Hi, anniekim.
The effect of electrolytes in retaining water in the blood is based on what is called osmosis. The basic idea is that when an electrolyte is present in water, it lowers what is called the chemical potential of the water itself, because there is less of it per unit volume of the solution. If there is a semipermeable membrane (a membrane that can pass water, but not electrolytes) separating two compartments that contain a water solution, there will be water molecules diffusing in both directions, but the rate of diffusion will be higher from the solution with lower concentration of electrolyte to the one with higher. Over time, the result will be to equalize the concentrations on both sides of the membrane, and this will equalize the chemical potential of the water on each side.
In the body, you can consider one of the solutions as being the blood, the other as being the urine, and the membrane as being the glomerulus, which is in the kidneys. It's more complicated than this, because the kidneys don't just function by diffusion, but do some active pumping. Nevertheless, the idea is that if the concentration of electrolytes is higher in the blood, it will cause the diffusion of water into the urine to be slower.
This is really just a temporary measure, and what is needed for a permanent fix is to get the hypothalamus/pituitary to put out more antidiuretic hormone. This signals the kidneys to do some active pumping to keep enough water in the blood. If this is not done, too much water goes out in the urine, and the person is constantly thirsty and can never catch up. It's like "their bucket has a hole in it." The thing to do is to fix the hole, not just keep adding water.
Vanguard, it's true that ADH plays a dual role. It is also called vasopressin, and it does affect constriction of blood vessels. But lack of it most certainly does cause low blood volume. I encountered one case in which the person was urinating over 7 liters per day. In ME/CFS, it is usually quite a bit less than this, but still significantly more than the average normal value of 1.5 liters per day. When water is being lost too fast to the urine, the person just can't keep up with it by drinking, and the total blood volume goes down. ADH has been measured and found to be low in ME/CFS patients. Total blood volume measurements have been made (using either a dye method or a radioisotope method) and found to be low. The late Dr. David Streeten worked on this.
Fixing the heart will not change the total blood volume, but it will increase the cardiac output (liters of blood per minute pumped out by the heart). Perhaps this is what Dr. Lerner was referring to.
In my view, the low cardiac output observed in ME/CFS by Peckerman and by Cheney is due partly to low total blood volume (and hence low venous return to the heart) and partly to diastolic dysfunction, which is caused by low ATP production in the mitochondria of the heart muscle cells, due to the vicious circle mechanism described by the GD-MCB hypothesis. If there is a viral infection in the heart, which Dr. Lerner treats, that would also contribute to lowering the cardiac output.
Best regards,
Rich
