Guest guest Posted January 31, 2006 Report Share Posted January 31, 2006 I'm interested in the reduced cardiac output idea. We go looking for all sorts of obscure reasons for this, but could it be because with all the fatigue and pain we are so much less active than we used to be? If we just don't move much for months at a time, of course the heart will pump less. And of course our muscles get smaller and weaker so we need less blood, so our heart pumps less, ending up in a vicious circle Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 1, 2006 Report Share Posted February 1, 2006 I have over the years in many different ways seen that there is a line/level/point of activity that varies greatly, which variation really characterizes the degree of how disabled you are by the disease at that time, which if you go above it instead of reconditioning you make yourself sicker and also sicker with shorter and longer rebounding effects. Though for myself I have some ideas about the specifics of what moves that point (really a range with more or less variation) but once it gets " lower, " i.e., allowing for much less activity and/or frequency before it triggers a flare) what it " really " is at a nonobservable level (metabolic, cellular, whatever) is a very central key to this illness. In fact, to make things more accurate but complicated, what constitutes activity that goes into what undermines you into a flare or general worsening can widen or at least change. Hence sometimes talking on the phone will do it while other times I actually can take more of that but it's carrying things and mostly walking or being active for a longer or shorter period with stopping for a rest, be it on a park bench or supine in bed on ice packs. Which of course is what's part of the outrage of the graduated excercise folks whose necks I could wring and who have an open invitation to be a fly on the wall of my life for a month or two and then see what they say. Rich that was a terrific description. Judith Wisdom > > > > I'm interested in the reduced cardiac output idea. > > We go looking for all sorts of obscure reasons for this, but could > it > > be because with all the fatigue and pain we are so much less active > > than we used to be? If we just don't move much for months at a > time, > > of course the heart will pump less. And of course our muscles get > > smaller and weaker so we need less blood, so our heart pumps less, > > ending up in a vicious circle > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 1, 2006 Report Share Posted February 1, 2006 Hi Judith. It's good to hear from you. I hope that your circumstances are improving. I agree with what you say. I have never technically tried to determine what my " range of allowable activity " is as a percentage of what my allowable activity would be if I didn't have CFIDS, but I would guess that it is low and narrow, maybe 10% to 15% maybe even lower and narrower. The range may seem wider to us, but it's a matter of perception. We are so limited in what we can do that very small improvements seem significant, but a healthy person probably wouldn't even notice that change in capability. Another thing that I have learned through repeated experience (as has almost every PWC) is that it is very important not to overdo things or get sick and let that range of allowable activity decrease. In other words, if I let my condition start getting worse (by overdoing or crahing or getting sick), it's very hard to get the momentum turned around and start getting better again. This is why PWCs (me at least, I can't speak for everyone) fear pushing against our limits too much. It's not that we have taken on a role as a sick person or some such idiotic psychobabble, it's a very well founded fear of making ourselves more disabled for long periods of time. I have been sick long enough that it is devastating to me when I get worse. I try to avoid it at all costs while staying as active as I can. Tom > > I have over the years in many different ways seen that there is a > line/level/point of activity that varies greatly, which variation > really characterizes the degree of how disabled you are by the > disease at that time, which if you go above it instead of > reconditioning you make yourself sicker and also sicker with shorter > and longer rebounding effects. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 2, 2006 Report Share Posted February 2, 2006 People hate to hear about deconditioning but the fact is is that if you are bedridden and do not or cannot get up and get some exercise, ie do some walking then you'll become deconditioned and that will add to your woes. Theres no around that - its physiogical fact. The question I have is how much exercise you need to do in order to avoid suffering from ills of deconditioning? I dont have any idea. With regard to exercise - every time you begin an exercise program you run up again increased oxidative stress. Your body is simply not ready for the increased oxidative stress occassioned by all that muscle activity. That is true for healthy people as well as CFS patients. In healthy people your body adjusts - antioxidant levels are higher than normal in people who exercise regularly. What happens with CFS patients? Nobody knows. There certainly is evidence of increased oxidative stress in CFS but antioxidant depletion? theres some evidence for it but not alot. Most studies indicate most CFS patients have normal levels of antioxidants. A more important question might be are they high enough to combat the increased oxidative stress? I just want to point out that everyone starting an 'exercise program' is going to feel worse at first and that if you can exercise ie " walk " you should and that people with CFS should try to do so. Deconditioning causes alot of bad stuff that you dont want to load on top of CFS. I am still not sold on Cheney's diastolic ideas. I think diastolic dysfunction is there but I think that anyone with the kind of diastolic dysfunction severe enough to cause the kind of disability in CFS would have been diagnosed long before. The problem with heart cells as I understand itis not the inability of all the heart cells to produce enough ATP but the death of some heart cells which causes increased stress on the remaining heart cells - this results in heart cell hypertrophy, heart enlargement, stiffening etc.. Perhaps CFS is different. rvankonynen <richvank@...> wrote: Hi, . The phenomenon you are referring to here is called " cardiovascular deconditioning " in the research literature. It is a very real phenomenon, observed in astronauts who go into weightless conditions as well as in people who are on extended bed rest, for examples. I think the basic issue in applying this to CFS is to determine which is the cart and which is the horse. As I understand it, after the astronauts are back down to earth for a few days, their cardiovascular systems adjust to the renewed demands on them, and they are able to function physically just fine. So this suggests that in their case the cardiovascular deconditioning indeed occurred in response to reduced demands while weightless, but that the cardiovascular system in these healthy people is able to bounce back and pick up the load again when it is applied, and this suggests that the cardiac output is adjusting to meet the demand. The picture appears to be different from this in CFS. A person with CFS cannot just get a little more exercise and recover their cardiovascular function. Most of them have a diastolic cardiomyopathy (as shown by Dr. Cheney's sensitive echocardiography), and the ability of the left ventricle to fill with blood is limited by the rate of production of ATP by the mitochondria of the heart muscle cells. In other words, the cardiac output is not adjusting to match the demands of the PWC's desired lifestyle. On the contrary, it is limiting it. When we correct what is limiting the ATP production rate in the heart muscle cells, the cardiac output is able to come up to what is required to support the person's chosen lifestyle. I think that's why things like magnesium, Co Q10, L-carnitine, D-ribose and B vitamins (as used by Dr. Myhill) help some PWCs. I don't think they will do the whole job, though, because I don't think they address the root cause of the diastolic cardiomyopathy, which in many cases is glutathione depletion. I think there are other PWCs who have systolic cardiomyopathies caused by viral infections (such as the ones Dr. Lerner works with), and probably others who have such cardiomyopathies as a result of mercury deposition in the heart muscle, secondary to glutathione depletion. The deconditioning argument has raged over the skeletal muscles in CFS for quite a few years, too. There is a school of thought in England and in the Netherlands, primarily, that holds that PWCs are physically unable to do as much as normal, healthy people because they are deconditioned from not doing as much as normal, healthy people, so they should just get out and do more. This argument has never gotten much traction with me. The PWCs I know would dearly love to go out and do more. But if you do it while you still have CFS, I think that's a good way to fry your cells with oxidizing free radicals. Rich > > I'm interested in the reduced cardiac output idea. > We go looking for all sorts of obscure reasons for this, but could it > be because with all the fatigue and pain we are so much less active > than we used to be? If we just don't move much for months at a time, > of course the heart will pump less. And of course our muscles get > smaller and weaker so we need less blood, so our heart pumps less, > ending up in a vicious circle > This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 2, 2006 Report Share Posted February 2, 2006 Hi, Cort. > With regard to exercise - every time you begin an exercise program you run up again increased oxidative stress. Your body is simply not ready for the increased oxidative stress occassioned by all that muscle activity. That is true for healthy people as well as CFS patients. In healthy people your body adjusts - antioxidant levels are higher than normal in people who exercise regularly. What happens with CFS patients? Nobody knows. There certainly is evidence of increased oxidative stress in CFS but antioxidant depletion? theres some evidence for it but not alot. Most studies indicate most CFS patients have normal levels of antioxidants. A more important question might be are they high enough to combat the increased oxidative stress? ***Well, as you know, I disagree with you here. I think there is quite a bit of evidence for decreased antioxidant function, either because of glutathione depletion, or because of genetic variations in the enzymes that use glutathione. But if you don't believe that, then I think the burden is on you to explain why there is oxidative stress, for which you do seem to accept the evidence. To get oxidative stress, you either have to raise the rate of production of oxidants (such as with ionizing radiation, or big loads of toxins, or free iron promoting the Fenton reaction, or some other mechanism), or you have to lower the antioxidant activity. Those are the only two choices. I go with lowered antioxidant activity. The problem with heart cells as I understand itis not the inability of all the heart cells to produce enough ATP but the death of some heart cells which causes increased stress on the remaining heart cells - this results in heart cell hypertrophy, heart enlargement, stiffening etc.. Perhaps CFS is different. ***What you're describing here is the mechanism of systolic cardiomyopathy. What Dr. Cheney is finding with his General Electric vivid 7 Echocardiograph is evidence for diastolic cardiomyopathy in over 80% of his patients. So, yes, CFS is different in this respect. Rich Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 Hi Cort, >>>I think diastolic dysfunction is there but I think that anyone with the kind of diastolic dysfunction severe enough to cause the kind of disability in CFS would have been diagnosed long before.<<<<< * Remember the part where Dr. Cheney said it is our CFS that is protecting/saving us? That it IS the inability to exert that's saving us from heart damage point he calls event horizon (need for transplant). * Then, in Clinic, he always said " unusual " form of Diastolic failure. It has to do with how fast or steady the pumping is. (My brain refuses to retain whether it is filling or emptying<<<that one I think) * You know the section better than me, but I'm told that he is finer and finer tuning just what is happening in that little area. * Then there's the part about Mitochondria damage. Part of why we cannot over-exert, in brain, muscles, limbs, etc but also maybe part of the heart problem. He said the heart contains the most Mitochondria of any of the body. So, maybe why this heart problem takes longer to show up? * A part of the reason for the Peckerman/Natleson study was that our level of dysfunction is matched almost only by " heart disease " . (I have seen that said numerous places over the years.) ANd that it was thought the study might result in a way to measure disability.(for benefits). * I still am confused about how us " living on Adrenaline " , (tho having the diastolic failure) are protected from the event horizon. Maybe we aren't. I will return in April, if still alive. Katrina > > > > I'm interested in the reduced cardiac output idea. > > We go looking for all sorts of obscure reasons for this, but could > it > > be because with all the fatigue and pain we are so much less active > > than we used to be? If we just don't move much for months at a > time, > > of course the heart will pump less. And of course our muscles get > > smaller and weaker so we need less blood, so our heart pumps less, > > ending up in a vicious circle > > > > > > > > > This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 My heart pains went away after getting away from the electrosmog. They came back when I visited my in-laws (there was a big cell phone mast several hundred kilometers from their house) and went away when I returned to the mountains. > > > > > > I'm interested in the reduced cardiac output idea. > > > We go looking for all sorts of obscure reasons for this, but could > > it > > > be because with all the fatigue and pain we are so much less active > > > than we used to be? If we just don't move much for months at a > > time, > > > of course the heart will pump less. And of course our muscles get > > > smaller and weaker so we need less blood, so our heart pumps less, > > > ending up in a vicious circle > > > > > > > > > > > > > > > > > This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 Hi Katrina, I think the unusual form of diastolic dysfunction is that it shows up when we are standing not necessarily when supine. That is very unusual; diastolic dysfunction or heart failure, as I understand it, is usually worse when lying down - that is when the heart has the most blood to pump and it is that position that oddly enough exerts the most stress on the heart. At least thats how I understand it. Given the circulatory problems in some CFS patients may Cheney's findings are not that surprising. Only time will tell about the mitocondrial stuff. (The new EBV study certainly is interesting though - EBV can attack the heart!). The heart does contain more mitochondria than any other organ but does it contain 'extra' mitochondria? Does it contain more than it needs or is it such an energy intensive muscle that it just needs more mitochondria? I dont know. It certainly has a large range of activity - that might be why it has so much mitochondria. I think the adrenaline (epinephrine) part is that in the face of reduced blood flow to the tissues because of poor cardiac output the sympathetic nervous system cuts in (with adrenaline, noradrenaline - I'm not sure which) and clamps down on the smaller blood vessels. this reduces blood flow to the outer part of the body but maintains it to the organs. Theres quite a few ways the body compensates for heart failure - all of them turn out to be bad for the heart in the long run. I'm sure Cheney is further and further refining his theory - hes always interesting to watch! Doyon <prd34@...> wrote: My heart pains went away after getting away from the electrosmog. They came back when I visited my in-laws (there was a big cell phone mast several hundred kilometers from their house) and went away when I returned to the mountains. > > > > > > I'm interested in the reduced cardiac output idea. > > > We go looking for all sorts of obscure reasons for this, but could > > it > > > be because with all the fatigue and pain we are so much less active > > > than we used to be? If we just don't move much for months at a > > time, > > > of course the heart will pump less. And of course our muscles get > > > smaller and weaker so we need less blood, so our heart pumps less, > > > ending up in a vicious circle > > > > > > > > > > > > > > > > > This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 rvankonynen <richvank@...> wrote: Hi, Cort. > With regard to exercise - every time you begin an exercise program you run up again increased oxidative stress. Your body is simply not ready for the increased oxidative stress occassioned by all that muscle activity. That is true for healthy people as well as CFS patients. In healthy people your body adjusts - antioxidant levels are higher than normal in people who exercise regularly. What happens with CFS patients? Nobody knows. There certainly is evidence of increased oxidative stress in CFS but antioxidant depletion? theres some evidence for it but not alot. Most studies indicate most CFS patients have normal levels of antioxidants. A more important question might be are they high enough to combat the increased oxidative stress? ***Well, as you know, I disagree with you here. I think there is quite a bit of evidence for decreased antioxidant function, either because of glutathione depletion, or because of genetic variations in the enzymes that use glutathione. But if you don't believe that, & & & & Rich why would I believe that? I dont know why you would believe otherwise. I believe you are very, very wedded to your depletion theory. Maybe the next string of studies will show GSH depletion in CFS patients but this one hasnt. There is almost as much evidence for increased GSH as their is for depleted GSH in CFS. I'm just reading the literature. I read it all the time and if someome says something contrary to what I'm reading then I'm going to say something. THis is from an earlier post: One study, the Krurup, found reduced levels of GSH but since the abstract did not mention a control group one wonders what it was in reference to. The Kennedy study found reduced levels of GSH in a SUBSET of obese hyptensive CFS patient. Since the other LARGER group of CFS patients who were not obese or hyptensive had normal GSH readings and since obesity is a risk factor for diseases associated with oxidative stress, the Kennedy group asserted the low GSH readings were due to that and were not an inherent part of CFS. The Study found reduced GSH readings in a SUBSET of CFS patients. The other two studies found NORMAL GSH readings. Jammes found a tendency for INCREASED GSH levels. McGregor (JCFS) has found INCREASED GSH levels in two studies examining blood erythrocytes. Thus of seven studies the one that found low GSH did not have a control group, one of the two that found low GSH in a subset of CFS patients believed it was due to their obesity. Two studies have found INCREASED GSH and one found a tendency for INCREASED GSH. The best study done on oxidative stress/antioxidant levels in CFS – the recent one by Kennedy – concluded that CFS was not a disease of reduced antioxidant levels but was a disease of increased oxidative stress. then I think the burden is on you to explain why there is oxidative stress, for which you do seem to accept the evidence. To get oxidative stress, you either have to raise the rate of production of oxidants (such as with ionizing radiation, or big loads of toxins, or free iron promoting the Fenton reaction, or some other mechanism), or you have to lower the antioxidant activity. Those are the only two choices. I go with lowered antioxidant activity. *** A chronic inflammatory reaction could produce high levels of oxidative stress. We know there's high levels of apoptosis in CFS; that in itself is a source of oxidative stress. recently found increased angiotensin activity in POTS patient - angiotensin activates NADPH oxidase which pumps out superoxide. Disturbed mitochondrial activity for whatever reason - did you see the recent EBV paper - can,instead of reducing oxidative stress, can also increase it. Toxins can also produce oxidative stress. The problem with heart cells as I understand itis not the inability of all the heart cells to produce enough ATP but the death of some heart cells which causes increased stress on the remaining heart cells - this results in heart cell hypertrophy, heart enlargement, stiffening etc.. Perhaps CFS is different. ***What you're describing here is the mechanism of systolic cardiomyopathy. What Dr. Cheney is finding with his General Electric vivid 7 Echocardiograph is evidence for diastolic cardiomyopathy in over 80% of his patients. So, yes, CFS is different in this respect. ***Those are findings from heart failure in general. Heart failure can come from diastolic or systolic cardiomyopathy or both. They often occur together but the PROCESS, when you come down to the individual cells, is the same. I'm obviously not an expert but I dont believe it matters what causes the problem, a virus, a heart attack due to blockage of the arteries or whatever a major problem remaining, uninjured heart cells cannot handle the increased load put on them and they compensate for this by enlargening. This works for awhile but in the end fails as fibrous material replaces the dead cells and it loses its elasticity and stiffens and becomes unable to eject blood from it (systolic) or to fill properly with blood (diastolic). Rich This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 Hi, . I take it that you meant to say meters instead of kilometers. Is that right? Rich > > My heart pains went away after getting away from the electrosmog. They > came back when I visited my in-laws (there was a big cell phone mast > several hundred kilometers from their house) and went away when I > returned to the mountains. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 3, 2006 Report Share Posted February 3, 2006 Hi, Cort, Rich: I think there is > quite a bit of evidence for decreased antioxidant function, either > because of glutathione depletion, or because of genetic variations > in the enzymes that use glutathione. But if you don't believe that, > & & & & Rich why would I believe that? I dont know why you would believe otherwise. I believe you are very, very wedded to your depletion theory. ***As long as it continues to match valid observations and have internal consistency from the standpoint of " known " biochemistry and physiology, yes, I will stick with it. Maybe the next string of studies will show GSH depletion in CFS patients but this one hasnt. There is almost as much evidence for increased GSH as their is for depleted GSH in CFS. I'm just reading the literature. I read it all the time and if someome says something contrary to what I'm reading then I'm going to say something. THis is from an earlier post: > One study, the Krurup, found reduced levels of GSH but since the abstract did not mention a control group one wonders what it was in reference to. The Kennedy study found reduced levels of GSH in a SUBSET of obese hyptensive CFS patient. Since the other LARGER group of CFS patients who were not obese or hyptensive had normal GSH readings and since obesity is a risk factor for diseases associated with oxidative stress, the Kennedy group asserted the low GSH readings were due to that and were not an inherent part of CFS. The Study found reduced GSH readings in a SUBSET of CFS patients. The other two studies found NORMAL GSH readings. Jammes found a tendency for INCREASED GSH levels. McGregor (JCFS) has found INCREASED GSH levels in two studies examining blood erythrocytes. > > Thus of seven studies the one that found low GSH did not have a control group, one of the two that found low GSH in a subset of CFS patients believed it was due to their obesity. Two studies have found INCREASED GSH and one found a tendency for INCREASED GSH. The best study done on oxidative stress/antioxidant levels in CFS – the recent one by Kennedy – concluded that CFS was not a disease of reduced antioxidant levels but was a disease of increased oxidative stress. ***I've commented before on the general problem with pretty much all the published experimental data on CFS, which results from the multitude of subsets that are subsumed by the Fukuda et al. case definition that is used to select subjects for research studies in CFS. I'm sorry that's the case, but it is. I think we have to take this into account whenever we read of experimental work that used this definition. It should not be assumed that glutathione depletion is not present in a substantial subset of PWCs because some of the studies, which averaged people from a variety of subsets together, didn't find it. I think you reported that your own glutathione level tested low, and that certainly has been the experience reported by many on this list. There's nothing magic about these published studies. They have a lot of problems, and their authors would probably be among the first to tell you that. I think it's a good idea to take them with a grain of salt. Concerning the Kennedy et al. study, I'm having an ongoing dialog with one of the authors about that. These experimenters are operating in good faith, but they have an incredible burden with the existing case definition. PWCs get pretty worked up about the name of this disorder, and that's certainly important for a lot of reasons, but the definition is what undermines the efforts of the experimentalists. I think it also drives good experimentalists away, because it prevents being able to work on a well-posed problem, and without that, it's very hard to get definitive results after all your hard work. ***As you point out, it's also true that some PWCs have elevated glutathione, and this would be expected if they have serious polymorphisms in their glutathione peroxidase or glutathione transferase genes. In that case, the demand for glutathione would be expected to drop, and the level of glutathione would then be expected to rise. I've only seen a very small number (maybe 3) like this so far (most people don't have the measurements), but I think this would explain why these PWCs have essentially the same symptomatology as the subset with depleted glutathione. Either way, they lack effective glutathione action, and go into a state of oxidative stress, which brings on the rest of the pathogenesis. > > then I think the burden is on you to explain why there is oxidative > stress, for which you do seem to accept the evidence. To get > oxidative stress, you either have to raise the rate of production of > oxidants (such as with ionizing radiation, or big loads of toxins, > or free iron promoting the Fenton reaction, or some other > mechanism), or you have to lower the antioxidant activity. Those > are the only two choices. I go with lowered antioxidant activity. > > A chronic inflammatory reaction could produce high levels of oxidative stress. We know there's high levels of apoptosis in CFS; that in itself is a source of oxidative stress. recently found increased angiotensin activity in POTS patient - angiotensin activates NADPH oxidase which pumps out superoxide. Disturbed mitochondrial activity for whatever reason - did you see the recent EBV paper - can,instead of reducing oxidative stress, can also increase it. Toxins can also produce oxidative stress. ***It's true that these mechanisms can produce oxidizing free radicals. To produce oxidative stress, though, they need to overwhelm the antioxidant system. I think we have to ask how this could have happened. How did the inflammation become chronic? What gave rise to the POTS? How were the toxins allowed to build up? The answers to these questions very likely are that there is something wrong with the glutathione function, since it forms the basis of the body's antioxidant system. ***Concerning the recent CDC paper, yes, I saw it, and thank you for posting it. I commented on it in another post a little while ago. As you can see from that post, I think this hypothesis fits some of the data reported in that paper. > > Heart failure can come from diastolic or systolic cardiomyopathy or both. They often occur together but the PROCESS, when you come down to the individual cells, is the same. I'm obviously not an expert but I dont believe it matters what causes the problem, a virus, a heart attack due to blockage of the arteries or whatever a major problem remaining, uninjured heart cells cannot handle the increased load put on them and they compensate for this by enlargening. This works for awhile but in the end fails as fibrous material replaces the dead cells and it loses its elasticity and stiffens and becomes unable to eject blood from it (systolic) or to fill properly with blood (diastolic). ***In terms of figuring out what to do about it, I think it matters very much what causes the problem. It may not be in CFS that heart muscle cells have been killed off, leaving the remaining ones with too large a task, as in conventionally understood heart failure. It may be that the heart muscle cells are still there in high enough numbers, but their mitochondria are not able to produce ATP fast enough to support normal diastolic function. I think that's what Dr. Cheney is suggesting. Rich Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 5, 2006 Report Share Posted February 5, 2006 rvankonynen <richvank@...> wrote: The problem is that as we get more studies with GSH it gets more and more difficult to find evidence at least in the scientific literature that it is depleted and your explanations to account for that have to get more and more convoluted - as in the definition is now the problem or that CFS patients have polymorphisms that inhibit GSH uptake. The definition certainly is a problem but as I noted in a earlier post that even with a problematic definition we are still finding some consistent abnormalities in CFS. That we are not finding anything approaching depleted GSH in studies of CFS patients suggests it is not a central finding in CFS - that it is not found in a 'substantial subset' of CFS patients. I was really surprised when you said that there are no epidemiology tests that will indicate whether the mercury in vaccines caused autism! You're just throwing science away at that point. If epidemiological studies continue to show no effects of mercury in vaccines - even if there are minor flaws in those studies - at some point the evidence becomes overwhelming and everybody, except for those who are sure, who know in their heart that mercury did it, will be convinced. ***It's true that these mechanisms can produce oxidizing free radicals. To produce oxidative stress, though, they need to overwhelm the antioxidant system. I think we have to ask how this could have happened. How did the inflammation become chronic? What gave rise to the POTS? How were the toxins allowed to build up? The answers to these questions very likely are that there is something wrong with the glutathione function, since it forms the basis of the body's antioxidant system. & & & I dont think its necessary that the antioxidant system be depleted for antioxidant stress to overwhelm it. There are limits to every system; theres only so much each system can do - thats why the body breaks down isnt it? SOme system, the immune system or whatever just can't deal successfully with whatever is perturbing it. Of course we have to ask how that happened. A 'smoldering' infection could cause chronic inflammation, there could be a problem with the lipid metabolism - I'm sure there are many things that could cause a chronic inflammatory state; there are many diseases in which that state exists; heart disease, arthritis, diabetes, neurological diseases - there are lots of them and there are separate answers for each. That doesnt mean some treatments won't be helpful for many of them. ***Concerning the recent CDC paper, yes, I saw it, and thank you for posting it. I commented on it in another post a little while ago. As you can see from that post, I think this hypothesis fits some of the data reported in that paper. > > Heart failure can come from diastolic or systolic cardiomyopathy or both. They often occur together but the PROCESS, when you come down to the individual cells, is the same. I'm obviously not an expert but I dont believe it matters what causes the problem, a virus, a heart attack due to blockage of the arteries or whatever a major problem remaining, uninjured heart cells cannot handle the increased load put on them and they compensate for this by enlargening. This works for awhile but in the end fails as fibrous material replaces the dead cells and it loses its elasticity and stiffens and becomes unable to eject blood from it (systolic) or to fill properly with blood (diastolic). ***In terms of figuring out what to do about it, I think it matters very much what causes the problem. It may not be in CFS that heart muscle cells have been killed off, leaving the remaining ones with too large a task, as in conventionally understood heart failure. It may be that the heart muscle cells are still there in high enough numbers, but their mitochondria are not able to produce ATP fast enough to support normal diastolic function. I think that's what Dr. Cheney is suggesting. & & & & There again - what a tricky problem! the heart cells are depleted enough so that they are functioning poorly but not depleted enough so that they die off. Thats a pretty fine line to walk. Idont think that anyone has suggested other that than CHeney. Who knows maybe he's right - thats the generalist chronic illness type of scenario. It is interesting that and somebody have benefited from chelation; who knows maybe we are all accumulating toxins that interfer with alot of bodily functions and that depending on where you store them is where you will get your symptoms. Could that BE CFS? Or is that a problem for anyone who has a chronic disease? Rich This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 6, 2006 Report Share Posted February 6, 2006 Hi, Cort. As always, I appreciate your honest comments. My responses are below. > > The problem is that as we get more studies with GSH it gets more and more difficult to find evidence at least in the scientific literature that it is depleted and your explanations to account for that have to get more and more convoluted - as in the definition is now the problem or that CFS patients have polymorphisms that inhibit GSH uptake. The definition certainly is a problem but as I noted in a earlier post that even with a problematic definition we are still finding some consistent abnormalities in CFS. That we are not finding anything approaching depleted GSH in studies of CFS patients suggests it is not a central finding in CFS - that it is not found in a 'substantial subset' of CFS patients. ***I think that whether it will be a substantial subset remains to be shown, but I do think it will turn out to be. Concerning the issue of my explanations getting more " convoluted " to account for the observations, this is actually the normal process of the scientific method. Rarely does a perfect theory pop out of someone's head at the first instance. The scientific method involves banging the hypothesis and the observed data together and changing the hypothesis and/or finding problems in the data until agreement is obtained. In some fields of study, the experimental data can be regarded as quite solid and reliable, and then the burden is on the theoretician to match it. In other fields of study (I would say that CFS is one of them, because of the " fuzzy " case definition problem) the bases for the experimental data are somewhat murky, and it's difficult to reach firm conclusions from them. In that case, it's helpful to use a more hypothesis-driven process to try to arrive at the truth, and to look at individual cases in detail, to see if the hypothesis fits at least some of them. > > I was really surprised when you said that there are no epidemiology tests that will indicate whether the mercury in vaccines caused autism! You're just throwing science away at that point. If epidemiological studies continue to show no effects of mercury in vaccines - even if there are minor flaws in those studies - at some point the evidence becomes overwhelming and everybody, except for those who are sure, who know in their heart that mercury did it, will be convinced. ***I normally don't dwell on things like this, but I think you may have a somewhat idealized picture of how scientific research is funded, carried out and published. Please bear in mind that on this thimerosol and autism issue there is a great deal at stake for some people who are in a position to influence what work gets funded and what work gets published. If it could be shown in a way that could be used in court that the thimerosol in vaccines is what caused the huge rise in autism cases, the liability would be tremendous for the vaccine manufacturers. Can you imagine the size of a class action suit when one out of 166 kids developed autism in the U.S.? Can you imagine the desire that would be expressed for someone to " pay " for the damage done to all those children? The CDC and its vaccine committee, which approved the vaccination recommendations, and the state institutions that endorsed them would also be in a very tough spot. The whole public health enterprise as well as all the pediatricians would likewise have a big problem, since they administered all these vaccinations. It also gets very political very fast. We are facing a possible avian flu pandemic. The government very much needs the cooperation of the vaccine manufacturers to prepare for that. The vaccine manufacturers are insisting that they can't do it unless the Congress puts liability protection for them into the law. There have been a couple of attempts already to slip a clause into one of the laws (including homeland security legislation) that would give them ex post facto liability protection, including from the autism cases. This is a very high stakes issue. In this kind of a climate, it's not easy to get funding to do a study on something like this, and if you are part of an institution, there are ways of putting pressure on your institution to discourage such work. If you write something and want to get it published, you have to get it past an editor and some " peer reviewers. " Some of those peer reviewers may have very good reasons why they don't want something like that published. There are also ways of putting pressure on editors. I don't think we should be surprised that there aren't a lot of good studies published on this issue. If you want to find out about some of the skullduggery that has gone on in this area, find the paper that F. Kennedy, Jr. wrote a while back about this. I think he has evidence for the things he says there. If he didn't, he would be in big legal trouble himself, because he's taking on some powerful interests. I noticed that the DAN! people don't dwell on the thimerosol--vaccines issue. I think they are wise. Their goal is to help the kids, not to get into expensive legal battles. They could put all their resources into a long, drawn-out, expensive legal battle, and meanwhile the kids would get older and less able to be helped significantly. I think the message about thimerosol has gotten across. It's out of most of the vaccines in this country, at least. The autism rate in California has dropped for the last two and a half years. I think there will be efforts made to fuzz out the correlation between pulling the thimerosol and seeing this improvement as much as possible, because of the factors I discussed above. > & & & I dont think its necessary that the antioxidant system be depleted for antioxidant stress to overwhelm it. There are limits to every system; theres only so much each system can do - thats why the body breaks down isnt it? SOme system, the immune system or whatever just can't deal successfully with whatever is perturbing it. Of course we have to ask how that happened. A 'smoldering' infection could cause chronic inflammation, there could be a problem with the lipid metabolism - I'm sure there are many things that could cause a chronic inflammatory state; there are many diseases in which that state exists; heart disease, arthritis, diabetes, neurological diseases - there are lots of them and there are separate answers for each. That doesnt mean some treatments won't be helpful for many of them. ***These things can be viewed either from the standpoint of the offense or the defense. Western conventional medicine has chosen to focus on the offense and ways of combatting it directly. Less focus is put on the defense, which normally protects the body. This goes under the name " terrain. " I think we need more focus on the terrain. I think a great deal of disease gets the upper hand because of a breakdown in the defensive powers of the terrain. > > & & & & There again - what a tricky problem! the heart cells are depleted enough so that they are functioning poorly but not depleted enough so that they die off. Thats a pretty fine line to walk. Idont think that anyone has suggested other that than CHeney. Who knows maybe he's right - thats the generalist chronic illness type of scenario. It is interesting that and somebody have benefited from chelation; who knows maybe we are all accumulating toxins that interfer with alot of bodily functions and that depending on where you store them is where you will get your symptoms. Could that BE CFS? Or is that a problem for anyone who has a chronic disease? ***I think these are good questions. I do think that the buildup of toxins plays a big role in CFS. It certainly does when glutathione is depleted, because glutathione normally provides one of the major Phase 2 detox pathways, as well as taking care of the free radicals produced by the Phase 1 cytochrome P450 enzymes. > ***Rich Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 6, 2006 Report Share Posted February 6, 2006 Well only time will tell how all these issues get sorted out. You certainly made a good case for the high stakes involved in thimerosal. I would think however that in such a high stakes case like this which is so closely watched on both sides that studies will be done that address both concerns? Maybe thats naive but I have to believe the patients have some pull; they must have some pull because they keep doing study after study even after the study results are underwhelming for the most part. It'll certainly be interesting to see how the autism cases do in California and elsewhere. This list is intended for patients to share personal experiences with each other, not to give medical advice. If you are interested in any treatment discussed here, please consult your doctor. Quote Link to comment Share on other sites More sharing options...
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