3 ms·

>The thought is her osteoporosis was likely caused by the cells leaching nutrients from the bones as they couldn't get them normally This is not how it works.

>The thought is her osteoporosis was likely caused by the cells leaching nutrients from the bones as they couldn't get them normally This is not how it works. When a cell has a metabolic defect, it is unable to use much of the substrates readily available in the blood stream (glucose, lipids). And of course such a cell cannot "leach" nutrients from the surrounds as its substrate absorption ability is seriously diminished. I suppose there is another process going on. It is an old good inflammation - in this case, an autoimmune reaction of the body to its own metabolically subpar cells. When such a "metabolic" inflammation occurs, it tends to target blood vessels of all sizes, causing the gradual dysfunction of their endothelium. With time, this induces a state similar to disseminated intravascular coagulation, although in a much milder form. This causes chronic problems with blood flow due to micro-clotting, which in turn affects nutrients delivery. This induces foci of tissue hypoxia, furtherly aggravating mitochondrial dysfunction at those areas. The immune system senses that and tries to "fix" it by inducing even more inflammation, but everything this does is causes such foci to spread even further. This is never a static process and it cannot be stopped without medications, causing a gradual quality decline of patient's life through months/years. Sometimes it affects bigger arteries and veins, causing more pronounced defects such as thrombophlebitis. But in any way, bone tissue needs nutrients delivered by the blood flow as well and when it is compromised on either level, bones start to degenerate. You can now see the whole picture of how a mitochondrial disease can induce such a seemingly unrelated condition as osteoporosis. Besides the bones, it can affect any organ in the body, especially those having high demands in energy (ATP), such as nervous system, liver, heart, muscles. Сhances are that your wife may have some other manifestations as well, especially neurological ones. The condition can be managed and even cured if the mitochondrial dysfunction is not caused by a genetic defect. If you are interested in details then let me know and I will provide the framework for a protocol.

Steve44 4y ago
That's really interesting thank you very much. I presume my leaching comment was a drastic oversimplification of how the nutrients are processed/diverted and shows my complete lack of knowledge in this field. Looking online we're not seeing any lumpy thrombophlebitis, but there is a possibility marks on the legs are similar to what seems to be referred to as Superficial Thrombophlebitis. I don't recall any of the doctors mentioning that but perhaps that's not something they are too worried about at this stage. > causing a gradual quality decline of patient's life through months/years. She's currently getting noticeably worse over a few weeks, including breathing, and we are doing what we can to expedite the diagnosis and hopeful treatment. > If you are interested in details then let me know and I will provide the framework for a protocol. Yes please, that's very kind and I am interested in trying to understand what's going on within my bounds.
- garganzol 4y ago
  > she's currently getting noticeably worse over a few weeks, including breathing, and we are doing what we can to expedite the diagnosis and hopeful treatment Please pay attention to lactate levels in her blood work. Difficulties with breathing tell me that she may have episodes of lactic acidosis, actually I'm pretty sure she has given the other manifestations. This also means that she is B1 and/or B12 deficient. Please note that the correct blood test for B1 deficiency is the test for transketolase activity which is rare and quite expensive. Not those quantitative B1 tests that show literally nothing. This may be a gotcha for lots of people with actual B1 deficiency but whose B1 quantitative levels are ok. This is a typical situation of concern for a condition known as mitochondrial dysfunction. The most widely-known cause of induced mitochondrial dysfunction is malnutrition, see Beriberi. Another common cause is the episodes of hypoxia or ischemia. The B12 deficiency can be detected quite easily in the widely accessible blood work. It leads to anemia and may induce mitochondrial dysfunction as well. Once mitochondrial dysfunction is induced there is no way out without the medical intervention. Here is the framework of a treatment for a patient with induced mitochondrial dysfunction: a) Slightly suppress the inflammation b) Slightly anti-coagulate the blood c) Fix the induced condition (osteoporosis) d) Fix other induced conditions. Heart, liver are most-commonly affected, a close attention should be paid to them. e) Gradually repair the damage of mitochondrial apparatus while reducing tissue hypoxia All these actions should be undertaken in parallel, not one by one. And here is a practical example of how I would treat her, for reference: 1. CoQ-10 60 mg + Alpha-lipoic acid 60 mg, should be taken at least 30 minutes before the first meal, daily. 2. Multivitamin*** + B1** (Thiamine Chloride, HCL) 250 mg + Benfotiamine 300 mg + Magnesium 100 mg + D3* 5000 I.U. + K2 MK7 100 mcg, right after the first meal, daily. 3. B3 (Nicothinamide Riboside or Nicothinamide) 100 mg, on an empty stomach between the first and second meals, daily. 4. Aspirin 300-500 mg or Ibuprofen 400 mg (but not both) right after the second meal, once in 2-4 days. These medicals represent a so-called mitochondrial cocktail with an addition of NSAID. Osteoporosis may require additional calcium supplementations. Besides the medicals, the diet correction is obligatory. Lower the consumed sugar levels to less than 50 grams per day. Exclude the foods with glycemic index >= 50 from the everyday diet. There should be 3 meals: morning, day, evening. Do not overeat and do not be hungry. Prioritize quality fat products to hydrocarbonates (look at ketogenic diets for inspiration). Recommended everyday products: milk, eggs, meat, tomatoes, cucumbers, peppers, paprika, avocado, fatty fumed/salted fish (salmon, trout), black rice (not brown and not white!), barley porridge, cheese. Totally exclude tea and coffee. Avoid processed foods as they are poor in nutrients and may contain things like MSG which would cause neurotoxicity in patients with mitochondrial dysfunction. Besides the medicals and diet, a life style corrections should be made. Everyday relaxed 45+ minutes walks are obligatory, but be sure that you have no bone pains in your feet. If you do, supplement with calcium and ensure that the specific pains go away before starting new physical activity sessions. Worries and responsibilities should be left behind. It is recommended to take at least 2 weeks sabbatical and devote it to the health. Treatment progress control: after the first paradoxical reactions a patient should start to feel considerably better, and should continue to do that week after week. Sometimes there will be bitter regressions, but the overall course of treatment should be positive. Blood work to pay attention to: lactic acid, transketolase, glucose, A1c, HOMA-IR, triglycerides, low-density lipoprotein (LDL), gamma-glutamyl transferase (GGT) and other hepatic markers. Be sure to exclude anemia. The closer the blood work to the norm, the better the person will feel. * Periodically check the D3 levels in blood work to not become higher than normal, if it is then exclude D3 and K2 MK7. ** Therapeutical doses of B1 vitamin and vitamins in general may cause strong paradoxical reactions. Paradoxical reaction is when a patient perceives an imaginary worsening despite the fact that his condition is being improved. This means that the very first vitamin doses should be very small, just the tiniest pieces of a tablet, you can scrape them with a knife. Then the doses should be gradually increased to the recommended levels [1]. *** Multivitamin should contain Manganese. For example [2]. This protocol is for reference only and works better when it is adjusted to the conditions of a particular patient. The treatment takes months and sometimes years, depending on the age of the condition. [1] https://www.hormonesmatter.com/refeeding-syndrome-thiamine-deficiency/ https://www.hormonesmatter.com/refeeding-syndrome-thiamine-d... [2] https://www.doppelherz.com/products/a-z-depot https://www.doppelherz.com/products/a-z-depot
Madmallard 4y ago
Is there somewhere I can message or email you? I suspect mine is not genetic as like I said I abruptly lost a lot after the fluoroquinolones. It has been 8 years since and I gradually developed what seems like a mast cell disorder on top of it causing severe difficulties not becoming malnourished. It sounds like it could be caused by the same process you described. As far as I’ve read about mito protocols, they were mostly shots in the dark rather than things that predictably worked. I’m talking about mito cocktails and such for mito patients, various forms of vitamin E and selenium, ketogenic diets, and exercise training.
- garganzol 4y ago
  Earlier today I stumbled upon the article describing an induced mitochondrial dysfunction after antibiotics intake: [1] [1] https://www.hormonesmatter.com/with-thiamine-paradox-symptoms-patience-is-key/ https://www.hormonesmatter.com/with-thiamine-paradox-symptom... P.S. If you want to chat write to: alex -at- zodiac.herald.icu

Steve44 4y ago

That's really interesting thank you very much. I presume my leaching comment was a drastic oversimplification of how the nutrients are processed/diverted and shows my complete lack of knowledge in this field. Looking online we're not seeing any lumpy thrombophlebitis, but there is a possibility marks on the legs are similar to what seems to be referred to as Superficial Thrombophlebitis. I don't recall any of the doctors mentioning that but perhaps that's not something they are too worried about at this stage. > causing a gradual quality decline of patient's life through months/years. She's currently getting noticeably worse over a few weeks, including breathing, and we are doing what we can to expedite the diagnosis and hopeful treatment. > If you are interested in details then let me know and I will provide the framework for a protocol. Yes please, that's very kind and I am interested in trying to understand what's going on within my bounds.

garganzol 4y ago
> she's currently getting noticeably worse over a few weeks, including breathing, and we are doing what we can to expedite the diagnosis and hopeful treatment Please pay attention to lactate levels in her blood work. Difficulties with breathing tell me that she may have episodes of lactic acidosis, actually I'm pretty sure she has given the other manifestations. This also means that she is B1 and/or B12 deficient. Please note that the correct blood test for B1 deficiency is the test for transketolase activity which is rare and quite expensive. Not those quantitative B1 tests that show literally nothing. This may be a gotcha for lots of people with actual B1 deficiency but whose B1 quantitative levels are ok. This is a typical situation of concern for a condition known as mitochondrial dysfunction. The most widely-known cause of induced mitochondrial dysfunction is malnutrition, see Beriberi. Another common cause is the episodes of hypoxia or ischemia. The B12 deficiency can be detected quite easily in the widely accessible blood work. It leads to anemia and may induce mitochondrial dysfunction as well. Once mitochondrial dysfunction is induced there is no way out without the medical intervention. Here is the framework of a treatment for a patient with induced mitochondrial dysfunction: a) Slightly suppress the inflammation b) Slightly anti-coagulate the blood c) Fix the induced condition (osteoporosis) d) Fix other induced conditions. Heart, liver are most-commonly affected, a close attention should be paid to them. e) Gradually repair the damage of mitochondrial apparatus while reducing tissue hypoxia All these actions should be undertaken in parallel, not one by one. And here is a practical example of how I would treat her, for reference: 1. CoQ-10 60 mg + Alpha-lipoic acid 60 mg, should be taken at least 30 minutes before the first meal, daily. 2. Multivitamin*** + B1** (Thiamine Chloride, HCL) 250 mg + Benfotiamine 300 mg + Magnesium 100 mg + D3* 5000 I.U. + K2 MK7 100 mcg, right after the first meal, daily. 3. B3 (Nicothinamide Riboside or Nicothinamide) 100 mg, on an empty stomach between the first and second meals, daily. 4. Aspirin 300-500 mg or Ibuprofen 400 mg (but not both) right after the second meal, once in 2-4 days. These medicals represent a so-called mitochondrial cocktail with an addition of NSAID. Osteoporosis may require additional calcium supplementations. Besides the medicals, the diet correction is obligatory. Lower the consumed sugar levels to less than 50 grams per day. Exclude the foods with glycemic index >= 50 from the everyday diet. There should be 3 meals: morning, day, evening. Do not overeat and do not be hungry. Prioritize quality fat products to hydrocarbonates (look at ketogenic diets for inspiration). Recommended everyday products: milk, eggs, meat, tomatoes, cucumbers, peppers, paprika, avocado, fatty fumed/salted fish (salmon, trout), black rice (not brown and not white!), barley porridge, cheese. Totally exclude tea and coffee. Avoid processed foods as they are poor in nutrients and may contain things like MSG which would cause neurotoxicity in patients with mitochondrial dysfunction. Besides the medicals and diet, a life style corrections should be made. Everyday relaxed 45+ minutes walks are obligatory, but be sure that you have no bone pains in your feet. If you do, supplement with calcium and ensure that the specific pains go away before starting new physical activity sessions. Worries and responsibilities should be left behind. It is recommended to take at least 2 weeks sabbatical and devote it to the health. Treatment progress control: after the first paradoxical reactions a patient should start to feel considerably better, and should continue to do that week after week. Sometimes there will be bitter regressions, but the overall course of treatment should be positive. Blood work to pay attention to: lactic acid, transketolase, glucose, A1c, HOMA-IR, triglycerides, low-density lipoprotein (LDL), gamma-glutamyl transferase (GGT) and other hepatic markers. Be sure to exclude anemia. The closer the blood work to the norm, the better the person will feel. * Periodically check the D3 levels in blood work to not become higher than normal, if it is then exclude D3 and K2 MK7. ** Therapeutical doses of B1 vitamin and vitamins in general may cause strong paradoxical reactions. Paradoxical reaction is when a patient perceives an imaginary worsening despite the fact that his condition is being improved. This means that the very first vitamin doses should be very small, just the tiniest pieces of a tablet, you can scrape them with a knife. Then the doses should be gradually increased to the recommended levels [1]. *** Multivitamin should contain Manganese. For example [2]. This protocol is for reference only and works better when it is adjusted to the conditions of a particular patient. The treatment takes months and sometimes years, depending on the age of the condition. [1] https://www.hormonesmatter.com/refeeding-syndrome-thiamine-deficiency/ https://www.hormonesmatter.com/refeeding-syndrome-thiamine-d... [2] https://www.doppelherz.com/products/a-z-depot https://www.doppelherz.com/products/a-z-depot

Madmallard 4y ago

Is there somewhere I can message or email you? I suspect mine is not genetic as like I said I abruptly lost a lot after the fluoroquinolones. It has been 8 years since and I gradually developed what seems like a mast cell disorder on top of it causing severe difficulties not becoming malnourished. It sounds like it could be caused by the same process you described. As far as I’ve read about mito protocols, they were mostly shots in the dark rather than things that predictably worked. I’m talking about mito cocktails and such for mito patients, various forms of vitamin E and selenium, ketogenic diets, and exercise training.

garganzol 4y ago
Earlier today I stumbled upon the article describing an induced mitochondrial dysfunction after antibiotics intake: [1] [1] https://www.hormonesmatter.com/with-thiamine-paradox-symptoms-patience-is-key/ https://www.hormonesmatter.com/with-thiamine-paradox-symptom... P.S. If you want to chat write to: alex -at- zodiac.herald.icu