Treatment Of Cirrhosis Of The Liver By A Nutritious Diet And Supplements Rich In Vitamin B Complex

Amazoniac

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Members that installed carpets at home to assist locomotion by gliding over colonies of microbes,

In this study, they randomly selected 54 hospitalized people and treated them with a "nourishing diet and supplements"*, then compared the outcome with 386 other hospitalized patients, and, as they noted, treated or not, they were more advanced cases. There was this premise that if infections (or other problems) were present (very common and varied), they were only accentuating the malnutrition; preceding and then contributing to the liver degeneration**. Treated patients were grouped by recovery, improvement (sometimes the length of monitoring was not long enough to consider the case a recovery) or failure. Regardless of the group, most of them were malnourished before admission, not just the ones that responded to the dietary intervention*** (crosses are scary).
In all groups there were some early deaths related or unrelated to degenerative processes.

TREATMENT OF CIRRHOSIS OF THE LIVER BY A NUTRITIOUS DIET AND SUPPLEMENTS RICH IN VITAMIN B COMPLEX

"Evidence of malnutrition was striking. [..] 81 per cent had eaten poor diets, and that 78 per cent had lost weight (allowing for ascites). Although careful dietary histories were taken, the data were not reliable enough to measure quantitatively."
"The most constant defects in the diets lay in the sparing use of meat and dairy products. Many patients gave histories of having subsisted entirely on alcoholic liquor for intervals of several days and of having refused all food during these sprees."

--
"It is known that the incidence of cirrhosis of the liver is high in certain countries where nutritional deficiencies are endemic (1, 2). Although malaria is blamed popularly for the high incidence of cirrhosis in these countries (3, 4), there is no direct evidence that malaria produces cirrhosis of the liver (5, 6)."

"It has been known that starvation renders the liver more vulnerable to injury by hepatotoxins (9). Lack of certain food factors contained in yeast are said to cause fatty changes in the liver (10) and impaired function (11)."

"It has also been shown that the feeding of excess fat (14) or of excess cystine (15) results in fibrotic changes in the liver."

"In a preliminary report on the treatment of 13 patients with alcoholic cirrhosis of the liver (21), it was noted that, in addition to signs of liver failure, there was evidence of specific malnutrition, notably of the vitamin B complex. These patients were fed a nutritious diet together with vitamin supplements. The improvement that followed treatment appeared to be outside chance expectations."

"The initial serum albumin value was low (below 4.0 grams per cent) in 96 per cent of the patients. The initial serum globulin value was high (above 3.0 grams per cent) in 83 per cent of the patients. ***It is noteworthy that the average initial value for serum albumin is higher in those patients who made clinical improvement than in those who failed to improve."

*
"In Table II is outlined the dietary regimen employed. The diet differs radically from that commonly advocated in this country for the treatment of cirrhosis of the liver, which is high in carbohydrate but low in protein and fat. The present diet contains a moderate amount of protein and fat. In addition to the protein of the diet (114 grams) the patients receive 50 grams of powdered Brewer's yeast 2 daily, of which the protein content is about 50 per cent. There has been no evidence of intolerance to fat in the amounts given. The stools do not contain excessive fat. Salt intake is restricted in patients with ascites and edema to the extent of omitting a salt shaker from the tray, and fluids are allowed up to 2,000 cc. daily. In the first group of 13 patients reported (21), vitamin B " complex " was provided daily in the form of autolyzed yeast (Vegex) or of aqueous liver extract (Valentine). Brewer's yeast was then substituted for these concentrates because it was found to be more palatable in large amounts. In addition to the yeast, the patients generally received intramuscular injections of concentrated liver extract, 5 cc. twice weekly (Lilly or Lederle), and of thiamin chloride,8 5 mgm [mg]. daily."
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"The typical patient with cirrhosis of the liver might be described as follows: Characteristically, he has been bedridden for weeks or months. He has lost much weight. At entry he is weak and tired, mentally dull and at times confused. Food is loathsome. He complains of thirst, of abdominal fullness and pain. There is often lowgrade fever. The pulse rate is rapid. Breathing is shallow because of an elevated diaphragm."

"Although jaundice usually is of low grade, it takes weeks or months for this to subside completely."

"Recovery from polyneuritis in these patients is slow and usually incomplete. Functional improvement is striking in most instances, but the return of vibratory sensation may be partial, and the tendon reflexes may fail to return even after several years of intensive treatment with vitamin B concentrates."

"Several patients, whose ascites had disappeared for considerable periods of time and who had made clinical recovery from cirrhosis, died from intercurrent illness or accident."

**
"Studies on the metabolism of vitamin A (50) and vitamin K (51), for example, indicate that cirrhosis of the liver may interfere with the utilization of these vitamins. However, in many instances our patients gave histories of deficiency disease long antedating the symptoms or signs of cirrhosis. From these observations it seems likely that nutritional deficiency precedes the development of cirrhosis, and that the cirrhotic process, once established, tends to perpetuate or even aggravate the state of nutritional deficiency."

"It is difficult to separate signs of general bodily improvement from those that pertain to the funiction of the liver alone."

"It is realized that cirrhosis of the liver often is discovered at autopsy in persons dying from other causes. In these cases cirrhosis may have been latent for many years. In a series of 245 autopsies that showed cirrhosis of the liver, McCartney (47) found that 35 per cent had no previous clinical manifestations of the disease."
 
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PakPik

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This is interesting, Mr. Amazon

It is my understanding that chronic diseased tissue/illness generates or worsens malnutrition, in a vicious cycle manner since the person ends up not being able to eat or digest food enough and utilize nutrients optimally, whilst the injured tissue imposes ever increasing nutritional needs the worse it gets.

"The initial serum albumin value was low (below 4.0 grams per cent) in 96 per cent of the patients. The initial serum globulin value was high (above 3.0 grams per cent) in 83 per cent of the patients.
So, in 1941 albumin below 4.0 was considered low. Nowaways the bottom value of the range is 3.5 or so, yikes! Maybe this "adjustment" reflects that more and more people in society are getting liver dysfunction. Peat was right on that one.

"The typical patient with cirrhosis of the liver might be described as follows: Characteristically, he has been bedridden for weeks or months. He has lost much weight. At entry he is weak and tired, mentally dull and at times confused. Food is loathsome. He complains of thirst, of abdominal fullness and pain. There is often lowgrade fever. The pulse rate is rapid. Breathing is shallow because of an elevated diaphragm."
cirrhosis may have been latent for many years.
This was me for years (except that my pulse was predominantly low, not rapid... more exactly, erratic). How can a person know if they have cirrhosis if it is not always clinically evident? Also, I've read having liver enzymes in the "normal" range doesn't exclude the possibility of liver disease.
 
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Amazoniac

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Pakpik!!
So, in 1941 albumin below 4.0 was considered low. Nowaways the bottom value of the range is 3.5 or so, yikes! Maybe this "adjustment" reflects that more and more people in society are getting liver dysfunction. Peat was right on that one.
It can be that it was low within the acceptable range, but it's indeed more likely that the range is now lower.
This was me for years (except that my pulse was predominantly low, not rapid... more exactly, erratic). How can a person know if they have cirrhosis if it is not always clinically evident? Also, I've read having liver enzymes in the "normal" range doesn't exclude the possibility of liver disease.
Since it develops as a slow progression and in stages, you should be able to feel that something is wrong there before any serious damage. I think that there are some posts on the forum discussing that..
 

PakPik

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I remember an interview where Peat said something to the effect that the range was narrower, 4-5 I think, in the old days, later changed to 3.5-5. Regarding diagnostics, maybe I'm missing something, but I've never read suggestions on the forum other than liver enzymes. Probably the gold standard is a liver biopsy :geek:... I'm opting out! Maybe the damage is not serious since I don't have the symptoms nowadays. Thanks for your response!
 

amethyst

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Members that installed carpets at home to assist locomotion by gliding over colonies of microbes,

In this study, they randomly selected 54 hospitalized people and treated them with a "nourishing diet and supplements"*, then compared the outcome with 386 other hospitalized patients, and, as they noted, treated or not, they were more advanced cases. There was this premise that if infections (or other problems) were present (very common and varied), they were only accentuating the malnutrition; preceding and then contributing to the liver degeneration**. Treated patients were grouped by recovery, improvement (sometimes the length of monitoring was not long enough to consider the case a recovery) or failure. Regardless of the group, most of them were malnourished before admission, not just the ones that responded to the dietary intervention*** (crosses are scary).
In all groups there were some early deaths related or unrelated to degenerative processes.

TREATMENT OF CIRRHOSIS OF THE LIVER BY A NUTRITIOUS DIET AND SUPPLEMENTS RICH IN VITAMIN B COMPLEX

"Evidence of malnutrition was striking. [..] 81 per cent had eaten poor diets, and that 78 per cent had lost weight (allowing for ascites). Although careful dietary histories were taken, the data were not reliable enough to measure quantitatively."
"The most constant defects in the diets lay in the sparing use of meat and dairy products. Many patients gave histories of having subsisted entirely on alcoholic liquor for intervals of several days and of having refused all food during these sprees."

--
"It is known that the incidence of cirrhosis of the liver is high in certain countries where nutritional deficiencies are endemic (1, 2). Although malaria is blamed popularly for the high incidence of cirrhosis in these countries (3, 4), there is no direct evidence that malaria produces cirrhosis of the liver (5, 6)."

"It has been known that starvation renders the liver more vulnerable to injury by hepatotoxins (9). Lack of certain food factors contained in yeast are said to cause fatty changes in the liver (10) and impaired function (11)."

"It has also been shown that the feeding of excess fat (14) or of excess cystine (15) results in fibrotic changes in the liver."

"In a preliminary report on the treatment of 13 patients with alcoholic cirrhosis of the liver (21), it was noted that, in addition to signs of liver failure, there was evidence of specific malnutrition, notably of the vitamin B complex. These patients were fed a nutritious diet together with vitamin supplements. The improvement that followed treatment appeared to be outside chance expectations."

"The initial serum albumin value was low (below 4.0 grams per cent) in 96 per cent of the patients. The initial serum globulin value was high (above 3.0 grams per cent) in 83 per cent of the patients. ***It is noteworthy that the average initial value for serum albumin is higher in those patients who made clinical improvement than in those who failed to improve."

*
"In Table II is outlined the dietary regimen employed. The diet differs radically from that commonly advocated in this country for the treatment of cirrhosis of the liver, which is high in carbohydrate but low in protein and fat. The present diet contains a moderate amount of protein and fat. In addition to the protein of the diet (114 grams) the patients receive 50 grams of powdered Brewer's yeast 2 daily, of which the protein content is about 50 per cent. There has been no evidence of intolerance to fat in the amounts given. The stools do not contain excessive fat. Salt intake is restricted in patients with ascites and edema to the extent of omitting a salt shaker from the tray, and fluids are allowed up to 2,000 cc. daily. In the first group of 13 patients reported (21), vitamin B " complex " was provided daily in the form of autolyzed yeast (Vegex) or of aqueous liver extract (Valentine). Brewer's yeast was then substituted for these concentrates because it was found to be more palatable in large amounts. In addition to the yeast, the patients generally received intramuscular injections of concentrated liver extract, 5 cc. twice weekly (Lilly or Lederle), and of thiamin chloride,8 5 mgm [mg]. daily."
View attachment 4412

"The typical patient with cirrhosis of the liver might be described as follows: Characteristically, he has been bedridden for weeks or months. He has lost much weight. At entry he is weak and tired, mentally dull and at times confused. Food is loathsome. He complains of thirst, of abdominal fullness and pain. There is often lowgrade fever. The pulse rate is rapid. Breathing is shallow because of an elevated diaphragm."

"Although jaundice usually is of low grade, it takes weeks or months for this to subside completely."

"Recovery from polyneuritis in these patients is slow and usually incomplete. Functional improvement is striking in most instances, but the return of vibratory sensation may be partial, and the tendon reflexes may fail to return even after several years of intensive treatment with vitamin B concentrates."

"Several patients, whose ascites had disappeared for considerable periods of time and who had made clinical recovery from cirrhosis, died from intercurrent illness or accident."

**
"Studies on the metabolism of vitamin A (50) and vitamin K (51), for example, indicate that cirrhosis of the liver may interfere with the utilization of these vitamins. However, in many instances our patients gave histories of deficiency disease long antedating the symptoms or signs of cirrhosis. From these observations it seems likely that nutritional deficiency precedes the development of cirrhosis, and that the cirrhotic process, once established, tends to perpetuate or even aggravate the state of nutritional deficiency."

"It is difficult to separate signs of general bodily improvement from those that pertain to the funiction of the liver alone."

"It is realized that cirrhosis of the liver often is discovered at autopsy in persons dying from other causes. In these cases cirrhosis may have been latent for many years. In a series of 245 autopsies that showed cirrhosis of the liver, McCartney (47) found that 35 per cent had no previous clinical manifestations of the disease."

This study makes perfect sense to me. Also, interestingly, they were given brewer's yeast. Brewer's yeast has lecithin in it as well as being a good source of B vitamins. Both are great for healing the liver, whether one has cirrhosis or not.
 
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Amazoniac

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I remember an interview where Peat said something to the effect that the range was narrower, 4-5 I think, in the old days, later changed to 3.5-5. Regarding diagnostics, maybe I'm missing something, but I've never read suggestions on the forum other than liver enzymes. Probably the gold standard is a liver biopsy :geek:... I'm opting out! Maybe the damage is not serious since I don't have the symptoms nowadays. Thanks for your response!
I think that it was Ray who mentioned that skin reflects the state of internal organs, considering that it didn't suffer much localized stress. I suppose that things like cracked heels and things alike are great indicators of hardening of soft tissue, just a guess though.
This study makes perfect sense to me. Also, interestingly, they were given brewer's yeast. Brewer's yeast has lecithin in it as well as being a good source of B vitamins. Both are great for healing the liver, whether one has cirrhosis or not.
Some extra selenium too..
 

PakPik

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I suppose that things like cracked heels and things alike are great indicators of hardening of soft tissue, just a guess though.
I did have very cracked heels for years. That could have well been a clue, as you suggest.
 

amethyst

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I think that it was Ray who mentioned that skin reflects the state of internal organs, considering that it didn't suffer much localized stress. I suppose that things like cracked heels and things alike are great indicators of hardening of soft tissue, just a guess though.

Some extra selenium too..
I read that brewer's yeast has selenium in it so that probably helped as well.
 
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Amazoniac

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All from the same author: Arthur Patek

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934006/pdf/bullnyacadmed00544-0057.pdf

"alcoholism is the most common antecedent factor in this disease in the Western hemisphere. I shall not cite the evidence for this observation, which is common knowledge. And yet, in about 30 per cent of cases seen at post-mortem examination there has been no story of alcoholism."

"The diet [that we provide] consists chiefly of meat, milk, eggs, fruit, and green vegetables. Meat is served twice daily; milk five times daily-three times with meals and two times with 25 grams of powdered brewer's yeast. It is advisable to feed the yeast in graded, increasing doses up to the final amount. Occasionally patients cannot tolerate brewer's yeast. For these, oral vitamin B complex has been substituted in the form of liquid yeast concentrates. In addition, thiamin chloride (5 mgm.) is injected i.m. daily and liver extract (5 cc.), twice weekly." More detailed below.

"In patients with ascites the salt intake is restricted only by the exclusion of a salt shaker from the tray, and fluids are allowed up to 2000 cc. daily. Too rigid restriction of salt and water is harmful to these patients, and has been observed to precipitate symptoms of hypochloremia."

"the incidence of signs of malnutrition in thirty-three patients with vitamin deficiency diseases is compared to that of fifty-four patients with Laennec's cirrhosis. There is a close similarity between the two groups." "The question may be raised as to whether such cases actually represent an early stage of Laennec's cirrhosis. I believe that they do."​

--
DIETARY TREATMENT OF CIRRHOSIS OF THE LIVER

"The present report is an analysis of results obtained in the treatment of 124 patients with cirrhosis of the liver by means of a diet rich in protein and supplemented by concentrates of the vitamin B complex. In 1937 a preliminary statement1 was made concerning favorable therapeutic results obtained in 13 patients who had been observed during the course of one year. The improvement appeared to exceed chance expectations. A more comprehensive report2 [original post above] in 1941 was made on 54 patients that had been studied over a four year period. The results tended to confirm the preliminary impression. With the new dietary regimen roughly one half of the patients showed signs of significant clinical improvement. These results were considerably better than those observed in a control series of 386 patients. However, since cirrhosis of the liver is a chronic disease and since its clinical course may vary considerably in different patients, the study was extended further in order to get a larger body of evidence and to get a clearer picture of the long term results of this therapeutic program."

"[The diet provided] contains 140 Gm. of protein,[5] 365 Gm. of carbohydrate and 175 Gm. of fat — a total of about 3,500 calories. The diet consists chiefly of meat, milk, eggs, fruit and green vegetables. Eggs are served with breakfast; meat, fish or poultry is served at dinner and supper; milk is served three times with meals and twice between meals, with 25 Gm. of yeast, in the form of milknog. If the patient eats these foods, considered basic to the program, the remainder of the diet is largely a matter of choice." "Yeast is fed in graded increasing dosage until 25 Gm. are fed twice daily. For patients who do not tolerate yeast (because of distention, diarrhea or nausea) an orally administered B complex preparation7 is substituted. Thiamine hydrochloride (5 mg. daily) and unconcentrated liver extract (5 cc. twice weekly) are injected intramuscularly. If the patient shows signs of severe polyneuritis or of mental confusion thiamine hydrochloride (100 mg.) and nicotinamide (300 mg.) are administered daily parenterally."

"[As an experiment, three out of six] patients received 4 to 6 Gm. daily of choline hydrochloride for six, eight and ten months respectively ; 5 patients received 3 to 4 Gm. daily of methionine for an average of three and six-tenths months. In 1 patient, who received methionine for seven months, slight clinical improvement was noted. No change was apparent in the others."

"The present studies indicate that Laennec's cirrhosis is not of necessity a progressive disease, since the process appears to be arrested in a significant number of patients. Improvement in symptoms and signs of the disease and increased period of survival are effected by a highly nutritious diet, rich in protein and supplemented with vitamin B concentrates. These observations have been substantiated in other reports,16 some of which describe more favorable results with the added use of specific substances."

"Experimental studies on animals have suggested that meat or meat juice may contain noxious substances that are not readily detoxified by the liver. However, in the patients under observation there was no apparent intolerance to animal proteins. On the basis of other studies, restriction of dietary fat has been advocated. The rationale stems from experiments which show that diets rich in fat, in conjunction with a low content of protein, predispose to hepatic injury. It may be pointed out that when adequate protein is fed, no such deleterious effects have been produced. Severe restriction of fat decreases the palatability of the diet and thus tends to reduce the caloric intake. In the present regimen a diet containing 170 Gm. of fat did not cause steatorrhea. Moreover, biopsy specimens of the liver obtained in the course of treatment did not reveal fatty changes in the liver. A recent report by Labby and Hoagland18 on the treatment of acute hepatitis also concluded that severe restriction of fat is not justified by clinical evidence."

"In recent years a number of reports have suggested that the administration of choline or methionine may produce effects apart from that provided by diet. For reasons stated, it is not easy to evaluate these reports. It is far more difficult to establish controls and to determine the role of a specific dietary factor in studies of human beings than in experiments with animals. Our own limited experience does not suggest that choline and methionine exert a specific effect in the late stage of hepatic failure. It would seem that their field of greatest usefulness might be in the precirrhotic fatty stage of the disease, since they are lipotropic agents. There appears to be no danger in administering these substances, but there may be harm in stressing their importance to the extent that other factors are neglected. Although observations on laboratory animals have established that choline and methionine protect against experimental cirrhosis produced by diets low in protein, the evidence for their curative effect has been less conclusive. Certainly, it has not been shown that these substances alone are adequate for repair or regeneration of the cirrhotic liver. It is possible that several factors may facilitate repair of the liver and restoration of function."

"The implications of the present study are essentially those stated in an earlier report.[2]:
The present data give no indication as to whether vitamin B concentrates, protein or some unknown substances are specifically effective in the treatment of cirrhosis. It is possible that, by maintaining patients in optimal nutrition and rest, the liver recovers "spontaneously." In other words, the present regimen may allow the patient to survive long enough for natural reparative processes to take effect. It is also possible that the present regimen provides a specific agent for recovery of the diseased liver. The fact that only a limited number of patients survive despite therapy does davetheauthor not rule out the latter possibility. When the diagnosis of cirrhosis of the liver can be made in the incipient stages, the mortality rate should become much reduced, for, unlike most other vital organs of the body, the liver has the capacity to regenerate. In this capacity lies the hope for an effective therapy."

"It generally required several months before substantial changes took place."​

@notjustanotherbrickinthewall
 

haidut

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It is possible that, by maintaining patients in optimal nutrition and rest, the liver recovers "spontaneously." In other words, the present regimen may allow the patient to survive long enough for natural reparative processes to take effect

I think this speaks volumes to the power of good diet and lack of stress to recover from "incurable" conditions. Adding some DHEA/progesterone would be the OTC method to help the process even more and for men adding some DHT should be ideal. The fact that choline and methionine are lipotropic agents is another reason to not indulge in eating too much of them.
 
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"Hepatic disease is often accompanied by hypovitaminosis due to an increased need for vitamins in the face of decreased intake (1), intestinal malabsorption (2), and reduced hepatic storage capacity (3). Clinical stigmata of vitamin deficiency also occur with normal tissue stores when liver dysfunction prevents conversion of vitamins into metabolically useful forms (4). Vitamin B complex depletion is common in hepatocellular disease, attributable to a) their release from necrotic cells without adequate replacement (5), and b) increased need for nucleic acid synthesis and liver regeneration (6-8). Reduced absorption of vitamins A (9), D (10), K (11), and E (12) is characteristic in patients with biliary obstruction or liver disorders with steatorrhea."

"Alteration in circulating levels of vitamins was regularly present in patients with either acute or chronic liver disease. An increase in vitamins was attributed to their release from the liver; while a decrease occurred with expansion of plasma volume or body depletion. The influence of liver disease on plasma protein and red blood cell metabolism may also be of importance in the abnormalities we encounter in clinical study. Studies of normal plasma revealed that alpha and beta globulins contain the bulk of the vitamins distributed on plasma proteins. Ascorbic acid, biotin, and vitamin B6 were found principally in the alpha globulin; vitamin A, thiamin, pantothenate, and reduced folate occurred mainly in the beta globulin fraction. Riboflavin and vitamin B12 are almost equally distributed between the alpha and beta globulins (14). Red blood cells in normal subjects were richer than plasma in riboflavin (3x), nicotinate (71x), thiamin (4x), pantothenate (2x), and reduced folate (2x). In contrast, ascorbate, A, E, biotin, B6, B12, and oxidized folyltri-glutamates are found mainly in plasma (15)."

"Marked elevation of blood pantothenic acid was characteristic of alcoholics hospitalized with acute fatty liver (18). Pantothenic acid was increased despite low circulating folic acid, thiamin, and vitamin B6, and was often accompanied by an increase in 24-hr urinary pantothenic acid. Pantothenate levels returned to normal over a 2- to 3-week period with mobilization of liver fat, which occurred on a regimen of a nutritious diet and abstinence from alcoholic beverages."

"Each of 140 patients with Laennec’s cirrhosis, 80% of the 10 patients with chronic viral hepatitis, and 75% of the 12 patients with biliary cirrhosis had low circulating levels of two or more vitamins." "The most common vitamin deficiency was folic acid, followed in frequency by low circulating levels of vitamin B6 and thiamin (Fig. 1). Vitamins A and E were often deficient in patients with biliary cirrhosis. History usually revealed an inadequate diet intake, which could account for the high incidence of vitamin deficiency. Occasionally, however, hypovitaminosis was present despite daily ingestion of therapeutic multivitamin capsules. Clinical stigmata of vitamin deficiency including glossitis, peripheral neuropathy, hyperkeratosis of the skin, reduced dark adaptation, and macrocytic anemia were encountered in 70% of these patients."

"Subcellular fractionation indicates vitamins occur primarily in the mitochondrial and supernatant fraction of the normal liver (22). Estimated total B-conhplex vitamin content of normal adult liver varies from 0.5 to 6.5 mg without a specific quantitative relationship to circulating levels (23) Cirrhosis was associated with an 80% reduction in total liver content of nicotinic acid (normal 6.5 mg), 60% reduction in vitanhin B12 (normal 0.8 mg), and folic acid (normal 5 mg), and 50% reduction in vitamin B6 (normal 6 mg)."

"Established daily minimal vitamin requirements for normal adults were not adequate for patients with active liver disease (24). Extra vitamins were needed to repair tissue damage and compensate for diminished hepatic storage capacity. Volunteers developed low circulating levels of folate, vitamin B6, thiamin, nicotinic acid, and riboflavin when steatonecrosis was induced by addition of 1-2 pints of vodka daily to a "normal" diet (24)."

"Symptoms of vitamin depletion were corrected by intensive therapy in 80% of the 72 patients with Laennec’s cirrhosis. Parenteral vitamins were given initially to correct acute deficits because of the uncertainty of intestinal absorption; a nutritious vitamin-supplemented diet was used to maintain vitamin balance. Parenteral administration of a single vitamin such as thiamin, folic acid, or pyridoxine in large amounts often corrected signs and symptoms of a specific deficiency state; laboratory evidence of other vitamin deficits, however, was not influenced by such therapy. In some instances, key symptoms attributed to a specific deficiency such as thiamin persisted until all vitamins were provided (20)."
@Valid

"Uptake, storage, and metabolism of vitamins remained abnormal until there was repair of liver cell damage. In some instances, vitamin therapy had a direct effect on morbidity and mortality. Thus, provision of folic acid, omitted from oral and parenteral vitamins given previously, interrupted aregenerative phases of hepatic injury and led to complete recovery in 16 malnourished alcoholics with steatonecrosis and progressive liver failure (26)."

"Vitamin depletion usually occurs in liver disease because intake is inadequate to meet needs imposed by tissue injury. Extra vitamins are needed with hepatic injury to protect uninjured liver cells, repair damaged cells, and produce new hepatocytes."

[Advanced damage]
"Clinical evidence of vitamin deficiency may persist in liver disease despite ingestion of a nutritious diet because of absorption defects or inability of the liver to convert vitamins into an active form."​
 
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Amazoniac

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Only for those that are considering adopting a sloth and naming it Klotho:

The Modern Treatment of Cirrhosis of the Liver - ScienceDirect

"Since alcoholic beriberi and pellagra had been shown to be similar to the endemic forms of these diseases, it seemed plausible to Patek that the correlation between alcoholism and cirrhosis of the liver might also be due to a coexisting nutritional deficiency. This hypothesis appeared particularly attractive in view of the high incidence of vitamin B-complex deficiency noted in patients with cirrhosis, as, for example, Wayburn and Guerard's3 report of multiple peripheral neuropathy in 17 per cent of a large series of cirrhotic patients. The trouble with the severe alcoholic is that he forgets to eat; thus it seems fair to assume that many of the various morbid states to which an alcoholic is subject are primarily manifestations of vitamin deficiency. Although alcohol conceivably may exert toxic effects in the face of a poor diet, it must play a minor role at best, since all of the deficiency syndromes may develop in total abstainers on deficient diets."

"Gyorgy and Goldblatt7 produced fatty livers with necrosis in rats maintained on a diet deficient in the vitamin B complex even though supplemented with thiamine, riboflavin and pyridoxine. The addition to the diet of yeast, a yeast extract, or 2 mg. of choline a day usually prevented the changes in the liver. Rich and Hamilton8 succeeded in reproducing true cirrhosis of the liver in rabbits fed a deficient diet. The development of this experimental cirrhosis was not prevented by the addition of thiamine, riboflavin, pyridoxine, nicotinic acid or vitamins A, D and E to the basal diet, whereas a daily supplement of 5 gm. of dry brewer's yeast gave full protection."

"His interest stimulated by Patek's [author above] original report on the dietary treatment of cirrhosis and the volume of suggestive experimental work already mentioned, Snell[12] began treating cirrhotic patients with a nutritious diet supplemented with various vitamins. His regimen differed materially from that recommended by Patek. The diet was high in carbohydrate (500 gm.), low in fat (about 60 gm.), and rich in proteins not derived from meat sources (110 gm.), providing roughly 3000 calories per day. The protein component of the diet was derived chiefly from vegetables, milk and egg-white, meat being kept at a minimum. The basis for this change in protein composition was Bollman's report that animals with experimentally produced hepatic injury are made worse by the administration of meat or meat extracts while tolerating protein from other sources without harmful effect. Snell supplemented his diet with various pure vitamins, crude oral liver extract, and yeast or yeast concentrates. In order to facilitate absorption of fat-soluble vitamins, patients were given animal bile salts, 0.3 to 1.0 gm. with each meal. This program gave very encouraging results in a group of fifty decompensated cirrhotic patients so treated. A few remarkable "cures" with disappearance of ascites were encountered, one of the most striking in a man aged 72 who after two years of almost weekly parencentesis remained free of ascites and in good health for one year. The results of treatment were regarded as "excellent" in 44 per cent of the entire group,13 although only 22 per cent were entirely free from ascites at the time of the report. Snell agrees with Patek that an even higher incidence of "cures" is to be expected among patients who present various degrees of fatty metamorphosis, degeneration and necrosis without extensive periportal fibrosis and great restriction of portal blood flow."

"In a recent report on the diagnosis and clinical course of fatty liver in seventy alcoholic patients, Keefer and Fries14 stress the therapeutic value of a high-carbohydrate, low-fat diet with a moderate amount of protein, supplemented with vitamin preparations and liver extract. They regard the fatty liver as the precursor of cirrhosis, but point out that ascites, jaundice, and death may occur during the stage when the liver is filled with fat and before actual fibrosis has developed. In some cases, the process appeared to be reversible. The recognition of this disorder in its early stages and the use of appropriate treatment was followed in many instances by recovery."

"For the past several years we have been keenly interested in the dietary treatment of cirrhosis at the johns Hopkins Hospital. To date too few patients have been so treated to justify any final conclusions, but we have seen sufficiently encouraging results to warrant a continuation of the regimen. In general, it has been our policy to adhere fairly closely to the Patek diet with the exception that the fat content of the diet has been considerably reduced for patients with jaundice or diarrhea. Since Snell's reasons for withholding meat are based on purely experimental grounds not necessarily applicable to the human liver and since meat is known to contain protein of "highest biologic value," we have not eliminated meat from our diet, but rather supplied it in liberal portions with complete impunity as far as we could ascertain. We have supplemented the diet with 30 to 50 gm. of brewer's yeast powder a day and polyvitamin capsules in numbers sufficient to supply at least twice the estimated normal adult requirement for the vitamins of proven importance in human nutrition, namely vitamins A, C, D, thiamine, nicotinic acid (or the amide), and riboflavin. Where hemorrhagic phenomena were observed with prolongation of the prothrombin time, vitamin K was administered either parenterally or orally along with bile salts to promote its absorption. Intramuscular injections of crude (rather than concentrated) liver extract have been given in some cases, especially when macrocytic anemia was present. Furthermore, the oral administration of crude liver extract powder has been employed in certain instances. In view of the experimental work on the lipotropic action and protective effects exerted by choline on the liver, it seemed plausible to Wintrobe and the writer to administer this substance to patients with cirrhosis as an additional supplement to the measures already outlined. At least ten patients have now received choline chloride, 1.5 gm. a day, administered in the form of a 10 per cent elixir prepared by the hospital pharmacy, in doses of 5 cc. after each meal. No untoward effects have been noted after the continued administration of choline for weeks or even months. It is as yet too early to speculate upon the possible merits of choline therapy in cirrhosis."

"Combating Secondary Vitamin Deficiency.- In addition to the highly suggestive evidence already presented that vitamin deficiency plays an important role in the etiology of liver disease, it has been firmly established that preexisting liver disease predisposes toward the development of numerous and varied manifestations of vitamin deficiency. Liver disease may contribute to the deficiency of the fat-soluble vitamins A and K in one of three ways: (1) failure of proper absorption in patients with jaundice; (2) failure of storage of the vitamins in the diseased liver; (3) disturuance of intermediary metabolism of the vitamins in the damaged liver. In patients with obstructive jaundice or hepatitis the dearth of bile salts in the intestinal tract results in poor absorption of fats and fat-soluble vitamins. Carotene furnishes the chief source of vitamin A in the average diet, and the normal liver converts carotene to vitamin A through the action of an enzyme, carotenase. Since a severely damaged liver will not effect this conversion, it is not surprising that low blood levels of vitamin A along with clinical manifestations of vitamin A deficiency (e.g., night blindness, keratomalacia, and epithelial metaplasia of various organs) have repeatedly been described in patients with cirrhosis or other forms of liver disease. Therapy or prophylaxis should consist in large doses of vitamin A administered orally with bile salts or large parenteral injections of vitamin A. Little improvement is to be expected from a high carotene intake in patients with severe liver damage."

"The recognition of the etiologic role of vitamin K deficiency in the hemorrhagic diathesis so common in patients with jaundice or severe liver damage represents one of the most important contributions to medical knowledge within the last decade. This hemorrhagic tendency has been conclusively shown to be due to lowered plasma prothrombin, which in turn results from inadequate absorption of vitamin K, failure of the severely damaged liver to utilize vitamin K in the formation of prothrombin, or a combination of these two conditions. The failure of jaundiced patients to absorb vitamin K may be controlled by the oral administration of the bile salts along with vitamin K preparations or the parenteral administration of a purified vitamin K derivative such as 2-methyl-l, 4-naphthoquinone (1 to 4 mg. a day intramuscularly). If the liver is so severely damaged that it cannot produce prothrombin in spite of an adequate supply of vitamin K, bleeding will not be influenced by either of these methods of administering vitamin K and the prognosis becomes extremely grave. Under such circumstances, transfusions of freshly drawn blood should be given to supply prothrombin directly."

"In addition to the special function of the liver with reference to vitamin A and K, the liver is known to serve as a storage depot for the majority of vitamins (A, B-complex, C, D, K) and probably provitamins as well. Hence, patients with severe liver disease are bound to have inadequate reserves and are, therefore, more likely to develop outspoken manifestations of vitamin deficiency under the added strain of any severe infection or curtailment of food. This situation affords still another reason for our advocating the liberal use of pure vitamins in addition to the high-vitamin diet and crude vitamin sources in the treatment of cirrhosis."

"Summary and conclusions
1. An abundance of experimental and clinical evidence points to dietary deficiency as a most important factor in the etiology of fatty liver and cirrhosis of the liver.
2. Treatment of fatty liver and cirrhosis by a nutritious diet high in calories, protein and vitamins, especially the vitamin B-complex, appears to be the most promising form of therapy for this disease, even after signs of hepatic decompensation such as jaundice, ascites and hem at emesis have developed.
3. This dietary treatment of cirrhosis has been discussed in some detail along with adjunctive therapeutic measures including various surgical procedures designed to relieve ascites and to prevent hematemesis.
4. Four cases are presented to illustrate the various aspects of dietary therapy. In one of these cases splenectomy was followed by dramatic relief from both ascites and hematemesis."​

@Yes, again, because of the extracts.
 

haidut

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Only for those that are considering adopting a sloth and naming it Klotho:

The Modern Treatment of Cirrhosis of the Liver - ScienceDirect

"Since alcoholic beriberi and pellagra had been shown to be similar to the endemic forms of these diseases, it seemed plausible to Patek that the correlation between alcoholism and cirrhosis of the liver might also be due to a coexisting nutritional deficiency. This hypothesis appeared particularly attractive in view of the high incidence of vitamin B-complex deficiency noted in patients with cirrhosis, as, for example, Wayburn and Guerard's3 report of multiple peripheral neuropathy in 17 per cent of a large series of cirrhotic patients. The trouble with the severe alcoholic is that he forgets to eat; thus it seems fair to assume that many of the various morbid states to which an alcoholic is subject are primarily manifestations of vitamin deficiency. Although alcohol conceivably may exert toxic effects in the face of a poor diet, it must play a minor role at best, since all of the deficiency syndromes may develop in total abstainers on deficient diets."

"Gyorgy and Goldblatt7 produced fatty livers with necrosis in rats maintained on a diet deficient in the vitamin B complex even though supplemented with thiamine, riboflavin and pyridoxine. The addition to the diet of yeast, a yeast extract, or 2 mg. of choline a day usually prevented the changes in the liver. Rich and Hamilton8 succeeded in reproducing true cirrhosis of the liver in rabbits fed a deficient diet. The development of this experimental cirrhosis was not prevented by the addition of thiamine, riboflavin, pyridoxine, nicotinic acid or vitamins A, D and E to the basal diet, whereas a daily supplement of 5 gm. of dry brewer's yeast gave full protection."

"His interest stimulated by Patek's [author above] original report on the dietary treatment of cirrhosis and the volume of suggestive experimental work already mentioned, Snell[12] began treating cirrhotic patients with a nutritious diet supplemented with various vitamins. His regimen differed materially from that recommended by Patek. The diet was high in carbohydrate (500 gm.), low in fat (about 60 gm.), and rich in proteins not derived from meat sources (110 gm.), providing roughly 3000 calories per day. The protein component of the diet was derived chiefly from vegetables, milk and egg-white, meat being kept at a minimum. The basis for this change in protein composition was Bollman's report that animals with experimentally produced hepatic injury are made worse by the administration of meat or meat extracts while tolerating protein from other sources without harmful effect. Snell supplemented his diet with various pure vitamins, crude oral liver extract, and yeast or yeast concentrates. In order to facilitate absorption of fat-soluble vitamins, patients were given animal bile salts, 0.3 to 1.0 gm. with each meal. This program gave very encouraging results in a group of fifty decompensated cirrhotic patients so treated. A few remarkable "cures" with disappearance of ascites were encountered, one of the most striking in a man aged 72 who after two years of almost weekly parencentesis remained free of ascites and in good health for one year. The results of treatment were regarded as "excellent" in 44 per cent of the entire group,13 although only 22 per cent were entirely free from ascites at the time of the report. Snell agrees with Patek that an even higher incidence of "cures" is to be expected among patients who present various degrees of fatty metamorphosis, degeneration and necrosis without extensive periportal fibrosis and great restriction of portal blood flow."

"In a recent report on the diagnosis and clinical course of fatty liver in seventy alcoholic patients, Keefer and Fries14 stress the therapeutic value of a high-carbohydrate, low-fat diet with a moderate amount of protein, supplemented with vitamin preparations and liver extract. They regard the fatty liver as the precursor of cirrhosis, but point out that ascites, jaundice, and death may occur during the stage when the liver is filled with fat and before actual fibrosis has developed. In some cases, the process appeared to be reversible. The recognition of this disorder in its early stages and the use of appropriate treatment was followed in many instances by recovery."

"For the past several years we have been keenly interested in the dietary treatment of cirrhosis at the johns Hopkins Hospital. To date too few patients have been so treated to justify any final conclusions, but we have seen sufficiently encouraging results to warrant a continuation of the regimen. In general, it has been our policy to adhere fairly closely to the Patek diet with the exception that the fat content of the diet has been considerably reduced for patients with jaundice or diarrhea. Since Snell's reasons for withholding meat are based on purely experimental grounds not necessarily applicable to the human liver and since meat is known to contain protein of "highest biologic value," we have not eliminated meat from our diet, but rather supplied it in liberal portions with complete impunity as far as we could ascertain. We have supplemented the diet with 30 to 50 gm. of brewer's yeast powder a day and polyvitamin capsules in numbers sufficient to supply at least twice the estimated normal adult requirement for the vitamins of proven importance in human nutrition, namely vitamins A, C, D, thiamine, nicotinic acid (or the amide), and riboflavin. Where hemorrhagic phenomena were observed with prolongation of the prothrombin time, vitamin K was administered either parenterally or orally along with bile salts to promote its absorption. Intramuscular injections of crude (rather than concentrated) liver extract have been given in some cases, especially when macrocytic anemia was present. Furthermore, the oral administration of crude liver extract powder has been employed in certain instances. In view of the experimental work on the lipotropic action and protective effects exerted by choline on the liver, it seemed plausible to Wintrobe and the writer to administer this substance to patients with cirrhosis as an additional supplement to the measures already outlined. At least ten patients have now received choline chloride, 1.5 gm. a day, administered in the form of a 10 per cent elixir prepared by the hospital pharmacy, in doses of 5 cc. after each meal. No untoward effects have been noted after the continued administration of choline for weeks or even months. It is as yet too early to speculate upon the possible merits of choline therapy in cirrhosis."

"Combating Secondary Vitamin Deficiency.- In addition to the highly suggestive evidence already presented that vitamin deficiency plays an important role in the etiology of liver disease, it has been firmly established that preexisting liver disease predisposes toward the development of numerous and varied manifestations of vitamin deficiency. Liver disease may contribute to the deficiency of the fat-soluble vitamins A and K in one of three ways: (1) failure of proper absorption in patients with jaundice; (2) failure of storage of the vitamins in the diseased liver; (3) disturuance of intermediary metabolism of the vitamins in the damaged liver. In patients with obstructive jaundice or hepatitis the dearth of bile salts in the intestinal tract results in poor absorption of fats and fat-soluble vitamins. Carotene furnishes the chief source of vitamin A in the average diet, and the normal liver converts carotene to vitamin A through the action of an enzyme, carotenase. Since a severely damaged liver will not effect this conversion, it is not surprising that low blood levels of vitamin A along with clinical manifestations of vitamin A deficiency (e.g., night blindness, keratomalacia, and epithelial metaplasia of various organs) have repeatedly been described in patients with cirrhosis or other forms of liver disease. Therapy or prophylaxis should consist in large doses of vitamin A administered orally with bile salts or large parenteral injections of vitamin A. Little improvement is to be expected from a high carotene intake in patients with severe liver damage."

"The recognition of the etiologic role of vitamin K deficiency in the hemorrhagic diathesis so common in patients with jaundice or severe liver damage represents one of the most important contributions to medical knowledge within the last decade. This hemorrhagic tendency has been conclusively shown to be due to lowered plasma prothrombin, which in turn results from inadequate absorption of vitamin K, failure of the severely damaged liver to utilize vitamin K in the formation of prothrombin, or a combination of these two conditions. The failure of jaundiced patients to absorb vitamin K may be controlled by the oral administration of the bile salts along with vitamin K preparations or the parenteral administration of a purified vitamin K derivative such as 2-methyl-l, 4-naphthoquinone (1 to 4 mg. a day intramuscularly). If the liver is so severely damaged that it cannot produce prothrombin in spite of an adequate supply of vitamin K, bleeding will not be influenced by either of these methods of administering vitamin K and the prognosis becomes extremely grave. Under such circumstances, transfusions of freshly drawn blood should be given to supply prothrombin directly."

"In addition to the special function of the liver with reference to vitamin A and K, the liver is known to serve as a storage depot for the majority of vitamins (A, B-complex, C, D, K) and probably provitamins as well. Hence, patients with severe liver disease are bound to have inadequate reserves and are, therefore, more likely to develop outspoken manifestations of vitamin deficiency under the added strain of any severe infection or curtailment of food. This situation affords still another reason for our advocating the liberal use of pure vitamins in addition to the high-vitamin diet and crude vitamin sources in the treatment of cirrhosis."

"Summary and conclusions
1. An abundance of experimental and clinical evidence points to dietary deficiency as a most important factor in the etiology of fatty liver and cirrhosis of the liver.
2. Treatment of fatty liver and cirrhosis by a nutritious diet high in calories, protein and vitamins, especially the vitamin B-complex, appears to be the most promising form of therapy for this disease, even after signs of hepatic decompensation such as jaundice, ascites and hem at emesis have developed.
3. This dietary treatment of cirrhosis has been discussed in some detail along with adjunctive therapeutic measures including various surgical procedures designed to relieve ascites and to prevent hematemesis.
4. Four cases are presented to illustrate the various aspects of dietary therapy. In one of these cases splenectomy was followed by dramatic relief from both ascites and hematemesis."​

@Yes, again, because of the extracts.

Thanks for this! It is interesting that they mentioned a small amount of choline helped protect/reverse the damage but then later on the text mentioned egg whites are used as protein source instead of egg yolks which are a rich source of (phosphatidyl)-choline and are known to repair liver damage.
 
OP
Amazoniac

Amazoniac

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Came across this:
Herb Doctors: Thyroid And Polyunsaturated Fatty Acidsnew
the liver is constantly detoxifying all the chemicals that you absorbed from your intestine. Anything in your bloodstream is processed through the liver. And if you're deficient in thyroid, the liver can’t handle the cholesterol or free fatty acids. If the liver treats the polyunsaturated fats as toxins and destroys them, causes them to be excreted, the cholesterol is recycled and used for making the digestive bile acids for reuse for making steroid hormones and such. But the liver can’t process these things without adequate protein and B vitamins. Thiamine, B1, is one of the essential vitamins for making the liver work efficiently. And a low thyroid function makes it impossible to use these B vitamins and protein. And so the liver, for any of these deficiencies, will fail to detoxify and will allow estrogen to accumulate. The estrogen activates the mobilization of free fatty acids, exposes your arteries to more oxidative damage, while suppressing your thyroid function and creating a vicious circle. So I usually advocate eating a high naturally rich in vitamin diet. And eggs and liver are probably the richest sources of all of the essential nutrients for liver function. But if you eat too much liver, it can act like too much muscle meat and suppress your thyroid. Too much carotene or vitamin A can also suppress your thyroid. So I recommend lots of liver and eggs in the diet, but only if you're balancing with the right amount of thyroid function, so that your liver has all of the actors that it needs to process out the toxins.
 
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Amazoniac

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Herb Doctors: Longevity
B vitamins act very quickly, so you can usually see an effect, sometimes - like with Vitamin B1 you can often feel an effect in the first hour, with Vitamin B6 you generally feel an effect in the first day. And with Vitamin B6, sometimes 10mg is all it needs and one dose will often take care of a problem that has lingered for a long time. And it's good if you can use a few doses of the supplements, because most of the supplements have impurities and excipients that aren't good in the long run.
 

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OP
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Sheila

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Another excellent find Monsieur,

As an alternative here, I have found that the somewhat expensive Swiss product A. Vogel BioStrath tablets well tolerated and efficacious in the past as a natural b vitamin-with-minerals yeast-based supplement. They grow their yeast for this on herbs and root vegetables then hydrolyse it. Some quite nice scientific data to support its use in those children with 'failure to thrive' which appears missing now from their websites, shame. I found it similarly useful, if dear. There is also a tonic which was designed to be palatable for children. 100% children I knew 'who expressed a preference' pronounced it: vile. Tabs were fine.

Although it is suggested that some react to natural yeast products, another cohort of course think nothing of reacting to even low dose synthetic b-vitamins - orally or topically. An organic liver extract (calves, not lambs! - worm burden eek!) from a trusted source might be the best of both worlds if Mr Haidut is feeling bored with his current range.

Thank you Amazoniac, you never fail to amaze with your finds.

Sheila
 

Nighteyes

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Another excellent find Monsieur,

As an alternative here, I have found that the somewhat expensive Swiss product A. Vogel BioStrath tablets well tolerated and efficacious in the past as a natural b vitamin-with-minerals yeast-based supplement. They grow their yeast for this on herbs and root vegetables then hydrolyse it. Some quite nice scientific data to support its use in those children with 'failure to thrive' which appears missing now from their websites, shame. I found it similarly useful, if dear. There is also a tonic which was designed to be palatable for children. 100% children I knew 'who expressed a preference' pronounced it: vile. Tabs were fine.

Although it is suggested that some react to natural yeast products, another cohort of course think nothing of reacting to even low dose synthetic b-vitamins - orally or topically. An organic liver extract (calves, not lambs! - worm burden eek!) from a trusted source might be the best of both worlds if Mr Haidut is feeling bored with his current range.

Thank you Amazoniac, you never fail to amaze with your finds.

Sheila

Thank you for mentioning This product! I have been looking for a good b-Complex here in Europe and did not even come across This till you mentioned it. Bought the drops today. Have not been able to find a complete list of nutrients contained and the amounts but I suppose the manufacturer cant know for sure?

The drops are in 32% vol alcohol but I suppose the amount of ethanol is very slight in ~30 drops. Did not get the pills as they have excipients
 

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