Cymatic
Member
- Joined
- Feb 15, 2017
- Messages
- 46
A typical conservative starting dose will be 50mcg T4 and 5mcg T3 1x dailyWhat ratio of T4 to T3 do you suggest and how often per day? Also what is your source for PEA?
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A typical conservative starting dose will be 50mcg T4 and 5mcg T3 1x dailyWhat ratio of T4 to T3 do you suggest and how often per day? Also what is your source for PEA?
You feel irritated after dhea because it is being converted to estrogen... I do not recommend normal dhea ...I do recommend 7-keto dehydroepiandrosterone(and only with pregnenolone) the one can't be converted into estrogen.... Beta alanine lowers serotonin in brain... Levothyroxine is t4 and I only recommend taken with triiodothyronine(t3)
Does the nicotine gum you take have any filler ingredients? Could you post a link. I have always had a flirtacious relationship with tobacco, but would much rather lean on a gum than a chew or a smoke.Yeah, niacinamide, nicotine, 5a-DHP and androsterone.
estrogen increases prolactin... and in short term prolactin makes you tired sleepy lacking energy... ready to go to bed or actually staying in bed.... It doesn't make you irritable in short term but we all know how bad prolactin is in medium long run...lack of libido and testosterone is one Its feature in physiological realmEven if it was still converting to estrogen after all that(?) then explain why when I eat soy or drink beer or do something that increases my estrogen levels I do not feel irritable like this at all, just tired and less libido.
What ratio of T4 to T3 do you suggest and how often per day? Also what is your source for PEA?
I use 12.5mcg of T3 and T4 ratio 1:1 and is great...and don't need coffee at all during the day... but you can use 1:2(12.5mcg triiodothyronine and 25mcg levothyroxine) or ratio or 1:3(12.5mcg triiodothyronine and 37.5 levothyroxine)
you have to see what is really best ratio for you but thyroid supplementation is essential for your issues
I buy PURE PEA brand from Germany... It is European brand that is sold as food supplement in pharmacies as well
estrogen increases prolactin... and in short term prolactin makes you tired sleepy lacking energy... ready to go to bed or actually staying in bed.... It doesn't make you irritable in short term but we all know how bad prolactin is in medium long run...lack of libido and testosterone is one Its feature in physiological realm
I didn't mean you will feel good in short term...I said prolactin will make you tired and not wanting to fight back... You will not feel irritable because you will not have brain energy to fight back... Harm avoidance in other words...So in the short term it makes you feel good but stay away because its long term effects? In essence you mean to say feel miserable because you'll live longer?
PEA sounds like it's worth trying... Has anyone else tried it?About PEA
PEA is palmitic acid + ethanolamine
Dr Raymond Peat wrote about It
"Another study in the brains of living rats found that a particular class of brain lipids, ethanolamine plasmalogens, had a turnover time of about 5 hours (Masuzawa, et al., 1984). (This type of lipid is an important component of the lipoproteins secreted by the liver into the serum [Vance, 1990], and is also a major lipid in the heart and brain.) Stresses such as the loss of sleep cause great distortions in phospholipid metabolism throughout the body, especially in the brain and liver."
"At birth, the baby's mitochondria contain a phospholipid, cardiolipin, containing palmitic acid, but as the baby eats foods containing polyunsaturated fatty acids, the palmitic acid in cardiolipin is replaced by the unsaturated fats. "
"The respiratory activity of the mitochondria declines as the polyunsaturated oils replace palmitic acid, and this change corresponds to the life-long decline of the person's metabolic rate."
In terms of my experience with PEA: Libido is high and wellbeing ... in terms of cognition... It boosts your thinking quite a lot and stress is better handle
I can't quite tell what it even is. But it (PEA) is readily available in US.PEA sounds like it's worth trying... Has anyone else tried it?
Key findings of the study include broad effects on plasma and cerebrospinal fluid (CSF) neuroactive steroid levels observed in 14 PFS patients, as compared to 25 controls. Statistically significant decreased levels of DHT, pregnenolone, progesterone, 17-beta estradiol and dihydroprogesterone (DHP), and increased levels of DHEA, testosterone and 3-alpha diol were observed in the CSF of PFS patients.
In plasma, statistically significant decreased levels of DHP and allopregnanolone, and increased levels of pregnenolone, DHEA and testosterone were observed.
Decreased plasma levels of allopregnanolone and decreased CSF levels of progesterone are common features of anxious/depressive symptomatology. Important physiologic effects of neuroactive steroids on brain function include neuroendocrine control of reproduction and sex behavior, synaptic plasticity, morphology of neurons and astrocytes, maintenance of cytoskeleton proteins and myelin, adult neurogenesis, and cognition-related functions
Peripheral neuropathy of the pudendal nerve, the major nerve supplying the genitals that is critical for peripheral neurogenic control of erection, in PFS patients is a novel finding that demonstrates for the first time involvement of the peripheral nervous system in PFS patients with severe ED.
it discovered that etifoxine worked through completely different mechanisms, i.e.. GABA(A) beta subtype selectivity and neurosteroid biosynthesis (purported to work through TSPO).
Etifoxine has been shown to stimulate the biosynthesis of endogenous neurosteroids, namely 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone and tetrahydroprogesterone.[12] Several studies have shown that the synthesis of neurosteroids is essential to the pharmacological actions of etifoxine. Inhibitors of neurosteroid biosynthesis reverse the anxiolytic and analgesic actions of etifoxine.
The new study mentioned by @JonnyCraig earlier in this thread is HUGE. A few significant quotes from the study:
1. Increased levels of testosterone in CSF and Plasma can be indicative of lowered 5ar activity.
2. Decreased levels of DHT and DHP in CFS, and decreased levels of DHP and Allopregnanolone in plasma can also be indicative of lowered 5ar activity.
3. Peripheral neuropathy of the pudendal nerve, a problem involving the nervous system.
The last point is exciting regarding an acknowledgment of a problem with the Nervous System, this has been my argument for the latter part of the thread. THIS GIVES US THE GUIDANCE THAT NEUROSTEROIDS AND 5AR SPECIFICALLY IN THE NERVOUS SYSTEM OUGHT TO BE TARGETED.
I posted a few studies earlier showing that PALMITOYLETHANOLAMIDE, and Vitamin C increases neurosteroids.
Etifoxine, an Anxiolytic drug which purportedly binds to the TSPO (translocator protein) increases neurosteroids.
From wiki:
PEONY ROOT has also been found to increase neurosteroids. I can't find the study at the moment I'll post it when I do. This is hugely exciting stuff.
I've just seen this thread. As I've just started a 6 week cycle of Pan/Andro, having read this it seems like as a PFS sufferer I'd be better off switching to a more pro 5AR combo like 5a-DHP/Andro/Diamant? Or can leave the Pan in as I don't seem to get the pro estrogen or prolactin effects of DHEA as some seem to here.
At the moment I'm on:
8mg Pan and Andro daily, application to the scrotum
Am I right in saying that I'd be better off switching to this combination:
4mg Pan/Andro scrotal application
5mg 5a-DHP/10mg Diamant to the inside elbow
8mg andro or Pan is a lot. That would make me feel terrible. How long have you been suffering from pfs? What is your diet like? Do you drink any caffiene?
I ahve gotten ebtter results from just 5adhp, aspirin, and niacinimide and caffee and famatodine
Interesting how estradiol is also found lowerred in that study. Why do you think that is?
And is anything that "increases neurosteroids" going to necessarily benefit?
Abstract
INTRODUCTION:
The treatment of anxiety disorders is still a challenge; novel pharmacological approaches that combine rapid anxiolytic efficacy with fewer side effects are needed. A promising target for such compounds is the mitochondrial translocator protein (18 kDa) (TSPO). TSPO plays an important role for the synthesis of neurosteroids, known to modulate GABAA receptors, thereby exerting anxiolytic effects.
We investigated the pharmacological profile of 2 well established TSPO ligands (XBD173 and etifoxine) compared to the benzodiazepine diazepam with regard to TSPO binding affinity, TSPO expression and neurosteroidogenesis.
. Radioligand binding assays revealed the highest binding affinity to TSPO for XBD173, followed by diazepam and etifoxine.