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| | From:  JamieDH4 (Original Message) | Sent: 7/27/2007 5:01 AM |
Hey Hans-
I didn't see a thread where people specifically asked you to evaluate their diets, so I guess I wanted to make one.
I guess, could you evaluate my diet, please?
Today I had the following:
Breakfast:
2 (homemade, no PUFA) toaster pastries. I make these, because they they freeze well and can be eaten on the run, but also have no PUFA.
The ingredients include butter, flour, corn syrup, cherries, and gelatin.
Lunch:
Coffee with Heavy Cream
Apple Pie (homemade, no PUFA)
Pasta w/ 1 tbsp butter, and parmesan cheese
Dinner:
Tomato Salad w/ Olive Oil and Oregano.
Feta Cheese stuffed spinach leaves.
1 cup 2% cottage cheese
1 cup Godiva Chocolate Spice Ice Cream. |
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| Hans, do you think the way I have been eating eggs for breakfast produces oxidized cholesterol ? First I boil cut fresh or can tomato on a fry pan with some salt. Then I add 2 whole eggs and mix them quickly. It takes less then 1 minute for the eggs to solidify because the tomato paste is already hot. Tomato also provides antioxidants (lycopene) so I thought the egg cholesterol doesn't oxidize. Finally I add coconut or extra virgin olive oil and eat it with bread, cottage cheese and blueberry jam. (In the old days I was adding flax seed or fish oil by tablespoons instead which I suspect led to my health problems) |
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The less time you fry something, the better, but I don't know if enough evidence is available on this. I did post a study about how bad it is to steam salmon, apparently, but studies have not been conducted in a systematic way. Here is something I did find:
QUOTE: Narrator: This is Science Today. Fast food may offer quick convenience and low cost, but it may also dramatically speed up clogging of the arteries. Ilona Staprans, a researcher at the University of California, San Francisco says animals fed the oxidized cholesterol found in fast foods had double the amount of clogged arteries.
Staprans: We can physically show the difference in arterial fat deposition that oxidized cholesterol or oxidized polyunsaturated fatty acids accelerate the process of fat deposition.
Narrator: Although this has yet to be tested in humans, Staprans says their findings are suggestive since heart disease is still the number one killer and fast food industries are booming. UNQUOTE
Source: http://www.ucop.edu/sciencetoday/pages/archive/transcripts/1998/sci533.html
Of course, this does not answer the question about how much of the cholesterol in the eggs get oxidized when fried.
The following tested the CLA content in eggs, which is probably more susceptible than the cholesterol, so it seems that a quick fry (without highly unsaturated oils) may not be so bad:
QUOTE: ...Either storage for 6 months or frying for 40 s did not significantly change the composition of CLA in egg yolk. However, the degradation of CLA was statistically significant, when the CLA mixture was fried under the same conditions at 160�?80 °C for 40 s, suggesting that other components of egg yolk protected CLA from degradation. It is concluded that CLA is well preserved in egg before it is consumed. UNQUOTE.
Source: Food Chemistry. Volume 86, Issue 4, August 2004, Pages 531-535.
On the internet: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T6R-4B428PM-5&_user=10&_coverDate=08%2F31%2F2004&_rdoc=
1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=30d6a7e26c52f681194ce30ba934626b
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| I counted my protein intake today, and it was 62 grams+ 4 grams of gelatin which I don't count. |
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This is the recipe I use.
Start by preheating the oven. By the time it's hot, the pie will be ready to bake.
Flaky, tender crust is " in the bag." This method of rolling the pastry inside a big plastic bag is a modern improvement on the old familiar method of rolling dough between sheets of waxed paper. It allows you to roll out pastry without adding extra flour to keep it from sticking even on a hot, humid day.
8 or 9-inch Double
* 3/4 cup Butter
* 5 tablespoons cold water
* 2 cups all-purpose flour
* 1 teaspoon salt
Preheat oven to 425°. Place butter, water, flour and salt in food processor bowl. Process just until dough clumps together - about 5 seconds.
Divide the dough in half and shape each half into a 6-inch pancake. Center one pancake inside a 13 by 15 inch plastic bag. Sprinkle a few drops of water on the countertop to hold the plastic bag in place. Smooth out the bag and begin rolling the pastry from the center out in alternating directions to form an even circle. After every few strokes, lift the top surface of the bag from the dough and smooth it down again flip the bag over and lift the other surface and smooth it down. Continue this "roll, lift, flip" pattern until your circle of dough is about one inch wider than the rim of your pie pan.
Loosen both sides of the plastic bag from the dough and slide the pie pan upside-down into the bag and center it over the circle of dough. Turn the pan and bag over so the dough rests in the pan and slide the pan and dough from the bag. Gently press the pastry into the pan and trim the edges about one half inch beyond the rim.
Filling
* 1/4 to 3/4 cup sugar (See Variety Note)
* 2 tablespoons flour
* 1 teaspoon cinnamon
* 1/4 teaspoon salt
* 7 cups (2 1/2 lbs) thinly sliced, pared tart apples (See Variety Note)
* 2 tablespoons butter
Variety Note
Exact amount of sugar depends on your taste and what apples you use. We like 1/2 cup sugar with a tart variety such as Jonathan. With sweet varieties such as Golden Delicious and Fuji, 1/4 cup sugar is plenty. Combine two or more varieties for best results.
Mix sugar, flour, cinnamon, and salt. Pare, core, and slice the apples with an apple peeler corer slicer. In a large bowl, toss the apple slices lightly with the sugar mixture then turn the filling into the bottom crust.
Cut the butter in small pieces and dot it over the filling.
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| If you are moderately active (with no major exercise), it sounds like you need more protein. I have been buying baked goods that are either very low in fat or else have a very high SFA content, relative to other FAs, to save some time. I eat a lot of ricotta with just small amounts of these baked goods. |
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Hello Hans.
Since yesterday I have my results for my hepatic enzymes ... and it's really frightening. I really don't know what to do now.
But first, a little introduction on me. I'm now 36 years old (almost 37).
HIV+ in march 2000.
Hepatitis C in april 2006.
Until now, I have never been ill (not even a cold since I use antioxidants since 2005). Until now my liver has never hurt me (except since yesterday but it's psychological, I think).
On the begin of the year 2005, thanks to internet, I discovered the AIDS dissidents, especially the Perth Group. Therefore, since the begin of 2005, I used antioxidants (for glutathione) and until now, it's still the same : N-acetylcysteine, Ester C (vitamin C), selenium ans R-lipoic acid.
But I was still having the same unhealthy life ... until I discovered in april 2006 that I was "infected" by the so-called virus of hepatitis C. I then stopped with poppers and anal sex without condom (except with my stable boyfriend).
RESULTS IN APRIL 2006 (when hepatitis C was discovered, but I had no apparent symptoms and until now, it's still the case) :
* For the liver (hepatic enzymes) :
- GOT (AST) : 179 (normal values : 10-37).
- GPT (ALT) : 348 (normal values : 9-40).
* For the cholesterol :
- Total cholesterol : 164
- Cholesterol HDL : 51
- Cholesterol LDL : 87
- Total cholesterol/HDL : 3,22
- Triglycerides : 128
* T4 : 178 (not much).
I then stopped with poppers and so on, and on the advice of the doctor :
- I didn't eat almost any milk and dairy product;
- I eat huge amount of fish oil and flax oil;
- I reduce a little bit the amount of SFA (more fish and a little bit less meat).
- I take supplements of iron (the doctor told me that I was a little bit deficient in iron).
And of course I use the same antioxidants (mentioned above, and it's still the case now).
RESULTS IN OCTOBER 2006 :
* For the liver : a clear improvement :
- GOT (AST) : 83
- GPT (ALT) : 154
* For the cholesterol :
- Total cholesterol : 141
- Cholesterol HDL : 42
- Cholesterol LDL : 69
- Total cholesterol/HDL : 3,36
- Triglycerides : 151
* T4 : 688 (! a very clear improvement)
Then the doctor told me :
- to eat less fish and oil fish (because my amount of omega 3 were "normal" in EPA and DHA),
- but to eat still more flax oil,
- to eat a little more dairy products, more eggs, more cooked prok meats and also an oil rich in omega 6 (I don't remember the specific name) because he had seen that I was slighty deficient in arachidonic acid and he told me that arachidonic acid is essential in order to live : 299,5 mol/l(and the "normal" values for arachidonic acid are : 324,5 - 552 mol/l). Until now, I haven't done the examination of arachidonic acid again because it's VERY and VERY expensive (in France). I will do that again next year (in 2008, if I still live ! LOL).
RESULTS IN MAY 2007 (no improvement) :
* For the liver :
- GOT (AST) : 88
- GPT (ALT) : 140
* For the cholesterol :
- Total cholesterol : 145
- Cholesterol HDL : 41
- Cholesterol LDL : 61
- Total cholesterol/HDL : 3,54
- Triglycerides : 219
* T4 : 418
* "Viral" load (HIV) : 14.757 (measured for the first time since 2005 : 24.051)
* I have two red marks on each side of my nose (the doctor tells me : it's the result of "HIV" infection ! LOL).
* I have white leukoplakia on my tongue (the doctor tells me : it's the result of "HIV" infection and maybe hepatitis C infection ! LOL).
* I have a begin of fungus in my mouth (the doctor tells me : it's the result of "HIV" infection ! LOL).
* I have a little more often cramps in my legs after my sport (I do approximately 8 hours per week body building [without supplementary products, except the antioxidants mentioned above] and jogging, whereas I drink at least one liter water at each session of sport.
In may, I discovered your website and decided not to listen any more to my doctor. I don't decide to eat more SFA (all the doctors tell me that SFA clog the liver and it's very dangerous for the liver) but I decided
- to stop all the vegetable oils (fish oil, flax oil and also an oil rich in omega 6 [I don't remember the name any more]),
- the only vegetable oil I used is extra virgin olive oil,
- to use for the hepatitis C that product : "Maximum Milk Thistle" (see here : http://www.maximummilkthistle.com/studiesindex.htm),
- and to stop definitely the supplements of iron.
In only one month, the results were really spectacular, especially for the liver :
RESULTS IN JUNE 2007 :
* For the liver :
- GOT (AST) : 66
- GPT (ALT) : 102
* For the cholesterol :
- Total cholesterol : 154
- Cholesterol HDL : 44
- Cholesterol LDL : 87
- Total cholesterol/HDL : 3,50
- Triglycerides : 115
* T4 : 534
* "Viral" load (HIV) : not measured
* "Viral" load (hepatitis C : measured for the first time [and only time until now]) : 700.000 (it's little in fact : < 1.000.000 ---> little; > 25.000.000 ---> enormous).
* I still have the two red marks on my face and white leukoplakia on my tongue, but I have less cramps in my legs and I haven't any more fungus in my mouth (and I haven't used drugs against the fungus in my mouth).
On the end of june 2007, I decide to eat more SFA (maybe, I have exaggerated).
- Extra virgin coconut oil : +/- 5-7 tablespoons each day.
- Butter only made with raw milk : +/- 10-15 grams each day.
- Swiss cheese only made with raw milk : +/- 100-200 grams each day.
- The (almost) only meat I eat are beef meat (very few PUFA) and chicken meat (there is unfortunately a little more PUFA in chicken meat than in beef meat), cooked in coconutoil, but no other meat (and especially no lard and no cooked prok meats); I don't eat eggs anymore because I have read that there is a little lot of arachidonic acid (and I have already arachidonic acid in the beef and chicken meat I eat).
I eat :
- Fish, only one time per week and no "fatty" fish;
- No vegetable oil, except of course extra virgin coconut oil and a little bit extra virgin olive oil;
- I avoid any food which contain even a little vegetable oil as ingredient;
- I try to avoid so often possible (but not always, it's not always possible, especially when you are invited by friends) food which contain more than a little PUFA (except chicken meat and not "fatty" fish); I surely now eat much less food with PUFA than before (I have no doubt about that).
- I drink fat free (but pasteurized) milk.
- I continue with the same amount of antioxidants (mentioned above) and also the same amount of "Maximum Milk Thistle".
How do I feel after only three months ?
- The two marks on my face are less red.
- My leukoplakia on my tongue is less serious and less white.
- I have no more cramps in my legs after the sport, whereas I drink LESS (!) water during the sport (maximum : 0,20 - 0,30 liter water now [and I do a little bit more sport than before]; before, I drank at least 1 liter water).
- I'm not bigger : I have the same weight and I could even say that I'm now more muscular (I take two tablespoons coconut oil just before the sport).
- I 'm not depressive anymore (except now with the results of the hepatic enzymes); in the morning, I can now stand up with no effort in order to go to work; I feel me happy and I have less stress.
- I now only sleep 6,30-7,30 hours each day and it's largely enough for me.
- I'm almost never tired, but when I go the bed, I sleep immediately (after 5 minutes; before, after +/- 20-30 minutes).
- I drink much less water than before.
- People think I'm maximum 27-30 years old (but I have always looked much less than my real age; I still don't have any wrinkle). And I'm almost 37 years old.
In one word, I only see advantages.
BUT ....
I have now the results for the hepatic enzymes (but my liver still doesn't hurt me), and it's really disastrous :
RESULTS ON 27 SEPTEMBER 2007 :
* For the liver :
- GOT (AST) : 167 (!)
- GPT (ALT) : 328 (!!)
* For the cholesterol :
- Total cholesterol : 161
- Cholesterol HDL : 55
- Cholesterol LDL : 79
- Total cholesterol/HDL : 2,93
- Triglycerides : 133
* T4 : 548
* "Viral" load (HIV) : 3.899
Hans,
I'm really a great and a enthusiastic supporter of your theory. Your theory seems to be very convincing. That's why I try to do your diet since june 2007. But I'm now VERY anxious about my liver. My liver could surely not live as that for a long time.
I know you have said that the cells release arachidonic acid when we eat large amounts of SFA (it's surely my situation) and very little PUFA (it's also surely my situation whereas I surely still eat a little more PUFA than you). But could you give me a scientific study which proves that (and wich proves that it's temporary) ? Sorry, maybe you have mentioned on your website a scientific study like that but your website is so big that I can't find that study (and I'm French, it's much more difficult for me).
Could you (or somebody else) give me studies which especially prove that arachidonic released by cells can make (very) worse the hepatic enzymes of the people (with or without hepatitis C) ? Or studies which prove that there is a strong association (or even causation) between arachidonic acid and hepatitis C ?
Maybe your theory is good for almost all the diseases ... except for the liver diseases (as hepatitis C) ?
I really don't know what to do know now. I don't want to stop my diet (I fell greater now) and maybe I have almost reached the aim, i.e. cells with very few arachidonic acid. But it seems to be now very risky. But I will maybe have regrets if I stop with the SFA. I'm maybe so close by the aim.
What I will surely do, is to check again my hepatic enzymes in two or three weeks. If I see that my hepatic enzymes have decreased, even a little bit, I will continue with your diet : it will surely mean that the worst time is behind me (it will surely mean that my body evacuates the arachidonic acid). But if my hepatic enzymes continue to increase, I'm afraid (and I'm very sad with that) that I will have no choice than to stop with the diet of SFA. Unless it will be temporary ?! (but I can't surely continue like that : lots of people with so huge hepatic enzymes must normally be hospitalized with so many hepatic enzymes, at least if they fill ill [but it's not my case]).
In one word : I really don't know what to do now.
Thanks a lot for your comments.
PS : I never drink even a drop of alcohol (and that, since I'm 19 years old). |
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What you have reported is what I would expect (due to AA release), for example:
QUOTE ...AST (SGOT) and ALT (SGPT) are sensitive indicators of liver damage from different types of disease. But it must be emphasized that higher-than-normal levels of these liver enzymes should not be automatically equated with liver disease. They may mean liver problems or they may not. The interpretation of elevated AST and ALT levels depends upon the whole clinical picture and so it is best done by doctors experienced in evaluating liver disease.
The precise levels of these enzymes do not correlate well with the extent of liver damage or the prognosis (outlook)... UNQUOTE.
You will need to decide whether you want to worry about temporary, indirect markers or not. And keep in mind how resilient the liver is. If you refrain from doing things that will damage it beyond what you've already done, I see no need to worry (I certainly would not). Interestingly, your "viral load" went down quite a bit, didn't it?
Source: http://www.medicinenet.com/liver_blood_tests/page2.htm#3whatare |
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I had time to do some more research since the last post, and the only interpretation of the evidence that makes sense is that this is related to AA release, or something else that would prompt the higher enzyme levels, but this does not mean it's a "bad" thing. I remember that coffee drinking was deemed to be unhealthy, due to studies that found things like:
"Cafetiere coffee raised alanine aminotransferase concentration by up to 80% above baseline values relative to filtered coffee..."
And: "Cafetiere coffee raised low density lipoprotein cholesterol concentrations by 9-14%..."
As I said, if you know what is dangerous and what is not, and you avoid the dangerous, then I see no reason to fear marker tests. I drink totally unfiltered coffee in small amounts each day now, and if I had that test done, and they said I had higher than "normal" ALT, it would not bother me at all. Note that in that particular study, they also found that:
"Triglyceride concentrations initially rose by 26% with cafetiere coffee but returned close to baseline values within six months."
Source: BMJ 1996;313:1362-1366 (30 November).
http://www.bmj.com/cgi/content/full/313/7069/1362
The kind of study that supports my view is the following:
"Oxidative stress is presumed to play an important role in hepatic fibrogenesis. Diets high in polyunsaturated fatty acids (PUFA) enhance fibrosis and have been associated with increased oxidative damage in some models of liver injury...
...high-PUFA diets have been shown to increase hepatic fibrosis in bile duct-ligated rats and in the continuous intragastric infusion model of alcoholic liver disease.[8,9] The alcohol model is particularly interesting because the addition of oils containing unsaturated fatty acids such as corn or fish oil to the alcohol-containing regimen results in fibrosis, while supplementation with saturated fat does not.[10] The high-PUFA diets have been shown to increase levels of oxidative damage in the liver...
...high-PUFA diets also exacerbate hepatic necrosis and inflammation induced by alcohol..."
Source: Liver Int 23(4):232-242, 2003. © 2003 Blackwell Publishing.
http://www.medscape.com/viewarticle/460549
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| Also, in case you are unaware, if you keep your PUFA consumption very low, your body simply cannot make AA, so it's not an issue of totally avoiding PUFAs, which is nearly impossible, but of avoiding any food that contains more than trace amounts. |
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Thanks a lot for your answers, Hans.
I'm now less anxious and I will continue with my present diet. But I will continue to check regularly the "markers" of my health.
I will tell you about the developments of my health in the next few weeks. |
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| I can't think of any reason why the liver enzymes would remain high, but I can't exactly when I think they would come down to around "normal," and I obviously cannot validate that you are not doing anything now to stress the liver (I'm assuming that you are not). It's disturbing how people have been led to worry about "bad" markers (the cholesterol stuff is a good example), even if they are in good health, or doing well in recovery from a "disease" with actual symptoms. There are some markers that are more than markers, in a sense, for instance TNF-alpha. Your body produces this and it is very dangerous, whereas the liver enzymes are often found "raised" in those with liver problems, and so they are making a connection that is not necessarily present. |
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Hello Hans.
I read again your posts and in the meanwhile I have done some new researches.
First, the good news. It's now very possible that my elevated hepatic enzymes are probably the result of an arachidonic acid deficiency ! Read this abstract ----> http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11934541&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
QUOTE :
Habitual food intake and polyunsaturated fatty acid deficiency in liver cirrhosis.
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OBJECTIVE: We compared the habitual food intake and plasma fatty acid composition in cirrhotic patients living in two different regions in Japan, Okayama and Toyama, and evaluated the effects of dietary polyunsaturated fatty acid and alpha-tocopherol intake on serum alanine aminotransferase (ALT) activity. METHOD: A quantitative food-frequency questionnaire method was used. RESULTS: The significantly higher intake of fish in the patients living in Toyama resulted in higher plasma levels of docosahexaenoic acid and lower levels of arachidonic acid. Serum ALT activity correlated negatively with plasma arachidonic acid (r = -0.456, P < 0.05) and alpha-tocopherol (r = -0.505, P < 0.05) levels. Dietary intakes of vitamin E and polyunsaturated fatty acids (mg/g) correlated negatively with serum ALT (r = -0.377, P < 0.05). Dietary intake of linoleic acid and the ratio of polyunsaturated to saturated fatty acid in dietary fat correlated significantly with serum ALT (r = 0.604, P < 0.01, and r = 0.622, P < 0.01, respectively). The amount of vegetable intake correlated with intake of vitamin E and polyunsaturated fatty acid (r = 0.527, P < 0.02). CONCLUSIONS: These findings suggest that habitual food intake affects the plasma fatty acid profile and that OBJECTIVE: We compared the habitual food intake and plasma fatty acid composition in cirrhotic patients living in two different regions in Japan, Okayama and Toyama, and evaluated the effects of dietary polyunsaturated fatty acid and alpha-tocopherol intake on serum alanine aminotransferase (ALT) activity. METHOD: A quantitative food-frequency questionnaire method was used. RESULTS: The significantly higher intake of fish in the patients living in Toyama resulted in higher plasma levels of docosahexaenoic acid and lower levels of arachidonic acid. Serum ALT activity correlated negatively with plasma arachidonic acid (r = -0.456, P < 0.05) and alpha-tocopherol (r = -0.505, P < 0.05) levels. Dietary intakes of vitamin E and polyunsaturated fatty acids (mg/g) correlated negatively with serum ALT (r = -0.377, P < 0.05). Dietary intake of linoleic acid and the ratio of polyunsaturated to saturated fatty acid in dietary fat correlated significantly with serum ALT (r = 0.604, P < 0.01, and r = 0.622, P < 0.01, respectively). The amount of vegetable intake correlated with intake of vitamin E and polyunsaturated fatty acid (r = 0.527, P < 0.02). CONCLUSIONS: These findings suggest that habitual food intake affects the plasma fatty acid profile and that elevated serum ALT may be related to arachidonic acid deficiency and vulnerability to lipid peroxidation in cirrhotic patients with hepatitis B and C viruses.
UNQUOTE
The end of that abstract says well :
QUOTE : ...that elevated serum ALT may be related to arachidonic acid deficiency ... UNQUOTE
According to your (really convincing) theory, I have now to be really happy because I have surely not any more an arachidonic acid overload but maybe well an arachidonic acid deficiency. But I'm not sure I have already a (big) arachidonic acid overload because I see no differences with the past when I cut myself (scar and so on).
BUT ...
That abstract says also :
QUOTE : ... that elevated serum ALT may be related to ..................... vulnerability to lipid peroxidation in cirrhotic patients with hepatitis B and C viruses UNQUOTE
I think that this consideration is very worrying. So, I have done some other researches and I have found some other scientific abstracts which seem to confirm that arachidonic acid deficiency promotes liver cirrhosis ... and that cirrhotic patients need PUFA and arachidonic acid in order to avoid liver fibrosis and cirrhosis !
See here : ---> http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2718770&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
QUOTE :
Lipid malnutrition of patients with liver cirrhosis: effect of low intake of dietary lipid on plasma fatty acid composition.
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The plasma fatty acid composition of cirrhotic patients and their dietary intake of fatty acids were determined. Significantly lower plasma arachidonic, docosahexaenoic, dihomo-gamma-linolenic and eicosapentaenoic acid levels were observed in cirrhotic patients than in healthy controls. A remarkably low dietary intake of polyunsaturated fatty acids supplied from fish, vegetable oil and pulses was shown in cirrhotic patients. Positive correlations were observed between plasma arachidonic acid concentrations and clearance rate of indocyanine green (KICG) (r = 0.826, p less than 0.05) and between dihomo-gamma-linolenic acid levels and cholinesterase activities (r = 0.841, p less than 0.05). From these results, we conclude that a supply of polyunsaturated fatty acids is necessary for the nutritional treatment of patients with liver cirrhosis.
UNQUOTE
And also here ---> http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12921881&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
QUOTE :
Arachidonic acid in mononuclear cells and its clinical significance in HCV cirrhotic patients.
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OBJECTIVES: An abnormal fatty acid pattern in patients with advanced liver cirrhosis (LC) has been reported in plasma phospholipids and some other tissues. To elucidate the significance of arachidonic acid deficiency on the clinical pathophysiology of LC and hepatocellular carcinoma (HCC), we analyzed the fatty acid compositions of mononuclear cell phospholipids, plasma alpha-tocopherol, and thiobarbituric acid-reactive substances and serum tumor necrosis factor-alpha (TNF-alpha) in cirrhotic patients infected with the hepatitis C virus with and without HCC. METHODS: Twelve cirrhotic patients without HCC (LC patients) and 11 with HCC (HCC patients) were enrolled. Fatty acids were analyzed with gas chromatography. alpha-Tocopherol and TNF-alpha were analyzed by high-performance liquid chromatography and enzyme-linked immunosorbent assay, respectively. Statistical analysis was performed by using the unpaired t test with Welch's correction and Spearman's rank-correlation analysis. RESULTS: Significantly low levels of linoleic, dihomo-gamma-linolenic, arachidonic, and eicosapentaenoic acids from mononuclear cell phospholipids were observed in LC and HCC patients compared with control subjects. Plasma alpha-tocopherol was lower and thiobarbituric acid-reactive substances were higher in HCC patients than in controls. Arachidonic acid molar percentage in mononuclear cell phospholipids correlated significantly with lymphocyte count (r = 0.460, P < 0.05) in the cirrhotic patients and with lymphocyte (r = 0.680, P < 0.01) and platelet (r = 0.763, P < 0.01) counts in all subjects. CONCLUSIONS: These results suggested that arachidonic acid in mononuclear cells may have an important role in the pathophysiology of hepatitis C virus associated with cirrhosis and that nutritional management preventing arachidonic acid deficiency may have some beneficial effects on the progression of LC.
UNQUOTE
You will surely understand that I'm again very anxious about my liver !
I know that in a previous post, you have found that (which says the exact opposite of "my" abstracts) :
QUOTE :
The kind of study that supports my view is the following:
"Oxidative stress is presumed to play an important role in hepatic fibrogenesis. Diets high in polyunsaturated fatty acids (PUFA) enhance fibrosis and have been associated with increased oxidative damage in some models of liver injury...
UNQUOTE
But lots of other studies have also come to the conclusion that PUFA and arachidonic acid seem to be necessary in order to prevent liver cirrhosis. Your abstract seems to be an exception (with also the case of alcohol, in which we have also to avoid PUFA).
Is it possible to reconcile the opposite conclusions of your abstract and of my abstracts ? Of maybe I don't understand anything ?
The question seems to be more difficult when I read also this abstract in which it is said (and it supports your view) that PUFA is very bad for the liver of "HIV-infected" subjects.
See here ---> http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16685065&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
QUOTE :
Polyunsaturated fatty acid intake is adversely related to liver function in HIV-infected subjects: the THUSA study.
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BACKGROUND: Dietary fat intake in the South African population is increasing. This population also has a high prevalence of HIV infection. However, information about metabolic effects of dietary fatty acids on HIV-infected subjects is lacking. OBJECTIVE: Our objective was to investigate the relation between dietary fatty acid intake and liver function in HIV-infected compared with HIV-uninfected subjects. DESIGN: This cross-sectional epidemiologic survey included a representative sample of 1854 apparently healthy black volunteers aged > or =15 y, who were recruited from 37 randomly selected sites throughout the North West province of South Africa. Data from 216 asymptomatic HIV-infected and 1604 HIV-uninfected subjects were used. RESULTS: Intakes of polyunsaturated fatty acids (PUFAs), linoleic acid (n-6), and the ratio of PUFAs to saturated fatty acids (SFAs) were positively associated with all the liver enzymes measured in HIV-infected subjects (R = 0.16-0.65). Most of these R values differed significantly from the R values for HIV-uninfected subjects. No associations were seen between liver enzymes and intakes of SFAs and monounsaturated fatty acids. Vitamin E intake was positively associated with serum gamma-glutamyl transpeptidase (R = 0.23), alanine aminotransferase (R = 0.37), and aspartate aminotransferase (R = 0.58) in HIV-infected subjects; these correlations differed significantly from those of the HIV-uninfected subjects because PUFA sources are the main carriers of vitamin E. CONCLUSIONS: The results suggest that n-6 PUFA intakes may be related to liver damage in these HIV-infected asymptomatic subjects. The reasons or mechanisms responsible are not clear, and further research is necessary to determine the optimal safe amounts for intake of n-6 PUFAs by HIV-infected subjects, especially in countries with traditionally high intakes of n-6 PUFA-rich vegetable oils.
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When I read all these abstracts, I have to think that PUFA is bad for the liver of "HIV-infected" patients but is good (and even necessary) for the liver of "Hepatitis C-infected" patients.
Then, what has a patient to do when he is "infected" simultaneously with "HIV" and "hepatitis C" ?
You will surely understand that I'm again VERY confused ! But I have maybe not good understood ?!
Thanks again for your advice. |
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Hans, what do you think about the nightshades? Is it safe to eat potatoes and tomato?
http://noarthritis.com/research.htm |
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I've seen all these studies before (or similar ones). What happens is that AA is released due to stressors, and so there is the claim that there is an "AA deficiency." It's complete nonsense as far as I'm concerned - "science" at its worst (the findings are accurate, but the interpretation is laughable). According to this notion, my liver should be destroyed by now.
As to the nightshades question, I think any vegetable with anti-nutritive qualities should be avoided except in small amounts or on rare occasions. If you don't eat the skin of potatoes, there should be no problems. The Irish had problems when they didn't have enough potatoes, not when they had too many, correct? |
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| There may be some need for AA if you overload your body with Omega-3s, because these strongly inhibit cell signalling, even that mediated by the Mead acid I guess. This may rarely happen in some Japanese villages consuming exclusively fish but not in the most of the metropolitan USA. It's like the experts are saying that you have to beat the Omega-6 overload by supplementing with Omega-3 but inverted. However this is playing a hazardous game with very unstable compounds with deleterious long term effects. So the best solution would be to avoid any Omega-3 in the first place and then you would have only minimal if any requirements for Omega-6/AA because the natural Mead acid signaling won't be inhibited. Also for proper liver functions make sure to have enough B vitamins. |
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