"I Have Liver Issues And I Am Not Making Progress"

[Amazoniac]

Regarding iron toxicity, especially for the hypopboyd, vit D supplements along with plenty of dairy is a synergistic program to deplete magnesium. And magnesium is required for the functioning of many nutrients that regulate iron, such as vitamin A and Bs for example. Cramps are not reliable unless vit D is coming from supplements, otherwise the body tries to adequate levels in a way that spares magnesium and prevents calcification. Magnesium stores can be very low without any cramp. Vit D supplements in this sense can be used to diagnose this imbalance. Dairy has a calcium and magnesium disparity that ain't good for the weak metabolism, it just can't afford unless supplemental is provided to compensate. Magnesium relieves body odor, same for dropping dairy in some cases, which is also another clue about their interaction with iron.
Based on Travis' articles published this year (still free for now), if dairy constipates you, it's one more aspect to consider because endotoxin enhances iron absorption.

Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload

"Consistent with these findings, magnesium deficiency in experimental animals affected status of thiamin (16), lipids (17), and minerals (18-21). Magnesium deficiency in rats decreased thiamin concentration in liver and kidney and the disappearance of injected radioactive 14C-thiamin from blood (22). Magnesium deficiency caused a decrease in tissue manganese concentrations and liver pyruvate carboxylase activity in rats (23). A decrease in bone calcium concentration and the reciprocal accumulation of calcium in kidney were found in magnesium deficient rats (24). Magnesium deficiency induces hyperlipidemia (25). Utilization of iron is affected by status of other nutrients, such as protein (26), pyridoxine, riboflavin (27), copper (28), or selenium (29). A preliminary study (19) found the accumulation of iron in liver, spleen, and kidney, and the elevated serum iron and percent saturation of iron binding protein of rats fed a magnesium-deficient diet, suggesting inefficient utilization of iron."

"The findings in the present study confirmed that magnesium deficiency affects iron metabolism. Cohlan et al. (38) reported microcytic anemia of the offspring of the magnesium-deficient rats. Tao et al. (39) observed anemia of magnesium-deprived Japanese quail. As was reported in a previous work (19), iron was accumulated in spleen, liver, heart, and muscle of magnesium deficient rats."

"In magnesium deficient rats, saturation of iron binding capacity was markedly decreased by iron deprivation and was extremely elevated by excess dietary iron. These results suggest the impairment of homeostatic control of transport iron in magnesium deficiency."

"These alterations in iron metabolism may imply that dietary magnesium deficiency causes inefficient utilization of iron and that iron overload with magnesium deprivation deteriorates rather than improves iron utilization.
The liver has the dominant role in plasma protein synthesis (46,47) and it represents the major source of plasma transferrin (48). A decrease of total iron binding capacity by magnesium deficiency may reflect general decline of protein synthesis rather than specific reduction of transferrin synthesis in liver because plasma albumin and choline esterase activity were decreased as well. In addition, magnesium deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and g-glutamate transaminase activities, indicating the impaired liver function."

"Magnesium deficiency with excess dietary iron may be an alternative model of hemochromatosis based on the pure dietary manipulation. Magnesium deficiency is compatible with the abnormalities in iron metabolism of hemochromatosis, i.e., iron deposition in liver, spleen, and other tissues; decreased total iron binding capacity; elevated saturation of iron binding capacity. In addition, magnesium-deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and 7-glutamate transaminase activities and a decreased plasma total protein, albumin, choline esterase activity, and total iron binding capacity, indicating liver cell damage and impairment of protein synthesis in liver. Magnesium-deficient rats had increased parathyroid hormone in plasma. Goldsmith (74) found the ectopic calcification in magnesium deficient rats. Kimura et al. (24) found a 24% decrease in the bone calcium concentration of magnesium deficient rats using 15% casein-based diet."

"Magnesium-deficient rats had increased calcium and phosphorus levels in kidney, suggesting the deposition of salt containing calcium and phosphorus. In addition, magnesium-deficient rats possessed the low alkaline phosphatase and inorganic phosphorus in plasma, and low magnesium concentration in kidney as well as plasma. Magnesium ion prevents the formation of calcium pyrophosphate crystal from the buffer solution containing calcium and pyrophosphate ions (75). Magnesium is an activator for alkaline phosphatase (76). Alkaline phosphatase possesses pyrophosphatase activity (77,78)."

"Magnesium-deficient rats in this study had the elevated parathyroid hormone concentration in plasma. The possible explanation to account for the rise in plasma parathyroid hormone in magnesium-deficient rats is a negative feedback control on parathyroid hormone secretion by magnesium. Shimada et al. (81) found an increase in plasma parathyroid hormone by low magnesium dialysate changed from normal magnesium dialysate in patients with chronic renal failure. Anast et al. (82) demonstrated an initial rise in plasma parathyroid hormone in magnesium-deficient rats followed by a fall below to normal. The second possibility is that the degradation of parathyroid hormone is secondarily reduced owing to the impaired liver function in magnesium-deficient rats."

"In conclusion, magnesium deficiency may evoke inefficient iron utilization and iron deposition in tissues that is reinforced by oral iron overload. The abnormalities of iron metabolism in magnesium deficiency are resembling the hemochromatotic conditions in the human."​

So, before embarking on aggressive chelation (not an indirect message to you, Regina), it's best to cover the basics.

And regarding copper, it should accumulate where there's excess iron, so it's protective in way. Biounavailable copper perhaps can be interpreted as iron toxicity instead.

Just some opinions.

 

[paymanz]

Magnesium deficiency caused a decrease in tissue manganese concentrations

Never thought that!

Thanks

 

[Amazoniac]

Never thought that!

Thanks

Yeah, increasing manganese reportedly protects against iron toxicity.

 

[paymanz]

Yeah, increasing manganese reportedly protects against iron toxicity.

Yeah,reportedly.

But I meant the Mg>Mn interaction...

 

[Regina]

Regarding iron toxicity, especially for the hypopboyd, vit D supplements along with plenty of dairy is a synergistic program to deplete magnesium. And magnesium is required for the functioning of many nutrients that regulate iron, such as vitamin A and Bs for example. Cramps are not reliable unless vit D is coming from supplements, otherwise the body tries to adequate levels in a way that spares magnesium and prevents calcification. Magnesium stores can be very low without any cramp. Vit D supplements in this sense can be used to diagnose this imbalance. Dairy has a calcium and magnesium disparity that ain't good for the weak metabolism, it just can't afford unless supplemental is provided to compensate. Magnesium relieves body odor, same for dropping dairy in some cases, which is also another clue about their interaction with iron.
Based on Travis' articles published this year (still free for now), if dairy constipates you, it's one more aspect to consider because endotoxin enhances iron absorption.

Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload

"Consistent with these findings, magnesium deficiency in experimental animals affected status of thiamin (16), lipids (17), and minerals (18-21). Magnesium deficiency in rats decreased thiamin concentration in liver and kidney and the disappearance of injected radioactive 14C-thiamin from blood (22). Magnesium deficiency caused a decrease in tissue manganese concentrations and liver pyruvate carboxylase activity in rats (23). A decrease in bone calcium concentration and the reciprocal accumulation of calcium in kidney were found in magnesium deficient rats (24). Magnesium deficiency induces hyperlipidemia (25). Utilization of iron is affected by status of other nutrients, such as protein (26), pyridoxine, riboflavin (27), copper (28), or selenium (29). A preliminary study (19) found the accumulation of iron in liver, spleen, and kidney, and the elevated serum iron and percent saturation of iron binding protein of rats fed a magnesium-deficient diet, suggesting inefficient utilization of iron."

"The findings in the present study confirmed that magnesium deficiency affects iron metabolism. Cohlan et al. (38) reported microcytic anemia of the offspring of the magnesium-deficient rats. Tao et al. (39) observed anemia of magnesium-deprived Japanese quail. As was reported in a previous work (19), iron was accumulated in spleen, liver, heart, and muscle of magnesium deficient rats."

"In magnesium deficient rats, saturation of iron binding capacity was markedly decreased by iron deprivation and was extremely elevated by excess dietary iron. These results suggest the impairment of homeostatic control of transport iron in magnesium deficiency."

"These alterations in iron metabolism may imply that dietary magnesium deficiency causes inefficient utilization of iron and that iron overload with magnesium deprivation deteriorates rather than improves iron utilization.
The liver has the dominant role in plasma protein synthesis (46,47) and it represents the major source of plasma transferrin (48). A decrease of total iron binding capacity by magnesium deficiency may reflect general decline of protein synthesis rather than specific reduction of transferrin synthesis in liver because plasma albumin and choline esterase activity were decreased as well. In addition, magnesium deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and g-glutamate transaminase activities, indicating the impaired liver function."

"Magnesium deficiency with excess dietary iron may be an alternative model of hemochromatosis based on the pure dietary manipulation. Magnesium deficiency is compatible with the abnormalities in iron metabolism of hemochromatosis, i.e., iron deposition in liver, spleen, and other tissues; decreased total iron binding capacity; elevated saturation of iron binding capacity. In addition, magnesium-deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and 7-glutamate transaminase activities and a decreased plasma total protein, albumin, choline esterase activity, and total iron binding capacity, indicating liver cell damage and impairment of protein synthesis in liver. Magnesium-deficient rats had increased parathyroid hormone in plasma. Goldsmith (74) found the ectopic calcification in magnesium deficient rats. Kimura et al. (24) found a 24% decrease in the bone calcium concentration of magnesium deficient rats using 15% casein-based diet."

"Magnesium-deficient rats had increased calcium and phosphorus levels in kidney, suggesting the deposition of salt containing calcium and phosphorus. In addition, magnesium-deficient rats possessed the low alkaline phosphatase and inorganic phosphorus in plasma, and low magnesium concentration in kidney as well as plasma. Magnesium ion prevents the formation of calcium pyrophosphate crystal from the buffer solution containing calcium and pyrophosphate ions (75). Magnesium is an activator for alkaline phosphatase (76). Alkaline phosphatase possesses pyrophosphatase activity (77,78)."

"Magnesium-deficient rats in this study had the elevated parathyroid hormone concentration in plasma. The possible explanation to account for the rise in plasma parathyroid hormone in magnesium-deficient rats is a negative feedback control on parathyroid hormone secretion by magnesium. Shimada et al. (81) found an increase in plasma parathyroid hormone by low magnesium dialysate changed from normal magnesium dialysate in patients with chronic renal failure. Anast et al. (82) demonstrated an initial rise in plasma parathyroid hormone in magnesium-deficient rats followed by a fall below to normal. The second possibility is that the degradation of parathyroid hormone is secondarily reduced owing to the impaired liver function in magnesium-deficient rats."

"In conclusion, magnesium deficiency may evoke inefficient iron utilization and iron deposition in tissues that is reinforced by oral iron overload. The abnormalities of iron metabolism in magnesium deficiency are resembling the hemochromatotic conditions in the human."​

So, before embarking on aggressive chelation (not an indirect message to you, Regina), it's best to cover the basics.

And regarding copper, it should accumulate where there's excess iron, so it's protective in way. Biounavailable copper perhaps can be interpreted as iron toxicity instead.

Just some opinions.

Thank you Amazoniac. I have upped my Mag and tempered dietary Calc a skooch. But I've been kind of a kuinone fiend. I have in my history a two year stretch on coumadin (following a rib-resection from a blood clot. Duhhh estrogen anyone? The good Drs thought rat poison a better idea). I think I rebuilt myself in 2017. Maybe that accounted for some weird iron metabolism and adjustments.

 

[Amazoniac]

Thank you Amazoniac. I have upped my Mag and tempered dietary Calc a skooch. But I've been kind of a kuinone fiend. I have in my history a two year stretch on coumadin (following a rib-resection from a blood clot. Duhhh estrogen anyone? The good Drs thought rat poison a better idea). I think I rebuilt myself in 2017. Maybe that accounted for some weird iron metabolism and adjustments.

I hope you keep improving. If you need a more intensive repletion, consider the occasional foot baths with magnesium chloride but with sodium bicarbonate. Travisterol (♥) or prosperol (↓) drops are optional.

 

[Giraffe]

I would not want to get people deficient in B5 but it would be interesting to see what the symptoms of deficiency are. Can you do a quick search? If deficiency causes increased oxygen consumption and uncoupling then I am all game

The was this study where they induced experimental pantothenic acid deficiency in man using a deficient diet (tube fed) and an antagonist.

Symptoms

"serious personality changes with irritability, restlessness, quarrelsomeness; and alternate periods of somnolence and insomia (Figure 3, 4). They began to complain of excessive fatigue after their daily walk. They would break out in a profuse sweat after trifling provocation or none at all. A little later the two men in the deficient group began to note similar complaints (Figure 5, 6). From this time on the condition of the deficient and the antagonist subjects became indistinguishable. All four men had a staggering gait and showed deterioration of their skill at pingpong. Frequently they refused to go for their daily walks, preferring to lie in bed all day. Gastrointestinal complaints became common, varying from epigastric burning to occasional regurgitation of small amounts of formula as they withdrew the tube. Loud abdominal rumblings occurred frequently, sometimes accompanied by abdominal cramping and occasionally by diarrhea. One subject developed paresthesias and "burning" of the soles of his feet which lasted only a few days and subsided spontaneously during the same phase of the test. Numbness of the hands, most distressing in the morning before arising, was fairly frequent in the two subjects receiving the antagonist. Physical examinations revealed few objective findings other than transient increase of the tendon reflexes and faulty coordination associated with tremor."

 

[Regina]

I hope you keep improving. If you need a more intensive repletion, consider the occasional foot baths with magnesium chloride but with sodium bicarbonate. Travisterol (♥) or prosperol (↓) drops are optional.

Yes. Thanks! Fortunately, the 'IF can aikido ELSE' gives me pretty reliable conditional logic feedback.

 

[Amazoniac]

IRON OVERLOAD AND CHELATION - Guidelines for the Management of Transfusion Dependent Thalassaemia (TDT) - NCBI Bookshelf

"Only a very small fraction of body iron is available for iron chelation at any moment of time. This is because iron chelators interact with low molecular weight 'labile' iron pools better than with iron stored as ferritin or haemosiderin. Labile iron is constantly being generated, so that the efficiency of chelation is better when a chelator is available at all times (chelator present 24 hours a day). 24h chelation also has the potential to remove toxic labile iron pools within cells continuously, which is particularly important in reversing heart failure. Chelatable iron is derived from two major sources: iron derived from the breakdown of red cells in macrophages (about 20 mg/day in healthy adults), and iron derived from the catabolism of stored ferritin iron within cells. Most of the storage iron in the body is in hepatocytes, and the ferritin in these cells is turned over less frequently (every few days). Iron chelated within the liver is excreted though the biliary system, or circulates back into plasma and is excreted in the urine. The extent to which this chelated iron is eliminated in faeces or urine varies with each chelator."

"Small quantities of storage iron are also deposited in the endocrine system and in the heart. Because these are not designed as cells for iron storage and release, unlike hepatocytes, storage iron is turned over in the lysosome compartment less frequently and a lower proportion of cellular iron is available for chelation at any moment. Thus it generally takes longer to remove iron from these tissues than from the liver."

"Vitamin C increases iron excretion by increasing the availability of chelatable iron, but if given in excessive doses may increase the toxicity of iron."​

--
Iron overload and non-alcoholic fatty liver disease - Minerva Endocrinologica 2017 June;42(2):173-83 - Minerva Medica - Journals

"Usually, subjects with NAFLD present with a dominant elevation of serum ferritin concentrations but transferrin saturation is mostly normal, close to the upper limit of normal or mildly raised.[42] The extent of body iron excess is overestimated by measurement of serum ferritin compared to the extent of body iron excess in hemochromatosis subjects with a similar degree of ferritin elevations in most interventional studies, the amount of iron removed ranged between 1.5g and 2.5g.[43-45]"​

--

https://chrismasterjohnphd.com/2017/01/27/need-manage-iron-status/
Let’s look at iron overload now. What should you do about it? Well, you could manage it dietarily and do everything that’s the opposite of what you do in anemia. So you could avoid liver and you could avoid clams and you could avoid red meat and you could always eat all of your meals with a lot of calcium and you could never supplement with vitamin C and you could avoid unrefined plant foods like all the ones that I listed before. Well, hey, while you’re at it, why don’t you give yourself a copper deficiency and a vitamin B6 deficiency too? Maybe that will help. I mean the problem with dietary management is, first of all, you have to restrict so many foods that (A) it’s like who on earth would want to manage all that dietary restriction just logistically? (B) All those foods are nutritious, so you’re restricting foods that are going to — any dietary restriction makes you more vulnerable to micronutrient deficiencies.

The last thing that you want is iron overload corresponding with other micronutrient deficiencies. For example, liver is yes, it’s high in iron. It’s high in copper. It’s high in B vitamins. It’s high in things that help you utilize that iron. Do you really want to eke away at dropping your iron stores by lowering your B vitamin status and your copper status and making you unable to use iron properly? That could make your situation worse because before you actually fix the iron overload now you can’t direct iron to where it needs to go into all the proteins that you need to use it for. You have that recipe that we talked about at the beginning where you have too much hydrogen peroxide and free iron running around increasing oxidative stress. So I’m not at all a fan of dietary management of iron overload, granted while you’re addressing it in other ways, maybe it makes sense to consider the iron cost of the food relative to the other benefit. For example, if we’re going to choose between liver and a hamburger, then yeah, you could cut your intake of hamburgers down while still consuming liver for its nutrient density.

But the real key to iron overload management is blood donation. Blood donation is a more specific way to get rid of iron that has much less risk than these other means. It’s much more effective because you’re actually getting rid of iron instead of just lowering your intake, and it also has a benefit to society in that we need blood donations.

--
Iron Overload in Patients With Chronic Liver Disease

 

[Amazoniac]

The was this study where they induced experimental pantothenic acid deficiency in man using a deficient diet (tube fed) and an antagonist.

Symptoms

"serious personality changes with irritability, restlessness, quarrelsomeness; and alternate periods of somnolence and insomia (Figure 3, 4). They began to complain of excessive fatigue after their daily walk. They would break out in a profuse sweat after trifling provocation or none at all. A little later the two men in the deficient group began to note similar complaints (Figure 5, 6). From this time on the condition of the deficient and the antagonist subjects became indistinguishable. All four men had a staggering gait and showed deterioration of their skill at pingpong. Frequently they refused to go for their daily walks, preferring to lie in bed all day. Gastrointestinal complaints became common, varying from epigastric burning to occasional regurgitation of small amounts of formula as they withdrew the tube. Loud abdominal rumblings occurred frequently, sometimes accompanied by abdominal cramping and occasionally by diarrhea. One subject developed paresthesias and "burning" of the soles of his feet which lasted only a few days and subsided spontaneously during the same phase of the test. Numbness of the hands, most distressing in the morning before arising, was fairly frequent in the two subjects receiving the antagonist. Physical examinations revealed few objective findings other than transient increase of the tendon reflexes and faulty coordination associated with tremor."

Giraffe!!

 

[Amazoniac]

Modern Pathology - Iron overload syndromes and the liver

"Normal values in the Mayo Metals Laboratory are 7.2–39.4

mol (400–2200

g) per gram dry weight in men and 1.8–28.6

mol (100–1600

g) per gram dry weight in women. The variation of repeated determinations on the same test sample is approximately 5%.

Mild to moderate iron overload (1–2+) generally correlates with quantitative iron values between 3000 and 10 000

g Fe/g dry weight liver (Figure 2). Grades 3 and 4 iron histologically generally reflect >10 000

g Fe/g dry weight liver (Figure 3). In uncomplicated HH, most patients with iron concentrations of 22 000

g Fe/g dry weight liver likely will have developed fibrosis as well.38"​

--
Quantification of Liver Iron with MRI: State of the Art and Remaining Challenges

"For cirrhotic livers, the coefficient of variation of LIC [liver iron concentration] measurements from two separate biopsies has been reported to be 41% (36); in nondiseased liver, average values of approximately 19% have been reported (37)." ​

You know what is in its state of art? An explanation for Travis' specific knowledge, such as the naming of enzymes.

 

[Giraffe]

Giraffe!!

 

[Amazoniac]

I still have some doubts about B5.

Zeus, check this out:

Pantothenic Acid: an Organ-Specific Pro-Oxidant Vitamin¶

"Coenzyme A is required for the initial activation of free fatty acids to fatty acyl-CoA thioesters prior to their oxidation or esterification to complex lipids 2,3. Consequently, it was expected that pantothenic acid deficiency would result in higher levels of free fatty acid in the liver, but not in the brain.
Surprisingly, however, analysis of tissue docosahexaenoic acid revealed that dietary pantothenic acid deficiency decreased the brain levels of this fatty acid by 30%, while virtually abolishing it in the liver (Fig 2). This finding can be explained based on the fact that pantothenic acid is also a structural element of the acyl carrier protein which is an essential component of the fatty acid synthetase complex 1."

"Pantothenic acid supplements to rats receiving pantothenic acid-deficient diet restored hepatic coenzyme A levels to control values (Fig 1), while increasing liver DHA levels by about 50%, supporting the conclusion that fatty acid synthesis is more susceptible to pantothenic acid than is its oxidation/esterification."

"In our study, brain and liver neuroprostane levels in control rats were 32+-4 ng/g and 29+-/4 ng/g, respectively (Fig 2). In parallel to the impact of pantothenic acid deficiency on tissue DHA, Pantothenic acid-deficient diet for 5 weeks did not change brain neuroprostane levels (Fig 2 ), while dramatically decreasing hepatic levels by 70% (Fig 2)."

"Similar to their effects on liver DHA concentrations, pantothenic acid supplements to these rats partially restored hepatic neuroprostane concentrations (Fig 2) ["Neuroprostanes result from free radical-induced peroxidation of DHA 5. This fatty acid is the most easily oxidizable naturally-occurring fatty acid"]. Whether or not longer duration of PA supplements to rats receiving PA-deficient diet would have completely restored hepatic DHA and neuroprostanes to control levels remains to be investigated.
These data show that dietary deficiency of PA has profound effects on hepatic coenzyme A and DHA levels, while exerting minimal or no effect on these metabolites in the brain. These organ-specific effects may be reflected in enhanced susceptibility of the liver to oxidative stress. This conclusion is evidenced by the diminished levels of neuroprostanes in livers of rats fed PA-deficient diet, coupled with undetectable changes in the brain levels of these sensitive markers of oxidative stress in the same rats."

"Animals and Diets
Male Sprague-Dawley rats (40-50 g; Sasco, Omaha, NE) were fed a PA-deficient diet (ICN Biomedicals, Costa Mesa, CA) for 5 weeks (PAD group), while control animals received regular rat chow for 5 weeks. Some rats receiving the PAD diet were supplemented with PA (100 mg/kg/d, orally) during the fifth week (PAD+PA group)."


(((

With the caveat that I have no idea what's ideal for a rat (if what they consider being deficient is correct for example), or how it's extrapolated to humanoids, a deficiency of the vitamin is out of question, so there's no point to use it as refence. Also I don't know why would the body use something valuable that was missing to synthesize something toxic. It makes no sense.

So we're left with this one:

Hepatocellular Lipid Changes Produced by Pantothenic Acid Excess

"An impressive and conspicuous initial histopathological observation is the appearance of intracellular fat due to the effects of injected d-pantetheine (20 mg.)."

But it was injected right into the muscles and the active form of the vit. I have no idea what this does to fatty acids and how it affects the liver compared to oral pantothenic acid.​

--
HEPATOPROTECTIVE EFFECTS OF PANTOTHENIC ACID ON CARBON TETRACHLORIDE-INDUCED TOXICITY IN RATS

 

[Amazoniac]

https://www.hindawi.com/journals/jnme/2015/760689/

 

[Amazoniac]

Based on Travis' work, mature coconuts are quite nutritious, unfortunately all is lost in coconut oil. Coconut milk should be superior to the oil if you're not allergic to it. You would expect that not only the characteristic way its fatty acids are metabolized can contribute to fatty liver, but also for being an oil devoid of nutrition because all in all it always comes down to excess energy or being incapable of processing, and both should be made worse when there's not enough nutrients being provided.
Now when it comes to being allergenic, it makes me think that it's doing its purpose. There are many foods with antimicrobial compounds that are "allergenic", but maybe they're doing exactly what they should. And perhaps if you insist while stimulating the metabolism, they can be effective. Something related to Koch's work anyway.
__
Travisord, if you're reading this, would you expect that the expectation of a mother that's expecting affects the life expectancy of the child in a negative way?

 

[Amazoniac]

Masticating juicers should be able to prepare an excellent fresh coconut milk without much mess.

 

[Wagner83]

You would expect that not only the characteristic way its fatty acids are metabolized can contribute to fatty liver

Sorry I must have missed something but where does that come from?

 

[Amazoniac]

Sorry I must have missed something but where does that come from?

"I Have Liver Issues And I Am Not Making Progress"
..or anesthesiology book.

 

[Wagner83]

"I Have Liver Issues And I Am Not Making Progress"
..or anesthesiology book.

Thanks.
Wouldn't we accumulate more fat (by not burning it and burning only sugar) by eating a ton of carbs and small amounts of fat of fat rather than something more balanced? I remember a member saying low fat high carb made him gain visceral fat, while an other said she lost waistline fat when she started eating balanced meals (macros), and people like JamesIV (with the caveat of a good muscle mass) lose weight by eating more avocadoes.. Also don't we burn fat when fasting and avoiding all carbs? What about the atkins diet? What about supplementing aspirin + niacinamide (inhibit lipolysis) and putting on more fat? What about life? Is the earth flat? My waist isn't.

 

[Amazoniac]

Thanks.
Wouldn't we accumulate more fat (by not burning it and burning only sugar) by eating a ton of carbs and small amounts of fat of fat rather than something more balanced? I remember a member saying low fat high carb made him gain visceral fat, while an other said she lost waistline fat when she started eating balanced meals (macros), and people like JamesIV (with the caveat of a good muscle mass) lose weight by eating more avocadoes.. Also don't we burn fat when fasting and avoiding all carbs? What about the atkins diet? What about supplementing aspirin + niacinamide (inhibit lipolysis) and putting on more fat? What about life? Is the earth flat? My waist isn't.

It's very difficult to gain visceral fat if the source of carbs is mainly glucose, the opposite has been noted many times in experiments. Since carbs have the preference for burning, then you'll always have the fat of the meal being stored and burned later on; so the more you eat, the more you'll have to burn later. To avoid this you would need to be eating little carbs. Regarding a more balanced ratio of macros, there can be many factors involved, such as satiation, improved digestion, and others responsible for a better outcome. Zeus was the guru that thought me for the first time that fat being stored away from organs is safer storage, I later read more about it in confirmation, if it's short term, it can be a sign that things are improving. Life ain't easy with Such giving you the silence punishment. Open anesthesiology book , then open Google Earth there and zoom out. Later on, if it makes you feel better, zoom in where I live and I'll go outside and wave at you.