Cardiomyopathy, Osteoporosis and the Deadlock Quartet

[Freddd]

I started checking out osteoporosis, I was amazed at what I found. As I continued looking for info on osteoporosis I found cardiomyopathy and all of usual of neurological diseases, all dependent upon multiple elements of the Deadlock Quartet. So then here we have CFS, FMS, MS, Pernicious anemia, ALS, Supra Nuclear Palsy, Subacute combined degeneration, Alzheimer’s, elevated MMA, elevated Hcy, B12 deficiency, folate deficiency are all associated with increased incidence and severity of osteoporosis and cardiomyopathy.

So how much cardiomyopathy and osteoporosis do we have around here?
I had congestive heart failure which can be a manifestation of cardiomyopathy.

l-Carnitine Fumarate and Isovaleryl-l-Carnitine Fumarate Accelerate the Recovery of Bone Volume/Total Volume Ratio after Experimetally Induced Osteoporosis in Pregnant Mice

http://link.springer.com/article/10.1007%2Fs00223-008-9109-6?LI=true

Abstract

Anabolic skeletal agents have recently broadened the therapeutic options for osteoporosis by directly stimulating bone formation and improving bone turnover, bone density, bone size, and bone microarchitecture. We recently demonstrated that two new l-carnitine derivatives, l-carnitine fumarate (LC) and isovaleryl-l-carnitine fumarate (Iso-V-LC), stimulated osteoblast proliferation and differentiation. We here investigated, by histomorphometry in a mouse model of osteoporosis, the impact of these compounds on the repair of trabecular bone and the osteoblast involvement in this process. Fifty-nine inbred adult female CD1 mice in pregnancy were assigned to four treatment groups: (1) controls, mice fed a standard normocalcemic pre- and postpartal diet; (2) Hypo, mice fed a low-calcium isocaloric prepartal diet and a standard postpartal diet; (3) LC, mice fed a group 2-type diet supplemented post-partum with LC; (4) Iso-V-LC, mice fed a group 2-type diet supplemented post-partum with Iso-V-LC. Bone volume/total volume ratio (BV/TV), bone perimeter, osteoblast surface/bone surface, and osteoblast number/bone surface were measured from sections of L3 and L4 vertebral bodies obtained from animals killed on the day of delivery (controls and Hypo) and on days 7, 14, and 21 after delivery (all groups). BV/TV and all osteoblast-based indexes were significantly higher in LC and Iso-V-LC than in Hypo mice at each time point, and Iso-V-LC at the end of the treatment attained levels observed in controls. In conclusion, Iso-V-LC and, to a lesser extent, LC accelerated the recovery of normal BV/TV level after a hypocalcemic diet.

L-Carnitine and Isovaleryl L-Carnitine Fumarate Positively Affect Human Osteoblast Proliferation and Differentiation In Vitro



http://link.springer.com/article/10.1007%2Fs00223-004-0147-4?LI=true

Abstract


Age-related bone loss is characterized by decreased osteoblast activity, possibly related to the reduction of energy production. Carnitine promotes energy availability and its concentration declines with age; Therefore, two Carnitine derivatives, L-carnitine fumarate (LC) and isovaleryl L-carnitine fumarate (Iso-V-LC), have been tested on several parameters of human osteoblasts in vitro. Both compounds significantly increased osteoblast activity, but the new compound Iso-V-LC was more efficient than LC at lower concentrations. They both significantly enhanced cell proliferation, [3H]-proline incorporation and the expression of collagen type I (COLLI), and the bone sialoproteins (BSPs) and osteopontin (OPN). The percentage of alkaline phosphatase (ALP)–positive cells and the secretion of osteocalcin were not modified by LC and Iso-V-LC. Both molecules increased the formation of mineralized nodules, but Iso-V-LC reached the maximum effect at a concentration 10-fold lower than that of LC. Furthermore, we showed that insulin-like growth factor (IGF)-I and IGF-II mRNA levels were not modified by the treatment. However, the two compounds induced an increase of insulin-like growth factor binding protein (IGFBP)-3 and a decrease of IGFBP-5 in both osteoblast lysates and the extracellular matrix (ECM). In conclusion these data suggest that carnitine and, in particular, its new derivative, Iso-V-LC supplementation in the elderly may stimulate osteoblast activity and decrease age-related bone loss.

Press on the “look inside” button and at the top of the right half of the page. It explains that osteoblast used to thought of as using glucose for energy. It turns out they use fatty acid (transported by LCF) oxidation in mitochondria with AdoCbl to produce the cells that grow bone. Another assumption hits the dust. A few years ago a study was published that linked MeCbl to decreased second hip fractures in elderly women, implied improved bone density. I hypothesized at the time it was increased osteoblast activity from better cell reproduction and methylation. This adds a whole new perspective. This was published in 2004. Put it together it sure looks like it’s the Deadlock Quartet that could possibly prevent or heal osteoporosis



From a study published in 1994

“We find that PD patients have a higher incidence of severe osteoporosis”

http://europepmc.org/abstract/MED/8190408

ABSTRACT

Bone mineral density (BMD) in 22 patients (three females, 19 males, aged 58-76 years) with idiopathic Parkinson's disease (PD) was measured by dual photon absorptiometry (DPA) using a M&SE OsteoTech 300 scanner. The BMDs of the 2nd to 4th lumbar vertebrae were measured and the mean density was presented as g cm-2. The BMD of the PD patients was compared with normal BMD values within the same age groups, and the patients were interpreted as normal, suffering mild osteoporosis or severe osteoporosis. The patients were divided into two groups according to (a) the Hoehn and Yahr (H-Y) scale as high or low, or based on (b) the duration of the disease as long or short, for comparison. The prevalence of abnormal BMD in each subgroup of patients was calculated. The results show that the BMD of all the PD patients was lower than those of the normal controls. The PD patients with a high H-Y scale had a higher prevalence of severe osteoporosis. However, the difference between any two groups, separated by the two criteria, is not significant by Fisher's test. We find that PD patients have a higher incidence of severe osteoporosis.



http://www.amjmed.com/article/S0002-9343(05)00151-8/abstract



Homocysteine as a predictive factor for hip fracture in elderly women with Parkinson’s disease

Abstract

Purpose

Incidence of hip fractures among elderly patients with Parkinson’s disease is high. Recent studies have found that levodopa induces hyperhomocysteinemia in Parkinson’s disease. Hyperhomocysteinemia is considered to be a risk factor for osteoporotic fractures in elderly men and women. Very high plasma homocysteine levels are a feature of homocystinuria, characterized by the early onset of osteoporosis. To determine the association between plasma homocysteine concentration and the risk of hip fracture in Parkinson’s disease patients receiving levodopa, we prospectively studied a cohort of elderly women with Parkinson’s disease.

Methods

We studied 199 elderly women with Parkinson’s disease receiving levodopa therapy, from whom blood samples had been obtained to measure plasma homocysteine. Age-adjusted incidence rates of hip fractures were calculated for quartiles of plasma homocysteine concentrations. Cox proportional-hazard regression was used to calculate hazard ratios for quartiles of homocysteine values.

Results

The mean duration of follow-up was 4.9 years. Hip fractures occurred in 66 patients. The age-adjusted incidence rates per 1000 person-years for hip fractures, from the lowest to the highest quartile of plasma homocysteine levels, were 1.59 (95% confidence interval [CI], 1.01-2.24), 1.57 (95% CI, 0.98-2.19), 1.21 (95% CI, 0.61-1.72), and 26.98 (95% CI, 16.48-37.24). The risk of hip fractures was greater in the highest quartile than that in the lowest, and the risk was almost 2.4 times higher.

Conclusion

These findings suggest that the homocysteine concentration is an important risk factor for hip fractures in Parkinson’s disease patients receiving levodopa.



The role of nutrition in osteoporosis.

http://europepmc.org/abstract/MED/7881322

low intakes of vitamin D--and possibly magnesium, boron, fluoride and vitamins K, B12, B6 and folic acid (particularly if co-existing)--may pre-dispose to osteoporosis

Osteoporosis-related bone fractures are a significant cause of mortality and morbidity, with women being particularly affected. Osteoporosis is a condition of bone fragility resulting from micro-architectural deterioration and decreased bone mass; adult bone mass depends upon the peak attained and the rate of subsequent loss; each depends on the interaction of genetic, hormonal, environmental and nutritional factors. An adequate supply of calcium is essential to attain maximum bone mass, and adult intakes below about 500 mg/day may predispose to low bone mass. Supplementation with calcium may conserve bone at some skeletal sites, but whether this translates into reduced fracture rates is not clear. Chronically low intakes of vitamin D--and possibly magnesium, boron, fluoride and vitamins K, B12, B6 and folic acid (particularly if co-existing)--may pre-dispose to osteoporosis. Similarly, chronically high intakes of protein, sodium chloride, alcohol and caffeine may also adversely affect bone health. The typical Western diet (high in protein, salt and refined, processed foods) combined with an increasing sedentary lifestyle may contribute to the increasing incidence of osteoporosis in the elderly.

http://www.biomedcentral.com/1471-2318/11/80/

Study protocol

Rationale and design of the B-PROOF study, a randomized controlled trial on the effect of supplemental intake of vitamin B12 and folic acid on fracture incidence


Osteoporosis is a major health problem, and the economic burden is expected to rise due to an increase in life expectancy throughout the world. Current observational evidence suggests that an elevated homocysteine concentration and poor vitamin B12 and folate status are associated with an increased fracture risk. As vitamin B12 and folate intake and status play a large role in homocysteine metabolism, it is hypothesized that supplementation with these B-vitamins will reduce fracture incidence in elderly people with an elevated homocysteine concentration.

The results of this study will be available later in 2013.



In the B-PROOF study, you can go read the protocol at the link above; they even apologize for using two nutrients, folic acid and B12. They leave out the apparently critical factor of l-carnitine fumarate and use the worst possible forms of folate and b12. No wonder research results are so inconsistent.

 

[dbkita]

Interesting. The last study would be of interest for sure. Sadly there is no correlation between BMD and fracture incidence despite all the papers. Went to a biopharmaceutical conference where that was made abundantly clear by clinicians. Ironic since people still keep popping the bisphosphonates. Much the discussion centered on vitamin D control, especially balance of inactive and active forms. It is good though to see more focus on stimulating osteoblasts as opposed to deactivating osteoclasts (which has been the norm so far and pretty unsuccessful sadly).

 

[MeSci]

I would guess that a correlation between CFS and osteoporosis could be due to our tendency to mineral deficiency. I had what appeared to be clear signs of deficiency-related tooth and bone problems after a severe episode of hyponatraemia that landed me in hospital, so I was clearly losing a lot of sodium, and probably other minerals too. I am pretty sure that the losses are largely due to excessive excretion in urine.

Since I've been taking a bone mineral + Vitamin D supplement, my generalised tooth pain is almost absent (but returned for a while recently after I inadvertently upped my carb intake), and my bones feel stronger too (they too felt worse when I was over-carbed). I have only ever had one fracture in my life, and that was during the time when my teeth were hurting and crumbling and I had hyponatraemia. The fracture occurred as a result of very minor fall.

Re bisphosphonates, I asked my GP if he would send me for a bone density scan, but made the mistake of telling him there and then that I did not want to take bisphosphonates. He said that in that case he was not prepared to refer me for a scan! As though these wretched drugs are the only solution to low bone density...

 

[Freddd]

Interesting. The last study would be of interest for sure. Sadly there is no correlation between BMD and fracture incidence despite all the papers. Went to a biopharmaceutical conference where that was made abundantly clear by clinicians. Ironic since people still keep popping the bisphosphonates. Much the discussion centered on vitamin D control, especially balance of inactive and active forms. It is good though to see more focus on stimulating osteoblasts as opposed to deactivating osteoclasts (which has been the norm so far and pretty unsuccessful sadly).

Hi Dbkita,

As I mentioned in the note I made a few years make a trial of MeCbl in elderly ladies who already had one hip fracture did succeed in reducing the rate of 2nd hip fractures. That may have occurred because that deficiency of MeCbl prevents the formation of those same osteoblasts. It takes all 4 of the Deadlock Quartet to be functional in the body to make all kinds of cells.

So it would be no surprise at all if lacking the Deadlock Quartet, who's lack prevents cell formation in muscles, epithelial tissues, endothelial tissues and nerves also prevents normal bone cell growth and causes heart problems. The heart is a muscle. My muscles aptrophied and I had congestive heart failure. I rapidly corrected the muscle atrophy when the right balance was reached in the Deadlock Quartet and otehr factors. The two key factors after both cobalamins was LCF and a large enough L-metafolin dose that I wasn't in paradoxical folate insufficiency all the time.

as opposed to deactivating osteoclasts (which has been the norm so far and pretty unsuccessful sadly).

Decades of non-success can often be caused by theories that don't work, that don't pan out. As that fits the pattern of the whole group of diseases caused by the lack of any one of the quartet, one miss after another in trying to figure them out. Has the incidence of osteoporosis gone up in the same way all these diseases have in the past 40 years?What other parts of the pattern do they fit. As the studies tell us those with the serious damage done by b12s/folate/LCF deficiencies, that usual group, has damage to all sorts of tiisue, adding bone and heart to that makes a lot of sense as they appear as a frequent comorbid condition. So perhaps the frequent comorbidity could point at a common cause.

Perhaps you will solve your tissue formation problems. It took me about 4-5 years to work through all the nutritional wrinkles and then the muscle rebuilding was turned on and I grew 40-50 pounds worth, rapidly at first and then slowing down as I reached a reasonable normality, and I also don't have the same congestive heart failure. My skin is, while a lot older, a lot better without all the problems. My lungs are not reactive and inflamed and easily infected. The burning veins in my head are gone. My gut is normal. 10 Years ago no tissues I could feel or see were normal in my body. Now they all are that I know of. From not being able to walk as far as 50 feet all at once I can walk 5-10 miles including 2000-4000 feet of vertical each up and down in doing so. My suggestion to test treatments with teams matched pair teams doing whatever protocols and then having a 5k race 3 days in a row, or a timed hill hike of 5-10 miles with lots of vertical, and whichever team wins illustrates the more (or most), any number of teams could be made for suitable matched sets, effective treatment. I was figuring that one for a 3 year time period. Two might be cutting it a little close to go from FMS/CFS/ME with the triple whammy, partial methylation block, methyltrap and partial ATP block with all the most severely affected people. I'm looking for some real money sponser for such a race. A team prize of $1,000,000 would attract real attention. It would be interesting to see the protocol choices for the different teams, as that is the real competition. If one team has a much more effective protocol they would win.

I used to jog 5-10 miles about 5 days a week. No problems. Now 40 years later I can do the hiking and vertical drop. My knees are not up to jogging any mor, too many injuries. I figure a race gets more attention for fund raising. What a TV moment, hundreds of people who 3 years before were totally disabled and not able to walk around the block doing hill climbs or road races. For anybody with these diseases going the distance once, slowly might be possible, but the cost would be great. However, doing it 3 days in a row, to me anyway, proves beyond the shadow of a doubt that the person could no longer be diagnosed or have the symtpoms of FMS/ME/CFS. Such a feat just wouldn't be possible.

Doesn't that sound like fun? A fundraiser for research race, may the best protocol at healing their team win. We could allow some healthy controls to participate for a fundraising donation.

 

[Freddd]

I would guess that a correlation between CFS and osteoporosis could be due to our tendency to mineral deficiency. I had what appeared to be clear signs of deficiency-related tooth and bone problems after a severe episode of hyponatraemia that landed me in hospital, so I was clearly losing a lot of sodium, and probably other minerals too. I am pretty sure that the losses are largely due to excessive excretion in urine.

Since I've been taking a bone mineral + Vitamin D supplement, my generalised tooth pain is almost absent (but returned for a while recently after I inadvertently upped my carb intake), and my bones feel stronger too (they too felt worse when I was over-carbed). I have only ever had one fracture in my life, and that was during the time when my teeth were hurting and crumbling and I had hyponatraemia. The fracture occurred as a result of very minor fall.

Re bisphosphonates, I asked my GP if he would send me for a bone density scan, but made the mistake of telling him there and then that I did not want to take bisphosphonates. He said that in that case he was not prepared to refer me for a scan! As though these wretched drugs are the only solution to low bone density...

Hi MeSci,

The biochemistry of the body gets totally messed up in CFS/FMS/etc. The lack of sufficient active b12s and folate and LCF makes hundreds if not thousands of things go wrong. If it directly fouls up 600 reactions, how many secondary reactions and tertiary reactions get screwed up too?

What I am wondering is how osteoporosis is represented in our population here and if anybody doing methylation etc protocols has had any improvment. Based on the research already done the prefered forms would be MeCbl and LCF at the least, as they have each demonstrated better cell formation. But then, comparing A-B-C-D variations can be very informative. For my loved ones to whom I'm giving advice I would place my real life "you bet your life" I would suggest the Deadlock Quartet on the chance that is the answer. I found all this going looking for what makes l-carnitine fumarate apparently more effective for more people with our disorders, but not everybody.

I started taking "Salmon oil" as soon as it was available, and watched it evolve to Omega3 oils and now 25 years later I know why it was a good idea. I'm still betting on mixed factor high gamma E. I started lecitihin 40 years ago. Now I know why it was a good idea. They were all just bets I placed on my future.

This testing thing you mention is a problem throughout medicine. When my doc suggested a sleep study and then wanted to prescribe one of the new at the time atypical antipsychotics, Zyprexa as a sleep aid. Without that agreement no sleep study. I refused Zyprexa as being outside my risk range. I didn't need more toxic drugs with horrid side effects, especially a couple of dozen that were already problem symtpoms. I did not want a cascade of drugs each additional for controling side effects of the previous bunch and introdiucing new ones. We settled on Provigil to keep me from falling asleep in approproately at dinner or driving. My pharmacy bill was already $1500/month self pay. Adequate pain treatment turned out to be a decent partial solution to my sleep proble and MeCbl and l-methylfolate and AdoCbl and LCF fixed all my sleep problems. My pharmacy bill now, not including vitamins, is under $75/month.

I also don't take any medications any more with a measurable "drop dead" rate these days. I used to take Dilantin for decades, controling neurological pain, quite well I may add. It had undesirable side effects including affecting folate/b12. It also had a 1:1,000,000 or so drop dead suddenly without obvious cause rate. So do many of these meds advertised on TV these days.

The problem I see is that IF the deadlock quartet is the answer, until all that b12 and folate research is repeated with the real active b12s and folate, researchers will come up with bisphosphonates and other similar things based on forcing certain things instead of normalizing them and causoing massive and terrible side effects in many cases and not working all that well. The pharmaceutical business is lookikng for the next billion dollar a year profit drug for maintenance of illness, not cures.

 

[alex3619]

On forcing cures: in heart disease angioplasty, stents etc, as well as drugs for arhythmia, were all touted as fantastic solutions - each corrected the problem they were designed to. Survival times either did not improve much or got worse, depending on the treatment. This is because they forced a solution on the body and secondary interactive factors were ignored. My bet is that Vioxx had the same issue - it was so effective it substantially eliminated a whole class of hormones. Drugs can work, but its overall improvement in the patient that is the primary marker for success, not just correcting the immediate problem. Medical researchers often do not use quality of life or overall survival time as markers.

Fixing the underlying problem is critical, but to be sure of fixing it we need to understand it and measure success. With methylation protocols we are getting there, but I don't think we are quite there yet. Ten or twenty years from now I do suspect many doctors will be talking about methylation protocols and prescribing methyl folate and B12 etc. It just requires research to get there - though that can be slow or lacking in natural products. However there is no reason a drug company cannot package all the nutrients in a single pill and patent the formula, presuming they can get around some of the absorption issues.

Freddd, you took salmon oil in 1988? That beats me by five years, I started trialing omega-3 fats for ME in about 1993.

 

[Freddd]

On forcing cures: in heart disease angioplasty, stents etc, as well as drugs for arhythmia, were all touted as fantastic solutions - each corrected the problem they were designed to. Survival times either did not improve much or got worse, depending on the treatment. This is because they forced a solution on the body and secondary interactive factors were ignored. My bet is that Vioxx had the same issue - it was so effective it substantially eliminated a whole class of hormones. Drugs can work, but its overall improvement in the patient that is the primary marker for success, not just correcting the immediate problem. Medical researchers often do not use quality of life or overall survival time as markers.

Fixing the underlying problem is critical, but to be sure of fixing it we need to understand it and measure success. With methylation protocols we are getting there, but I don't think we are quite there yet. Ten or twenty years now I do suspect many doctors will be talking about methylation protocols and prescribing methyl folate and B12 etc. It just requires research to get there - though that can be slow or lacking in natural products. However there is no reason a drug company cannot package all the nutrients in a single pill and patent the formula, presuming they can get around some of the absorption issues.

Freddd, you took salmon oil in 1988? That beats me by five years, I started trialing omega-3 fats for ME in about 1993.

Hi Alex,

Freddd, you took salmon oil in 1988? That beats me by five years, I started trialing omega-3 fats for ME in about 1993.

I'm not sure of the year but it was the year it came out. I started lecithin back in the mid to late 70s. You might say I married into it. My MIL Had a complete collection of the old Rodale Prevention and all the Adelle Davis books. I started witth vitamin C 2 grams in 1972, which put a complete stop to a drug resistant a persistant urinary tract infection I had for almost 2 years and incidently decreased my incidence of streps by about 90%. I've been working on this for that long, thanks to my MIL. It was Adelle Davis that headed me towards the desiccated liver and the b12/folate questions research for my symptoms.


Ten or twenty years now I do suspect many doctors will be talking about methylation protocols and prescribing methyl folate and B12 etc. It just requires research to get there - though that can be slow or lacking in natural products

I was astonishingly naive back in 1979, when I found out that it was the 20th annaversery of the discovery of the two REAL b12s, that CyCbl was a lab error that has cost millions our health and trillions of healthcare dollars. I was already consulting to HMOs then, mostly about how to use computers to collect the info needed for data mining, converting all medical records to forms that could give to results oriented data, much as they are STILL trying to do. I don't find any convincing argument that we can expect any change loke that in 10 or 20 more years. I expected that in 1979. It has been 54 years that science has known of the real b12. We still don't have any proper A-B trials. Researchers have no idea of the Deadlock Quartet and the most limiting factor idea. The osteoblast "proliferation" I think is misinterpreted. Instead I would say that with the LCF there was now the possibility of building mitochondria and hence a cell. This is what happens with muscle cells, and I woulld bet my bottom dollar that applies to cardiac muscle as well, and osteoblasts that FINALLY are understood to produce much of their own ATP for what they do, and they need a LOT of energy. So do cardiac muscle cells. Instead of proliferating the use of AdoCbl, MeCbl and L-methylfoalte they are trying to bury them forever with Codex Alimentaris and in the USA a regression of supplments to 1992 before any of them were available. That avoids the embarassment of how stupidly the researchers have been researching all this coming to the conclusion that CyCbl, HyCbl and folic acid is all we ought to be able to get without prescriptions that would rarely be available. We have been one senate vote away from being able to continue to use these things for years now. That is one good thing Senator Hatch has done, protect our right to use supplements. Much of the Senate is for taking that away from us. That would drive MeCbl. AdoCbl and maybe L-methylfolate underground. However, as l-methylfolate has been through the full pharmaceutical treatment it might survive. That is the one loophole in the pre 92 law. A correspondent of mine in Norway has told be that her calcium supplement that used to cost $3/month at the supermarket now costs $88/month as a prescription. I can't afford $400/month for the MeCbl injections and whatever AdoCbl would cost. That is much worse because it is completely unstable in aqeous solution. I can't afford $4000/month or whatever for what I take. The doses would also be very limited by law and to get effective substances and amounts would require a prescription for each one. It would make it impossible to do trials as we ahave been doing.

In looking at how long it takes to understand and use properlly the vitamins involved takes about 70 years. So now 70 years in we know how BAD folic acid is. MeCbl and AdoCbl were intoduce in 1998 or later. Let's see, that comes out to 2068 when we might expect it to be as effective used as everybody here knows even if they don't believe it. Doing all the trials I have done in a peer journal acceptable manner (but NOT acceptable to Institutional Review Boards) would take more than 100 years. I talk to researchers. I have presented designs to them. I have been told that they would very much like to do such BUT it would never get by the IRB. The problems is SO MANY DIFFERENT THINGS. The FDA is all about testing ONE PURE SUBSTANCE. That is one reason cannabis is a problem but will end up being dozens of big money drugs. Then to have everything done by titration, to recognize induced deficiencies and make adjustments in doses would have to have each separate item done 1 at a time each taking several years at best. You have no idea how barricaded the system is against these things. Expecting 1 pure item is what led them astray in the 40s figuring out what "protein mystery factor" acutally was that gave miraculous effects. Then when I tell them that they should select their trial population so as to get 95%+ results they tell me that first the selection system has to be validated and the links proven.

Right now from a questionaire I can predict a response to MeCbl, AdoCbl, L-methylfolate and LCF at least at a 95% rate. I'm saying "response", not whether the person thinks it is healing or "detox" or any other name for the response. People without symptoms, selected for the control group, would be needed to show NO RESPONSE without appropriate symptoms. The problem is right now I say there are 400 relevant symtpoms, not 10-30. So what are all the rest, mystery disease? People get upset and say it must be crookedly rigged to get near 100% response. Why would it? I call that a demonstration of understanding the basis of the problem. I think we need to make this what "everybody knows" before the lawmakers and chemical industry make it illegal. The manufacturers wrote Codex Alimentarus. It is NOT for your or my good health. It protects markets, not health


Medical researchers often do not use quality of life or overall survival time as markers.

I know. That is one of the worst design flaws. For those of us living in hell, which I'm not any more, but I have a lot of empathy for all that are having spent way to much of my life in that way. That is part of the problem of going after "proof" like a specific test result of a one specific biological reaction. They get drugs that may completly wipe out a pathway causing all sorts of other problems worse than it fixes. And of course since what they are tweaking isn't a cause but a secondary or teriatary reaction from the real problem, there don't solve the problem and cause all sorts of side effects. In this real naked eye healing is what we, the afflicted want. We want to live a good life not in misery. We want to be ABLE to "Life, Liberty and the pursuit of happiness".

 

[alex3619]

Freddd, I suspect I may be too optimistic as well. Psychogenic illness has been promoted for a century of a half, given privilege under law by virtue of considering the doctors diagnosing it as experts, and generally making life hell for those misdiagnosed with it. Helicobacter pylori took 108 years to be recognized as the cause of gastrointestinal ulcers, as I describe in one of my blogs. However with some solid findings by Dr. Barry Marshall it only took 10-20 years for H. pylori to go from an obscure bacteria to the known cause and be treated accordingly. Thats what it takes. One brave researcher who stands up to the system and proves how wrong everyone else is. He shared a Nobel prize for that. I keep hoping to see more researchers like him, but they are a rare breed.

 

[Freddd]

Hi Alex,

Medicine as a whole has been far more effective and efficient on bacterial caused illness than on nutrition research, but not until they are recognized. Ulcers, Lyme, Legionaires, and some others were denied or ignored for years.

Yes, they tell people sufferring from b12 deficiency caused mood and personality changes and all sorts fo neuropsyc problems and tell the purson "it's all in your head", which it literally is but not pschologically caused or psychosomatic. So their dismissal of IAIYH is useless rather than saying "Oh, b12 deficiency, duh!" which is functional and helpful.