Caffeine Reduces Fatty Liver But Increases FFA

maillol

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Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice.
Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice. - PubMed - NCBI

For those that don't have access to the full article the summary included this statement:

In summary, we have demonstrated that caffeine has a potent effect in lowering levels of hepatic lipids by activation of autophagy in cell culture and in vivo. This mobilization and hydrolysis of TGs to free fatty acids (FFAs) through the autophagy‐lysosomal pathway led to increased delivery of FFAs to the mitochondria.

Lowering hepatic lipids is good but increased delivery of FFAs to the mitochondria is bad right?
 

Jam

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milkboi

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Not if these are mostly SFAs.

No it's still mostly bad.

But it's common knowledge around here that caffeine has the potential to do that, as thyroid has. It increases metabolism and therefore the need for fuel, if the extra calories aren't supplied from food the body will take em from your adipose tissue.
 
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maillol

maillol

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No it's still mostly bad.

But it's common knowledge around here that caffeine has the potential to do that, as thyroid has. It increases metabolism and therefore the need for fuel, if the extra calories aren't supplied from food the body will take em from your adipose tissue.
Do you think that means caffeine would only improve fatty liver if taken without food?
 

milkboi

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Do you think that means caffeine would only improve fatty liver if taken without food?

Pheww, that's above my pay grade tbh, but no, I would think it helps even with food, at least I think that is what @haidut would say. Caffeine Reverses Stress, Insulin Resistance, Hypertension

Also, maybe my above statement is wrong, and the FFAs that stem from liver fat are actually a sign of the liver leaning up, and therefore are actually a good thing.
 

Jam

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No it's still mostly bad.

I'm getting tired of such statements being thrown around with absolutely no explanation, evidence or citations.
According to recent (and not-so-recent) studies, long-chain saturated fatty acids, especially stearic acid, promote mitochondrial health. See this for example:

Abstract

Mitochondria are involved in a variety of cellular functions, including ATP production, amino acid and lipid biogenesis and breakdown, signalling and apoptosis. Mitochondrial dysfunction has been linked to neurodegenerative diseases, cancer and ageing. Although transcriptional mechanisms that regulate mitochondrial abundance are known, comparatively little is known about how mitochondrial function is regulated. Here we identify the metabolite stearic acid (C18:0) and human transferrin receptor 1 (TFR1; also known as TFRC) as mitochondrial regulators. We elucidate a signalling pathway whereby C18:0 stearoylates TFR1, thereby inhibiting its activation of JNK signalling. This leads to reduced ubiquitination of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function. We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo. Intriguingly, dietary C18:0 supplementation can counteract the mitochondrial dysfunction caused by genetic defects such as loss of the Parkinson's disease genes Pink or Parkin in Drosophila. This work identifies the metabolite C18:0 as a signalling molecule regulating mitochondrial function in response to diet.
 

Hans

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Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice.
Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice. - PubMed - NCBI

For those that don't have access to the full article the summary included this statement:



Lowering hepatic lipids is good but increased delivery of FFAs to the mitochondria is bad right?
Caffeine increases cellular function and stimulates lipolysis. I've seen a study that shows that only a fraction of the fat that are released through lipolysis are oxidized and the rest were re-esterified.
Caffeine does not promote insulin resistance just because it increases FFAs. Thyroid also stimulates lipolysis and fatty acid oxidation.
 
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jb116

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I think it's important to bring up one of Ray's points on certain substances having a seemingly not great effect but in total metabolic support they are good substances. Such as coconut oil as previously mentioned on the forum. it can lower DHT but has overall very good metabolic and health promoting effects. It's all about net effect. Caffeine is no exception as an overall supportive substance.
 
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maillol

maillol

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Good good. I got some slightly elevated liver enzyme results today so I'm thinking of trying caffeine pills. I see this is usually suggested with K2. Is the K2 really necessary?
 

mangoes

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Good good. I got some slightly elevated liver enzyme results today so I'm thinking of trying caffeine pills. I see this is usually suggested with K2. Is the K2 really necessary?

I had slightly elevated liver enzymes once and I high dosed k2 and they normalised. I don’t really do too great on coffee. It could’ve been just time/something else that normalised them but it seemed like the k2 alone worked for me
 

Jem Oz

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I had slightly elevated liver enzymes once and I high dosed k2 and they normalised. I don’t really do too great on coffee. It could’ve been just time/something else that normalised them but it seemed like the k2 alone worked for me
What dose of k2 and for how long?
 

brocktoon

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What dose of k2 and for how long?
I have a fatty liver. Over the last year, I was able to lower my high liver enzymes by trying K2, caffeine and (perhaps most effectively) dry vitamin E succinate. That said, after a year I had another MRI and a FibroScan, only to find that despite the lowered enzymes my liver was still chock full of fat. No sign of fibrosis (yet), which is good, but my battle with NAFLD has been such a frustrating one.
 

Jem Oz

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I have a fatty liver. Over the last year, I was able to lower my high liver enzymes by trying K2, caffeine and (perhaps most effectively) dry vitamin E succinate. That said, after a year I had another MRI and a FibroScan, only to find that despite the lowered enzymes my liver was still chock full of fat. No sign of fibrosis (yet), which is good, but my battle with NAFLD has been such a frustrating one.
Interesting (and unfortunate). I'm going for a liver scan next week, might be in same boat. Do you know if a period of very low fat would be of benefit?
 

Gl;itch.e

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I have a fatty liver. Over the last year, I was able to lower my high liver enzymes by trying K2, caffeine and (perhaps most effectively) dry vitamin E succinate. That said, after a year I had another MRI and a FibroScan, only to find that despite the lowered enzymes my liver was still chock full of fat. No sign of fibrosis (yet), which is good, but my battle with NAFLD has been such a frustrating one.
Are you currently overweight?
 
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I have a fatty liver. Over the last year, I was able to lower my high liver enzymes by trying K2, caffeine and (perhaps most effectively) dry vitamin E succinate. That said, after a year I had another MRI and a FibroScan, only to find that despite the lowered enzymes my liver was still chock full of fat. No sign of fibrosis (yet), which is good, but my battle with NAFLD has been such a frustrating one.
From what I read about PUFA and sugar, it's not possible for fatty liver to progress into fibrosis unless you have inflammation( PUFA) in the liver. So, if the fat in your liver is saturated or monounsaturated, then it won't get worse. There was a study on rats which showed that even if they fed enough sucrose to fatten up the rat's liver, it would still show no signs of increased inflammation( the fats that we produce from sugar are palmitic acid and oleic acid).

What has your diet been like?

Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice.
Caffeine stimulates hepatic lipid metabolism by the autophagy-lysosomal pathway in mice. - PubMed - NCBI

For those that don't have access to the full article the summary included this statement:



Lowering hepatic lipids is good but increased delivery of FFAs to the mitochondria is bad right?
Perhaps using caffeine to release fat from the liver, then waiting a while then using niacinamide to push the fat into the fat tissues is a good idea. If the FFAs are PUFA and they stay in the blood for a long time, they will cause damage.
 

Jem Oz

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Also, what dose Vitamin E did you try? There's a study floating around, or maybe an anecdotal story, about someone using 800 IU a day for 6 months and completely reversing fatty liver
 
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mangoes

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What dose of k2 and for how long?

sorry it was years ago, I can’t remember exactly. I did definitely get the idea from here tho so the suggestion is probably somewhere in one of the liver threads
 

brocktoon

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Also, what dose Vitamin E did you try? There's a study floating around, or maybe an anecdotal story, about someone using 800 IU a day for 6 months and completely reversing fatty liver
I've usually used 800 IU, alternating between the dry E and a Tocovit-like product. Yes, E is one of the very few natural substances that has a clinical record of efficacy re: fatty liver.
 

brocktoon

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Are you currently overweight?
Over the last year I've dropped some weight, from 201 to 187. I'm 5'11". Now that I'm slimmer, I can see that while I'm less doughy, I've lost a good bit of muscle tone in recent years. Such are the pitfalls of being a guy at 52 with low T, I suppose.:neutral:
 
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brocktoon

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I asked Haidut about vitamin K, mk4 and how it works re: the liver/NAFLD. Quote: "Lower doses (of) niacinamide should be OK and in fact beneficial. I think up to 500mg daily would be fine. Vitamin K can be used in any dose and its effects are mostly anti-fibrotic to prevent NAFLD becoming NASH or cirrhosis. I'd say 15mg-30mg daily should be enough. Caffeine seems optimal in 200mg-400mg daily doses."
 
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