(MAC/MAI) Mycobacterium Avium Complex Pulmonary Disease: Join us

@ling123 That was exactly my thought process when I read Karl's post.

@windwalker, I'm not gonna argue with anyone. All I have to go on is Mayo and the doctors who have diagnosed me. But there is a big difference between simple or acute bronchiectasis, and Chronic Bronchiectasis. Simple bronchi... is the result of bacterial infection. it is hard to control, and can be deadly. But if you can control, even kill, the bacteria, no more damage will be done. Chronic, on the other hand, owes its existence to misfolding and dying prions of protein. These prions, or proteins with autoimmune problems, often clone themselves a few times before they die. Then each clone repeats, and so on, putting their clone out into the blood stream. When they die, their carcasses work their way into body tissue, stack themselves into tiny water tubes called fibrils, and START doing their damage to the tissue. For instance, if the fibrils get into the lung tissues, it is these dead carcases that leatherize the tissues or make them enlarge, or mess up skin, or corneas, or stack themselves in the brain, or whatever. They are tiny, about a thousandth the width of a human hair. But because they are already dead, their existence is chronic and cannot now be stopped as bacteria can. At this point in time, science has no way to get them out of the body if the kidneys fail, and no way to stop them from forming. The fibrils only live for 2-3 hours, not long enough to take a hammer and beat the little buggers into submission. So they just keep doing their damage until after the person is dead. That is the difference. Nothing stops them, especially not their death. With the bacteria, they may be difficult to kill, but they can be stopped, at least theoretically. Acute bronchi.... is dangerous only as long as the bacteria is alive. Amyloid fibrils are dangerous only after they are dead. Then localized fibrils attach whatever tissue they can attach to. Some can go only to heart walls, or blood vessel linings. Some go after these, and kidneys, and toenails and corneas, for instance. It depends on their exact shape, elasticity, size, atomic weight, whatever, after they are dead and reformed into fibrils. If bacteria, it lives to damage. If protein prions, they die to damage.

Thank you for this valuable info.

What recommendations do members have regarding drinking water? Is tap water safe for someone with MAC? Would water through a Brita filter pitcher be better?

What recommendations do members have regarding drinking water? Is tap water safe for someone with MAC? Would water through a Brita filter pitcher be better?

@windwalker, I'm not gonna argue with anyone. All I have to go on is Mayo and the doctors who have diagnosed me. But there is a big difference between simple or acute bronchiectasis, and Chronic Bronchiectasis. Simple bronchi... is the result of bacterial infection. it is hard to control, and can be deadly. But if you can control, even kill, the bacteria, no more damage will be done. Chronic, on the other hand, owes its existence to misfolding and dying prions of protein. These prions, or proteins with autoimmune problems, often clone themselves a few times before they die. Then each clone repeats, and so on, putting their clone out into the blood stream. When they die, their carcasses work their way into body tissue, stack themselves into tiny water tubes called fibrils, and START doing their damage to the tissue. For instance, if the fibrils get into the lung tissues, it is these dead carcases that leatherize the tissues or make them enlarge, or mess up skin, or corneas, or stack themselves in the brain, or whatever. They are tiny, about a thousandth the width of a human hair. But because they are already dead, their existence is chronic and cannot now be stopped as bacteria can. At this point in time, science has no way to get them out of the body if the kidneys fail, and no way to stop them from forming. The fibrils only live for 2-3 hours, not long enough to take a hammer and beat the little buggers into submission. So they just keep doing their damage until after the person is dead. That is the difference. Nothing stops them, especially not their death. With the bacteria, they may be difficult to kill, but they can be stopped, at least theoretically. Acute bronchi.... is dangerous only as long as the bacteria is alive. Amyloid fibrils are dangerous only after they are dead. Then localized fibrils attach whatever tissue they can attach to. Some can go only to heart walls, or blood vessel linings. Some go after these, and kidneys, and toenails and corneas, for instance. It depends on their exact shape, elasticity, size, atomic weight, whatever, after they are dead and reformed into fibrils. If bacteria, it lives to damage. If protein prions, they die to damage.

@lch713 We installed an osmosis filter system under our kitchen sink. I really don't drink much water. I drink wine, soda, tea from water I have boiled....I mostly take baths, but do occasionally shower. we turned up the water temp on our water heater to 140 degrees, that is suppose to kill the mac. There is a topic on the Discussion Board. You can find the discussion board at the Connect Mac Group home page.

@windwalker, I'm not gonna argue with anyone. All I have to go on is Mayo and the doctors who have diagnosed me. But there is a big difference between simple or acute bronchiectasis, and Chronic Bronchiectasis. Simple bronchi... is the result of bacterial infection. it is hard to control, and can be deadly. But if you can control, even kill, the bacteria, no more damage will be done. Chronic, on the other hand, owes its existence to misfolding and dying prions of protein. These prions, or proteins with autoimmune problems, often clone themselves a few times before they die. Then each clone repeats, and so on, putting their clone out into the blood stream. When they die, their carcasses work their way into body tissue, stack themselves into tiny water tubes called fibrils, and START doing their damage to the tissue. For instance, if the fibrils get into the lung tissues, it is these dead carcases that leatherize the tissues or make them enlarge, or mess up skin, or corneas, or stack themselves in the brain, or whatever. They are tiny, about a thousandth the width of a human hair. But because they are already dead, their existence is chronic and cannot now be stopped as bacteria can. At this point in time, science has no way to get them out of the body if the kidneys fail, and no way to stop them from forming. The fibrils only live for 2-3 hours, not long enough to take a hammer and beat the little buggers into submission. So they just keep doing their damage until after the person is dead. That is the difference. Nothing stops them, especially not their death. With the bacteria, they may be difficult to kill, but they can be stopped, at least theoretically. Acute bronchi.... is dangerous only as long as the bacteria is alive. Amyloid fibrils are dangerous only after they are dead. Then localized fibrils attach whatever tissue they can attach to. Some can go only to heart walls, or blood vessel linings. Some go after these, and kidneys, and toenails and corneas, for instance. It depends on their exact shape, elasticity, size, atomic weight, whatever, after they are dead and reformed into fibrils. If bacteria, it lives to damage. If protein prions, they die to damage.