halcyon
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It seems to be a topic of active interest at NINDS, with several of the study members publishing on it previously.
Investigating the Investigators of the Upcoming Post-Infectious NIH Study
- Thread starter Valentijn
- Start date
Full text is available at http://www.neurology.org/content/47/6/1410.full . The P-value differences between the CFS patients and depressed controls was 0.068 on one measurement and 0.059 on another. Meaning a larger sample or fewer comparisons could have resulted in statistical significance. No mention of that possibility in the paper though
4 of the 18 controls were the investigators, who would have known to put a lot more effort into the exercise.
Based on their research, it sounds like Hallett & Maurer would be the ones pushing for that.
No, a null result does not mean a researcher is bad. Sabotaging a study to ensure a null result means a researcher is bad. Results are often null because there is really no correlation between the disease being investigated, and the biological factor being investigated. Null results are a normal and healthy part of science.
She sounds great. I'd also be curious to hear what she thinks about about the effects of three small controls groups on the statistical power of the study.
I'm relieved to see we're up to 10 investigators who look pretty good. I was a little worried at first with all the quacks appearing after a bit of digging I'm also not too bothered by the borderline "uncertain" ones. Those two don't seem like they really bring anything to the table, but they also don't seem like they'd be any sort of disruption either.
I'll look into Drinkard today. Which leaves 11 investigators to be investigated!
I'm also not too bothered by the borderline "uncertain" ones. Those two don't seem like they really bring anything to the table, but they also don't seem like they'd be any sort of disruption either.I'll look into Drinkard today. Which leaves 11 investigators to be investigated!
taniaaust1
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- Sth Australia
thanks. I'll edit that post then and take the second part out.
Bart Drinkard looks like he's done a couple dozen studies involving the CPET in various disease. One involves ME/CFS (and RA and polymyositis).
Straus was a co-author, but deceased long before the paper was submitted. Basically they were looking to better describe and measure fatigue, by comparing questionnaire answers (fatigue and activity) with maximal CPET results. There's some talk of "Moods" in the POMS-fatigue subscale, but it's just asking "have you been weary/fatigued/sleepy/tired/etc the past week". So I think they're referring to "moods" as a potentially temporary/passing state, compared to chronic fatigue or chronically reduced activity.
In describing the three diseases, they are generally using the same sort of terminology. There's no apparent attempt to contrast CFS with the "real" diseases. CFS did get singled out a bit in reported activity not correlating nicely with CPET performance - CFS patients did a bit better than expected. But the authors didn't really emphasize this or make it sound like the CFS patients were exaggerating or catastrophizing.
There was some talk of deconditioning, but in pretty neutral terms, not as a value judgement or the cause of illness, and CFS was not singled out. I was impressed that they mentioned that low CPET values from bedrest in healthy volunteers plateau at around 70% of normal, whereas all three groups in the study were at 58.2% on average (CFS = 56.1%, polymyositis = 53.8%, and RA = 64.3%). They concluded that that indicates the diseases are impacting the results, separately from any deconditioning which may have also impacted the results.
They were also very upfront about the problems with the small sample sizes (29 patients total), clearly labeled it as a pilot study, and included a "trend" p-value of 0.15.
In short, I'm certain he's capable of running maximal CPET testing, could understand the importance of a 2-day CPET, and wouldn't attempt to spin any outcomes. He's conducting exercise trials in some of his other research, but does seem to approach the diseases as being distinct, without touting exercise as the grand panacea for everyone.
http://www.sciencedirect.com.sci-hub.cc/science/article/pii/S1934148209004365
Straus was a co-author, but deceased long before the paper was submitted. Basically they were looking to better describe and measure fatigue, by comparing questionnaire answers (fatigue and activity) with maximal CPET results. There's some talk of "Moods" in the POMS-fatigue subscale, but it's just asking "have you been weary/fatigued/sleepy/tired/etc the past week". So I think they're referring to "moods" as a potentially temporary/passing state, compared to chronic fatigue or chronically reduced activity.
In describing the three diseases, they are generally using the same sort of terminology. There's no apparent attempt to contrast CFS with the "real" diseases. CFS did get singled out a bit in reported activity not correlating nicely with CPET performance - CFS patients did a bit better than expected. But the authors didn't really emphasize this or make it sound like the CFS patients were exaggerating or catastrophizing.
There was some talk of deconditioning, but in pretty neutral terms, not as a value judgement or the cause of illness, and CFS was not singled out. I was impressed that they mentioned that low CPET values from bedrest in healthy volunteers plateau at around 70% of normal, whereas all three groups in the study were at 58.2% on average (CFS = 56.1%, polymyositis = 53.8%, and RA = 64.3%). They concluded that that indicates the diseases are impacting the results, separately from any deconditioning which may have also impacted the results.
They were also very upfront about the problems with the small sample sizes (29 patients total), clearly labeled it as a pilot study, and included a "trend" p-value of 0.15.
In short, I'm certain he's capable of running maximal CPET testing, could understand the importance of a 2-day CPET, and wouldn't attempt to spin any outcomes. He's conducting exercise trials in some of his other research, but does seem to approach the diseases as being distinct, without touting exercise as the grand panacea for everyone.
http://www.sciencedirect.com.sci-hub.cc/science/article/pii/S1934148209004365
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LiveAgain
Senior Member
- Messages
- 103
I think Joshua Milner can go on the 'looks good' list. He's been studying a newly defined disease having to do with mast cell, joint hypermobility, & dysautonomia (linked below) and based on some of his other papers, he seems to find biomarkers. See second link for selected publications.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016972/
http://irp.nih.gov/pi/joshua-milner
Joshua David Milner, M.D., S.B.
Senior Investigator
Genetics and Pathogenesis of Allergy Section
NIAID/DIR
Building 10, Room 5-3950
10 Center Drive
Bethesda, MD 20892
301-827-3662
jdmilner@niaid.nih.gov
Biography
Joshua Milner graduated with an S.B. in biology from the Massachusetts Institute of Technology (MIT) in 1995 and an M.D. with distinction in immunology from the Albert Einstein College of Medicine in 2000. He was the recipient of the Pediatric Scientist Development Program Fellowship and did his fellowship in allergy and immunology at NIAID. He completed a postdoctoral fellowship with Dr. William Paul, NIAID, examining issues of mouse T-cell receptor repertoires. He was in the NIAID Clinical Research Transition Program immediately prior to being named chief of AIU as a clinical tenure-track investigator in NIAID.
Research Topics
The Genetics and Pathogenesis of Allergy Section is a basic, translational, and clinical lab focused on understanding the immunology of atopic disease through patients with genetic diseases associated with atopic manifestations, patients with immune deficiency and atopy, and patients with severe atopic dermatitis. Through studies of patients and mouse models, we hope to gain better insights into the mechanisms of immunodysregulation that lead to atopic inflammatory disease. Josh Milner and an NIAID research team have found that wet wrap therapy combined with education on long-term skin care can dramatically improve the lives of children with severe eczema.
Investigation of Defects in T-Cell Receptor Signaling and Repertoires
Weak T-cell receptor (TCR)-mediated signaling of yet-undifferentiated naïve T cells can lead to inappropriate Th2 differentiation in mouse models. Insufficient TCR diversity can lead to impaired regulation of T cells by other T cells due to insufficient TCR specificity overlap of effector and regulatory populations or due to the absence of competition between T cells leading to the inappropriate emergence of weakly signaling TCRs specific for a given antigen. Our lab is developing and applying techniques to determine whether certain human disorders of atopy may be caused by defects in TCR diversity or signaling function.
Analysis of Patients With Known Genetic Diseases Associated With Atopy
Via the study of selected genetic diseases that have allergic symptoms as an associated manifestation, we hope to derive lessons in the pathophysiology of atopy from the known affected pathways. Examples of diseases studied include the autosomal dominant hyper-immunoglobulin (IgE) syndrome due to mutations in STAT3, Wiskott-Aldrich Syndrome, adenosine deaminase (ADA)-deficiency severe combined immunodeficiency disease (SCID) associated with high IgE and others.
Search for Novel Genetic Diseases Associated With Atopy
AIU is also centrally focused on defining and understanding new genetic diseases of atopy in order to find novel pathways in the pathogenesis of allergy from these unique diseases. One example is PLCG2-associated antibody deficiency and immune dysregulation (PLAID), which we recently described. Patients with PLAID have cold urticaria, atopy, immune deficiency, and autoimmunity. Research is ongoing into the pathophysiology of PLAID and into the role of the PLCG2 and its pathway in other related disorders.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016972/
http://irp.nih.gov/pi/joshua-milner
Joshua David Milner, M.D., S.B.
Senior Investigator
Genetics and Pathogenesis of Allergy Section
NIAID/DIR
Building 10, Room 5-3950
10 Center Drive
Bethesda, MD 20892
301-827-3662
jdmilner@niaid.nih.gov
Biography
Joshua Milner graduated with an S.B. in biology from the Massachusetts Institute of Technology (MIT) in 1995 and an M.D. with distinction in immunology from the Albert Einstein College of Medicine in 2000. He was the recipient of the Pediatric Scientist Development Program Fellowship and did his fellowship in allergy and immunology at NIAID. He completed a postdoctoral fellowship with Dr. William Paul, NIAID, examining issues of mouse T-cell receptor repertoires. He was in the NIAID Clinical Research Transition Program immediately prior to being named chief of AIU as a clinical tenure-track investigator in NIAID.
Research Topics
The Genetics and Pathogenesis of Allergy Section is a basic, translational, and clinical lab focused on understanding the immunology of atopic disease through patients with genetic diseases associated with atopic manifestations, patients with immune deficiency and atopy, and patients with severe atopic dermatitis. Through studies of patients and mouse models, we hope to gain better insights into the mechanisms of immunodysregulation that lead to atopic inflammatory disease. Josh Milner and an NIAID research team have found that wet wrap therapy combined with education on long-term skin care can dramatically improve the lives of children with severe eczema.
Investigation of Defects in T-Cell Receptor Signaling and Repertoires
Weak T-cell receptor (TCR)-mediated signaling of yet-undifferentiated naïve T cells can lead to inappropriate Th2 differentiation in mouse models. Insufficient TCR diversity can lead to impaired regulation of T cells by other T cells due to insufficient TCR specificity overlap of effector and regulatory populations or due to the absence of competition between T cells leading to the inappropriate emergence of weakly signaling TCRs specific for a given antigen. Our lab is developing and applying techniques to determine whether certain human disorders of atopy may be caused by defects in TCR diversity or signaling function.
Analysis of Patients With Known Genetic Diseases Associated With Atopy
Via the study of selected genetic diseases that have allergic symptoms as an associated manifestation, we hope to derive lessons in the pathophysiology of atopy from the known affected pathways. Examples of diseases studied include the autosomal dominant hyper-immunoglobulin (IgE) syndrome due to mutations in STAT3, Wiskott-Aldrich Syndrome, adenosine deaminase (ADA)-deficiency severe combined immunodeficiency disease (SCID) associated with high IgE and others.
Search for Novel Genetic Diseases Associated With Atopy
AIU is also centrally focused on defining and understanding new genetic diseases of atopy in order to find novel pathways in the pathogenesis of allergy from these unique diseases. One example is PLCG2-associated antibody deficiency and immune dysregulation (PLAID), which we recently described. Patients with PLAID have cold urticaria, atopy, immune deficiency, and autoimmunity. Research is ongoing into the pathophysiology of PLAID and into the role of the PLCG2 and its pathway in other related disorders.
LiveAgain
Senior Member
- Messages
- 103
I'm looking into Luigi Ferrucci next.
LiveAgain
Senior Member
- Messages
- 103
Luigi Ferrucci, M.D., Ph.D.
Senior Investigator
Longitudinal Studies Section
NIA
Scientific Director
Biography
Dr. Luigi Ferrucci is a geriatrician and an epidemiologist who conducts research on the causal pathways leading to progressive physical and cognitive decline in older persons. In September 2002, he became the Chief of the Longitudinal Studies Section at NIA and the Director of the Baltimore Longitudinal Study on Aging.
http://irp.nih.gov/pi/luigi-ferrucci for research interests, full bio and selected publications.
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Researches the biologic process of aging and age related illness/ disability and also idiopathic fatigue. Found a few references to "chronic fatigue syndrome" in projects/ articles he's involved in - nothing alarming, he seems okay.
In this article he talks about biological mechanisms of fatigue. Thankfully they separate CFS out from regular fatigue or fatigue from causes like cancer. http://www.boston.com/news/health/articles/2008/10/13/way_too_tired/?page=full
In a research agenda for Idiopathic Fatigue and Aging, CFS is separated out as a disease: "DISEASE-BASED MODELS OF FATIGUE A number of diseases are known to cause fatigue and may serve as models for how underlying impaired physiological processes contribute to fatigue, particularly those in which energy utilization may be an important factor, but the link between these underlying mechanisms and self-reported or performance-based fatigue has not necessarily been clarified in each disease model below. A number of relevant disease models are also not represented here, notably neurodegenerative disease (e.g., multiple sclerosis) and rheumatological diseases (e.g., fibromyalgia and chronic fatigue syndrome)."
Under recommendations for future fatigue research it says: "Conduct fatigue recovery studies in different populations, including younger adults, older adults, patients with chronic fatigue syndrome, and patients with various diseases and conditions." Seems like a good sign the report acknowledges "CFS" as a disease, no question. Cant link but it's: Bedside-to-Bench Conference: Research Agenda for Idiopathic Fatigue and Aging, ALEXANDER ET AL. MAY 2010–VOL. 58, NO. 5
From one edited by Ferrucci: "Although lack of energy in nonelderly adults has received considerable attention, and severe forms that are persistent and unexplained (e.g., chronic fatigue syndrome) have invoked considerable clinical and research interest (35,36), relatively little research has focused on lack of energy in older individuals." Again "CFS" taken seriously, but not sure they realize it's about much more than fatigue.
http://biomedgerontology.oxfordjournals.org/content/63/7/707.full
Senior Investigator
Longitudinal Studies Section
NIA
Scientific Director
Biography
Dr. Luigi Ferrucci is a geriatrician and an epidemiologist who conducts research on the causal pathways leading to progressive physical and cognitive decline in older persons. In September 2002, he became the Chief of the Longitudinal Studies Section at NIA and the Director of the Baltimore Longitudinal Study on Aging.
http://irp.nih.gov/pi/luigi-ferrucci for research interests, full bio and selected publications.
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Researches the biologic process of aging and age related illness/ disability and also idiopathic fatigue. Found a few references to "chronic fatigue syndrome" in projects/ articles he's involved in - nothing alarming, he seems okay.
In this article he talks about biological mechanisms of fatigue. Thankfully they separate CFS out from regular fatigue or fatigue from causes like cancer. http://www.boston.com/news/health/articles/2008/10/13/way_too_tired/?page=full
In a research agenda for Idiopathic Fatigue and Aging, CFS is separated out as a disease: "DISEASE-BASED MODELS OF FATIGUE A number of diseases are known to cause fatigue and may serve as models for how underlying impaired physiological processes contribute to fatigue, particularly those in which energy utilization may be an important factor, but the link between these underlying mechanisms and self-reported or performance-based fatigue has not necessarily been clarified in each disease model below. A number of relevant disease models are also not represented here, notably neurodegenerative disease (e.g., multiple sclerosis) and rheumatological diseases (e.g., fibromyalgia and chronic fatigue syndrome)."
Under recommendations for future fatigue research it says: "Conduct fatigue recovery studies in different populations, including younger adults, older adults, patients with chronic fatigue syndrome, and patients with various diseases and conditions." Seems like a good sign the report acknowledges "CFS" as a disease, no question. Cant link but it's: Bedside-to-Bench Conference: Research Agenda for Idiopathic Fatigue and Aging, ALEXANDER ET AL. MAY 2010–VOL. 58, NO. 5
From one edited by Ferrucci: "Although lack of energy in nonelderly adults has received considerable attention, and severe forms that are persistent and unexplained (e.g., chronic fatigue syndrome) have invoked considerable clinical and research interest (35,36), relatively little research has focused on lack of energy in older individuals." Again "CFS" taken seriously, but not sure they realize it's about much more than fatigue.
http://biomedgerontology.oxfordjournals.org/content/63/7/707.full
It looks like he's involved in looking at the neurological impact of diseases associated with infections, such as Ebola, MS, HTLV-1, etc. He works directly on Avi Nath's team as a "Staff Clinician", and has published with him.
http://www.neurology.org/content/84/14_Supplement/P5.235
There's many other Bryan Smiths who are doctors and researchers. I'm pretty sure this one isn't the one who does molecular imaging (turns up in NIH searches due to a fellowship) and he's probably not the one at John Hopkins (does HIV + stroke stuff, but very very recently with no mention of dual affiliations).
Dr. Stephen Sinclair is a Clinical Psychologist at the NIMH. His specialty is "Affective Cognitive Neuroscience", which generally seems to involve the neurological mechanisms of emotions and thought.
His research deals with behavioral disorders in youths, attempting to find cognitive or brain abnormalities which correlate with them. The team he works with does seem genuinely interested in finding abnormalities, and presents null results prominently instead of hiding them. The research also seems completely focused on the discovery of abnormalities, with little or no interest in promoting particular treatments.
However, I don't know if their imaging results support their conclusions, since it's not an area I know anything about. I'm also not particularly enthusiastic about investigators specializing in behavioral disorders analyzing ME/CFS brain scans in general, but if it's going to happen, this is probably a good person to be doing it.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941702/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491633/
http://ajp.psychiatryonline.org.sci-hub.cc/doi/full/10.1176/appi.ajp.2015.15020250
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632075/
His research deals with behavioral disorders in youths, attempting to find cognitive or brain abnormalities which correlate with them. The team he works with does seem genuinely interested in finding abnormalities, and presents null results prominently instead of hiding them. The research also seems completely focused on the discovery of abnormalities, with little or no interest in promoting particular treatments.
However, I don't know if their imaging results support their conclusions, since it's not an area I know anything about. I'm also not particularly enthusiastic about investigators specializing in behavioral disorders analyzing ME/CFS brain scans in general, but if it's going to happen, this is probably a good person to be doing it.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941702/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491633/
http://ajp.psychiatryonline.org.sci-hub.cc/doi/full/10.1176/appi.ajp.2015.15020250
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632075/
This may be of interest in general: http://clinicalcenter.nih.gov/about/news/newsletter/2008/nov08/newsletter.html
The article is half way down the page.
Note that all three in this picture are on the study. From left to right: Dr. Fred Gill, Stacey Solin (middle), and Dr. Penelope Friedman
As far as I can tell from the article, the Internal Medicine Consult Service is supposed to be involved in all studies, and is for patients who require treatment/care for any health problems they may have during the trial. Unless this is a coincidence and all three are part of this study in a different capacity, they are probably included by default.
The article is half way down the page.
Note that all three in this picture are on the study. From left to right: Dr. Fred Gill, Stacey Solin (middle), and Dr. Penelope Friedman
As far as I can tell from the article, the Internal Medicine Consult Service is supposed to be involved in all studies, and is for patients who require treatment/care for any health problems they may have during the trial. Unless this is a coincidence and all three are part of this study in a different capacity, they are probably included by default.
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It looks like Fred Gill, Stacey Solin and Penelope Friedman have been working together at the Internal Medicine Consult Service since at least 2008. There is info about a clinical elective program for students at the IMCS on the NIH website, which lists all three under staff and is dated 2015.
Perhaps unsurprisingly, I have found nothing else about Stacey Solin, no documented research participation, no speeches/talks/educational material by her, whether related to ME/CFS or not.
I've looked into Penelope/Penny Friedman as well and haven't found anything remarkable either.
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If the IMCS is a standard part of NIH clinical research and that's the reason why Gill, Solin and Friedman show up as investigators, then they aren't really involved in the study per se and there is little reason to worry about their influence I think.
On the other hand, trial participants who need medical help would understandably be concerned about not being taken seriously if they are seen by IMCS staff, given Fred Gill's position.
Perhaps unsurprisingly, I have found nothing else about Stacey Solin, no documented research participation, no speeches/talks/educational material by her, whether related to ME/CFS or not.
I've looked into Penelope/Penny Friedman as well and haven't found anything remarkable either.
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If the IMCS is a standard part of NIH clinical research and that's the reason why Gill, Solin and Friedman show up as investigators, then they aren't really involved in the study per se and there is little reason to worry about their influence I think.
On the other hand, trial participants who need medical help would understandably be concerned about not being taken seriously if they are seen by IMCS staff, given Fred Gill's position.
Neal Young, M.D.
Senior Investigator, Cell Biology Section, Chief of the NHLBI's Intramural Research Hematology Branch
His research focus is on bone marrow failure diseases and he conducted research on immuno-suppressive drugs for aplastic anemia which resulted in the first effective treatment for the disease. He also studies parvovirus B19 (anemia) and diseases related to the telomere (lung fibrosis, liver cirrhosis). In his review article on parvovirus B19 (2004) he wrote the following, citing a paper/case report of 3 fibromyalgia patients:
Avindra Nath said he involved Neal Young because of his expertise in immunology. From the MEAction's transcript of his talk on 15 Feb:
He's also authored a paper together with Ioannidis, who has written the famous paper "Why Most Published Research Findings Are False", on publication bias/distortion of research results and science.
And for what it's worth, this Washington Post article describes him as someone who likes to solve a mystery:
Couldn't find any red flags, so he seems all right.
Jay H. Chung, Ph.D., M.D.
Senior Investigator
Laboratory of Obesity and Aging Research
From the NIH website:
The NIH site lists his publications as well. It's all purely biomedical and highly technical. He wants to understand the biological mechanisms of metabolism in humans, how it changes with age and its relationship with diseases. For instance:
I still went ahead and tried to find a connection to anything BPS-related, but unsurprisingly nothing came up. Jay Chung passes PR's quality assurance test.
I'll do Dr. Eugene Major next.
As for Elizabeth Unger, do we need to look into her? If I remember correctly, her position has been discussed quite extensively elsewhere, and it's a bit of a mixed bag, but not to the extent that it can be considered detrimental to the study. I might be wrong, so corrections are welcome.
As for Elizabeth Unger, do we need to look into her? If I remember correctly, her position has been discussed quite extensively elsewhere, and it's a bit of a mixed bag, but not to the extent that it can be considered detrimental to the study. I might be wrong, so corrections are welcome.