Daily Mail 20th March: CFS, thyroid hormones, PACE and the Lightning Process

[Countrygirl]

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

Debilitating chronic fatigue syndrome could be caused by low levels of thyroid hormones, finds study

• The findings shed new light on the truth behind the condition, which is incurable
• CFS, or ME, has prompted uproar among the medical community in recent years
• Skeptics dismiss the extreme tiredness and lethargy as merely psychological
• However, angry patients are adamant the condition has a biological cause
• And the new Dutch research backs up the claims that it is a physical problem

By Stephen Matthews For Mailonline

PUBLISHED: 14:07, 20 March 2018 | UPDATED: 10:33, 21 March 2018
Chronic fatigue syndrome (CFS) could be caused by having low levels of thyroid hormones, a new study suggests.

The findings shed new light on the truth behind the debilitating condition, which has prompted uproar among the medical community in recent years.

Skeptics dismiss the extreme tiredness and mental lethargy as merely psychological, but angry patients are adamant it's biological.

And the new Dutch research, conducted on 197 adults, backs up claims that it is a physical problem and not made up in the head of sufferers.

Scientists today announced hope of finding the root cause of CFS, which may allow doctors to move away from treatments that involve psychologists.

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The findings shed new light on the truth behind the condition, which has prompted uproar among the medical community in recent years

Treatment for CFS is delivered by psychologists and involves therapy, which has only angered sufferers more by suggesting it is all in their head.

The new study comes after Bristol University research in September, published in the Archives of Disease, revealed that a controversial treatment for children with debilitating CFS can actually help in some cases.

The Lightning Process - a course which claims to retrain the brain to improve physical health - worked when combined with specialist medical care.

The £620 course has been praised by celebrities such as Martine McCutcheon and the wife of England rugby union player Austin Healey.

But some experts and campaigners have condemned the £620 course – which is not available on the NHS - as pseudoscience' and 'quack medicine'.

Dr Charles Shepherd, honorary medical adviser at the ME Association, said: 'This new research into thyroid gland hormones in ME/CFS represents an important advance in our understanding of hormonal abnormalities in this illness.

'We already know that there are abnormalities involving the hormone cortisol in ME/CFS.

'However, routine blood tests for thyroid function in ME/CFS have always indicated that thyroid gland hormones are not affected.

'Consequently, thyroid hormone treatment is not recommended for ME/CFS - as this can cause serious side effects in people who have normal thyroid function.

 

[alex3619]

The problem is that the thyroid issue in ME and CFS is not measured by routine tests. Its about reverse T3, which is rarely tested. So its not about a deficiency as such, or at least that is my current interpretation and presuming its about the rT3 paper. Its about too much of a thyroid hormone variant that induces thyroid resistance.

If this were insulin, and not thyroid hormone, then its more like we have type 2 diabetes (or one of the five subtypes now considered to comprise type 2) rather than type one diabetes. The issue is the normal levels of hormone do not work.

A similar story possibly applies to cortisol via the beta cortisol receptor, but that paper is way overdue for publication unless I missed it.

 

[hixxy]

The problem is that the thyroid issue in ME and CFS is not measured by routine tests. Its about reverse T3, which is rarely tested. So its not about a deficiency as such, or at least that is my current interpretation and presuming its about the rT3 paper. Its about too much of a thyroid hormone variant that induces thyroid resistance.

Also how many people actually have major improvement when supplementing T3? It did nothing for me despite very high rT3.

 

[pattismith]

Also how many people actually have major improvement when supplementing T3? It did nothing for me despite very high rT3.

Maybe the T3 dose was not acurate?

The other thing to do could be to improve D1 activity and to lower D3 activity

 

[FMMM1]

The problem is that the thyroid issue in ME and CFS is not measured by routine tests. Its about reverse T3, which is rarely tested. So its not about a deficiency as such, or at least that is my current interpretation and presuming its about the rT3 paper. Its about too much of a thyroid hormone variant that induces thyroid resistance.

If this were insulin, and not thyroid hormone, then its more like we have type 2 diabetes (or one of the five subtypes now considered to comprise type 2) rather than type one diabetes. The issue is the normal levels of hormone do not work.

A similar story possibly applies to cortisol via the beta cortisol receptor, but that paper is way overdue for publication unless I missed it.

I know next to nothing about this but I'm interested in seeing these findings replicated.

Check out OMF "Experts Blog" which looks at an improvement to tests which rely on the use of antibodies ("proximity ligation assay"). On the face of it, it may be possible to replicate these tests using the improved technique i.e. to improve detection limits/reduce false negatives/positives etc.

I can see that you might find different (presumably higher) levels of rT3 in people with ME/CFS; however, I'm not clear how you prove that this is the cause. Can you test the receptors to see if they are functioning correctly? In diabetes I assume that they give you glucose and test how long it takes to clear; is there an equivalent for the HPT axis?

Jonas Bergquist has been funded by OMF to carry out research on the "roles of hormones, proteins, and antibodies in ME/CFS"; maybe that study will turn up something. Also, maybe this paper will provide the basis for a further study on the HPT axis.

 

[hixxy]

Maybe the T3 dose was not acurate?

The other thing to do could be to improve D1 activity and to lower D3 activity

The dose was okay. It brought my levels back in line just fine but there were absolutely no benefits clinically.

 

[alex3619]

The dose was okay. It brought my levels back in line just fine but there were absolutely no benefits clinically.

Yeah, but that is the problem. Normal levels wont work if rT3 is high. Getting rT3 back to normal might help.

It is also correct to say that its far from proven that rT3 causes ME or is any more than a minor factor. Lots more research is needed. On forums we have been discussing rT3 for many years now. I first became interested more than five years ago.

If there is a general suppression of energy production in ME then we might expect issues with cortisol, thyroid hormone and even insulin and glucose. Which appears to be the case. We do not however know how important these issues are, and its possible all of them are secondary problems when they occur.

 

[hixxy]

Yeah, but that is the problem. Normal levels wont work if rT3 is high. Getting rT3 back to normal might help.

Yep. That's what I meant by brought my level back in line.

 

[char47]

A similar story possibly applies to cortisol via the beta cortisol receptor, but that paper is way overdue for publication unless I missed it.

Interesting Alex, is this about 'cortisol resistance' like insulin resistance? I have always wonder why i have remarkable improvement in ALL my symptoms when i am very anxious/stressed (i assume it's the effect of adrenaline/cortisol).

Probab;y revealing my ignorance there but hey ho


The DM article is written in a biased way (look at the way the box detailing the argument between Coyne etc from the JHP twists it a bit to appear as if Coyne was in the wrong). Typical, but we've seen much worse from them so i guess small mercies n all that.

 

[alex3619]

Interesting Alex, is this about 'cortisol resistance' like insulin resistance? I have always wonder why i have remarkable improvement in ALL my symptoms when i am very anxious/stressed (i assume it's the effect of adrenaline/cortisol).

There was a comment on a video from a UK research a year or two back (Bansal?) that he had found elevated beta cortisol receptor in ME patients. This receptor acts as a decoy, binding cortisol but not leading to cellular responses. Its a way the body can make individual cells unresponsive to cortisol ... except in us the problem was more general. This would magnify the effect of the otherwise mild cortisol problems found using conventional cortisol testing methods. Since I do not think it was published we are still in the dark about the quality of the finding.

Cortisol was a standard treatment for ME for a while, or at least post viral fatigue, some decades back. It helped, but then the side effects mounted up, as these were immunosuppressive doses.

 

[pattismith]

Yeah, but that is the problem. Normal levels wont work if rT3 is high. Getting rT3 back to normal might help.

It is also correct to say that its far from proven that rT3 causes ME or is any more than a minor factor. Lots more research is needed. On forums we have been discussing rT3 for many years now. I first became interested more than five years ago.

rT3 causes my ME/CFS, I reversed it with a tiny T3 dose. I don't need a big dose, because I have a very low TTSI (hypersensitivity to TH). When I took the T3 it was like if I had suddenly switch on the ligh, the effect started withinan hour, and lasted 8 hours.

For people with high TTSI (high TH resistance), the T3 dose needed may be much higher.

rT3 has no effect to block any genomic function of TH, but it has the ability to block the non genomic effect of TH on sodium membranes' currents:

http://forums.phoenixrising.me/inde...e-a-cancer-support-hormone.58039/#post-961858

So the antithyroid effect of rT3 is very particular, it affects the brain and the muscles, modifying sodium currents and intracellular Ca levels.

 

[hixxy]

@pattismith Doesn't the dose just have to be high enough to bring rT3 back to a normal level? If rT3 causes your ME/CFS then are you back to normal?

 

[pattismith]

@pattismith Doesn't the dose just have to be high enough to bring rT3 back to a normal level? If rT3 causes your ME/CFS then are you back to normal?

My case shows that you can outstrip the rT3 blocking effect in less than one hour by taking T3.

The T3 intake is not able to lower rT3 just in one hour, so it means that you can revert the situation with T3 very quickly in some case.

Lowering rT3 is a much longer process, it can be achieved by lowering T4/TSH, or/and improving 5'deiodinase activity (D1 and D2, but D1 is the most important in that case), and down-regulating D3. (N acetyl cysteine seems able to down regulate D3, I posted some studies about it yesterday)

 

[mermaid]

I was diagnosed with autoimmune hypothyroidism many years before I ended up with the CFS diagnosis. As Thyroxine/T4 worked for me for the first few years, it didn't occur to me for a long time that it could be down to that. My annual blood checks were mostly OK so the GP didn't think to question it, and FT3 is rarely done in the UK now.

Eventually I paid privately to have it done, and it was below range, or low in range when the NHS retested it afterwards. I was allowed to start on some Liothyronine/T3 with the T4 but it didn't help. I was lucky enough to be permitted to use T3 only on the NHS (would not happen now but this was 5 years ago). I didn't improve immediately but over time I began to feel better than I was, and eventually my stamina was much improved, and even my stubbon immune issues slowly began to shift.

Unfortunately then the NHS began to review people on T3 due to the cost - in late 2016, and my health began to slide again as they wanted me to either reduce or add in T4, with the complication of having osteoporosis thrown into the mix, and it being used as a reason to reduce. Last year I agreed to try T4/T3 again but got even iller, so eventually put my foot down and now my GP has supported me in what makes me feel best, which is T3 only.

Even that has hit a glitch recently as I was given a different brand of T3 - Teva, after being on the same one for 5 years, and all the same hypothyroid symptoms came back. I am now trying to get back onto the original one, to attempt to get my health back on track. I have heard of many having issues with Teva, including their Thyroxine, so I now wonder if their T4 impacted badly on me when the Endocrinologist was trying to get me to add it back in, as when I was on T4 before it was not Teva being used.

Incidentally, I know of many people who are definitely hypothyroid, but for whom Thyroxine ceases to work for them over time. There are so many nuances with this illness, that are not understood properly, it seems, even though Endos and Drs will have it that one tablet (ie Thyroxine) solves all of our problems.

 

[clive powney]

Also how many people actually have major improvement when supplementing T3? It did nothing for me despite very high rT3.

Hi hixxy. Have you tried running your thyroid panel results through the SPINA software? There are a few posts on the forum that may help you understand (and also help to evaluate the usefulness of the software)
http://forums.phoenixrising.me/inde...and-intracellular-hypothyroidism.57031/page-6
The result may indicate why t3 did not work. I have taken T3 for a few years and have had good results. The SPINA software seems to have told me why

 

[char47]

There was a comment on a video from a UK research a year or two back (Bansal?) that he had found elevated beta cortisol receptor in ME patients. This receptor acts as a decoy, binding cortisol but not leading to cellular responses. Its a way the body can make individual cells unresponsive to cortisol ... except in us the problem was more general. This would magnify the effect of the otherwise mild cortisol problems found using conventional cortisol testing methods. Since I do not think it was published we are still in the dark about the quality of the finding.

Cortisol was a standard treatment for ME for a while, or at least post viral fatigue, some decades back. It helped, but then the side effects mounted up, as these were immunosuppressive doses.

Thank you, so it's watch n wait then