with our nerves and with other cells in a number of ways, some of which are not understood at all. What is known is that cells in a sac that are still receiving arterial blood actually transfer oxygen and nutrients to cells that aren't. This keeps those cells alive, but the donor will not have enough of either to metabolize properly, and the recipient won't either.

It is cell metabolism that creates the heat that keeps our bodies warm. Impaired metabolism means that cells don't generate enough heat in RSD/IRI affected areas. This is why cold affects us so terribly in affected limbs; the limb is not able to heat itself.

Nerves need oxygen and nutrients too. I won't try to describe research into ischemia (blockage of arterial blood flow), but I know from reading this research that if you take a blood pressure cuff and apply it to your arm, raise the pressure to above your normal diastolic blood pressure, then wait just a few minutes, the touch of an ice cube to your hand will cause intense burning pain. This is the allodynia we suffer.

Sensory nerves that don't get enough oxygen and nutrients can't function properly. I have not read any research explaining how ischemia affects our pain sensory nerves (nociceptors), but I suggest that they don't like it and they tell the brain that in no uncertain terms, using the only language they have; pain messages. The constant burning pain of RSD.

Bones need the same things as other cells, and they need lots of calcium, all of which is delivered by the blood. Some bone cells get enough calcium, others don't; this is the cause of patchy osteoporosis.

Nails and hair follicles need these things supplied by the blood too. You can look at how slowly your nails grow, how the hair on your limbs disappears. I think you know what I am telling you causes this.

There is another thing you can look for, cyanosis; that blue to purplish -- or sometimes blanched or gray -- skin color that corresponds almost exactly with the areas you feel pain.

What you are looking at are MVS very close to the skin surface. They are filled with oxygen depleted blood that can't pass through the MVS and into the veins because the venules are plugged.

Finally, our skin radiates excess heat generated by cell metabolism or absorbs heat when the body isn't warm enough. The capillaries that carry too warm blood to the skin aren't carrying warm blood, and so our skin temperature is lower and we are hypersensitive to cold.

Every sign and symptom of RSD can be fully explained by the known disease process I just described to you. This is why, after years of reading the literature on RSD, the immune response to trauma and IRI, I reached the inevitable conclusion that this disease is not the result of a nerve injury; it is the result of physical trauma to tissue. It is an ischemia-reperfusion injury.

If you read my post 4-1/2 years of being wrong, this explanation of IRI is about as brief as I can make it. If I had time, I could fine-tune it a little; and I will in future posts, but I am anxious to get this posted after such a long delay.

Bare-bones as it is, from my point of view, it is enough for today. If you care to read this post carefully and skeptically, I think you must be further down the road to understanding what RSD really is. I hope you will.

I will follow this post with a (hopefully) shorter post on how HBOT affects RSD/IRI. I can't promise it will be shorter because I believe that current HBOT protocols involve too much oxygen at too high an atmospheric pressure.

I not only need to explain how HBOT can successfully treat RSD/IRI, but I also need to explain why many RSD patients who have undergone this therapy got better and then got catastrophically worse. I know why. I have shared this with others who decided to try HBOT, and none of them suffered that catastrophic relapse. I look forward to sharing it with you...Vic