Seems great but if it is so great what can we expect to be the downsides?

@natureman Overdosing effects sound scary I wonder what qualifies as overdosing. 100mcg T3? 300mcg T4?

@oj Can't resist, sorry not sorry 😬
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You have all the needed sources within reach https://bioenergetic.forum/topic/4/ray-peat-resource-thread

@Lothric Im glad that worked out for you! I find that i have much more consistent energy doing it that way too.

@cs3000
May be key to use IR light that includes 8-10 uM wavelength , IR-C
https://www.nature.com/articles/s41598-019-48187-0
which is weird because only a tiny amount of IR-C comes from the sun, and doesnt penetrate skin as well as ir-A or B. but was the wavelengths that worked on mitochondria in epithelial cells

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humans might emit infrared around 9-10 uM though which matches the mitochondria study https://www.researchgate.net/post/What_is_the_IR-radiation_emitted_by_the_human_body

& the embryo study used a lamp "at wavelengths ranging from 1 μm to 14 μm, with a peak at 2.9 μm."

@cs3000

in response to stimulation with 1,25[OH]₂ D, upregulation of the inactivating enzyme CYP24A1 curtailed the functional effects of vitamin D in DCs, but not macrophages.

rifampin fixes 1,25 excess in sarcoidosis through inducing CYP 3a4 enzyme

So CYP 3a4 can be used to lower the 1,25 excess coming from macrophages

side note 24,25 vit D increases bone strength / fracture repair where 1,25 does not have this effect https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6063485/

Insightful studies below that highlight 24,25 aka 24r,25 looks to be the commonly desirable form of vitamin D.
If in good health it's supposed to rise in ratio to 1,25 as 25 vit D goes up, https://www.nature.com/articles/s41598-019-43462-6

24r,25 form of vit D is likely protective in MS / brain atrophy https://pubmed.ncbi.nlm.nih.gov/21047880/ lower 24,25 compared to 25 = worse outcome

and it actually DECREASES the VD Receptor

Vitamin D3 is metabolized in the liver and kidney in addition to localized tissue-specific biosynthesis. Bone cells are known to metabolize 25(OH)D3 into both 1α,25(OH)2D3 and 24R,25(OH)2D3 via 1α-OHase and 24-OHase, respectively

24,25 DECREASES vdr expression and can lower 1,25,
it inhibits stem cell proliferation like 1,25 also does, but unlike 1,25 it stimulates stem cell maturation / enables their differentiation ,
increasing bone repair / strength https://pubmed.ncbi.nlm.nih.gov/24597546/

(but by my experience cannot get this increased enough simply through vit D without worsening the issue from extra 1,25 in people with this excess issue,
was thinking maybe there isnt enough 24a1 enzyme producing 24,25 here, but upregulating doesnt work to counter 1,25 in macrophages)

targeting less 1,25 through CYP 3a4 should have effect but also degrades 25 vit D though, so losing 24,25.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310418/

Thyroid hormone also increases cyp3a4
(another connection to hypothyroid & vitamin D problems)
and also decreases CYP27B1 , lowering 1,25 (at least in the kidneys, wonder if this also has effect in macrophages keratinocytes etc https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077994/table/T1/?report=objectonly)

lowering Cyp27b1 is a major target for lowering 1,25, it stays expressed even when macrophages are removed from IFN-y inducing environment https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077994/

How was it that synthetic 1-hydroxylating activity in macrophages harvested from humans with active disease persisted ex vivo in culture even in the absence of conditioning IFNs? Some of the questions have been answered and some are still coming to light. For example, it is now known that there exists a single gene that encodes the 1-hydroxylase, CYP27B1 [11] and the 24-hydroxylase, CYP24A1 [12]. Further, it is now clear that persistence of mTB in macrophages is an explanation for the continual expression of the CYP27B1 in human macrophages even after their removal from the host and conditioning cytokines present in the inflammatory microenvironment in the host.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6508960/
(thyroid hormone & iron key players) & upping 24,25

In this work, we demonstrate that THs induce a significant increase in CYP3A4 mRNA levels, protein expression and metabolic activity through the membrane receptor integrin αvβ3 and the activation of signalling pathways through Stat1 and NF-κB.

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@basebolt Thanks! Wow 150mcg I'm only at a sip and im on my second week and this morning I experienced a stress response. Woke up with a beating heart and sweating. I already have high heart beats from estrogen and adrenaline. I can't imagine getting to 150mcg from the get go. Will staying on T3 deplete T4 too much or should that not be an issue since my liver is dysfunctional and overburdened? I am on high dose progesterone for 6 months, so its certain the T3 caused the stress response. What does my reaction to T3 tell you about my situation?

@Kvirion Yes! I read the same too about methylation from another forum and that if one was to start B vitamins, they would need to start low and slow also. But high doses are advertised everywhere.

@yerrag said in Heart failure report showing t4 solo vs t4:t3 in action for full recovery (edema too):

By the way, I have fully recovered from heart failure but thanks to the knowledge gained from the bioenergetic orientation of being immersed in a thought subculture revolving around Ray Peat's writings I am back to mybold healthy thriving self.

💪 💪 💪

@rosenstein if the liver can’t store glycogen then sleep will be affected, (no fuel during sleep-which ironically is a metabolically demanding process). Stress in the form of overtraining will raise cortisol which can lead to fatty liver and decreased glycogen storage/muscle catabolism. Some of us with favorable body composition might be able to skirt this for a time because muscles can store glycogen too, (my personal theory is that they do so when subjected to the stress of training as localized glycogen storage tanks to deal with stress more immediately-especially if liver function is impaired).

I don’t do the caffeine before bed, (sorry for any confusion there). I take my last dose around 3pm. My reasoning for the caffeine and vitamin K supplementation is due to a number of studies Haidut posted on the old forum regarding their leaning out the liver and assisting in glycogen storage. When I started “Peating” I couldn’t drink black coffee without cold hands and feet. Now I can drink a double espresso on an empty stomach with no stress response, (suggesting my glycogen storage is much improved).

In the studies, I believe glycogen storage was improved with a certain amount of caffeine mg/kg. In my initial experiments I used 1200mg split in three doses of 400mg each with lots of food for two weeks. Since then I’ve found I prefer 200mg twice a day for longer periods. This also assisted in improved metabolism as I dropped body fat while increasing calories and maintaining training regime. My weight went from about 235 to 205, (and the weight loss wasn’t instant, it continued after ceasing the caffeine over the course of the next few months).

K in studies was found to lower liver enzymes dramatically at 15mg over a few weeks, or 45mg over a few days.

@bhspeat

I believe it was anywhere from a couple weeks or a month maybe. I switched to Armour after that.

I personally wouldn't start with an NDT product like that. I think it will probably just be confusing to figure out what's going on without the ability to be precise. If your temp and pulse are both low and you want to look into thyroid as a tool to get it up, I'd definitely use something like Armor, or Cynomel/Cynoplus.

If you haven't seen this article by Danny, it's very helpful.

There's a lot of good info on this page as well.

@Shar_to_the_dae I hope I don’t have a dead batch

@Master Too bad but thanks anyway Master.

So I got a blood test today. I didn't get a full thyroid panel due to the cost.

My results are as below:

Total cholesterol: 183 mg/dl. Before starting thyroid it was 180, and Ray said for someone on thyroid even 160 is acceptable, so I'm good here;

Ferritin: 32.8 μg/l. I test that because one time I did get a result in the low teens and adding more iron helped somewhat. I need to eat liver more regularly, I felt better when it was around 50.

Vitamin D (25-OH): 22.8 ng/ml. This is what I get for being a cheapskate. When starting thyroid I reasoned that the test is expensive, and I already had a vit D supplement on hand, so I assumed taking 2000 IU daily will be enough to avoid this problem. Today I took 10 000 IU and there's already some improvement in my mood; I assume this might be the main reason for my recent difficulties;

TSH: 2.2 μU/mL. So I'm definitely not experiencing a thyroid storm and my TSH is not being suppressed by excess T3. However, this is puzzling because my TSH was actually lower (1.2) before starting NDT.

Does anyone know why taking thyroid might increase someone's TSH? Is it because exogenous hormones have suppressed my natural production, but due to vitamin D deficiency (or some other deficiencies) it fails to increase metabolism and thus the pituitary signals for even more? Or maybe my TSH was suppressed by cortisol (after all, 1.2 is kind of low for someone with waking temperatures in the low 97s), the NDT has lowered cortisol, so now TSH can reach its natural level? Or maybe NDT just isn't for me and I need more T3?

My plan for now is to eat liver at least once and preferably twice a week, blast Vitamin D like there's no tomorrow, and stay on the five drop dose until the worst issues go away.

@MJ_LZ I started the T3 three days ago now but have noticed zero anything. My resting heart rate has dropped in fact. I’m taking 5mg twice a day with meals. When did you feel symptoms improve?