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From Our Readers: Comments and Suggestions - 7/16/14

  [ 3 votes ]   [ Discuss This Article ]
www.ProHealth.com • July 14, 2014


From Our Readers: Comments and Suggestions - 7/16/14. Image
Image" pixbox77, freedigitalphotos.net
Re: Breaking the BDNF Blues: Dr. Courtney Craig D.C. on Natural Ways to Raise BDNF Levels in Chronic Fatigue Syndrome

Vitamin D also affects BDNF levels 

While sunlight is a major influence over BDNF, Vitamin D3 is a potent inducer of BDNF expression and it contributes to the regulation of BDNF in vivo (1, 2.). Vitamin D3 also enhances glial cell–derived nerve factor (GDNF) mRNA in vitro and in vivo. Rats pretreated with vitamin D3 had up-regulated cortical GDNF

1. Naveilhan, P., Neveu, I., Wion, D., and Brachet, P. (1996) 1,25-Dihydroxyvitamin D3, an inducer of glial cell linederived neurotrophic factor. 
Neuroreport 7(13), 2171–2175.

2. Naveilhan, P., Neveu, I., Baudet, C., Funakoshi, H., Wion, D., Brachet, P., and Metsis, M. (1997) 1,25-
Dihydroxyvitamin D3 regulates the expression of the low-affinity neurotrophin receptor. 
Brain Res. Mol. Brain Res. 44(1), 178. ~Posted by: IanH, Jun 19, 2014


Re: Plague: An Interview With Judy Mikovits

Non-HIV AIDS!

"Let's talk retro viruses, non-HIV/AIDS, ME/CFS, Lyme, Fibromyalgia, politics, and more!"

60-minutes w/ Judy Mikovits 

There's tons of research if you simply google "NON HIV AIDS" ~ Posted by: cfsboston, Jun 2, 2014
 ____________________

I don't know what happened to Dr. Mikovitz, but I have ordered her book to get her perspective. Pioneers often look and sound over the edge because they are reacting to the very real oppression they are seeing around them. After 40 years of suffering, I am not interested in being polite and not rocking the boat. As someone who once aspired to be a scientist, I couldn't be more disillusioned with the profession as a whole. ~ Posted by: anomar. Jun 18, 2014
Xenograft - graft of tissue taken from one species and grafted into another species 

John Coffin was able to produce replication competent retroviruses in only 10 days from Pre-XMRV1,2, and human kidney cells. Generation of Multiple Replication-Competent Retroviruses through Recombination between PreXMRV-1 and PreXMRV-2 – This research from Dr. John Coffin and Dr. Vinay Pathak showed that replication competent murine leukemia retroviruses can be produced in a relatively short period of time. From their abstract, “To determine their potential to generate RCRs,we transfected PreXMRV-1 and PreXMRV-2 into 293T cells and used the virus produced to infect fresh cells; the presence of reverse transcriptase activity at 10 days indicated the presence of RCRs." 

Or how about the fact they are finding Infectious MLV retroviruses in xenograft cell lines and cell lines that are just housed in the same building: Frequent Detection of Infectious Xenotropic Murine Leukemia Virus (XMLV) in Human Cultures Established from Mouse Xenografts - This research suggests that the murine leukemia retroviruses have the potential to become airborne. In their conclusion the team warned, “Laboratories working with xenograft-derived human cultures should be aware of the risk of contamination with potentially bio-hazardous human-tropic mouse viruses and their spread to other cultures.”

Another: Xenotropic MLV Envelope Proteins Induce Tumor Cells to Secrete Factors that Promote the Formation of Immature Blood Vessel - the results suggest that xenograft approaches commonly used in the study of human cancer promote the evolution of novel retroviruses with pathogenic properties.

Oh and this one is very important. It is the 1995 National Academies analysis for xenotransplantation (still in use today), which includes xenografting human and animal cells - Infectious Disease Risk to Public Health Posed by Xenografting, The possibility that infections can be transmitted from animals to humans is of concern not only because of the threat to the health of the recipient, but also because such infections may be transmissible to others, creating a public health hazard. Further, such infections may be due to previously unrecognized organisms, making detection difficult if not impossible. If the time from infection to clinical symptoms is long, the risk of widespread transmission is greater, because during this time the new organism may silently spread from person to person, as happened with human immunodeficiency virus (HIV).

Emergence of a new public health risk appears to be a two-step process (Morse, 1995). First, a new infectious agent is introduced into a given human population from other human populations, animals, or environmental exposures. Frequently these new agents are zoonoses, defined as animal microbes that can infect humans as well as the animal species from which they come. The second step is establishment and dissemination of organisms that prove to be infective and transmissible from person to person. The first step, introduction of a potentially transmissible agent into a human, could be accomplished by transplanting an organ that was infected with the agent. It is the second step of establishment and dissemination, however, that raises public health concerns, particularly if the agent is viral since current therapies for viral illnesses are limited.

Basis For Public Health Concern

Historic experience with many zoonotic diseases suggests that the potential for human infection with xenogeneic pathogens has implications for the community that extend beyond the individual transplant recipient.

“examples demonstrate that some zoonotic infections have the potential to extend beyond the individual and into the community. Thus, the risk of xenotransplant-associated infection is not restricted to the xenotransplant recipient alone. The potential for xenogeneic infections to be transmitted through human populations is real and poses a public health concern. Further, the risk for health care workers in close contact with the xenograft recipient is probably higher than for the community at large.”

The potential for the introduction of a new retrovirus into human hosts via implanted xenogeneic tissue is of public health concern due to the long period of clinical latency associated with all known human retroviral infections. This long latency period provides the opportunity for silent person-to-person transmission to occur before pathogenicity is evident.

There are concerns that xenogeneic viruses may recombine or reassort with viruses latent in human tissues and result in variants that possess either a broader host range or an increased pathogenic potential. What options are available for risk management of xenotransplant-associated infectious public health risk? One option is to eliminate all risk by avoiding all use of xenogeneic tissue in humans.

Conclusions and Recommendations

Xenotransplantation may also be valuable for the treatment of human diseases. However, it is well recognized that infectious agents can be transmitted from animals to humans and that organisms benign in one species can be fatal when introduced into other species. Further, it is known that the pathogenicity of infectious organisms can change under a variety of conditions and that the effects of infection by some organisms, such as the human immunodeficiency virus, are delayed for years or even decades. Because xenotransplants involve the direct insertion of potentially infected cells, tissues, or organs into humans, there is every reason to believe that the potential for transmission of infectious agents (some of which may not even now be recognized) from animals to human transplant recipients is real. If established in the recipient, the potential for transmission to caregivers, family, and the population at large must be considered a real threat.

However, all members of the committee agreed that some mechanism is needed to ensure attention to and reduction of the risk of infectious disease transmission. ~Posted by: Robyn_E, Jun 20, 2014


Re: Brain imaging reveals clues about chronic fatigue syndrome

Clarification needed

I'm wondering which definitions was used by the researchers? The Cdn definition is highly restrictive. Persons diagnosed with ME are usually experiencing a more severe form of the disease. If persons with depression show the same areas of the brain as inflamed this would make the study unuseful for understanding and treating ME. It was the last paragraph that raised the issue of study on depressed persons that made me wonder how valid and reliable the research is. Could we have this claried? ~ Posted by: Beverlyjthomson@me.com, Jun 21, 2014

Re: Call for Congressional Hearing on Treatment for ME/CFS

I want to testify

More than that, I HAVE to testify. If I do not do something to publically express the tragedy of this disease and how it has limited my professional and personal, I conspire in my destruction, I join the ranks who feel we are expendable. ~ Posted by: anomar, Jun 20, 2014

Re: ME/CFS Appears to Be a Disease Affecting the Basal Ganglia & Dopamine Metabolism

Is Dopamine the Culprit? I THINK SO!

Dopamine or, more likely, problems with processing dopamine is now my primary suspect for my Chronic Fatigue Syndrome. I'll tell you why - this certainly isn't a fully formed scientific theory, but it adds up for me now. The light bulb went off when I recently had a negative reaction to a medication, Nuvilgil, that was similar to what I experienced with my first big, debilitating crash and similar to withdrawal symptoms I had experienced from antidepressants. I've taken Nuvigil sporadically for a few months. Sporadically because I find it very strong and was only using it every once in awhile to give an extra boost when I thought I would need it. But recently, I began using it every day, only about 1/8 of the full tablet. What I noticed was a sharp uptick in energy, mental and physical that lasted about a week, a reduction in energy the next week, a flatlining if you will, a complete crash with lack of energy and increased pain the next week, and finally, severe pain that was obviously withdrawal symptoms after not taking it for 1-2 days. So basically a very quick cycle of up, then down, then way down. Rewind back a few years when all of this began. I went to a sleep doctor and was diagnosed with sleep apnea. I had been under a lot of stress from work and life and had gone an extended period of time with only sleeping 3 or 4 hours a night. When a CPAP machine didn't seem to cure my tiredness, the doctor prescribed Wellbutrin and Provigil, medications that both work on dopamine. Instead of getting better, I was getting worse. I then went to a psychiatrist and tried med after med to try to address the fatigue and pain. Nothing worked and eventually I had the big crash which let to be not being able to work and fully function or even take care of myself. What I now believe happened is that my dopamine receptors were already malfunctioning or burned out because of the stress and lack of sleep and the medication that was meant to help by increasing dopamine backfired because my body was already overwhelmed by too much and couldn't process it. I don't think my problem was/is not enough dopamine, it's that my body can't process it correctly. So my question is what happens to the dopamine or other neurotransmitters that cannot be processed? I think it may be treating it like a virus and would explain an immune system that is constantly in overdrive. I read someone said it was something like being in state of withdrawal from drugs 24/7 , and I thought that's it! It is like being in detox/withdrawal constantly and I think the body is doing something with the excess dopamine, etc. that cannot be processed normally by properly working dopamine receptors. I would love for someone to comment on this, because after years of dealing with this horrible condition, I think it comes close to explaining it for me. Thanks. ~Posted by: prohealthnelg, Jun 29, 2014

Re: “Flowers” in the blood: A novel paired erythrocyte arrangement in a patient with chronic fatigue syndrome following infectious mononucleosis


Fascinating!!! 

What a great confirmation of Simpson's earlier work. Now we can see why the A-V shunts are activating and developing. Oversized erythrocytes and agglutinated erythrocytes cannot penetrate the capillary bed. They then bank up. Such "back-pressure" activates the A-V shunt or where there is no shunt one develops. The more the shunts are activated the less perfusion of muscle, skin, peripheral nerve and possibly even internal organs and glands.

As a consequence we have poor oxygenation, poor ROS and NOS clearance and reduced mitochondrial performance because of lowered mitochondrial membrane potential. Things are starting to add-up.Now we need to show why/how the immune system (infection) causes the change in erythrocyte behaviour and morphology. ~Posted by: IanH, July 11, 2014

Re: VIDEO: Julia Newton Talks About Neurocognitive problems in ME/CFS

Blood pressure and neurocognitive effects 

I don't agree with Prof. Newton when she proposes that the neuro-cognitive and memory problems are due to low BP. I know of many people with ME/CFS whose BP is normal to high and they have just as significant problems with their dysautonomia and cognitioin/memory.

I do agree that blood flow is part of the problem but it isn't BP. As was recently discussed the microcirculation in the periphery is disrupted in ME/CFS by faulty erythrocyte morphology (worse than it is in severe depression). The brain is subject to this same microcirculation and flow would be disrupted in the same way by enlarged/flattened and "flowered" red cells.

Postural orthostatic problems would exacerbate the low flow and more easily cause vertigo and blackout but it isn't the drop in BP per se, it is the drop in BP (normal) on top of the already starved tissue. Some ME people with highish BP do suffer from these same postural orthostatic problems for the same reason.

Some people with ME seem to have high frequency of A-V shunting, others do not. If you have a high degree of shunting then BP might not be raised. If you have a low degree of shunting then BP would be expected to be raised because of "occlusion" of the capillary bed causing a "rise in pressure". ~Posted by: IanH, July 13, 2014
____________________


Microcirculation and excitotoxicity 

Does impeded microcirculation cause hypoxia? Even a mild level of hypoxia, decreases glutamate transporters expression, resulting in cytotoxicity and reduced tolerance to glutamate exposure. In turn mitochondrial function is mildly compromised. Glutamate induced cytotoxicity leads to the activation of Ca2+ permeable NMDA receptors on myelin sheaths and oligodendrocytes, leaving oligodendrocytes susceptible to Ca2+ influxes and subsequent excitotoxicity. One of the damaging results of excess calcium in the cytosol is initiating apoptosis through cleaved caspase processing.

Another damaging result of excess calcium in the cytosol is the opening of the mitochondrial permeability transition pore, a pore in the membranes of mitochondria that opens when the mt absorb too much calcium. Opening of the pore may cause mitochondria to swell and release reactive oxygen species and other proteins. The pore can also cause mitochondria to release more calcium. In addition, production of adenosine triphosphate (ATP) may reduced or even stopped, and ATP synthase may in fact begin hydrolysing ATP instead of producing it.

These excitotoxic consequences are known to occur in hypoxia. The question is whether impeded microcirculation (in the brain) results in mild or intermittent hypoxia. It is reasonable to assume it does and even at a low level it must cause some of the above consequences resulting in cognitive and particularly memory dysfunction. ~Posted by: IanH, July 13, 2014


ReNorwegian ‘Woulds’ (and ‘Wouldn’ts’): The ME/CFS Survey

Necessary to factor in that ME/CFS Can Improve Doing Nothing But Rest 

It is important to note that while lots of people improved over their first several years doing all kinds of things, some of us improved by doing nothing but going to bed and restings full time. I got sick in 1986 prior to antivirals, had a documented case of Epstein-Barr virus that nothing could be done for at the time and was bedridden for several years before I got a minimal improvement allowing me to sit in a recliner and occasionally go out though that led to a crash. I remain ill after 28 years. 

In those days, around 1990, once I became able to read up on it, people were crediting their improvements to all kinds of things. But it would be helpful to know how many people were able to improve just on rest. This would give us a baseline to judge treatments against. I was also supported by a doctor who said I had Chronic EBV around the time the name CFS was given to our illness. So I also had a bit of support at the beginning which was no doubt helpful as well for the first 3 years or so after which I moved. ~ Posted by: siebertesther,Jul 12, 2014



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