fish oil

[Guest guest]

Mike,

I assume you mean Udo's Oil.

Flora products are available at all fine health food stores.To locate a store near you please contact our Customer Service Department at 1-800-446-2110.

---------------------------------------------------------------------

> Where do you buy the Uli oil?>

[Guest guest]

I use both types of oils. I use Udo's or Flax (5ml) throughout my six meals (unless I have added fat from another source) and then before I go to bed, I take one capsule of the Salmon Oil. I find taking the Udo's or Flax easier if I take the oil rather than the capsules as it is easier than downing 5 football size black pills 6 x a day. The one tsp is much faster and easier (mixed with a little juice).

I get mine in a healthfood store and it is always refrigerated.

Fish Oil>>>I went to the health food store today and I saw>- Salmon oil capsules>- fish oil capsules>>but no Uli Oil.>>Which is better? Where do you buy the Uli oil?>>Mike>

[Guest guest]

I have been using hemp seed oil. (Imported from Canada

to Amsterdam, NL. For some reason it seems strange

that it needs to be imported and is not available

here. Maybe I just havn't found it.)

Check out www.freshhempfoods.com for nutritional

information, etc.

Bill Staniewicz

Amsterdam, NL

--- Phosphor <phosphor@...> wrote:

>

> When you have finished reading Dr Harve's commercial

> spiel on Eskimo 3

> [thought MD's were forbidden from advertising?]

> people may want to get cod

> liver oil for about 1/10 of the price.

>

__________________________________________________

[Guest guest]

> Eskimo-3 is manufactured under strict quality controls to guarantee potency,

> purity and freshness. It is purified by processes that remove environmental

>

> Harvey Maron, M.D.

> Steamboat Springs, CO

When you have finished reading Dr Harve's commercial spiel on Eskimo 3

[thought MD's were forbidden from advertising?] people may want to get cod

liver oil for about 1/10 of the price.

Mooloolaba QLD

Australia

[Guest guest]

Dr. Harvey,

I first read about fish oils in " The Zone " . Dr. Sears emphasized oils which

had the heavy metals removed by what he called " molecular distillation " .

Since then, I've seen fish oil capsules labeled as processed by molecular

distillation.

Is this process sufficient to render fish oils safe?

Skip Dallen

Covina

_________________________________________________________

[Guest guest]

From: " Phosphor " <phosphor@...>

> When you have finished reading Dr Harve's commercial spiel on Eskimo 3

> [thought MD's were forbidden from advertising?] people may want to get cod

> liver oil for about 1/10 of the price.

>

> Mooloolaba QLD

> Australia

I have no financial or commercial interests in any company. I have been

retired from Medicine for over 12 years.

Cod liver oil is fish oil and can be grossly contaminated by PCB's etc.

I was merely trying to give people a respected source for safe fish oil !

Harvey Maron, M.D.

Steamboat Springs, CO

[Guest guest]

From: " Skip Dallen " <skipdallen@...>

Re: fish oil

> Dr. Harvey,

>

> I first read about fish oils in " The Zone " . Dr. Sears emphasized oils which

> had the heavy metals removed by what he called " molecular distillation " .

> Since then, I've seen fish oil capsules labeled as processed by molecular

> distillation.

>

> Is this process sufficient to render fish oils safe?

>

> Skip Dallen

> Covina

It certainly is.

Harvey Maron, M.D.

Steamboat Springs, CO

[Guest guest]

I haven't read THE ZONE, but that was my first thought at the mention

of cod liver oil too. I am reluctant to eat the organ meats of any

animal, particularly the liver or the kidneys - especially from

predator (I don't know whether a cod is a predator). This is a place

where vast amounts of environmental toxins can be concentrated. Can

that process remove PCB's?

Wilbanks

Madison, WI

> Dr. Harvey,

>

> I first read about fish oils in " The Zone " . Dr. Sears emphasized

oils which

> had the heavy metals removed by what he called " molecular

distillation " .

> Since then, I've seen fish oil capsules labeled as processed by

molecular

> distillation.

>

> Is this process sufficient to render fish oils safe?

>

> Skip Dallen

> Covina

>

>

> _________________________________________________________

>

[Guest guest]

I remember in survival training we were told never to eat a polar

bear's liver, since it contains enough toxins to kill a person.

Personally, I don't recommend eating any organs, wheter they belonged

to cods or polar bears. It's about as appetizing - and probably as

healthy - as draining pasta through my dryer's lint catcher.

Christian Cernovich

Malibu, CA

[Guest guest]

> I remember in survival training we were told never to eat a polar

> bear's liver, since it contains enough toxins to kill a person.

>

> Christian Cernovich

The reason you should not eat polar bear liver is not that it contains

" toxins " , but that it contains a toxic overdose of Vitamin A. Polar bear

meat can be dangerous because it is a cause of trichinosis.

Harvey Maron, M.D.

Steamboat Springs, CO

[Guest guest]

Christian Cernovich wrote:

>

>I remember in survival training we were told never to eat a polar

>bear's liver, since it contains enough toxins to kill a person.

Oddly enough, the toxin is retinol (vitamin A). The quote is from the WHO

site, and deals with the interactions of Vitamin A and vaccines. Too much of

a good thing.....

http://www.who.int/vaccines-diseases/safety/infobank/vita.htm

" This does not result from public health intervention programmes. Rather,

toxicity has been associated with the abuse of vitamin A supplements and

with diets extremely high in preformed vitamin A (i.e. foods of animal

origin). Toxic reactions provoked by large doses of vitamin A are well-known

to occur following either intake of liver rich in vitamin A (e.g. polar

bear, halibut or whale) or by excessive administration of vitamin A

preparations ( & , 1982). "

Bob Bowman

Missoula, MT

[Guest guest]

> I remember in survival training we were told never to eat a polar

> bear's liver, since it contains enough toxins to kill a person.

> Personally, I don't recommend eating any organs, wheter they belonged

> to cods or polar bears. It's about as appetizing - and probably as

> healthy - as draining pasta through my dryer's lint catcher.

>

Do you think dosage might be an issue? The toxins in polar bear liver are

two kinds..

1. vitamin A. Only toxic in extremely high amounts. It is rare. Whale liver

is considered a prized meat in polar tribes.

2. PCBs and other environental toxins. They tend to accumulate in polar

animals due to condensation in cold air. Curious that some consider fish

oil from polar regions safer than cod liver oil. Up to you.

Mooloolaba QLD

Australia

[Guest guest]

You aren't taking the liquid form are you?? KathyLiz <elwilkinson@...> wrote:

I am taking fish oil because heart disease is in my family. I'll take it for 1 year before my big 50th year cleaning out process. It isn't for everyone like Deb said.

Take care of yourself,

Liz

Kathy Brunow

[Guest guest]

Fish oil can definitely make you queasy and result in the dreaded

" fish burp. " Most of us use flax oil, ground flax seeds, or Udo's oil

blend instead of fish oil. If you decide to switch to a plant source

for your EFAs, keep in mind that it takes about 14 capsules to equal 1

tablespoon of oil.

On 9/23/05, Lizzy <jadelizzard@...> wrote:

> Hi Everyone,

> I have been taking the EAS fish oil caplets and I was wondering if

> they mess with your stomache. I havn't been eating any differently but

> for the past week I have been having stomache problems while taking

> them.

> Lizzy

[Guest guest]

Hillbilly Tim <knoxweb1@...> wrote: NEW YORK (Reuters Health) - Fish oil could potentially save more lives than cardiac defibrillators, devices used to revive individuals whose hearts have stopped beating and to prevent and treat life-threatening heart arrhythmias, researchers estimate in a new report. ADVERTISEMENT Past research has linked the omega-3 fatty acids found in oily fish to a lower risk of fatal heart rhythm disturbances. This latest study tried to estimate the potential public health impact of raising adults' omega-3 levels with fish oil supplements. Using a computer-simulated community of 100,000 Americans and data from past medical studies, the researchers calculated that raising omega-3 levels would save 58 lives each year. This amounts to a 6.4-percent total death reduction -- mostly by preventing sudden cardiac death in apparently people, according to the study authors, led by Dr. E. Kottke of the Heart Center at Regions Hospital in St. , Minnesota. Conversely, the researchers estimate that far fewer lives would be saved by defibrillators, devices that deliver a "shock" to restart the heart or to resolve

ventricular fibrillation, an otherwise fatal heartbeat irregularity in which the heart quivers instead of contracting normally. For example, the study found, even if automated external defibrillators (AEDs) were available in every home and public area, the devices would lower a community's annual death rate by less than 1 percent. AEDs are portable devices that can be used by lay people to shock someone in cardiac arrest. They are frequently available in public places such as large stores or on airplanes. Though the devices do save lives, the researchers note that AEDs would make little difference in the overall rate of sudden cardiac death. Kottke's team estimates that implantable defibrillators would lower the cardiac death rate by 3.3 percent, still not as much as the 6.6-percent lower death rate achieved by increasing the use of fish oil supplements. Though the implantable devices are effective, the researchers point out

that about half of adults who die suddenly from cardiac arrest have no warning signs beforehand -- and would, therefore, never be candidates for an implanted defibrillator. The study, which is published in the American Journal of Preventive Medicine, has its limitations, as a computer simulation. Though the researchers based their estimates of fish oil benefits on two large studies, it's not yet clear that omega-3 fatty acids prevent sudden cardiac death in apparently healthy people. Ongoing trials in Italy and England may help answer this question, Kottke and his colleagues note. If fish oil is as effective against fatal heart arrhythmias as evidence suggests, the researchers conclude, it would have more widespread benefits than either AEDs or implanted defibrillators. SOURCE: American Journal of Preventive Medicine, October 2006. Email Story IM Story Discuss Printable View RECOMMEND THIS STORY Recommend It: Average (321

votes) » Recommended Stories Health News Spinach pulled from stores across U.S. AP Study: Annual shot of drug helps bones AP Japan's centenarians at

record 28,395 AP Psychotherapy, gene pioneers honored AP Dr.: Va. teen cancer patient improving AP Most Viewed - Health Shoppers avoid spinach in E. coli scare AP British minister says ban scrawny models AP Study: Annual shot of drug helps bones AP Alcohol use helps boost income: study AFP Japan's centenarians at record 28,395 AP Health Video Childhood obesity on the rise CNN - 2 hours, 35 minutes ago Deadly Spinach: E. Coli Outbreak Grows

ABC News - Fri Sep 15, 9:31 PM ET Treating Seniors for Depression ABC News - Fri Sep 15, 6:01 PM ET Health Minute: Youth smoking CNN - Fri Sep 15, 12:08 PM ET Elsewhere on the Web CNN.comShoppers shun spinach as

E. coli cases top 100 CNN.comFDA: Don't eat bagged spinach ABC Newss' Death Highlights Rise in Esophageal Cancer On CNN Kids in sports More kids are playing, and more parents are worrying. » Parents' checklist » Find the right sport On Health What Defines You? Explore your life with women bloggers from around the world. » More on Health Full Coverage Bird Flu Get the latest news, video and photos. From Y! Health Health Questions? Find answers on Health: » More from Y! Health Tim Parsons knoxville,tn 37931 865-588-2465 x107 work www.knoxville1.com All-new - Fire up a more powerful email and get things done faster. Tim Parsons knoxville,tn 37931 865-588-2465 x107 work

www.knoxville1.com

Messenger with Voice. Make PC-to-Phone Calls to the US (and 30+ countries) for 2¢/min or less.

[Guest guest]

Tim Fish oil is an amazing thing and the more they look at it, the more they find ways to use it safely in all sorts of medical conditions...thanks for posting it!Hillbilly Tim <knoxweb1@...> wrote: Hillbilly Tim <knoxweb1 > wrote: NEW YORK (Reuters Health) - Fish oil could potentially save more

lives than cardiac defibrillators, devices used to revive individuals whose hearts have stopped beating and to prevent and treat life-threatening heart arrhythmias, researchers estimate in a new report. ADVERTISEMENT Past research has linked the omega-3 fatty acids found in oily fish to a lower risk of fatal heart rhythm disturbances. This latest study tried to estimate the potential public health impact of raising adults' omega-3 levels with fish oil supplements. Using a computer-simulated community of 100,000 Americans and data from past medical studies, the researchers calculated that raising omega-3 levels would save 58 lives each year. This amounts to a 6.4-percent total death reduction -- mostly by preventing sudden cardiac

death in apparently people, according to the study authors, led by Dr. E. Kottke of the Heart Center at Regions Hospital in St. , Minnesota. Conversely, the researchers estimate that far fewer lives would be saved by defibrillators, devices that deliver a "shock" to restart the heart or to resolve ventricular fibrillation, an otherwise fatal heartbeat irregularity in which the heart quivers instead of contracting normally. For example, the study found, even if automated external defibrillators (AEDs) were available in every home and public area, the devices would lower a community's annual death rate by less than 1 percent. AEDs are portable devices that can be used by lay people to shock someone in cardiac arrest. They are frequently available in public places such as large stores or on airplanes. Though the devices do save lives, the researchers note that AEDs would make little difference in the overall rate of sudden

cardiac death. Kottke's team estimates that implantable defibrillators would lower the cardiac death rate by 3.3 percent, still not as much as the 6.6-percent lower death rate achieved by increasing the use of fish oil supplements. Though the implantable devices are effective, the researchers point out that about half of adults who die suddenly from cardiac arrest have no warning signs beforehand -- and would, therefore, never be candidates for an implanted defibrillator. The study, which is published in the American Journal of Preventive Medicine, has its limitations, as a computer simulation. Though the researchers based their estimates of fish oil benefits on two large studies, it's not yet clear that omega-3 fatty acids prevent sudden cardiac death in apparently healthy people. Ongoing trials in Italy and England may help answer this question, Kottke and his colleagues note. If fish oil is as effective against

fatal heart arrhythmias as evidence suggests, the researchers conclude, it would have more widespread benefits than either AEDs or implanted defibrillators. SOURCE: American Journal of Preventive Medicine, October 2006. Email Story IM Story Discuss Printable View RECOMMEND THIS STORY Recommend It: Average (321 votes) » Recommended Stories Health News Spinach pulled from stores across U.S. AP Study: Annual shot of drug helps bones AP Japan's centenarians at record 28,395 AP Psychotherapy, gene pioneers honored AP Dr.: Va. teen cancer patient improving AP Most Viewed - Health Shoppers avoid spinach in E. coli scare AP British minister says ban scrawny models AP Study: Annual shot of drug helps bones AP Alcohol use helps boost income: study AFP Japan's centenarians at record 28,395 AP Health Video Childhood obesity on the rise CNN - 2 hours, 35 minutes ago Deadly Spinach: E. Coli Outbreak Grows ABC News - Fri Sep 15, 9:31 PM ET Treating Seniors for Depression ABC News - Fri Sep 15, 6:01 PM ET Health Minute: Youth smoking CNN - Fri Sep 15, 12:08 PM ET Elsewhere on the Web CNN.comShoppers shun spinach as E. coli cases top 100 CNN.comFDA: Don't eat bagged spinach ABC Newss' Death Highlights Rise in Esophageal Cancer On CNN Kids in sports More kids are playing, and more parents are worrying. » Parents' checklist » Find the right sport On Health What Defines You? Explore your life with women bloggers from around the world. » More on Health Full Coverage Bird Flu Get the latest news, video and

photos. From Y! Health Health Questions? Find answers on Health: » More from Y! Health Tim Parsons knoxville,tn 37931 865-588-2465 x107 work www.knoxville1.com All-new - Fire up a more powerful email and get things done faster. Tim Parsons knoxville,tn 37931 865-588-2465 x107 work www.knoxville1.com Messenger with Voice. Make PC-to-Phone Calls to the US (and 30+ countries) for 2¢/min or less. Jackie

[Guest guest]

HI TIM,

THIS IS GOOOOD INFO FOR ME. I'LL HAVE TO HIT THE HEALTH FOOD STORE!!!!!

ALSO FOR THOSE THAT ARE ON TX. FLAX SEED OIL IS VERY GOOD @ HELPING REDUCE THE SYMPTONS OF CHEMO AND GIVES LONGEVITY TO PATIENTS THAT ARE TERMINAL. INTERFERON HAS SIMILAR SIDE EFFECTS TO CHEMO. THE ONE THING THAT YOU NEED TO WATCH FOR W/FLAX SEED OIL IS THAT THE BEST KIND IS IN THE FRIDGE IN A DARK COLORED BOTTLE AND MUST BE KEPT IN THE FRIDGE. I KNOW THAT THEY SELL CAPLETS IN DRUG STORES AND SUCH BUT THAT STUFF IS CRP. IT'S A LITTLE MORE PRICEY BUT BELEIVE THE OLD ADAGE THAT YOU GET WHAT YOU PAY FOR . GOING HOLISTIC IS A GREAT COMPLIMENT TO CONVENTIONAL MEDICINE!!!!!

> > NEW YORK (Reuters Health) - Fish oil could potentially save more lives than cardiac defibrillators, devices used to revive individuals whose hearts have stopped beating and to prevent and treat life-threatening heart arrhythmias, researchers estimate in a new report. > ADVERTISEMENT> > Past research has linked the omega-3 fatty acids found in oily fish to a lower risk of fatal heart rhythm disturbances. This latest study tried to estimate the potential public health impact of raising adults' omega-3 levels with fish oil supplements.> Using a computer-simulated community of 100,000 Americans and data from past medical studies, the researchers calculated that raising omega-3 levels would save 58 lives each year.> This amounts to a 6.4-percent total death reduction -- mostly by preventing sudden cardiac death in apparently people, according to the study authors, led by Dr. E. Kottke of the Heart Center at Regions Hospital in St. , Minnesota.> Conversely, the researchers estimate that far fewer lives would be saved by defibrillators, devices that deliver a "shock" to restart the heart or to resolve ventricular fibrillation, an otherwise fatal heartbeat irregularity in which the heart quivers instead of contracting normally.> For example, the study found, even if automated external defibrillators (AEDs) were available in every home and public area, the devices would lower a community's annual death rate by less than 1 percent.> AEDs are portable devices that can be used by lay people to shock someone in cardiac arrest. They are frequently available in public places such as large stores or on airplanes. Though the devices do save lives, the researchers note that AEDs would make little difference in the overall rate of sudden cardiac death.> Kottke's team estimates that implantable defibrillators would lower the cardiac death rate by 3.3 percent, still not as much as the 6.6-percent lower death rate achieved by increasing the use of fish oil supplements.> Though the implantable devices are effective, the researchers point out that about half of adults who die suddenly from cardiac arrest have no warning signs beforehand -- and would, therefore, never be candidates for an implanted defibrillator.> The study, which is published in the American Journal of Preventive Medicine, has its limitations, as a computer simulation. Though the researchers based their estimates of fish oil benefits on two large studies, it's not yet clear that omega-3 fatty acids prevent sudden cardiac death in apparently healthy people.> Ongoing trials in Italy and England may help answer this question, Kottke and his colleagues note.> If fish oil is as effective against fatal heart arrhythmias as evidence suggests, the researchers conclude, it would have more widespread benefits than either AEDs or implanted defibrillators.> SOURCE: American Journal of Preventive Medicine, October 2006. > > > Email Story > IM Story > Discuss > Printable View > RECOMMEND THIS STORY [input] [input] [input] [input] [input] [input] [input] [input] [input] Recommend It: > > > > Average (321 votes)> > > » Recommended Stories > > > > > Health News > Spinach pulled from stores across U.S. AP > Study: Annual shot of drug helps bones AP > Japan's centenarians at record 28,395 AP > Psychotherapy, gene pioneers honored AP > Dr.: Va. teen cancer patient improving AP > Most Viewed - Health > Shoppers avoid spinach in E. coli scare AP > British minister says ban scrawny models AP > Study: Annual shot of drug helps bones AP > Alcohol use helps boost income: study AFP > Japan's centenarians at record 28,395 AP > > > > Health Video > Childhood obesity on the rise CNN - 2 hours, 35 minutes ago > Deadly Spinach: E. Coli Outbreak Grows ABC News - Fri Sep 15, 9:31 PM ET > > Treating Seniors for Depression ABC News - Fri Sep 15, 6:01 PM ET > Health Minute: Youth smoking CNN - Fri Sep 15, 12:08 PM ET > > > > > > > > Elsewhere on the Web CNN.comShoppers shun spinach as E. coli cases top 100 > CNN.comFDA: Don't eat bagged spinach > ABC Newss' Death Highlights Rise in Esophageal Cancer > > > > > > > On CNN Kids in sports > More kids are playing, and more parents are worrying.> » Parents' checklist> » Find the right sport > > On Health What Defines You?> Explore your life with women bloggers from around the world.> » More on Health > > Full Coverage Bird Flu> Get the latest news, video and photos.> > From Y! Health Health Questions?> Find answers on Health: [input] [input] > » More from Y! Health> > > > > > Tim Parsons > > knoxville,tn 37931 > > 865-588-2465 x107 work> > > www.knoxville1.com> > ---------------------------------> All-new - Fire up a more powerful email and get things done faster. > > > > > Tim Parsons > > knoxville,tn 37931 > > 865-588-2465 x107 work> > > www.knoxville1.com> > > ---------------------------------> Messenger with Voice. Make PC-to-Phone Calls to the US (and 30+ countries) for 2¢/min or less.>

[Guest guest]

You can also get significant omega-3's from grass-fed beef (must be grass-fed, not just organic beef) and organic eggs (the eggs may be forbidden). The ruminant process of digestion in cows fed grass produces highly signficant quantities of conjugated linoleic acid, an omega 3 fatty acid. It may not be as good as the DHA from fish oils, but it's helpful.

Moral- if your kitchen floor has blood stains on it instead of yellow stains from the fish oil (ours has both), the problem is probably not the fish oils.

Fish oil

Btw- we use Coromega. It’s a cream- kinda like ketchup or pudding. It comes in packets and might be neater than the other oils. Plus, no fish burps. I love that cause I HATE fish with a passion. After hearing the fish oil disaster comments I thought I would share that info. Oh ya- and it’s orange flavored.Ps- I do not own stock in the Coromega co. (but wish I did)

[Guest guest]

I have tried 3 different brands,, and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002@...> wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn> wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily sardines. A lot of research recommends eating fish like three times a week and I won't eat it at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> > Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia>

> Oxidative stress is implicated as a cause of liver injury in a range > of liver diseases including viral hepatitis, alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> > Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated

inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading to impaired nucleotide > and protein synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> > Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function. Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of

protective mechanisms that ameliorate or > attenuate the effect of ROS including the up-regulation of a range of > endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols > (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of

the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to describe any combination of compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the phospholipid bilayer > of the cell membranes where it has a major biological role in > protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of

conditions. These factors appear > particularly important in the pathogenesis of NASH. Hyperinsulinemia > and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous > antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies

> have been mixed. In population studies, there seems to be a lack of > benefit from vitamin E in preventing cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E > in liver disease. A recent Cochrane review concluded that data was > too limited to assess the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients

with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but did not affect > liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E > appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been repeated in larger cohorts.> > Why might vitamin E supplementation not translate into clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to >

a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful neuroprotective, anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the plasma concentrations of > other vitamin E analogs such as y-tocopherol and ¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental

a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm the ability of supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an > animal model of hyperphagia, obesity, and hepatic steatosis that > occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to >

glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be protected from > necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral > administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but there was no histological evidence of apoptosis. > Pretreatment with a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation,

although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on > generation of ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role > in this model. The second observation is that pretreatment with -> tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of

experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and > lipid peroxidation. ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related compounds need > to be resolved. Soden and colleagues have shown that parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further

exploration of the > role of vitamin E supplementation in liver disease.> > > > > > Jackie > > > > Jackie > > > > Jackie>Jackie Building a website is a piece of cake. Small Business gives you all the tools to get online. Jackie

[Guest guest]

I stopped all for a time while I detoxed, then started adding things back slowly, had been using Puritan or Vitacost brand and even Walmart at times, but will sure be checking labels closer.. Jackie on <redjaxjm@...> wrote: I have tried 3 different brands,,

and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002 > wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn>

wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily sardines. A lot of research recommends eating fish like three times a week and I won't eat it at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> > Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia> > Oxidative stress is implicated as a cause of liver injury in a range > of liver diseases including viral hepatitis, alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden

et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> > Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading to impaired nucleotide > and protein synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> >

Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function. Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of protective mechanisms that ameliorate or > attenuate the effect of ROS including the up-regulation of a range of > endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols

> (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to describe any combination of compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E

makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the phospholipid bilayer > of the cell membranes where it has a major biological role in > protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of conditions. These factors appear > particularly important in the pathogenesis of NASH. Hyperinsulinemia > and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous >

antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies > have been mixed. In population studies, there seems to be a lack of > benefit from vitamin E in preventing cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis

suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E > in liver disease. A recent Cochrane review concluded that data was > too limited to assess the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but did not affect > liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E >

appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been repeated in larger cohorts.> > Why might vitamin E supplementation not translate into clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to > a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful neuroprotective, anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This

approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the plasma concentrations of > other vitamin E analogs such as y-tocopherol and ¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm the ability of supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model

of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an > animal model of hyperphagia, obesity, and hepatic steatosis that > occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to > glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be protected from > necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral >

administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but there was no histological evidence of apoptosis. > Pretreatment with a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation, although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on > generation of ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile

acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role > in this model. The second observation is that pretreatment with -> tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and > lipid peroxidation. ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of

supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related compounds need > to be resolved. Soden and colleagues have shown that parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further exploration of the > role of vitamin E supplementation in liver disease.> > > > > > Jackie > > > > Jackie > > > > Jackie>Jackie Building a

website is a piece of cake. Small Business gives you all the tools to get online. Jackie

Fussy? Opinionated? Impossible to please? Perfect. Join 's user panel and lay it on us.

[Guest guest]

I believe I have used Puritan as one of the 3 I have tried... there was one and I wish I could remember the name, but it said on the label that it was WILD caught cold water fish oil on it and it had NONE of the Murcury or other metals in it.. it was a bit expensive but I did feel like it was the best brand, if I can find it again, I will buy it and then give you the name of it if you are interested... Fish oil is VERY important for us heppers because our livers need the EPA and DHA..Sheena <mom4possums2002@...> wrote: I stopped all for a time while I detoxed, then started adding things back slowly, had been using Puritan or Vitacost brand and even Walmart at times, but will sure be checking labels closer.. Jackie on <redjaxjm > wrote: I have tried 3 different brands,, and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002 > wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn> wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily

sardines. A lot of research recommends eating fish like three times a week and I won't eat it at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> >

Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia> > Oxidative stress is implicated as a cause of liver injury in a range > of liver diseases including viral hepatitis, alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> >

Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading to impaired nucleotide > and protein synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> > Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function.

Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of protective mechanisms that ameliorate or > attenuate the effect of ROS including the up-regulation of a range of > endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols > (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized

by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to describe any combination of compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the

phospholipid bilayer > of the cell membranes where it has a major biological role in > protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of conditions. These factors appear > particularly important in the pathogenesis of NASH. Hyperinsulinemia > and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous > antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose

metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies > have been mixed. In population studies, there seems to be a lack of > benefit from vitamin E in preventing cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E

> in liver disease. A recent Cochrane review concluded that data was > too limited to assess the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but did not affect > liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E > appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been

repeated in larger cohorts.> > Why might vitamin E supplementation not translate into clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to > a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful neuroprotective, anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the

plasma concentrations of > other vitamin E analogs such as y-tocopherol and ¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm the ability of supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an

> animal model of hyperphagia, obesity, and hepatic steatosis that > occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to > glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be protected from > necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral > administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but

there was no histological evidence of apoptosis. > Pretreatment with a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation, although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on > generation of ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role >

in this model. The second observation is that pretreatment with -> tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and > lipid peroxidation. ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related

compounds need > to be resolved. Soden and colleagues have shown that parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further exploration of the > role of vitamin E supplementation in liver disease.> > > > > > Jackie > > > > Jackie > > > > Jackie>Jackie Building a website is a piece of cake. Small Business gives you all the tools to get online. Jackie Fussy? Opinionated? Impossible to please? Perfect. Join 's user panel and lay it on us. Jackie

[Guest guest]

Still looking in Google under "cold water" fish oil gel caps and not coming up with much yet. I do know liquid Carlson's is highly recommended, but I'd also rather take the gel caps.. Jackie on <redjaxjm@...> wrote: I believe I have used Puritan as one of the 3 I have tried... there was one and I wish I could remember the name, but it said on

the label that it was WILD caught cold water fish oil on it and it had NONE of the Murcury or other metals in it.. it was a bit expensive but I did feel like it was the best brand, if I can find it again, I will buy it and then give you the name of it if you are interested... Fish oil is VERY important for us heppers because our livers need the EPA and DHA..Sheena <mom4possums2002 > wrote: I stopped all for a time while I detoxed, then started adding things back slowly, had been using Puritan or Vitacost brand and even Walmart at times, but will sure be checking labels closer.. Jackie on <redjaxjm > wrote: I have tried 3 different brands,, and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002 > wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO

aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn> wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily sardines. A lot of research recommends eating fish like three times a week and I won't eat it at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> > Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia> > Oxidative stress is implicated as a cause of liver injury in a range

> of liver diseases including viral hepatitis, alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> > Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading

to impaired nucleotide > and protein synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> > Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function. Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of protective mechanisms that ameliorate or > attenuate the effect of ROS including the

up-regulation of a range of > endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols > (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to

describe any combination of compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the phospholipid bilayer > of the cell membranes where it has a major biological role in > protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of conditions. These factors appear > particularly important in the pathogenesis of NASH.

Hyperinsulinemia > and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous > antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies > have been mixed. In population studies, there seems to be a lack of > benefit from

vitamin E in preventing cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E > in liver disease. A recent Cochrane review concluded that data was > too limited to assess the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but

did not affect > liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E > appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been repeated in larger cohorts.> > Why might vitamin E supplementation not translate into clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to > a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful

neuroprotective, anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the plasma concentrations of > other vitamin E analogs such as y-tocopherol and ¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm

the ability of supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an > animal model of hyperphagia, obesity, and hepatic steatosis that > occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to > glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be

protected from > necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral > administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but there was no histological evidence of apoptosis. > Pretreatment with a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation, although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on

> generation of ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role > in this model. The second observation is that pretreatment with -> tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and

> lipid peroxidation. ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related compounds need > to be resolved. Soden and colleagues have shown that parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further exploration of the > role of vitamin E supplementation in liver disease.> > > > >

> Jackie > > > > Jackie > > > > Jackie>Jackie Building a website is a piece of cake. Small Business gives you all the tools to get online. Jackie Fussy? Opinionated? Impossible to please? Perfect. Join 's user panel and lay it on us. Jackie

Ready for the edge of your seat? Check out tonight's top picks on TV.

[Guest guest]

try this http://www.enerex.ca/products/wild_fish_oil.htmSheena <mom4possums2002@...> wrote: Still looking in Google under "cold water" fish oil gel caps and not coming up with much yet. I do know liquid Carlson's is highly recommended, but I'd also rather take the gel caps.. Jackie on <redjaxjm > wrote: I believe I have used Puritan as one of the 3 I have tried... there was one and I wish I could remember the name, but it said on the label that it was WILD caught cold water fish oil on it and it had NONE of the Murcury or other metals in it.. it was a bit expensive but I did feel like it was the best brand, if I can find it again, I will buy it and then give you the name of it if you are interested... Fish oil is VERY important for us heppers because our livers need the EPA and DHA..Sheena <mom4possums2002 > wrote: I stopped all for a time while I detoxed, then started

adding things back slowly, had been using Puritan or Vitacost brand and even Walmart at times, but will sure be checking labels closer.. Jackie on <redjaxjm > wrote: I have tried 3 different brands,, and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002 > wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn> wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily sardines. A lot of research recommends eating fish like three times a week and I won't eat it

at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> > Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina

Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia> > Oxidative stress is implicated as a cause of liver injury in a range > of liver diseases including viral hepatitis, alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> > Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number

of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading to impaired nucleotide > and protein synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> > Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function. Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair

membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of protective mechanisms that ameliorate or > attenuate the effect of ROS including the up-regulation of a range of > endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols > (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a

saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to describe any combination of compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the phospholipid bilayer > of the cell membranes where it has a major biological role in >

protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of conditions. These factors appear > particularly important in the pathogenesis of NASH. Hyperinsulinemia > and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous > antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by

decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies > have been mixed. In population studies, there seems to be a lack of > benefit from vitamin E in preventing cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E > in liver disease. A recent Cochrane review concluded that data was > too limited to assess

the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but did not affect > liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E > appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been repeated in larger cohorts.> > Why might vitamin E supplementation not translate into

clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to > a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful neuroprotective, anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the plasma concentrations of > other vitamin E analogs such as y-tocopherol and

¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm the ability of supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an > animal model of hyperphagia, obesity, and hepatic steatosis that >

occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to > glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be protected from > necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral > administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but there was no histological evidence of apoptosis. > Pretreatment with

a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation, although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on > generation of ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role > in this model. The second observation is that pretreatment with ->

tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and > lipid peroxidation. ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related compounds need > to be resolved. Soden and colleagues have shown that

parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further exploration of the > role of vitamin E supplementation in liver disease.> > > > > > Jackie > > > > Jackie > > > > Jackie>Jackie Building a website is a piece of cake. Small Business gives you all the tools to get online. Jackie Fussy? Opinionated? Impossible to please? Perfect. Join 's user panel and lay it on us. Jackie Ready for the edge of your seat? Check out tonight's top picks on TV. Jackie

[Guest guest]

Thanks, those look really good, and yep, Arctic would sure be COLD water, LOL.. Have to order from Canada, looks like. Jackie on <redjaxjm@...> wrote: try this http://www.enerex.ca/products/wild_fish_oil.htmSheena

<mom4possums2002 > wrote: Still looking in Google under "cold water" fish oil gel caps and not coming up with much yet. I do know liquid Carlson's is highly recommended, but I'd also rather take the gel caps.. Jackie on <redjaxjm > wrote: I believe I have used Puritan as one of the 3 I have tried... there was one and I wish I could remember the name, but it said on the label that it was WILD caught cold water fish oil on it and it had NONE of the Murcury or other metals in it.. it was a bit

expensive but I did feel like it was the best brand, if I can find it again, I will buy it and then give you the name of it if you are interested... Fish oil is VERY important for us heppers because our livers need the EPA and DHA..Sheena <mom4possums2002 > wrote: I stopped all for a time while I detoxed, then started adding things back slowly, had been using Puritan or Vitacost brand and even Walmart at times, but will sure be checking labels closer.. Jackie on <redjaxjm > wrote: I have tried 3 different brands,, and as long as they say "wild cold water fish", Im happy with it,, and as long as each capsule has 1000 mg in each so I only have to take 2 per day,, what brand are you taking?Sheena <mom4possums2002 > wrote: Are you taking any particular brand, Jackie?Jackie on <redjaxjm > wrote: I take 2 grams of fish oil in 2 gelcaps myself Lee and I have NO aftertaste at all,, and I can tell that my inflammation is down from taking it along with my cholesterol, CRP, SED etc,, all from fish

oil! When I fail to take it, I can tell because I start to hurt alot more!Lee <leecuatemsn> wrote: I've been taking the Fish oil caps for a while now, mainly because I can't stand eating fish. Especially the ones that are supposed to be good for you like oily sardines. A lot of research recommends eating fish like three times a week and I won't eat it at all.Beleive me that it doesn't give you any fishy aftertaste at all in the gelcaps.Lee> Is vitamin E beneficial in chronic liver disease? EDITORIAL> > Hepatology Aug 2007> > Ingrid Hickman 1, Graeme Macdonald 1 2 *§> 1The Diamantina Institute for Cancer, Immunology and Metabolic > Medicine, The University of Queensland, Brisbane, Australia> 2Department of Gastroenterology and Hepatology, Princess andra > Hospital, Brisbane, Australia> > Oxidative stress is implicated as a cause of liver injury in a range > of liver diseases including viral hepatitis,

alcoholic liver disease, > and nonalcoholic steatohepatitis (NASH). Vitamin E is the most widely > studied antioxidative, particularly in NASH. In the current issue of > HEPATOLOGY, Soden et al.[1] have examined the role of vitamin E in an > animal model of liver disease.> > Abbreviations> GCDC, glycochenodeoxycholic acid; NASH, nonalcoholic steatohepatitis; > ROS, reactive oxygen species.> > Oxidative stress is mediated by reactive oxygen species (ROS) > generated in the liver by a number of mechanisms involving induction > of microsomal CYP2E1[2] and H2O2 production from peroxisomal -> oxidation of fatty acids, consequently resulting in cytokine release > as well as recruitment of activated inflammatory cells.[3] ROS react > with a range of molecules in the cell, leading to impaired nucleotide > and protein

synthesis, which in turn injure organelles and activate > hepatic stellate cells.[4] ROS are responsible for inducing apoptosis > and cell death and interfere with repair mechanisms.> > Polyunsaturated fatty acids are major constituents of cell membranes. > They are particularly susceptible to free-radical-mediated oxidation > which results in lipid peroxidation and disturbances in membrane > structure and function. Oxidative stress and lipid peroxidation may > change the physical state of plasma membranes and impair membrane > function, including insulin signaling.[5] In patients with NASH, > markers of lipid peroxidation are positively correlated with insulin > resistance.[6]> > There are a number of protective mechanisms that ameliorate or > attenuate the effect of ROS including the up-regulation of a range of >

endogenous antioxidants, such as coenzyme Q10 and ubiquinones. There > is also a range of exogenous antioxidants including vitamins E and C, > carotenoids (beta carotene and lycopene), and polyphenols > (flavonoids). Vitamin E is of particular interest because it can > limit membrane injury by ROS.> > There are 8 naturally occurring vitamin E compounds, 4 tocopherol > homologs and 4 tocotrienols, which are synthesized by plants from > homogenistic acid. The 4 tocopherol homologs (da-, db-, d¥-, dy-) > have a saturated 16-carbon phytol side chain, whereas the > tocotrienols (da-, db-, dy-, d¥-) have 3 double bonds on the side > chain. All are derivatives of 6-chromanol and differ in the number > and position of the methyl groups on the ring structure (Fig. 1). The > term vitamin E can be used to describe any combination of

compounds; > however, a-tocopherol is the most abundant in nature and in human > plasma, and the most widely used in supplements and biomedical > research studies.> > The structure of vitamin E makes it a highly effective antioxidant, > readily donating the hydrogen from the hydroxyl group on the ring > structure to free radicals, and rendering them inactive. Vitamin E is > fat soluble and is primarily located within the phospholipid bilayer > of the cell membranes where it has a major biological role in > protecting polyunsaturated fats and other components of the cell > membranes from oxidation by free radicals.> > Obesity has been linked to insulin resistance, hepatic steatosis, and > liver injury in a range of conditions. These factors appear > particularly important in the pathogenesis of NASH. Hyperinsulinemia >

and hyperglycemia have been linked with increased oxidant stress[5] > and a decrease in a-tocopherol independent of body weight.[7] Central > obesity is associated with depletion of the body's endogenous > antioxidants.[8] As a consequence, the liver may be more vulnerable > to injury. Vitamin E supplementation with d1-a-tocopherol (900 mg/day > for 4 months) improves total body glucose disposal and nonoxidative > glucose metabolism in lean subjects, and in type 2 diabetes.[9] > Vitamin E may have dual benefits by decreasing oxidative stress and > improving insulin sensitivity and is an attractive therapeutic agent > for NASH and other liver diseases.> > Despite the encouraging in vitro work, results from clinical studies > have been mixed. In population studies, there seems to be a lack of > benefit from vitamin E in preventing

cardiovascular disease.[10][11] > Randomized trials of supplemental vitamin E to date have been small > and have not shown substantial beneficial effects on mortality > endpoints. A recent meta-analysis suggested there may be a small > increase in the risk of all-cause mortality with high-dose -> atocopherol supplementation (>400 IU/day).[12]> > A number of studies have examined the role of supplemental vitamin E > in liver disease. A recent Cochrane review concluded that data was > too limited to assess the effectiveness of Vitamin E in NAFLD,[13] > and the only study to assess the histological effect of a-tocopherol > supplementation in NASH showed no histological improvement compared > to placebo.[14] In patients with chronic hepatitis C, high-dose a-> tocopherol significantly reduced oxidative stress but did not affect

> liver enzymes or histological features of liver injury,[15] whereas > in a randomized, placebo-controlled study of alcoholic hepatitis, > there was no beneficial effect with 1000 IU/day.[16] Vitamin E > appears more promising in hepatitis B, where it was associated with > improved alanine aminotransferase levels and suppressed viral > replication in nearly half the patients treated[17]; however, these > studies have not been repeated in larger cohorts.> > Why might vitamin E supplementation not translate into clinical > benefit? First, the term vitamin E is used collectively for 8 > compounds, each potentially with its own biological effects. Most > research used tocopherol (99% of vitamin E papers on PubMed relate to > a-tocopherol)[18] rather than tocotrienols. However, tocotrienols > exhibit powerful neuroprotective,

anticancer, and some cholesterol-> lowering properties that are not necessarily shared by tocopherols.> [18]> > Second, the method of administration has been predominantly oral > supplementation. This approach is straightforward and allows greater > dosage than is possible from dietary sources. However, the oral > bioavailability of supplemental tocopherols are not precisely known > and high-dose a-tocopherol may reduce the plasma concentrations of > other vitamin E analogs such as y-tocopherol and ¥-tocopherol due to > competition for uptake and transfer in key tissues.[19] The changes > to bioavailability of other tocopherols and tocotrienols may in part > account for the null effects in studies of supplemental a-tocopherol.> > Finally, the production of ROS in different disease states may > overwhelm the ability of

supplemental vitamin E to ameliorate lipid > peroxidation and cellular injury.> > In this issue of HEPATOLOGY, Soden et al.[1] report the results of > subcutaneous administration of -tocopherol in an animal model of > steatocholestasis. This group has a long history of studying toxicity > of bile acids and the effects of vitamin E and other antioxidants.[20-> 22] They recently extended their studies to the Zucker fatty rat, an > animal model of hyperphagia, obesity, and hepatic steatosis that > occurs as a consequence of a mutation in the leptin receptor.[22] > These animals develop hepatic steatosis without inflammation or > fibrosis. Hepatocytes isolated from these animals and exposed to > glycochenodeoxycholic acid (GCDC) undergo necrosis, which is mediated > in part by ROS. The isolated hepatocytes could be protected from

> necrosis by exposure to antioxidants, including -tocopherol.> > In their current study, the effects of GCDC and vitamin E were > studied in vivo. Animals were loaded with a-tocopherol by parenteral > administration for a week prior to exposure to GCDC. Treatment with > the bile acid resulted in necrosis and inflammation, particularly in > the obese animals. This was associated with evidence of lipid > peroxidation, but there was no histological evidence of apoptosis. > Pretreatment with a-tocopherol led to a significant increase in > vitamin E concentration in the liver, and a significant reduction in > hepatocyte necrosis and inflammation. There was no beneficial effect > on lipid peroxidation, although in their earlier in vitro studies, > the authors were able to show a beneficial effect of a-tocopherol on > generation of

ROS.[22]> > The first observation from this study is that hydrophobic bile acids > can stimulate necroinflammation in an animal model of hepatic > steatosis, at least with short-term exposure. Thus, these bile acids > may be an important second hit in the evolution of NASH. An important > caveat is that leptin signaling has been shown to be relevant in > hepatic responses to injury[23] and leptin resistance may play a role > in this model. The second observation is that pretreatment with -> tocopherol can ameliorate, but not abrogate, this liver injury. > Although not shown in the current study, this may be mediated through > reduction in ROS and lipid peroxidation.> > In summary, a range of experimental studies have shown that vitamin E > can play a role in protecting cells from injury caused by ROS and > lipid peroxidation.

ROS and depleted antioxidants have been > implicated in insulin resistance and obesity and may play a role in > the pathogenesis of disease such as NASH. However, to date there is > little data to support the use of supplemental vitamin E in treating > liver disease. The possible therapeutic utility is made complex > because vitamin E is a group of compounds, and issues related to > bioavailability and interactions between these related compounds need > to be resolved. Soden and colleagues have shown that parenteral > vitamin E ameliorates liver injury in an animal model of obesity and > hepatic steatosis, by protecting animals from hydrophobic bile acid. > These observations provide support for further exploration of the > role of vitamin E supplementation in liver disease.> > > > > > Jackie > >

> > Jackie > > > > Jackie>Jackie Building a website is a piece of cake. Small Business gives you all the tools to get online. Jackie Fussy? Opinionated? Impossible to please? Perfect. Join 's user panel and lay it on us. Jackie Ready for the edge of your seat? Check out tonight's top picks on TV. Jackie

Luggage? GPS? Comic books?

Check out fitting gifts for grads at Search.

[Guest guest]

Does anyone recommend a specific fish oil to their patients if they are having trouble eating fish or just don’t like it? I currently recommend Nordic Naturals, but wanted to see if anyone else knew of a good brand that has some solid

research to back up the quality of it.

Thanks,

Abby