I have been running HGH for several years and usually have been cruising it at 2iu and then ramp it and blast it with my cycle between 4-6iu split.
Currently right now I’m off HGH after being on it for a year straight which is recommended to help bringing back your BG to baseline, as well to prevent insulin sensitivity and most importantly to avoid developing antibodies for using it over a prolonged period of time. I’ll be getting bloods in a few weeks to get my base before starting back up on my next cycle.
Anyway, one of the biggest tools I utilize while on HGH has always been BerBerine especially above 4iu in order to keep my BG in check. It has always provided what studies have shown is to promote the ability to provide positive effects on blood sugar, cholesterol, heart disease, blood pressure, autoimmune disease, inflammation, weight control. As well as lowering your A1-C.
I have always preferred BerBerine versus utilizing Metaformin due to the vast amount of side effects it could bring.
What I didn’t know, is that there have been multiple studies on BerBerine’s negative side effects in regards to how it can effect pretty much the protein synthesis being decreased in your body over time and increased muscle degradation as well. It also seems to have an impact on your IGF-1 Levels and is not recommended for long term use.
What I am wondering is the extent this has on an individual and if we are obviously on an AAS cycle and working out etc if it’s enough to counterbalance the negative effects as well.
Perhaps @opti @mands @Dr JIM or anyone else familiar with additional studies and its correlation could provide some more insight.
I apologize if the following is quite lengthy but a very informative read I can assure you.....
This is an excerpt from one of the many studies I was reviewing:
“RESEARCH DESIGN AND METHODS We evaluated whether berberine ameliorates muscle atrophy in db/db mice, a model of type 2 diabetes, by measuring protein synthesis and degradation in muscles of normal and db/db mice treated with or without berberine. We also examined mechanisms for berberine-induced changes in muscle protein metabolism.
RESULTS Berberine administration decreased protein synthesis and increased degradation in muscles of normal and db/db mice. The protein catabolic mechanism depended on berberine-stimulated expression of the E3 ubiquitin ligase, atrogin-1. Atrogin-1 not only increased proteolysis but also reduced protein synthesis by mechanisms that were independent of decreased phosphorylation of Akt or forkhead transcription factors. Impaired protein synthesis was dependent on a reduction in eIF3-f, an essential regulator of protein synthesis. Berberine impaired energy metabolism, activating AMP-activated protein kinase and providing an alternative mechanism for the stimulation of atrogin-1 expression. When we increased mitochondrial biogenesis by expressing peroxisome proliferator–activated receptor γ coactivator-1α, berberine-induced changes in muscle protein metabolism were prevented.
CONCLUSIONS Berberine impairs muscle metabolism by two novel mechanisms. It impairs mitochonidrial function stimulating the expression of atrogin-1 without affecting phosphorylation of forkhead transcription factors. The increase in atrogin-1 not only stimulated protein degradation but also suppressed protein synthesis, causing muscle atrophy.
There is evidence that an herbal compound, berberine, improves insulin-mediated glucose metabolism and enhances insulin sensitivity in mice (1–3). For example, Lee et al. (1) reported that administering berberine to insulin-resistant db/db mice led to a decrease in body fat and significant improvement in glucose tolerance. Because catabolic conditions associated with insulin resistance can lead to progressive muscle atrophy, we examined whether berberine improves muscle protein metabolism. This was of interest because successful inhibition of mechanisms causing loss of muscle mass in diabetic mice might be extended to other catabolic conditions that cause muscle atrophy (4–8). However, we found that berberine actually promoted muscle atrophy in both wild-type and db/db mice. This led us to examine potential mechanisms causing berberine-induced muscle atrophy.
Muscle atrophy induced by several catabolic conditions (e.g., cancer, cachexia, diabetes, chronic kidney disease, cardiac failure, sepsis) share a common group of biochemical and transcriptional adaptations (7–12). In atrophying muscles, there is a higher level of expression of the E3 ubiquitin ligase, atrogin-1/MAFbx, which has been closely linked to stimulation of muscle protein degradation by the ubiquitin-proteasome system (UPS) (13–17). The mechanism that increases atrogin-1 expression has been linked to defects in insulin/IGF-1 signaling, specifically, suppression of insulin receptor substrate (IRS)-1–associated phosphatidylinositol 3-kinase (PI3K) activity and a reduction in p-Akt (14–16). The decrease in p-Akt, in turn, reduces phosphorylation of the forkhead transcription factors (FoxOs) that can enter the nucleus to stimulate atrogin-1 expression. The focus on atrogin-1 in conditions stimulating muscle atrophy arises because atrogin-1 expression causes a proportional increase in muscle protein degradation (17).”
Here is the link for the entire study:
diabetes.diabetesjournals.org
Currently right now I’m off HGH after being on it for a year straight which is recommended to help bringing back your BG to baseline, as well to prevent insulin sensitivity and most importantly to avoid developing antibodies for using it over a prolonged period of time. I’ll be getting bloods in a few weeks to get my base before starting back up on my next cycle.
Anyway, one of the biggest tools I utilize while on HGH has always been BerBerine especially above 4iu in order to keep my BG in check. It has always provided what studies have shown is to promote the ability to provide positive effects on blood sugar, cholesterol, heart disease, blood pressure, autoimmune disease, inflammation, weight control. As well as lowering your A1-C.
I have always preferred BerBerine versus utilizing Metaformin due to the vast amount of side effects it could bring.
What I didn’t know, is that there have been multiple studies on BerBerine’s negative side effects in regards to how it can effect pretty much the protein synthesis being decreased in your body over time and increased muscle degradation as well. It also seems to have an impact on your IGF-1 Levels and is not recommended for long term use.
What I am wondering is the extent this has on an individual and if we are obviously on an AAS cycle and working out etc if it’s enough to counterbalance the negative effects as well.
Perhaps @opti @mands @Dr JIM or anyone else familiar with additional studies and its correlation could provide some more insight.
I apologize if the following is quite lengthy but a very informative read I can assure you.....
This is an excerpt from one of the many studies I was reviewing:
“RESEARCH DESIGN AND METHODS We evaluated whether berberine ameliorates muscle atrophy in db/db mice, a model of type 2 diabetes, by measuring protein synthesis and degradation in muscles of normal and db/db mice treated with or without berberine. We also examined mechanisms for berberine-induced changes in muscle protein metabolism.
RESULTS Berberine administration decreased protein synthesis and increased degradation in muscles of normal and db/db mice. The protein catabolic mechanism depended on berberine-stimulated expression of the E3 ubiquitin ligase, atrogin-1. Atrogin-1 not only increased proteolysis but also reduced protein synthesis by mechanisms that were independent of decreased phosphorylation of Akt or forkhead transcription factors. Impaired protein synthesis was dependent on a reduction in eIF3-f, an essential regulator of protein synthesis. Berberine impaired energy metabolism, activating AMP-activated protein kinase and providing an alternative mechanism for the stimulation of atrogin-1 expression. When we increased mitochondrial biogenesis by expressing peroxisome proliferator–activated receptor γ coactivator-1α, berberine-induced changes in muscle protein metabolism were prevented.
CONCLUSIONS Berberine impairs muscle metabolism by two novel mechanisms. It impairs mitochonidrial function stimulating the expression of atrogin-1 without affecting phosphorylation of forkhead transcription factors. The increase in atrogin-1 not only stimulated protein degradation but also suppressed protein synthesis, causing muscle atrophy.
There is evidence that an herbal compound, berberine, improves insulin-mediated glucose metabolism and enhances insulin sensitivity in mice (1–3). For example, Lee et al. (1) reported that administering berberine to insulin-resistant db/db mice led to a decrease in body fat and significant improvement in glucose tolerance. Because catabolic conditions associated with insulin resistance can lead to progressive muscle atrophy, we examined whether berberine improves muscle protein metabolism. This was of interest because successful inhibition of mechanisms causing loss of muscle mass in diabetic mice might be extended to other catabolic conditions that cause muscle atrophy (4–8). However, we found that berberine actually promoted muscle atrophy in both wild-type and db/db mice. This led us to examine potential mechanisms causing berberine-induced muscle atrophy.
Muscle atrophy induced by several catabolic conditions (e.g., cancer, cachexia, diabetes, chronic kidney disease, cardiac failure, sepsis) share a common group of biochemical and transcriptional adaptations (7–12). In atrophying muscles, there is a higher level of expression of the E3 ubiquitin ligase, atrogin-1/MAFbx, which has been closely linked to stimulation of muscle protein degradation by the ubiquitin-proteasome system (UPS) (13–17). The mechanism that increases atrogin-1 expression has been linked to defects in insulin/IGF-1 signaling, specifically, suppression of insulin receptor substrate (IRS)-1–associated phosphatidylinositol 3-kinase (PI3K) activity and a reduction in p-Akt (14–16). The decrease in p-Akt, in turn, reduces phosphorylation of the forkhead transcription factors (FoxOs) that can enter the nucleus to stimulate atrogin-1 expression. The focus on atrogin-1 in conditions stimulating muscle atrophy arises because atrogin-1 expression causes a proportional increase in muscle protein degradation (17).”
Here is the link for the entire study:
Atrogin-1 Affects Muscle Protein Synthesis and Degradation When Energy Metabolism Is Impaired by the Antidiabetes Drug Berberine
OBJECTIVE. Defects in insulin/IGF-1 signaling stimulate muscle protein loss by suppressing protein synthesis and increasing protein degradation. Since an herbal
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