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3-Iodothyronamine ( T1AM ) administered to rodents induce a hypometabolic state

Iritu1021

Breaking Through The Fog
Messages
586
I've tried DL-phenylalanine at doses around 4000 mg, but again did not notice much, except perhaps a very mild mood boost (I was hoping it would have a useful antidepressant effect, since depression is one of the comorbidities I have with my ME/CFS).

I don't think I ever tried phenylalanine with selegiline though.

But my brain may not be the best one for testing out selegiline: I used selegiline on and off for 20 years as an effective mood booster and smart drug (before I developed ME/CFS from a viral infection). But after I was hit with a nasty episode of chronic organophosphate pesticide poisoning, just prior to getting ME/CFS, I noticed that selegiline was never again able to boost my mood. So selegiline seemed to permanently lose its antidepressant effect after my organophosphate exposure. I have not been able to figure out why.
that's a great mystery of life why things work and then stop. I find too that I'm never able to step into the same water twice.

I read that dopamine dimerizes with TAAR so if you TAAR is down-regulated or blocked by excess T1AM you might not be able to get the same dopamine boosting effect. That's of course just one possible explanation but I thought I'd mention that since this is a thread on T1AM.
 

Hip

Senior Member
Messages
17,824
that's a great mystery of life why things work and then stop. I find too that I'm never able to step into the same water twice.

I never really had the issue of drugs stopping working until I developed the ill health that lead to ME/CFS. I'd previously been a big explorer of nootropic drugs and (healthy) athletic performance enhancing supplements, and always found their effects consistent over the years.

But since developing ME/CFS, drugs and supplement seem to have become more fickle, with some working for a short period, and then ceasing to work for no apparent reason. This phenomenon seems not uncommon in ME/CFS, as other patients report this too.

I've even joked that ME/CFS is an intelligent adaptive disease process, which when you find a medication that helps, the disease will adaptively respond so as to negate the benefits you get from the medication!
 
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Iritu1021

Breaking Through The Fog
Messages
586
I never really had the issue of drugs stopping working until I developed the ill health that lead to ME/CFS. I'd previously been a big explorer of nootropic drugs and (healthy) athletic performance enhancing supplements, and always found their effects consistent over the years.

But since developing ME/CFS, drugs and supplement seem to have become more fickle, with some working for a short period, and then ceasing to work for no apparent reason. This phenomenon seems not uncommon in ME/CFS, as other patients report this too.

I've even joked that ME/CFS is an intelligent adaptive disease process, which when you find a medication that helps, the disease will adaptively respond so as to negate the benefits you get from the medication!
@Hip and others, you might be interested in reading my latest blog post on dopamine-thyroid connection which also has some of my personal story in it:
http://www.chronicfatiguediagnosis.com/2018/06/03/dopamine-vs-thyroid-hormone/
 

sb4

Senior Member
Messages
1,654
Location
United Kingdom
@Iritu1021 Interesting blog post. You talk about technology at the end. I have read countless times that blue light (and nnEMF) destroy dopamine. "Blue light activates an enzyme that is designed to lower dopamine called MOA-B". I thought blue light also stimulated dopamine though, as this is what happens when you see blue sky in the morning, perhaps it's UV that stimulates dopamine. Either way, have you tried blue blocking glasses or removing the blue out of your computer screen? It should help in this regard.
 

Iritu1021

Breaking Through The Fog
Messages
586
@Iritu1021 Interesting blog post. You talk about technology at the end. I have read countless times that blue light (and nnEMF) destroy dopamine. "Blue light activates an enzyme that is designed to lower dopamine called MOA-B". I thought blue light also stimulated dopamine though, as this is what happens when you see blue sky in the morning, perhaps it's UV that stimulates dopamine. Either way, have you tried blue blocking glasses or removing the blue out of your computer screen? It should help in this regard.
@sb4 thanks for reading! hmm... I have to look into that, it's an interesting topic. I do have some software that changes the brightness and colors in my computer starting late afternoon to help with sleep. However, I'm not sure if it's blue light or not. I do like the idea of "happy blue shades".
I'm also worried about EMF from wireless -especially with its Class 2B carcinogen classification but I haven't really been proactive about that either. It just feels like a vain effort at this point since EMF is everywhere we go.
It's interesting that you note blue sky in the morning as I do notice a circadian correlation in my states, I always feel better when the days are longer and when I get lots of bright light.
 

sb4

Senior Member
Messages
1,654
Location
United Kingdom
Yeah I think circadian rhythm, particularly strong sun light, is way over looked when it comes to health.

As for EMF, yeah it's very difficult. Good thing is it's power drops off exponentially the further you move away. So getting everything wired instead of wireless, sitting away from worst offenders, and putting phone in airplane mode is a good start.
 

Iritu1021

Breaking Through The Fog
Messages
586
I wonder if one can decrease T1AM level by taking bile acid binders like cholestyramine. These drugs are contraindicated for those who take levothyroxine because they bind thyroxine molecule in the gut lumen.

I have no idea as to how valid this hypothesis might be but if we were assume that T1AM is produced in the gut lumen - which is where the latest evidence points - and that T1AM and T4 are very structurally similar than I guess in theory it could work.

I've heard of a number of people who recovered by taking these drugs for what's supposed to be a "mold problem" but maybe mold was just "the red herring" and they were actually getting rid of T1AM.

I don't think I have T1AM problem since I'm able to tolerate T4 without problem now so I can't test it on myself but maybe someone else wants to try.
 

Gondwanaland

Senior Member
Messages
5,092
@Iritu1021 do you think that high T1AM underlies dairy intolerance in Hashi's sufferers?

There is someone I follow in the social media, she started reporting depression from eating dairy and then discovered she was hypothyroid
 

Iritu1021

Breaking Through The Fog
Messages
586
@Iritu1021 do you think that high T1AM underlies dairy intolerance in Hashi's sufferers?

There is someone I follow in the social media, she started reporting depression from eating dairy and then discovered she was hypothyroid
There are at least three ways of how I can link dairy and hypothyroidism.

1) At least half of adults are lactose intolerant. They are usually able to get around it when they are euthyroid but once your metabolism is altered it becomes a bigger issue that can lead to gut problems, malabsorptiona and nutrient deficiencies.

2) Milk contains iodine and excess iodine can lower deiodination. If you are early stage hypothyroid and depend on high -GD for maintaining tissue T3 levels than you have very limited tolerance.

3) Increased histamine release (which seems to be an issue in people with higher than optimal T3 levels) and is probably related to T1AM metabolite that causes histamine release from mast cells. When my histamine was high I was sensitive to literally everything.

http://www.chronicfatiguediagnosis.com/2018/02/26/t1am-and-histamine-connection/

That being said dairy is an excellent source of sphingolipids which have been shown to be a primary deficiency in the majority of CFS patients and is probably responsible for a lot of brain dysfunction.

http://www.chronicfatiguediagnosis.com/2018/03/02/lipid-rafts-the-new-frontier-in-neurochemistry/

I went through a "dietary obsession" phase in my disease - because I reacted so strongly to food - but now, in hindsight, I came to view food intolerance a consequence rather than the cause of my disease. Now, as long as I keep my T4/T3 ratio in the tight narrow range that my body wants it to be I can eat everything I want without any problem.
 

frozenborderline

Senior Member
Messages
4,405
I wonder if one can decrease T1AM level by taking bile acid binders like cholestyramine. These drugs are contraindicated for those who take levothyroxine because they bind thyroxine molecule in the gut lumen.

I have no idea as to how valid this hypothesis might be but if we were assume that T1AM is produced in the gut lumen - which is where the latest evidence points - and that T1AM and T4 are very structurally similar than I guess in theory it could work.

I've heard of a number of people who recovered by taking these drugs for what's supposed to be a "mold problem" but maybe mold was just "the red herring" and they were actually getting rid of T1AM.

I don't think I have T1AM problem since I'm able to tolerate T4 without problem now so I can't test it on myself but maybe someone else wants to try.
Have you tried TUDCA? People say it helps with T3 levels but is bile acid
 

frozenborderline

Senior Member
Messages
4,405
I never really had the issue of drugs stopping working until I developed the ill health that lead to ME/CFS. I'd previously been a big explorer of nootropic drugs and (healthy) athletic performance enhancing supplements, and always found their effects consistent over the years.

But since developing ME/CFS, drugs and supplement seem to have become more fickle, with some working for a short period, and then ceasing to work for no apparent reason. This phenomenon seems not uncommon in ME/CFS, as other patients report this too.

I've even joked that ME/CFS is an intelligent adaptive disease process, which when you find a medication that helps, the disease will adaptively respond so as to negate the benefits you get from the medication!
I swear! I get this too. Got it with mixed tocopherols, emodin, and now it seem
Yeah I think circadian rhythm, particularly strong sun light, is way over looked when it comes to health.

As for EMF, yeah it's very difficult. Good thing is it's power drops off exponentially the further you move away. So getting everything wired instead of wireless, sitting away from worst offenders, and putting phone in airplane mode is a good start.
So using phone with wireless off is fine? I tend to use it as an ipod since all my ipods are broken--i tend to need something to listen to when resting
 

sb4

Senior Member
Messages
1,654
Location
United Kingdom
So using phone with wireless off is fine? I tend to use it as an ipod since all my ipods are broken--i tend to need something to listen to when resting

I'm not sure how ipads work but if it's anything like your phone, putting in airplane mode will turn off wifi, bluetooth, and the microwaves put out from pinging with towers so you should be fine.
 

frozenborderline

Senior Member
Messages
4,405
Abstract
Obesity is a complex disease associated with environmental and genetic factors. 3-Iodothyronamine (T1AM) has revealed great potential as an effective weight loss drug. We used metabolomics and associated transcriptional gene and protein expression analysis to investigate the tissue specific metabolic reprogramming effects of subchronic T1AM treatment at two pharmacological daily doses (10 and 25 mg/kg) on targeted metabolic pathways. Multi-analytical results indicated that T1AM at 25 mg/kg can act as a novel master regulator of both glucose and lipid metabolism in mice through sirtuin-mediated pathways. In liver, we observed an increased gene and protein expression of Sirt6 (a master gene regulator of glucose) and Gck(glucose kinase) and a decreased expression of Sirt4 (a negative regulator of fatty acids oxidation (FAO)), whereas in white adipose tissue only Sirt6 was increased. Metabolomics analysis supported physiological changes at both doses with most increases in FAO, glycolysis indicators and the mitochondrial substrate, at the highest dose of T1AM. Together our results suggest that T1AM acts through sirtuin-mediated pathways to metabolically reprogram fatty acid and glucose metabolism possibly through small molecules signaling. Our novel mechanistic findings indicate that T1AM has a great potential as a drug for the treatment of obesity and possibly diabetes. View Full-Text
 

frozenborderline

Senior Member
Messages
4,405
I've heard of a number of people who recovered by taking these drugs for what's supposed to be a "mold problem" but maybe mold was just "the red herring" and they were actually getting rid of T1AM
its an interesting thought but I’ve heard of way more people recovering using mold avoidance without drugs or with few drugs than people feeling relief from the cholestyramine. In fact a lot of the mold avoidance people criticize shoemaker for emphasizing the binders and pharmaceutical treatment and not as much extreme avoidance
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Abstract
Obesity is a complex disease associated with environmental and genetic factors. 3-Iodothyronamine (T1AM) has revealed great potential as an effective weight loss drug. We used metabolomics and associated transcriptional gene and protein expression analysis to investigate the tissue specific metabolic reprogramming effects of subchronic T1AM treatment at two pharmacological daily doses (10 and 25 mg/kg) on targeted metabolic pathways.

...

Our novel mechanistic findings indicate that T1AM has a great potential as a drug for the treatment of obesity and possibly diabetes. View Full-Text
This is a study using mice. It might be wise to ponder this:

http://www.slate.com/articles/health_and_science/the_mouse_trap/2011/11/the_mouse_trap.html

The title is "The Mouse Trap: The dangers of using one lab animal to study every disease."