TUDCA

Ras

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Has anyone been able to try TUDCA and Taurine for a while and compare them?
 
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Has anyone been able to try TUDCA and Taurine for a while and compare them?

I've been taking Taurine for well ove a year and started TUDCA a few weeks ago. TUDCA stimulates bile flow a lot better that Taurine in my experience. Taurine does it, but it's not as consistent and as pronounced as TUDCA. Not sure how its affecting liver numbers, dont have the money for tests at the moment, just relying on subjective experiences. Taurine is good for GABA though, better than TUDCA I'd say.
 

Ras

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Sep 12, 2015
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I've been taking Taurine for well ove a year and started TUDCA a few weeks ago. TUDCA stimulates bile flow a lot better that Taurine in my experience. Taurine does it, but it's not as consistent and as pronounced as TUDCA. Not sure how its affecting liver numbers, dont have the money for tests at the moment, just relying on subjective experiences. Taurine is good for GABA though, better than TUDCA I'd say.
Thank you.
What benefits are you hoping to get from TUDCA?
 
Joined
Jan 4, 2017
Messages
260
Thank you.
What benefits are you hoping to get from TUDCA?

I have a feeling my liver isn't where it needs to be. I feel like utter crap if I drink a moderate amount of alcohol and I tend to benefit from Progesterone a lot, which along with other signs, tells me I have estrogen issues. I'm hoping improving liver function will help me not rely on Progesterone as much and also help my body function better overall.
 

Dezertfox

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Aug 15, 2017
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I started on TUDCA yesterday and got a headache, had it with lunch and headache..Not sure why any thoughts?
 

Dobster

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Feb 11, 2016
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What is a good brand to take ? Also would a choline supplementation be needed whilst taking TUDCA? Thanks
 

BigChad

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From what I've read that's way, way too much for the average user. That dose was used on people with severe cirrohsis or some other pathological condition they were experimentally treating with TUDCA. For reducing ER stress and liver protection, 500mg/day is plenty, and 250mg/day would probably be fine.

I'm finding I'm actually getting a nice little boost out of TUDCA, and am wondering now if it doesn't work in much the same way as Ray says coffee works. And without the side effect of AChE inhibition that caffeine brings, that rattles some of us so much. I'm still looking into it and not sure if my fogbrain will be able to connect the dots, but if TUDCA turns out to be for me what I'm thinking it might, I might not have to worry about the demon coffee any more. That's a pretty big if at this point, but right now I'm encouraged. Only time will tell.

Also, I don't think TUDCA is something that should be taken long term. In some studies they've had people take it for up to a year but for everyday users it might be best to cycle it, like a couple months on, couple months off, or similar.

what are the risks with doing 250mg tudca a day, year round? why does it need to be cycled
 

bdawg

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as Haidut mentioned, Bile Acid -> FXR activation for the win - can overcome type 2 generated by HFD by increasing our cholesterol use for the good stuff (steroidogenesis)

The study mentions both saturated and PUFA as bad tho (Oleic and Palmitic) but largely follows Rays line on the havoc FFA can cause

Steroidogenic acute regulatory protein (StAR) overexpression attenuates HFD-induced hepatic steatosis and insulin resistance - ScienceDirect

Steroidogenic acute regulatory protein (StAR), one of the mitochondrial cholesterol delivery proteins, transfers cholesterol from the outer mitochondrial membrane to the inner mitochondrial membrane, which plays an important role in the maintenance of intracellular lipid homeostasis [28]. Our previous in vivo investigations showed that StAR played an important role in regulating cholesterol and triglyceride levels in the process of atherosclerosis [29]. Thus, targeting StAR- bile acid synthesis pathway may significantly contribute to a decrease in cholesterol accumulation in the liver and potentially reduce liver damage.
Other than disorders in lipid content, increased FFA levels also led to glucose disorders, resulting in more gluconeogenesis and less glycogen synthesis and glucose consumption [30], [31], the main symptoms and manifestations of insulin resistance.
In the present study, we provided insight into the effect of StAR on hepatic lipid/glucose metabolism and insulin resistance, using both in vitro and in vivo models for NAFLD.
According to the most widespread and prevalent “two-hit” model for NAFLD, while the “first hit” refers to lipid accumulation (including FFA, cholesterol and triglyceride) in the hepatocytes [32], the second is subsequent hepatic injury, inflammation and fibrosis. Consistent with this theory, our models of NAFLD induced by OA/PA overloading or HFD feeding resulted in marked up-regulation of lipid accumulation, de novo lipogenesis, and inflammatory response. At the same time, the expression of StAR were significantly decreased whether in FFA-overloaded hepatocytes or in livers of NAFLD mice and patients, indicating that StAR played an important role in preventing the development of NAFLD. Furthermore, we introduced the adenovirus encoding StAR gene to rival this inhibitory effect. Our data demonstrated that StAR overexpression decreased the levels of hepatic lipids and maintained the hepatic glucose homeostasis in FFA-overloaded hepatocytes and livers of NAFLD mice induced by HFD. Expressions of genes involved in hepatic lipid metabolism (HMGCR, SREBP1c, FASN, ACC1), inflammatory response (TNF-α, MCP-1, IL-β) as well as gluconeogenesis genes (Pcx, G6PC) were decreased, while genes involved in glycogen synthesis (GSK-3β, Gys2) were increased significantly in hepatocytes by StAR overexpression.
Insulin resistance is suggested to be the key pathogenic factor in the development of hepatic steatosis [33]. It is well established that the insulin signaling pathway plays a central role in regulating glucose, lipid, and energy metabolism [34]. Phosphorylation of insulin receptor subsrate-1 (IRS-1) and Akt is a marker of insulin signaling pathway [25]. Diacylglycerol (DAG), a second messenger signaling lipid, and its target phosphorylated PKCε are among the main negative regulators for insulin signaling that may induce serine phosphorylation of IRS-1[26], [35], [36]. The data from this study showed that the content of intracellular DAG and phosphorylated PKCε were significantly decreased after StAR overexpression, indicating that the inhibited insulin signaling in NAFLD was reversed by StAR. As a result, the tyrosine phosphorylation of IRS-1 and Akt were markedly increased by StAR overexpression.
LIPIN1 is a mammalian phosphatidic acid phosphatase for diacylglycerol (DAG) synthesis. Knockdown of LIPIN1 ameliorates hyperglycemia and insulin resistance by reducing DAG and PKCɛ activity in db/db mice [19], which is consistent with our study. Our present data showed that StAR overexpression decreased expression of LIPIN1 in livers of NFALD mice. These data suggested that StAR could improve insulin signaling and inhibit the progression of NAFLD by reducing activity of DAG and PKCɛ.
In addition, StAR plays a critical role in bile acid synthesis by enhancing the delivery of substrate cholesterol into mitochondria via the “acidic” pathway [8]. It was demonstrated that bile acids lowered TG synthesis via activating FXR-SHP-SREBP-1c regulatory cascade. Bile acids activate FXR to induce SHP synthesis, and SHP suppresses the transcriptional function of SREBP-1c, leading to the suppression of lipogenic gene expression [12]. Moreover, Ishimoto et al. demonstrated that SREBP-1c mediated the transcription of LIPIN1 gene [37]. In our study, hepatic overexpression of StAR significantly increased both serum and hepatic bile acid levels in mice, which was consistent with previous studies [38], [39]. Furthermore, the expression of FXR downstream genes such as SHP, SREBP-1c and LIPIN1 was regulated by StAR overexpression, indicating that FXR was activated by bile acid, although the expression of FXR gene was not affected. FXR activation might control lipogenesis through both SREBP-1c-dependent and -independent mechanisms. Several other mechanisms have been implicated in the TG-lowering effect of FXR activation. FXR ligands induce the expression of PPARα, which is a key player in hepatic lipid metabolism, and its target gene pyruvate dehydrogenase kinase-4 (PDK4) [40]. Our study indicated FXR activation by StAR overexpression resulted in PPARα up-regulation in NAFLD mice.


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Our findings indicate that supraphysiological bile acid levels as observed in cholestasis stimulate steroidogenesis via an S1PR2‐ERK‐SF‐1 signalling pathway.

This one says FXR represses CYP17A1 steroidogenesis in the liver in a fed state but not in ketogenesis when DHEA is formed in the liver and hits PPARa

Steroidogenic control of liver metabolism through a nuclear receptor-network - ScienceDirect

By contrast, the FXR is activated postprandially by bile acids returning to the liver from the intestine [6]. As such, FXR and PPARα can directly drive expression of genes involved in anabolic and catabolic processes, respectively, in the liver.
However, FXR can also act as a trans-repressor of gene expression. In the bile-acid synthesis pathway, for example, FXR induces the expression of the small heterodimer partner (SHP), which represses expression of Cyp7a1 by preventing binding of the liver receptor homologue 1 (LRH1) to its promoter [10]. Intriguingly, FXR is also expressed in steroidogenic cells of the gonads [11], many of its target-genes are P450-enzymes, and bile acids themselves are steroid-like molecules that provide feedback on its activity [12]. As such, FXR may potentially represent a previously unexplored integrator of metabolic and steroidogenic processes.

Here, we have discovered that the steroidogenic enzyme Cyp17a1 is repressed by FXR-action in the liver in the fed-state. However, during starvation, Cyp17a1 is de-repressed and produces a hormone-ligand (DHEA) for PPARα.
 

Lokzo

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I have been using TUDCA at around 250mg the last couple of weeks.

This stuff makes you POOP!

I can't believe how often it makes you.

Im usually a once in the morning kind of guy, but this has ramped it up to like 3 times a day.


I have noticed energy increases from it as well. I feel like my workout performance is better and that my Urine colour is less dark than usual.

Overall, I think TUDCA is very therapeutic. I think it needs to be cycled, and also very low doses are probably still very good for liver support.

Yet again, learning so much from the Ray Peat forum. Thanks, everyone.
 

Goobz

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Mar 2, 2019
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I have been using TUDCA at around 250mg the last couple of weeks.

This stuff makes you POOP!

I can't believe how often it makes you.

Im usually a once in the morning kind of guy, but this has ramped it up to like 3 times a day.


I have noticed energy increases from it as well. I feel like my workout performance is better and that my Urine colour is less dark than usual.

Overall, I think TUDCA is very therapeutic. I think it needs to be cycled, and also very low doses are probably still very good for liver support.

Yet again, learning so much from the Ray Peat forum. Thanks, everyone.

Thanks for the report!

You’re in Aus too aren’t you? If you can divulge, where do you source your Tudca?
 

Momado965

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Aug 28, 2016
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TUDCA is not much different than taurine when it comes to liver or metabolic effects, as it is in fact a taurine-conjugated bile acid. Taking taurine will stimulate its synthesis, as well as the synthesis of all other bile acids. All stimulators of bile acids or bile acids themselves will have a pro-metabolic effect as activating the bile acid receptor increases conversion of T4 into T3. That is how taurine helps diabetes, CVD, cholesterol, etc.
How Pregnenolone And Progesterone Raise Metabolism
How Taurine May Treat Diabetes

While it is interesting to experiment with, if you look at the animal studies that compared it to taurine you will see that it does not have that much more benefit to offer. Taurine has other benefits too that TUDCA does not - i.e. GABA agonism and decreasing catecholamines.




Does regular taurine have the same insulin sensitizing benefits if tudca?


Insulin sensitivity was increased in obese but non-diabetic men and women after 1,750mg daily ingestion of TUDCA for 4 weeks. Muscle and liver tissue became more insulin sensitive, but adipose (fat) tissue did not. The degree of improvement was approximately 30% improvement, which rivals current anti-diabetic pharmaceuticals such as thiazolinediones and metformin."

Tauroursodeoxycholic Acid - Scientific Review on Usage, Dosage, Side Effects | Examine.com
 

Motif

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Nov 24, 2017
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Does regular taurine have the same insulin sensitizing benefits if tudca?


Insulin sensitivity was increased in obese but non-diabetic men and women after 1,750mg daily ingestion of TUDCA for 4 weeks. Muscle and liver tissue became more insulin sensitive, but adipose (fat) tissue did not. The degree of improvement was approximately 30% improvement, which rivals current anti-diabetic pharmaceuticals such as thiazolinediones and metformin."

Tauroursodeoxycholic Acid - Scientific Review on Usage, Dosage, Side Effects | Examine.com
I have a feeling my liver isn't where it needs to be. I feel like utter crap if I drink a moderate amount of alcohol and I tend to benefit from Progesterone a lot, which along with other signs, tells me I have estrogen issues. I'm hoping improving liver function will help me not rely on Progesterone as much and also help my body function better overall.
Were you able to improve your liver health meanwhile ?
 

Ἀπόλλων

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Jun 28, 2021
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Where can one get TUDCA in Europe? From reputable company if possible.
An old question, but as I've been looking for the same and found an EU source (within EU, not UK) here it is: amazon.de:

TUDCA Liver Support, Detoxification, Cleansing 60 Vegan Capsules, 250 mg High Strength
Amazon productView: https://www.amazon.de/dp/B08VN9KSPY/

(non-affiliate link)

You can find the same on Amazon.FR, Amazon.ES, etc. That's about the only source I've been able to find that is not totally shady.
 

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