Higher prevalence of ‘low T3 syndrome’ in patients with chronic fatigue syndrome: A case-control study (2018) Ruiz-Núñez et al.

More evidence that this is a hypometabolic syndrome? Is this reliable work?

 

Very interesting, but I'm dubious about the iodide suggestion. Low iodine is a cause of hypothyroidism in parts of the world where iodine is low in the soil that crops are grown in. But elsewhere in the world giving iodine to iodine-replete patients is likely to suppress thyroid activity, not give it a boost.

 

My subtype is hypo for many different types of hormones. I doubt what I have resembles what Whitney has. I think what the evidence tells us it is that there are many subtypes, and thats why the current style of academic scientific research, one that collects massive amounts of data, is failing us.

 

What else can u do though? There`s not any obvious place to narrow down the research

 

I don’t have answers ATM, but I feel this topic of discussion needs to be addressed, possibly after the MillionsMissing May 12 protests. I think that advocacy for May needs to be our top priority now.

 

You could start with the narrowest definition of ME, find out what rules seem to apply to that group, and then see if other groups are different. Hyde or Ramsay ME are the strictest definitions (Ramsay seems looser than Hyde). With MS, they use very narrow criteria to start with, for example, and in FMS studies they often use only women without co-morbid illnesses. Perhaps that's how we start, instead of the kitchen sink approach, and see what defines the 'classic' post-viral, acute onset ME patients with demonstrable CNS injury. Then look at, say, gradual onset, or autoimmune ME, or ME possibly caused by chemicals. See how they compare or not.

Younger seems to think there are at least three broad subgroups (viral, autoimmune, metabolic), but until we see his study it's hard to see how he's reached this conclusion.

 

MEA Website: Frontiers Press Release: Chronic fatigue syndrome possibly explained by lower levels of key thyroid hormones

http://www.meassociation.org.uk/201...levels-of-key-thyroid-hormones-20-march-2018/

 

What might be the implications for someone whose ME began when they contracted a flu bug whilst recovering from a thyroid operation, but never then recovered their energy levels again. Been on thyroid treatment ever since.

 

Byron Hyde noted more thyroid issues in his patients. I know MEA says they've not seen evidence of a link before (from their survey, I think?), but I wonder if many patients at the higher end of the 'normal' range (bear in mind some US docs treat when TSH > 3, whereas here we wait until it's >4.5) might unknowingly have issues with T3 production?

My thinking, however, is that any thyroid issues will be like the HPA issues--i.e., secondary to mitochondrial or some other dysfunction. It's quite clear that few systems are entirely untouched in ME, since it seems to cause a cascade of problems.

 

Opening section from the MEA's article.

 

I gather the Dutch are, like the UK, usually quite obsessed with the BPS model of ME. Although that seems to be (slowly) changing. I'm not sure why it's included in the MEA write-up, however.

 

this could link to hypometabollic state?
see also potential for ROS activation-

https://www.ncbi.nlm.nih.gov/pubmed/9633610-
3,5,3'-triiodothyronine induces mitochondrial permeability transition mediated by reactive oxygen species and membrane protein thiol oxidation.

http://www.tiredthyroid.com/rt3-4.html

 

The Press Release was written by Frontiers:

It had an embargo until 10.00am this morning. The BBC were going to write about it and we had given them comment from Dr Shepherd, but then they changed their mind, so we went ahead with the Frontier's release in its entirety.

 

Worth noting they used the 'CBO criteria' which is based on Fukuda 'with the exclusion criteria of Reeves' which does at least seem to rule out some kinds of psychiatric disorder. But (from my read at least) I think you're right in that PEM might not be mandatory. My impression is that the authors do not try and come down on a specific side on whether it it has an immunological/metabolic/neurological/psychiatric pathology.

Still, it's an interesting study and I'm pleased the MEA is looking to fund any applicants who want to try and replicate it.

 

Many doctors in the UK won't treat hypothyroidism until TSH is > 10 and Free T4 is below the reference range. It is institutionalised torture for many people.

From this link (NICE Clinical Knowledge Summaries, which carry approximately zero weight): https://cks.nice.org.uk/hypothyroidism#!diagnosissub:1

• Arrange investigations including:
  • Blood tests for thyroid stimulating hormone (TSH) and free thyroxine (FT4):
    • Diagnose overt hypothyroidism (OH) if TSH is greater than 10 mU/L and FT4 is below the reference range.
    • Suspect subclinical hypothyroidism (SCH) if TSH is above the reference range and FT4 is within the reference range. In non-pregnant people repeat TSH and T4 (ideally at the same time of day) 3–6 months after the initial result to exclude transient causes of a raised TSH (such as intercurrent illness) and to confirm the diagnosis of SCH.
    • Suspect secondary hypothyroidism if the clinical features are suggestive and T4 is low without raised TSH. Be aware that in secondary hypothyroidism TSH may also be low, normal, or slightly elevated due to circulation of bio-inactive forms of TSH.

 

Daily Mail coverage of this:

http://www.dailymail.co.uk/health/article-5522831/Could-cause-chronic-fatigue-syndrome.html

Some good:

Some mixed to bad: