CoolTweetPete

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Last week I ordered a 20 oz coffee. Half way through I thought "oh crap, did I say decaf?" Sure enough, I did not. No worries though because I felt great. Never had the slightest hint of stress response from it which is very unusual for me. It had to be defibron or niacinamide, or the combo.

I started using DeFibron about the same time I started on high dose beef liver supplementation. I'm thinking with improved liver function caffeine is a breeze, so it's pro-dopamine effects can be fully exploited. I'm up around 1.5g of caffeine per day and still sleeping like a baby when it comes time for bed. Barely using any DeFibron right now (after running through 3 bottles quickly) also, so the effect lasts.
 

aarfai

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I started using DeFibron about the same time I started on high dose beef liver supplementation. I'm thinking with improved liver function caffeine is a breeze, so it's pro-dopamine effects can be fully exploited. I'm up around 1.5g of caffeine per day and still sleeping like a baby when it comes time for bed. Barely using any DeFibron right now (after running through 3 bottles quickly) also, so the effect lasts.
Funny I just ordered Perfect Desiccated Liver in hopes to improve my own liver issues. May I ask what you've noticed with the liver supplementation and DeFibron combo? Can you tell whether your liver has improved?
 

CoolTweetPete

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Funny I just ordered Perfect Desiccated Liver in hopes to improve my own liver issues. May I ask what you've noticed with the liver supplementation and DeFibron combo? Can you tell whether your liver has improved?

That's the same brand I'm using. To be fair I use quite a few other things but DeFibron was the latest addition along with the beef liver.

It's hard to know for sure without any tests but it seems like glycogen storage has improved.

My subjective measures for this are 1) improved caffeine tolerance 2) able to sleep through the night without waking up to eat 3) generally calmer mood

Has really been a breakthrough.
 

denise

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That's the same brand I'm using. To be fair I use quite a few other things but DeFibron was the latest addition along with the beef liver.

It's hard to know for sure without any tests but it seems like glycogen storage has improved.

My subjective measures for this are 1) improved caffeine tolerance 2) able to sleep through the night without waking up to eat 3) generally calmer mood

Has really been a breakthrough.
There must be something in the air! Just today I ordered a bottle of the Perfect Desiccated Liver AND I restarted my caffeine/K routine, AND I'm trying to ramp up my Defibron doses. I'm looking forward to seeing what this combo does for me.
 

managing

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There must be something in the air! Just today I ordered a bottle of the Perfect Desiccated Liver AND I restarted my caffeine/K routine, AND I'm trying to ramp up my Defibron doses. I'm looking forward to seeing what this combo does for me.
Is there something you expect to get from dessicated liver that is different from fresh? Or simply a matter of convenience and availability?
 

CoolTweetPete

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Is there something you expect to get from dessicated liver that is different from fresh? Or simply a matter of convenience and availability?

My choice came from convenience and dislike of the taste. I find chicken liver palatable but quality sources are hard to find. The brand we mentioned comes from grass-fed cows and doesn't have any nasty fillers.
 

Raytoo

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My choice came from convenience and dislike of the taste. I find chicken liver palatable but quality sources are hard to find. The brand we mentioned comes from grass-fed cows and doesn't have any nasty fillers.

I agree, I've been using those for a few years now.
 
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aarfai

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Yup can we please get some updates about this product? Have old injuries healed? Better liver function? Etc...
 

Scenes

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Yup can we please get some updates about this product? Have old injuries healed? Better liver function? Etc...

I stopped using it a week or so ago and haven't noticed any change, possible placebo effect when on...not sure.

I commented earlier in the thread that I already eat a lot of sat fats so perhaps this product isn't that necessary for me.

I'd say it helped me sleep through the night (retain liver glycogen) within a few days of using it. I never used to have problems with that before peating the last few months, but DeFibron helped.

Was giving me very minor acne around my nose and on my upper back, nothing else could have caused that from my observations.

No noticeable dopamine effect, which was probably the main thing I was hoping for. Others mentioned they got a lot more of the pro-dopamine actions.
 

managing

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The biggest single impact of anything I've ever taken. That sums it up.

The main attractions for me are liver and intestinal. Dramatically "normalized" bowels such that I really don't notice them anymore. Much stronger liver glycogen storage. Much. Although I felt effects from day 1, it just keeps getting better in subtle ways. I'm about 2 mos in.
 

Wagner83

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The biggest single impact of anything I've ever taken. That sums it up.

The main attractions for me are liver and intestinal. Dramatically "normalized" bowels such that I really don't notice them anymore. Much stronger liver glycogen storage. Much. Although I felt effects from day 1, it just keeps getting better in subtle ways. I'm about 2 mos in.
How have you seen other benefits on mood , energy levels , creative endeavours etc..?
 

Raytoo

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The biggest single impact of anything I've ever taken. That sums it up.

The main attractions for me are liver and intestinal. Dramatically "normalized" bowels such that I really don't notice them anymore. Much stronger liver glycogen storage. Much. Although I felt effects from day 1, it just keeps getting better in subtle ways. I'm about 2 mos in.
Are you taking orally ? And how much?
 

managing

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How have you seen other benefits on mood , energy levels , creative endeavours etc..?
Mood and energy--pretty significant. Call it 5. Creativity? I would express it as focus and attention span which can apply to many things.
 
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Would you mind expanding on this @ecstatichamster? Curious...

Macrophages are necessary of course, but they are also implicated in fibrotic and cancer states.

Potential role of apoptotic macrophages in pulmonary inflammation and fibrosis
Induction of apoptosis has been associated with a variety of exposures which result in inflammatory and fibrotic lung disorders. Macrophages are key regulatory cells in the lung; however, the role of apoptotic macrophages in those pulmonary disorders is not well characterized. In the present investigation, apoptotic macrophages were instilled into the lungs of rats to study directly the pulmonary responses to apoptotic cells. The effects of apoptotic macrophages on lung inflammation and fibrosis, as well as associated protein expression of TNF-α, TGF-β, and matrix metalloproteinases (MMPs) were examined. Induction of macrophage apoptosis was carried out in vitro using a variety of known apoptosis inducers. Intratracheal administration of apoptotic macrophages (5 × 106 cells/rat) into the lung of rats caused an increase in pulmonary infiltration of macrophages and lung cell apoptosis 4 weeks after the treatment as indicated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. In contrast, pulmonary instillation of saline or normal control macrophages had no effect. Histological analysis of lung sections showed collagen deposition and fibrotic lesions after apoptotic cell treatment but not in control groups. Immunohistochemical studies revealed increased expression of TNF-α, TGF-β, MMP2, and MMP9 in the treatment group 4 weeks after the treatment. These results suggest a role for macrophage apoptosis in the initiation of these lung disorders. This study provides direct evidence that apoptotic macrophages can induce lung inflammation and fibrosis and that this induction may be associated with increased expression of TNF-α, TGF-β, MMP2, and MMP9.

Anti-inflammatory and antifibrotic effects of methyl palmitate - ScienceDirect
Methyl palmitate (MP) has been shown earlier to inhibit Kupffer cells and rat peritoneal macrophages. To evaluate the potential of MP to inhibit the activation of other macrophages, RAW cells (macrophages of alveolar origin) were treated with varying concentrations of MP (0.25, 0.5, 1 mM). Assessment of cytotoxicity using MTT assay revealed that 0.25 and 0.5 mM are not toxic to RAW cells. MP was able to inhibit the phagocytic function of RAW cells. Treatment of cells with MP 24 hours prior to LPS stimulation significantly decreased nitric oxide release and altered the pattern of cytokines release; there was a significant decrease in TNF-α and a significant increase in IL-10 compared to the controls. However, there is a non-significant change in IL-6 level. Furthermore, phosphorylation of inhibitory kappa B (IκBα) protein was significantly decreased in RAW cells treated with 0.5 mM MP after LPS stimulation. Based upon the in-vitro results, it was examined whether MP treatment will be effective in preventing bleomycin-induced lung inflammation and fibrosis in-vivo. Bleomycin given by itself caused destruction of the lung architecture characterized by pulmonary fibrosis with collapse of air alveoli and emphysematous. Bleomycin induced a significant increase in hydroxyproline level and activated NF-κB, p65 expression in the lung. MP co-treatment significantly ameliorated bleomycin effects. These results suggest that MP has a potential of inhibiting macrophages in general. The present study demonstrated for the first time that MP has anti-inflammatory and antifibrotic effect that could be through NF-kB inhibition. Thus MP like molecule could be a promising anti-inflammatory and antifibrotic drug.
 
L

lollipop

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Macrophages are necessary of course, but they are also implicated in fibrotic and cancer states.

Potential role of apoptotic macrophages in pulmonary inflammation and fibrosis
Induction of apoptosis has been associated with a variety of exposures which result in inflammatory and fibrotic lung disorders. Macrophages are key regulatory cells in the lung; however, the role of apoptotic macrophages in those pulmonary disorders is not well characterized. In the present investigation, apoptotic macrophages were instilled into the lungs of rats to study directly the pulmonary responses to apoptotic cells. The effects of apoptotic macrophages on lung inflammation and fibrosis, as well as associated protein expression of TNF-α, TGF-β, and matrix metalloproteinases (MMPs) were examined. Induction of macrophage apoptosis was carried out in vitro using a variety of known apoptosis inducers. Intratracheal administration of apoptotic macrophages (5 × 106 cells/rat) into the lung of rats caused an increase in pulmonary infiltration of macrophages and lung cell apoptosis 4 weeks after the treatment as indicated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. In contrast, pulmonary instillation of saline or normal control macrophages had no effect. Histological analysis of lung sections showed collagen deposition and fibrotic lesions after apoptotic cell treatment but not in control groups. Immunohistochemical studies revealed increased expression of TNF-α, TGF-β, MMP2, and MMP9 in the treatment group 4 weeks after the treatment. These results suggest a role for macrophage apoptosis in the initiation of these lung disorders. This study provides direct evidence that apoptotic macrophages can induce lung inflammation and fibrosis and that this induction may be associated with increased expression of TNF-α, TGF-β, MMP2, and MMP9.

Anti-inflammatory and antifibrotic effects of methyl palmitate - ScienceDirect
Methyl palmitate (MP) has been shown earlier to inhibit Kupffer cells and rat peritoneal macrophages. To evaluate the potential of MP to inhibit the activation of other macrophages, RAW cells (macrophages of alveolar origin) were treated with varying concentrations of MP (0.25, 0.5, 1 mM). Assessment of cytotoxicity using MTT assay revealed that 0.25 and 0.5 mM are not toxic to RAW cells. MP was able to inhibit the phagocytic function of RAW cells. Treatment of cells with MP 24 hours prior to LPS stimulation significantly decreased nitric oxide release and altered the pattern of cytokines release; there was a significant decrease in TNF-α and a significant increase in IL-10 compared to the controls. However, there is a non-significant change in IL-6 level. Furthermore, phosphorylation of inhibitory kappa B (IκBα) protein was significantly decreased in RAW cells treated with 0.5 mM MP after LPS stimulation. Based upon the in-vitro results, it was examined whether MP treatment will be effective in preventing bleomycin-induced lung inflammation and fibrosis in-vivo. Bleomycin given by itself caused destruction of the lung architecture characterized by pulmonary fibrosis with collapse of air alveoli and emphysematous. Bleomycin induced a significant increase in hydroxyproline level and activated NF-κB, p65 expression in the lung. MP co-treatment significantly ameliorated bleomycin effects. These results suggest that MP has a potential of inhibiting macrophages in general. The present study demonstrated for the first time that MP has anti-inflammatory and antifibrotic effect that could be through NF-kB inhibition. Thus MP like molecule could be a promising anti-inflammatory and antifibrotic drug.
Very cool. Thank you :):
 
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