Discussion in 'Phoenix Rising Articles' started by Firestormm, Sep 12, 2013.
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Great article guys! Exciting to hear about the signs of immune activation and also interesting to me to hear about the increase in Leptin, i have to admit I overlooked it intially but reading the article it stand out to me as a very interesting upregulation to see. It makes a lot of sense to have upregulation of a molecule such as this given the evidence of mitochondrial and ATP production problems!
I think it's worth mentioning too that these findings given important evidence for both the autoimmune theory that Fluge and Mella are working on and indeed the pathogen theory that Lipkin himself believes. Hopefully some of these abnormalities hold up to further scrutiny!
Well done, Simon - great article! And well done, Russ - great transcript!
Yes, I was intrigued by that too, though I that line is pretty-much the extent of my knowledge of Leptin.
Yes, and I think they key thing is replication, which is very much what Ian Lipkin plans to do. I have to say, these broad findings are probably consistent with many different theories so I will be very interested in what the future work turns out: certainly Ian Lipkin's main focus now seems to be to find what is responsible for these changes.
Overactive immune system has been known for at least 2 decades.
This is remarkable. I think it's interesting that this study makes ME/CFS somewhat similar to MS, particularly in the "hit and run scenario". A virus-like infection comes in shortly, disrupts the immune system, and it's all downhill from there.
Also, how do we pressure for more research funds? How do we organize and lobby to get these researchers what they need?
Indeed it has but we now seem to be getting to the bare bones of the issue with what exactly is wrong with strong evidence to support these initial claims - if nothing else these findings are good clues as of where to look next!
Sometimes finding nothing at all is the best outcome. In terms of viruses as a central causation, this somewhat conclusively shows little significance in the commonly held perpetrators which means we can move on to newer ideas without the baggage that these old ideas bring with them.
An analogy I made in a previous thread earlier today seems to also be relevant here I feel with regards to the 'hit and run' idea many people discuss. The reference to autoimmunity is however just a personal opinion I hold and for the purpose of this topic should be interchangeable with immune activation.
The interesting part here is the specifics of the immune activation - certainly not all of these will prove to be repeatable but if just a handful do we could be looking at a good trace of why the immune response has turned so aberrant.
Thank you Simon and Firestormm for the hard work putting this clear review together and supplying a transcript for us. I had listened in to the meeting but, apparently missed a lot of the details.
It is clear to me that Lipkin found enough abnormalities/biomarkers for him to be excited to plunge in deeper for further studies. Any study showing differences between patients and controls is promising. It remains to be shown/proven what this will lead to.
Their finding of the three year marker showing differences in the results is intriguing. I wonder why three? As he stated though, they were not looking for that, it just has seemed to appear when comparing results.
I wish I could understand in layman's terms what these abnormalities in cytokines mean or what this Leptin issue means.
I almost wish I had gone through medical school in order to understand and follow these developments.
Great news! Thanks for the article. I truly hope that they advance the understanding of the disease mechanisms. It's fascinating that some inflammatory markers were even low. I also hope that microbiome analysis gets a lot cheaper through better implementation of computers and resulting automation.
In addition to regulating the hunger-response, Leptin controls the release of toxins from the fatty tissues.
Lipkins findings of Leptin is consistent with "the elusive biomarker for CFS" that we have known about for about fifteen years now.
With regard to Leptin, I think it is a very interesting find and it's more interesting that it has been found in the past. I'm not sure it will prove to be a causative agent in the disease pathology of ME but certainly it would be interesting to know why it appears to be getting up-regulated - I suspect it could be due to its role in metabolism considering the findings of dysfunctional mitochondria and Lactate build-up in the muscles - presumably through increased anaerobic respiration during trivial exertion.
Help in understanding, so is there an up- regulation in Leptin if you have CFS?
Checked SNPedia and there are Leptin related genes/snps for those who wish to travel down that rabbit hole.
As you might expect....It's complicated.
Leptin stimulates MSH "Melanocyte Stimulating Hormone"
Which in turn regulates the innate immune system.
High Leptin and low MSH is seen in illnesses where toxins are stored in the fatty tissues.
The high Leptin makes weight loss extremely difficult.
Since CFS researchers have yet to make the connection between this phenomenon and CFS, the connection remains to be explored. But for Lipkin to see it makes it more likely that CFS researchers will take an interest.
I wonder if the genes associated with Leptin will be determined to play any role. For now I checked three of the SNPs associated with Leptin and I have the common variety so they dont explain my expereince. I am one of the 'fighting this battle longer than three years' group. I still suspect when I had mono in 1995 that was the start of it all even though I did not recognize the long periods between crash and recovery as being related. The last 6-7 years I know realize the unmistakable relation. I am just coming out of another crash (6-7 weeks) and there is a difference, more function (although not sure I'll ever get back to 100%), not as sick all the time, symps not as severe. I wish I understood this crash and recovery element to whatever is causing this . Do others also experience this crash and recovery I am describing? There are some symps I have all the time but when I crash I am more disabled, other symps added and the ones I usually have seem worse then like a cloud lifting I enter a day or week that I realize I am much better. It is so friggen madding the inconsistency. I blame that most for the reason I lost my career, how can I or my employer count on me when I dont know one day to the next if I can function. Sorry for the derail I just want answers, to heal and get my life back!!!!
The variability was in my quote from Dr Ramsay.
Yes, I know what controls the crash phenomenon, and it is linked to leptin signaling.
It seems that he did find bugs. He reported that he found both anellovirus sequences and also retroviral sequences. He said he didn't know what it meant of if it would lead anywhere. Given the craziness that happened last time a researcher tried to associate a viral cause with CFS I don't blame him for being cautious and wanting more evidence before making any claims. But he did state he felt the cause still seemed like an infection and that all of the findings (bugs or not) should be followed up.
Also, I have a hard time reconciling the claims about IL-8. Several other studies have shown IL-8 to be significantly elevated in patients with CFS. My own IL-8 is one of the most consistently elevated markers, and I have participated in several of these studies through my CFS doctor (including this one). I'll admit though, I don't know the intricacies of testing for cytokines. Perhaps they vary based on time of day, or processing method or something.
You bring a very good point. I noticed he mentioned the anellovirus and traces of some retrovirus, but qualified it quickly as needeing more research. After the xmrv debacle, you can't blame any researcher for being utterly cautious.
I think the title is not necessarily misleading, but leaning heavily on Dr Lipkin's cautious approach to the findings.
Dr. Lipkin is even more emphatic on this earlier in the call...
Montoya's recently released results from a small (10 participants, I believe) study: They obtained blood draws for 25 consecutive days from these patients, who also, I believe, kept journals indicated their fatigue levels. The only finding that correlated directly with fatigue levels in most (not all) of these patients was the hormone leptin. I think that the overall levels were not abnormal, but the changes in leptin tracked the fatigue level changes.
I imagine the details of this are discussed somewhere in the forum, but I haven't had a chance to track it down yet.
You can also try a Google Site Search
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