Fair enough. Id love to see that, and its important. Whether we will soon im not sure, due to the cutting edge of this study. But I agree it would be very helpful and important.
Chronic presence of deranged lipids in adult humans are potentially dangerous and contribute significantly in autoimmune and chronic inflammatory diseases (such as Rheumatoid Arthritis) to dying prematurely from Myocardial Infaction (Heart Attack).
Some with ME (who privately test) are also finding out they have a chronic inflammatory disease state.
Lipids also have a protective effect, so we don't want them too low, or too high. Too low, and the Mitochondria won't work, too high and you run a risk of premature:
Vascular Dementia
Adverse Cardiac and Neurological events inc TIA + Stroke
Two potentially useful blood tests I would suggest when inflammation and 'ME' are present are Lp-PLA2 + Oxidised LDL. (I would also add HS-CRP into the mix for cardiovascular 'risk', as usually, CRP alongside ESR doesn't show anything much in ME unless an acute infection or other autoimmune disease has developed).
In case you're interested, I've linked some research below.
Research:
Association between Lp-PLA2 and coronary artery disease: focus on its relationship with lipoproteins and markers of inflammation and hemostasis. http://www.ncbi.nlm.nih.gov/pubmed/16115490
Elevated Lp-PLA2 levels add prognostic information to the metabolic syndrome on incidence of cardiovascular events among middle-aged nondiabetic subjects. http://www.ncbi.nlm.nih.gov/pubmed/17431184
Increased serum level of Lp-PLA2 is independently associated with the severity of coronary artery diseases: a cross-sectional study of Chinese population. http://www.ncbi.nlm.nih.gov/pubmed/25879827
.....Fourth: They concluded that ME is a hypometabolic state, with a profile similar to the medically recognised survival state of "dauer", which occurs when humans experience extreme circumstances where it may die if it not change its metabolism. E.g. in extremely cold conditions, or in states of extreme hunger. ME could in other words be a evolutionary conserved hypometabolic state remniscent of this, that for some reason occurs in response to other triggers together with genetic predispositions.
Yes, in basic form you need to switch off the CDR, but we don't know if this is possible, in case the pathogens in the patients, then worsen the disease. Dr Cheney proposed ages ago, that the 'effect' of extreme exhaustion in 'CFS' may well be protective, e.g. by making you able to do nothing, this is happening for a reason and keeping you alive.
He may well be correct.
So before we have out cutting edge treatment that enables us to go down a gym, we need to see that it's safe to turn off the CDR, as previously mentioned.. for this we need cutting edge pathogen studies, in the correct group of patients, with this proposed Novel defect discovered, they would indeed, by the correct group (what we've always lacked).
Hopefully in the next few years, scientists, doctors and even Government Health Agencies (enablers of harm to ME CFS sufferers) giving charlatan F48.0 psychiatrists a planet wide exclusion zone they must stick to, to avoid further harm to the patients.
I thought this quote from the paper was worth citing..
....The low sphingolipid profile in CFS appears to be an adaptive response that is opposite to the increased sphingolipids observed in metabolic syndrome (11) and the acute cell danger response (CDR) (7) and ultimately may represent a fundamental response to oppose the spread of persistent viral and intracellular bacterial infections....
"Eighty subjects were from California". Can we find out if there is a relationship to where the subjects lived/worked (number of months) and known government reported toxic areas?
Here is a map, that can be used to identify sources of toxic waste. The data is derived from US Gov't sources. If we were able to get a data feed from Terradex and reference it with subject self reports (geographic locations) then we could see if the toxic chemical exposures had any impact on the study participants. If there was a relationship, then we could look at specific chemicals that are detailed about each site.
Maybe Ron is already doing this research? It might be a conflict of interest, since one of the offending sites was formerly occupied by Hewlett Packard (OptoElectronic Division) located in Palo Alto, on Page Mill Road; the land is owned (maybe still is owned?) by Stanford University.
"Eighty subjects were from California". Can we find out if there is a relationship to where the subjects lived/worked (number of months) and known government reported toxic areas?
Here is a map, that can be used to identify sources of toxic waste. The data is derived from US Gov't sources. If we were able to get a data feed from Terradex and reference it with subject self reports (geographic locations) then we could see if the toxic chemical exposures had any impact on the study participants. If there was a relationship, then we could look at specific chemicals that are detailed about each site.
Maybe Ron is already doing this research? It might be a conflict of interest, since one of the offending sites was formerly occupied by Hewlett Packard (OptoElectronic Division) located in Palo Alto, on Page Mill Road; the land is owned (maybe still is owned?) by Stanford University.
.....Flavin Adenine Dinucleotide (FAD) Was Decreased. Plasma FAD was decreased in both males and females with CFS (Tables 2 and 3). FAD is synthesized from riboflavin (vitamin B2) and ATP. The gastrointestinal absorption, distribution, and transporter-medi-ated uptake of FAD are carefully regulated during health and disease (19). FAD is mobilized from tissues, increased in the plasma, and renal secretion is increased under conditions of stress or infection (20). FAD is an important cofactor for fatty acid oxidation and sterol synthesis and is required for activation and oxidation of vitamin B6 (pyridoxine); lipoic acid metabolism (E3 subunit) needed for pyruvate, alpha-ketoglutarate, and branched chain amino acid oxidation; vitamin A activation; 5-methyltetrahydrofolic acid synthesis; niacin and NAD synthe-sis; and glutathione reduction.....