-
By using this site you agree to the terms, rules, and privacy policy.
-
Charlie's Restoration Giveaway #2 (Entire Home EMF Mitigation & Protection Along With Personal Protection) - Click Here To Enter
-
Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
Rest the rest of this post by clicking here
-
The Forum is transitioning to a subscription-based membership model - Click Here To Read
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
Ray Peat Diet Gave Me A Fatty Liver?
- Thread starter leonardo
- Start date
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
This is my opinion and perhaps there are some doses where it might do what you say, but I feel that all of its flavors of action point to one thing, and it does not involve fat.
kineticz
Member
I have eye floaters, and cleared out a load of dark coloured stools with things like carnitine and quercitin.
Ray Peat mentioned somewhere serotonin causes cataracts. Is this the same as eye floaters?
I'm not sure if I have fatty liver or just high serotonin.
I can tell you that low thyroid, low pregnenolone synthesis and high prolactin induced-cortisol are likely to cause fatty liver, due to adrenaline liberating unused fatty acids due to suffocated mitochondria entry.
Ray Peat mentioned somewhere serotonin causes cataracts. Is this the same as eye floaters?
I'm not sure if I have fatty liver or just high serotonin.
I can tell you that low thyroid, low pregnenolone synthesis and high prolactin induced-cortisol are likely to cause fatty liver, due to adrenaline liberating unused fatty acids due to suffocated mitochondria entry.
kineticz
Member
Like I say, quercetin really cleaned out some gloopy sludge in my liver.
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
RPDiciple said:
No, I'm saying it goes well with carbohydrates.
kineticz
Member
Such Saturation, you seem experienced. Can you advise what eye floaters can mean.
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
kineticz said:
Not really but I can almost tell you their nicknames after twenty-three years with them
BobbyDukes
Member
- Joined
- Jan 6, 2015
- Messages
- 345
Such_Saturation said:
Oh, so you're implying that everyone here megadoses vitamins and takes aspirin? And those who don't, don't get fatty liver disease?
So no. That doesn't really sound very straight forward to me, because I know it's BS. I'm sure there are people in this thread that have an issue with fatty liver disease and don't do those things you're taking about.
I bet you as well, that there might be some peeps here who eat a lot of fat (100g + per day), take high dose aspirin (many grams per day) and take a ***t load of supps and have no fatty liver).
Although, it's nice that the little regimen you've adopted works for you.
Me personally, I don't have a clue what state of health my liver is in. But I know that the state of my health can be dependant upon my liver working correctly, or not.
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
BobbyDukes said:
Well this certainly is an excellent point and I can only agree, but those are indeed some of the ways aspirin does its magic, that's all I was saying. Anyway I'd still like to put an ultrasound to those people's bellies. My blood enzymes are awesome and I still have a "slightly hyperreflective" liver.
Parsifal
Member
- Joined
- Aug 6, 2015
- Messages
- 1,081
Such_Saturation said:
Why did you take T4 instead of T3? How is your fatty liver now?
Maybe a genetic fructose intolerance may contribute to this issue?
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
Parsifal said:
I don't know how it is now. I took T4 mainly because Ray Peat said it would be enough in young people when the liver has enough energy. It's also inversely associated with the steatosis, unlike free T3 or TSH, as I said in post #9.
Amazoniac
Member
I haven't been following your thread but what about the organism having to preserve/spare protein (if you're not eating enough or digesting properly), that can affect the function of lipoproteins; lipids enter faster than they are expelled. Am I hallucinating?
Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
I can't cram any more protein than 100g, if that's what you're saying 
Parsifal
Member
- Joined
- Aug 6, 2015
- Messages
- 1,081
It seems that thyroid hormones do trigger lipolysis so randle cycle? Why would something good for energy production interfere with energy production? 
Oh and how would higher protein diets help fatty liver?
Oh and how would higher protein diets help fatty liver?
Nicholas
Member
- Joined
- Apr 25, 2015
- Messages
- 666
Parsifal said:
because the carb ratio is lower. diets have to be arrived at on a cellular level, which is indicated by temp/pulse/ and how you feel. You don't just decide to heal fatty liver. You decide to meet the demands of your cells....and if this is achieved, then the cells heal the fatty liver. Bringing balance to the cells and regulating blood sugar regulates all systems. in the situation of fatty liver, it makes sense that the cells will naturally indicate to you to lower your carb ratio or opt for starch and get higher protein because your liver cannot deal with fructose in the amount you are eating. People with compromised livers will likely have higher protein demands than they will have carb demands.
Last edited by a moderator:
Such_Saturation said:
I'm working on my liver, Such, with your ideas about aspirin and such.
I haven't looked at a lot of studies on liver and T3,
but just in perusing I see this kind of thing
(I copied just the "discussion"...
http://www.fasebj.org/content/22/8/2981.full.pdf
DISCUSSION
The notable findings made in this study with a nutritional
model of NAFLD are that 1) T3 exerts a strong
inhibitory effect on the development of steatosis; 2) T3
causes a rapid regression of fully established steatosis;
and 3) similar effects are exhibited by the potent TR
selective agonist GC-1.
It has been suggested that a diminished export of
lipids from the liver via very low-density lipoproteins,
along with an increased intake of dietary fat and a
limited capacity to oxidize excess fatty acids, is the cause
of steatosis in the CMD-diet model (37, 38). It has also
been shown that cofeeding PPAR agonists with the
CMD diet to mice prevents the development of steatohepatitis,
presumably through effects of PPAR stimulation
diverting fatty acid utilization for hepatic synthesis
of TG (13, 14). PPAR- is a key regulator of lipid
metabolism, influencing expression of lipid metabolic
enzymes, lipid transporters, and apolipoproteins (39);
and PPAR-null mice have hepatic steatosis, elevated
serum cholesterol and TG levels (40), reduced capacity
to metabolize fatty acids, depletion of glycogen, and
reduced cellular uptake of lipids (41, 42). Notably, TR
and PPAR- share the heterodimerization partner,
retinoid X receptor (RXR), required for optimal DNA
binding and activation (43, 44), are coexpressed in
many tissues, and both regulate a number of genes
relevant to metabolism, including malic enzyme, bifunctional
enzymes, uncoupling protein (UCP) 3, andCPT-I (45–50).
Finally, both PPAR- agonists and T3
are strong inducers of hepatocyte proliferation (17, 18,
51). How exactly TR activation mimics PPAR- activation
is unclear, but this suggests a potential interaction
between the two nuclear receptors. Irrespective of the
mechanisms underlying the nature of the potential
crosstalk between TR and PPAR- in the context of fatty
liver, our present finding that cofeeding T3 with a CMD
diet results in a prevention of steatosis that is associated
with induction of ACO mRNA suggests that T3 prevents
accumulation of TGs by inducing fatty acid oxidation,
with a consequent impairment of TG synthesis and of
TG accumulation in the liver. Our results also showed
that T3 decreased the expression of L-FABP, an abundant
protein in the cytosol of hepatocytes that facilitates
fatty acid transport and utilization. Genetic disruption
of L-FABP expression has been shown to impair
the ability of the liver to efficiently import and transfer
fatty acids to glycerolipid biosynthesis (27). Moreover,
ablation of L-FABP completely blocks the accumulation
of TGs in mouse liver (28) and protects against Western
diet-induced hepatic steatosis (52). Taken together, the
results of the present study suggest that increased
degradation of fatty acids together with their reduced
transfer into glycerolipid biosynthesis may be the mechanisms
by which T3 coadministration prevents CMDdiet-induced
steatosis.
Chronic feeding of a CMD diet leads to steatohepatitis.
The CMD diet therefore seems to be a simple and
reproducible animal model of fatty liver disease with
inflammation and injury that morphologically resembles
the group of human disorders known as NASH.
PPAR- agonists not only prevent CMD-induced steatosis
but also rapidly reverse CMD-diet-induced steatohepatitis,
as shown by strong reductions in fat accumulation,
hepatic lipoperoxide levels, and serum ALT
levels (10, 14). Similar to PPAR- agonists, T3 administration
for only 1 wk, following 10 wk of CMD diet,
dramatically reduced levels of liver TGs and the expression
of COX-2; down-regulated pathways, such as JNK
and STAT3 pathways, usually activated in inflammatory
processes; and reduced the severity of liver injury, as
determined by serum levels of transaminases. Whether
TR activation may also result in the reduction of
hepatic fibrosis is at present unknown and will need
additional studies, requiring a more prolonged time of
exposure to the CMD diet.
Finally, our results also show that the capability of T3
to prevent and reverse steatosis is shared by GC-1, a
recently developed selective agonist of the -isoform of
TR. Notably, animal studies (53) revealed that treatment
with GC-1 cause an even greater reduction in TG
levels than that produced by equimolar doses of T3.
Even more significant was the finding that GC-1 can
elicit these effects at doses that have no significant side
effects on heart rate and do not cause muscle loss or an
increase in the overall catabolic state (54). Because of
the “selective hyperthyroidism” generated by GC-1, this
compound has the potential to be developed as a new
therapeutic agent for the treatment of a variety of
thyroid hormone-related metabolic disorders, such as
lipid disorders and obesity (55). Our finding that GC-1
is also capable of preventing steatosis and of inducing a
rapid and dramatic reduction of preaccumulated hepatic
TG makes this member of the new class of
halogen-free thyroid hormone agonists an ideal one for
therapy against fatty liver disease and suggests that
activation of specific TR isoforms may have important
applications in future strategies in therapy of liver
damage.
My understanding is that increasing thyroid hormone generally increases the rate of fuel use, and so it takes less time to use up the available sugars. If the increased metabolism is to be sustained, the energy has to come from somewhere. If the sugar is used up, then more fat will be burned. When there is insufficient fat available, more will be liberated, and more protein turned to sugar. For those of us whose liver does not currently succeed in storing a large amount of glycogen, either because we don't eat enough carbs or because it is not so good at storing it, the sugar will run out faster, and lipolysis and gluconeogenesis will occur sooner.Parsifal said:post 109535 It seems that thyroid hormones do trigger lipolysis so randle cycle? Why would something good for energy production interfere with energy production?
If gluconeogenesis takes protein from our organs faster than we can rebuild them, this eventually weakens them. If it breaks down muscle tissue, some of the amino acids released will inhibit metabolism. We have probably evolved this feedback mechanism as a good way to improve the odds of surviving famines. You have such mechanisms to thank for not yet dying of starvation despite a very low calorie diet.
This is one important reason why I so often advise to eat enough before considering supplementing thyroid. Thyroid alone will not raise metabolism for long - you need to supply adequate nutrition to support it, or the body will often respond in various ways to reduce the thyroid function again. The alternative (that the body allows the BMR to stay high during starvation) is worse.
Last edited by a moderator:
Nicholas said:
Thats interesting. I always thought it would be the other way around that people with compromised livers may not deal with a big intake of protein and would benefit from a higher carb diet of mainly starch or sucrose containing foods. Why would the liver have higher protein demands, Nicholas?
Last edited by a moderator:
EMF Mitigation - Flush Niacin - Big 5 Minerals
Similar threads
