63 replies to this topic

[hbar]

http://www.bbc.co.uk...health-17443454
http://www.thelancet...1654-1/fulltext

"Taking a low (75-300mg) daily dose of the drug appeared to cut the total number of cancer cases by about a quarter after only three years - there were nine cancer cases per 1,000 each year in the aspirin-taking group, compared with 12 per 1,000 for those taking dummy pills.

It also reduced the risk of a cancer death by 15% within five years (and sooner if the dose was higher than 300mg)

And if patients stayed on aspirin for longer, their cancer death risk went down even further - by 37% after five years.

Low-dose aspirin also appeared to reduce the likelihood that cancers, particularly bowel, would spread (metastasise) to other parts of the body, and by as much as half in some instances.

In absolute numbers, this could mean for every five patients treated with aspirin one metastatic cancer would be prevented, the researchers estimate.

At the same time, aspirin cut the risk of heart attacks and strokes, but it also increased the risk of a major bleed.

However this elevated bleeding risk was only seen in the first few years of aspirin therapy and decreased after that."

--

Does any of this change peoples' opinions on aspirin? A few people on this board have expressed strong positive opinions towards aspirin, yet it still seems to be rarely mentioned in regimens or on "top supplements" lists. I've posted this before about aspirin, because it seems to me that of all the supplements we take that have anti-cancer effects, I can't think of anything else besides maybe Vit D that is showing such significant (and actually documented, not hypothesized) effects on cancer.

So...how close are we to the point that low-dose aspirin can be recommended for use in healthy individuals with no family history of cancer? Have we already reached it? I know people will respond to this with the same arguments about GI bleeding, but the article even mentions that the risk of GI bleeds decreases after being on aspirin for several years. When will we be able to definitively say that the cancer reduction is worth the increased bleeding risk?

[PWAIN]

Asprin seems to be something of a wonder drug. It really seems to have good effects. I've been taking it for about 18 months now and don't see myself discontinuing. I think that it is the one thing in my regime that has a lot of science behind it.

There is risk with this and it is very real risk, however, I think to at least a certain extent this can be reduced a little. First up use a low dose (75 - 90 mg), then get the enteric coated version and then probably safer to either take it with food or milk. I try to drink a fair bit at the same time with the hope that the water will dilute it as it dissolves.

Anyone got other ideas about how to make it a bit safer to take?

[Tomas E]

How safe is aspirin together with fish oils, if anyone got any safety margins on doses from both in combination. I took before 250mg of aspirin daily but after reading the interaction with fish-oil ive stopped taking it.

[niner]

There is risk with this and it is very real risk, however, I think to at least a certain extent this can be reduced a little. First up use a low dose (75 - 90 mg), then get the enteric coated version and then probably safer to either take it with food or milk. I try to drink a fair bit at the same time with the hope that the water will dilute it as it dissolves.

Anyone got other ideas about how to make it a bit safer to take?

I don't think that it's going to make much difference if the aspirin is enterically coated or buffered. The problem is that aspirin inhibits the COX enzyme responsible for a step of the synthesis of certain prostaglandins that have a protective effect for the GI mucosa. Since this is a systemic phenomenon, it wouldn't matter how the aspirin got in. A lower dose should be better, though a higher dose is better for cancer protection. If the aspirin is also acting as an irritant, and it might, then maybe the enteric coating would help, but it wouldn't eliminate all danger. Generally speaking, you can protect your stomach by not assaulting it when you have no food. Watch out for things like coffee, liquor, and irritating drugs or supplements, including aspirin.

The good news, sort of, is that the biggest danger of a bleed is in the GI tract, so you can keep an eye on things by observing the color of your poop. Also watch for symptoms of anemia. Unfortunately, GI bleeds can also come on very quickly; you could be fine one day and in the hospital the next, so it's a mixed bag.

The worst case scenario would be a cerebral hemorrhage. I'd rather have cancer than a bad stroke. However, I think that Aspirin's mechanism here is not making a bleed more likely, but rather making it less likely to stop because of anti-platelet action. I don't know how to counter this, but I think the odds of it are low compared to a GI problem. Obviously, you'd want to seek medical attention at the first sign of any problem.

How safe is aspirin together with fish oils

They both have anti-platelet effects, and it's conceivable that they could be more than additive, though I don't know that to be the case. I don't advise fish oil megadoses whether you take aspirin or not, but I think almost everyone should take a gram or two of fish oil. I don't see a big risk in combining low dose fish oil with low dose aspirin, unless you have a bleeding disorder or are anticipating surgery or a bar fight.

[platypus]

I don't see a big risk in combining low dose fish oil with low dose aspirin, unless you have a bleeding disorder or are anticipating surgery or a bar fight.

I'm already on standard doses of fish oil, aged garlic extract, curcumin, ginkgo biloba, K-vitamins, E-vitamins, lycopene etc. which all affect blood clotting. How can I know whether adding a baby-aspirin would be safe?

[DeadMeat]

I hope they hurry up a bit with the new NOSH aspirin.
http://www.scienceda...20308132812.htm

The fly in the ointment has been that prolonged use of aspirin posed its own dangers: side effects ranging from bleeding ulcers to kidney failure. To resolve this, the researchers created a hybrid of two earlier formulations, which they have called "NOSH-aspirin." They used the aspirin as a scaffold to support two molecules that have been shown to increase the drug's safety and potency.

One arm of the hybrid aspirin releases nitric oxide (NO), which helps protect the stomach lining. The other releases hydrogen sulfide (H2S), which the researchers have previously shown enhances aspirin's cancer-fighting ability. The researchers suspected that the hybrid would be more effective than either of the two components alone to boost aspirin's safety and power against cancer.

"The hybrid is more potent -- and it is more potent by orders of magnitude -- compared to aspirin," said Kashfi. Only 24 hours after treating a culture of cancer cells, the NOSH-aspirin demonstrated 100,000 times greater potency than aspirin alone. "At 72 hours it is about 250,000 times more potent in an in-vitro cell culture against human colon cancer," Kashfi added. "So you need a lower amount to get the same result."

[Tomas E]

Now that was interesting, thanks for sharing.

[gizmobrain]

Another thing I've read is that CoQ10 would interfere with the effects of aspirin, negating its positive effects. Given that CoQ10 is becoming more and more mainstream, I wonder how many people are combining the two.

I hope they hurry up a bit with the new NOSH aspirin.
http://www.scienceda...20308132812.htm

Me too.

Edited by zrbarnes, 22 March 2012 - 09:20 PM.

[niner]

Another thing I've read is that CoQ10 would interfere with the effects of aspirin, negating its positive effects. Given that CoQ10 is becoming more and more mainstream, I wonder how many people are combining the two.

I don't think there is any interaction between aspirin and CoQ10.

I hope they hurry up a bit with the new NOSH aspirin.
http://www.scienceda...20308132812.htm

It sounds good, but don't hold your breath. Maybe 10 years, with the odds of it making it to the end of the process about 5%? If it does get approved, expect it to cost a fortune. Or.... You could have it made for a song by a Chinese synthesis house, and have it in a matter of weeks.

[gizmobrain]

I don't think there is any interaction between aspirin and CoQ10.

I thought I remembered seeing something about CoQ10 undoing what aspirin did to help your heart. Maybe it was just Warfarin in combo with CoQ10? I can't seem to find it again.

[hbar]

niner, do you take aspirin? I don't think I've seen you mention it much, nor have a lot of the other long-time posters (doesn't seem like it's in MR's regimen either). The only person I can recall who seemed to be a big aspirin supporter was ajnast4r, but it still seems to me like a lot of people are shying away from it for cancer prevention unless they're also taking it for heart health.

I guess I'm just confused when people (not saying this about you, you seem to be pretty conservative in your approach to supplements) will latch onto exotic supplements that have little or no demonstrated ability to do much of anything. Yet aspirin, which by all accounts is an incredibly well-studied compound that seems to have huge anti-cancer benefits (and cancer is the disease that scares me more than probably any other) is ignored.

I guess part of it is that while other supplements may not have such large demonstrated benefits, being less well-studied also means their negative effects haven't been exposed yet. But aspirin's downside is well-known. Still, given a choice between GI bleeding and cancer, I'd take the former in a heartbeat.

I'm hoping that people who are more knowledgeable about this topic will chime in on whether or not we've reached the point with aspirin where the benefits outweigh the risks. I was taking it for a few months but then stopped after reading some (probably alarmist) stuff about bleeding, but I'd really like to know what the current thinking is in the supplement community right now regarding taking it solely for cancer prevention.

[niner]

I don't take aspirin. Historically, my stomach has been a bit of a weak link. I had a bleed a long time ago that put me in the hospital. Admittedly, at the time I had been abusing my stomach horribly, so I probably should discount that. Considering the benefits, I probably ought to take it. I have to admit the data looks pretty compelling. I never thought I had much of a cardiovascular risk, but since I recently found out that I have dangerously high lp(a), maybe I'll end up taking aspirin for heart health. If I got a two-fer like that, it would change the risk/reward profile.

[PWAIN]

Owing to its effect on the stomach lining, manufacturers recommend people with peptic ulcers, mild diabetes, or gastritis seek medical advice before using aspirin. Even if none of these conditions is present, there is still an increased risk of stomach bleeding when aspirin is taken with alcohol or warfarin

That looks like an easy one to avoid and would probably account for a fair few of the cases of GI bleeds.

Aspirin use has been shown to increase the risk of gastrointestinal bleeding. Although some enteric coated formulations of aspirin are advertised as being "gentle to the stomach", in one study enteric coating did not seem to reduce this risk. Combining aspirin with other NSAIDs has also been shown to further increase this risk. Using aspirin in combination with clopidogrel or warfarin also increases the risk of upper gastrointestinal bleeding.

In addition to enteric coating, "buffering" is the other main method companies have used to try to mitigate the problem of gastrointestinal bleeding. Buffering agents are intended to work by preventing the aspirin from concentrating in the walls of the stomach, although the benefits of buffered aspirin are disputed. Almost any buffering agent used in antacids can be used; Bufferin, for example, uses MgO. Other preparations use CaCO3.

This seems to backup what Niner said.

Taking it with vitamin C is a more recently investigated method of protecting the stomach lining. According to research done at a German university, taking equal doses of vitamin C and aspirin decreases the amount of stomach damage that occurs compared to taking aspirin alone.

It is reported that deglycyrrhizinated licorice (DGL), an extract of the popular herb licorice, helps relieve the symptoms of gastritis. In a 1979 research study, a dose of 350 milligrams of DGL was shown to decrease the amount of gastrointestinal bleeding induced by three adult-strength aspirin tablets (750 milligrams).

Seem that a Vit C at the same time might not be a bad idea - cheap and not dangerous - seems like a must. Anyone know anything about DGL?

A dose of 500 milligrams of S-adenosyl-methionine (SAMe, an amino acid naturally formed in the body) given together with a large dose of aspirin (1300 milligrams) in a research study reduced the amount of stomach damage by 90 percent.

Also worth considering but a bit more expensive. I think it would be worth looking into this more before jumping on board but definitely worth the investigation.

A study found that, in contrast to oral aspirin, intravenous injection of aspirin did not produce detectable histological damage or significantly alter gastric mucosal potential difference, and concluded that high blood levels of circulating salicylate did not acutely damage gastric mucosa, so that gastric mucosal damage produced acutely after single oral doses of aspirin are due to its topical, rather than systemic, action.

This last bit seems to be important. As I read it, it is contradicting what you were saying about systemic damage Niner. If this is accurate, does it mean that intravenous injection at least in large part reduces the risk of GI bleed? If this is indeed the case, then injection may be the way to go or at least finding ways to reduce the histological damage when taking the pills would be a good way to go.

Niner, I would appreciate your comments about intravenous injection, is this an extreme course of action and how great are the risks of infection? I have to admit the idea of injecting is very off putting and looks like something that would be hard to arrange but I want to continue with aspirin but also want to reduce the risks.

[PWAIN]

I also came across this:

http://www.scienceda...10912104830.htm

The key here being that they say:

In patients who took proton pump inhibitors (PPIs), bleeding risk decreased

But then Wikipedia ( http://en.wikipedia....pump_inhibitors ) says:

High dose or long-term use of PPIs carry a possible increased risk of bone fractures

Bone fractures are probably better than bleeds, cancer or heart attack but still not desirable.

Edited by PWAIN, 23 March 2012 - 05:22 AM.

[niner]

A study found that, in contrast to oral aspirin, intravenous injection of aspirin did not produce detectable histological damage or significantly alter gastric mucosal potential difference, and concluded that high blood levels of circulating salicylate did not acutely damage gastric mucosa, so that gastric mucosal damage produced acutely after single oral doses of aspirin are due to its topical, rather than systemic, action.

This last bit seems to be important. As I read it, it is contradicting what you were saying about systemic damage Niner. If this is accurate, does it mean that intravenous injection at least in large part reduces the risk of GI bleed? If this is indeed the case, then injection may be the way to go or at least finding ways to reduce the histological damage when taking the pills would be a good way to go.

Niner, I would appreciate your comments about intravenous injection, is this an extreme course of action and how great are the risks of infection? I have to admit the idea of injecting is very off putting and looks like something that would be hard to arrange but I want to continue with aspirin but also want to reduce the risks.

That's interesting. It's not completely consistent with the study that found enteric coating not to be helpful, unless that meant that the enteric coating was failing. It does suggest that the irritant nature of aspirin is a significant factor, and/or that avoiding a high aspirin concentration in the stomach is good, but then why the poor results with the enteric coating? As for iv injection, I wouldn't consider it for a lifetime daily drug like aspirin. Even if you had infection risk totally under control, there would still be the potential for injury and scarring of the veins. There's the classic picture of the junky who shoots up in all kinds of crazy places because all the easy veins are wrecked. You could probably dodge most of that by using a fresh needle every time, and having really good technique, but still...

In patients who took proton pump inhibitors (PPIs), bleeding risk decreased

But then Wikipedia ( http://en.wikipedia....pump_inhibitors ) says:

High dose or long-term use of PPIs carry a possible increased risk of bone fractures

Bone fractures are probably better than bleeds, cancer or heart attack but still not desirable.

I'd rather have the typical GI bleed than a fracture. A vertebral fracture might mean a lifetime of pain, but you can heal an ulcer. PPIs have other downsides, too, like affecting your nutrient absorption. The PPI results tell us that the risk of bleeds is a function of stomach acidity, which kind of goes without saying. If you take care of your stomach, only putting in harsh substances when you have some food on board, being careful with alcohol and coffee, and avoiding tobacco, you will have better luck with bleeds.

Vitamin C is dangerous by itself because of its acidic nature, but seems fine with food. Interesting that it's helpful- I wonder what the mechanism is? Good to know at any rate. I recall some sort of significant negative with SAMe, but don't remember exactly what it was. It's never really been on my radar screen for some reason. Don't know anything about DGL.

[mikeinnaples]

I have been taking 81mg doses for years with no issues. My understanding of some of the studies I read is that there was very little additional benefit over that amount. In addition, I also came to understand that you had to take the aspirin for a long period of time for it to reduce overall risk. I would think staying in the dosage of a baby aspirin or two would give the best risk:benefit.

[brunotto]

Anyone got other ideas about how to make it a bit safer to take?

I take it (100 mg/day) on empty stomach with 200 mcg/day misoprostol (cytotec) and a lot of other supps & cup of tea with little milk in the morning... really zero gastric problems... also short action of time so acid secretion is fully restored after maybe 2 hours (half life 20–40 minutes)...

http://en.wikipedia....iki/Misoprostol

Bone fractures are probably better than bleeds, cancer or heart attack but still not desirable.

Misoprostol is a substance that is much similar of the natural one (PGE2) that aspirin inhibits in the stomach so leading to gastric problem... I would say it's the most "natural" solution... much different story would be taking h2 inhibitors or PPIs (much less "natural")... those are -unnecessary for aspirin- long actions substances that easly leads to cronic malabsorbtion of minerals due to low acid secretion of the stomach (osteoporosis).

http://www.ncbi.nlm....pubmed/21688629

Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.

http://www.ncbi.nlm....pubmed/11191738

A synthetic prostaglandin E1 (PGE1) analogue, misoprostol, was investigated for its effects on the growth of colon cancer in two in vivo models. Human colon cancer cell lines C170, LIM2412 and LIM2405 were grown as subcutaneous xenografts on T-lymphocyte deficient ARC(s) nu/nu mice. Tumour volumes were found to be significantly inhibited compared with control in misoprostol-treated animals with two cell lines. C170 was inhibited by 70.5% (P = 0.0001) and LIM2412 by 68.2% (P = 0.01). LIM2405 was inhibited by 33% (P = 0.14) which was not significantly different from the control. In a second experiment, colon cancers were induced in Sprague-Dawley rats using 1,2 dimethyl-hydrazine (DMH). After 10 weeks of treatment, rats were randomized to receive a 5 week course of 20 micrograms/kg per day of oral misoprostol. Misoprostol-treated rats were found to have a similar tumour incidence and staging compared with control animals. Oral administration of misoprostol has an inhibitory effect on early tumour growth of some colonic cancers, but not on established tumours.

http://www.ncbi.nlm..../pubmed/8117200

In patients with underlying renal impairment, administration of nonsteroidal anti-inflammatory drugs (NSAID) can produce a marked reduction of renal function via inhibition of renal prostaglandin (PG) synthesis. Recent findings indicate that administration of misoprostol can at least partially prevent NSAID induced nephrotoxic effects, suggesting a role for exogenous PG in this setting. These agents may also have important immunomodulatory effects. Other recently reported data show that use of misoprostol in renal transplant patients receiving immunosuppressive therapy with cyclosporine and prednisone was associated with a significant reduction in the incidence of acute graft rejection, as well as improved graft function irrespective of the occurrence of rejection.

http://www.ncbi.nlm..../pubmed/1903809

Acute infusion of cyclosporine in rats causes intense renal vasoconstriction and decreased glomerular filtration rate, effects that persist during short-term daily administration. We tested whether the orally active prostaglandin E1 analog misoprostol could reverse cyclosporine-induced renal vasoconstriction and restore the glomerular filtration rate. Male Sprague-Dawley rats were infused with cyclosporine (10 mg/kg) and then given an oral dose of misoprostol (100, 500, or 1000 micrograms/kg). Cyclosporine caused large decreases in glomerular filtration rate and renal blood flow and a large increase in renal vascular resistance. Misoprostol decreased renal vascular resistance and increased renal blood flow and glomerular filtration rate to near normal levels. The two highest doses of misoprostol caused severe hypotension only in cyclosporine-treated animals. However, when it was given in a dose of 100 micrograms/kg hypotension was not a serious problem. This dose of misoprostol resulted in an increase in glomerular filtration rate from 341 +/- 57 to 669 +/- 104 microliter/min (P less than 0.005) and renal blood flow from 2.23 +/- 0.36 to 4.25 +/- 0.65 ml/min (P less than 0.01), as well as a decrease in renal vascular resistance from 73.7 +/- 23.8 to 29.4 +/- 5.8 mmHg/ml/min (P less than 0.05) in cyclosporine-treated animals. When given to control animals, misoprostol had no effects on renal hemodynamics or renal function. In summary, acute cyclosporine-induced renal vasoconstriction and renal dysfunction in the rat were substantially reversed by oral administration of the prostaglandin E1 analog misoprostol.

http://www.ncbi.nlm..../pubmed/3132763

Edited by brunotto, 23 March 2012 - 01:50 PM.

[brunotto]

How safe is aspirin together with fish oils

Really strong -IMHO positive- antinflammotory (also in some way immunomodulatory) combo becouse of resolvins...

I use aspirine + fish oil becouse of this: "An important third mechanism has recently been discovered that produces lipoxins of different stereochemistry, i.e. the epi-lipoxins, sometimes termed the aspirin-triggered lipoxins (‘ATL’), as the reaction is initiated by aspirin and requires the cyclooxygenase COX-2 in the first step. As discussed in the Introduction to these pages, COX-2 is induced in endothelial and epithelial cells in response to a variety of stimuli. The effect of aspirin is to acetylate the enzyme, switching its catalytic activity (and its chirality) from prostanoid biosynthesis to production of 15R-HETE rather than the S-enantiomer. This is in turn converted to 5S,6S-epoxy-15R-hydroxy-ETE, as described above for lipoxins, by the action of the 5-lipoxygenase in leukocytes and thence to epi-lipoxins, i.e. epi-LXA₄ and epi-LXB₄ with 15R-stereochemistry. 15(R)-HETE produced by the action of a cytochrome P450 enzyme in the absence of aspirin can also be converted to 15-epi-lipoxins"


http://lipidlibrary....k/index.htm#epi

http://lipidlibrary....resol/index.htm

Acute inflammation in response to infection or tissue damage is usually characterized by heat, redness, swelling and pain at a simple observational level, and by oedema, accumulation of leukocytes, and then by accumulation of monocytes and macrophages at a cellular level. Leukotrienes (especially LTB₄) and prostaglandins (PGE₂ and PGD₂) derived from arachidonic acid are important in the early stages of the inflammatory process. As tissues return to health, resolvins and protectins, together with lipoxins and maresins, promote resolution of the inflammation through removal of the leukocytes together with cellular debris, ideally without leaving remnants of the host defences or of the invading microorgansms or other inflammatory initiators.

The resolvins and neuroprotectins are distinctive and highly stereospecific lipids, which are endogenous local mediators with strong anti-inflammatory effects in addition to some immunoregulatory activities at picomolar to nanomolar concentrations. They are part of the molecular mechanisms that contribute to removal of inflammatory cells and restoration of tissue integrity once the need for the inflammatory response is over, i.e. they actively assist in the resolution of inflammation, once thought to be a passive process. It is evident that the presence of aspirin uniquely facilitates the resolution of inflammation. Thus, at local sites of inflammation, aspirin treatment enhances the conversion of the omega-3 fatty acids EPA and DHA to 18R-oxygenated products, i.e. resolvins of the E and D series, which carry potent anti-inflammatory signals. So far two receptors have been identified that mediate the activities of RvE₁.

During inflammation, polymorphonuclear neutrophils are produced which have generally beneficial effects in countering disease, but in the longer term or if malfunctioning they may eventually cause trauma and tissue damage through infiltration into tissues. The resolvins, like the lipoxins, appear to have an important role in regulating and indeed inhibiting these harmful effects. In so doing they oppose the effects of some of the pro-inflammatory prostanoids. For example, nanomolar concentrations of resolvin E1 dramatically reduce dermal inflammation, peritonitis, dendritic cell migration and interleukin production. RvE1 blocks excessive platelet aggregation, and it also limits the effects of certain human pathogens by enhancing phagocytosis by polymorphonuclear leukocytes. Similarly, RvD2 has extremely potent regulatory actions on neutrophil trafficking in the picogram range in vivo by stimulating resolution and enhancing innate host defense mechanisms via a specific receptor.

The (neuro)protectins appear to operate in the same way as the resolvins in brain tissue. Thus, (N)PD1 has anti-inflammatory effects and protects retinal epithelial cells from apoptosis induced by oxidative stress. In addition, it has protective effects in animal models of stroke and of Alzheimer's disease. Amongst its activities in non-neuronal tissues, it promotes apoptosis of T cells and it has beneficial effects towards asthma in nanogram amounts. It is evident that such compounds and their metabolism have considerable potential for therapeutic intervention in acute inflammation or chronic inflammatory disease. They may also mitigate the affects of sepsis.

It is now well established that administration of lipoxins, resolvins and protectins in vivo in animal models can aid the process of recovery from inflammation without compromising host defences by causing immune suppression.

It is evident that these lipids or synthetic analogues have considerable therapeutic potential in managing chronic inflammatory diseases, including arthritis, cardiovascular disease, asthma and even cancer. From a nutritional or health standpoint, it has been suggested that dietary supplements of the precursor omega-3 fatty acids, taken together with aspirin, may ameliorate the clinical symptoms of many inflammatory disorders by regulating the time course of resolution via the production of resolvins and protectins

[Mind]

After so many years of positive studies, I finally started taking low dose aspirin last month. Its cheap. Risks are low.

[Tomas E]

What dose are people taking aspirin?

[Mind]

81mg for me

[maxwatt]

Thee is also a genetic factor. Many people have an SNP which inhibits the effectiveness of an enzyme that metabolizes aspirin, so it stays around longer, and they need half the dose of aspirin and other NSAIDS that others do. As for bleeding, I've read that whether you have symptoms or not, the standard 200 mg aspirin dose will cause two or three teaspoons of blood to leak into the intestines. The COX inhibition resulting in reduced generation of prostaglandins can be compensated with EPA supplements, or eating high omega-3 fish two or three times a week.

I take 100 mg of aspirin about four times a week with no problem. I also eat a few pieces of pickled herring with breakfast. which has more EPA than a like amount of Salmon or Tuna according to the Cron-o-Meter calculation, and it adds some vitamin D.

A question: does taking vitamin K2 as MK7 make up for the increased risk of bleeding from aspirin and fish oil? I suspect it does by decreasing clotting time.

[niner]

Thee is also a genetic factor. Many people have an SNP which inhibits the effectiveness of an enzyme that metabolizes aspirin, so it stays around longer, and they need half the dose of aspirin and other NSAIDS that others do. As for bleeding, I've read that whether you have symptoms or not, the standard 200 mg aspirin dose will cause two or three teaspoons of blood to leak into the intestines. The COX inhibition resulting in reduced generation of prostaglandins can be compensated with EPA supplements, or eating high omega-3 fish two or three times a week.

A question: does taking vitamin K2 as MK7 make up for the increased risk of bleeding from aspirin and fish oil? I suspect it does by decreasing clotting time.

That's a lot of occult blood; is that supposed to be a daily amount? The usual aspirin doses are 81mg (baby aspirin) and 650mg, the latter being two 325mg tablets; the famed 'take two aspirin and call me in the morning' dose. Seems like too much blood to not notice.

This is the first I've heard of fish oil being helpful. Is it on the pathway for whichever prostaglandin is protective? All I ever hear is that since they are both "blood thinners", you should be careful when mixing.

Vitamin K beyond normal requirements doesn't help; it is involved in the clotting cascade, but once there is enough, my understanding is that that's it; more K doesn't make you clot more because all of the GLA proteins are already carboxylated. If you had a deficiency, it would be a different story, as your clotting would be compromised. Warfarin works by inducing a vitamin K deficiency, so K is considered an antidote to it.

[gamesguru]

I take white willow bark, 240 mg salicin daily (which metabolizes to roughly 87 mg aspirin). White willow bark probably has independent anti-inflammatory mechanisms too. It's also been around for at least 10x longer, not that that guarantees anything.

[maxwatt]

The salicylic acid in willow bark, by itself would cause more bleeding and gut problems than acetylated salicylic acid, known as aspirin.

[Tomas E]

Thats great, as I take both fish oil, aspirin and vitamin k ....... Probally one day without fish oil and stack on aspirin twice a week.

[gamesguru]

I do believe that willow bark contains salicin, which is metabolized after absorption into salicylic acid, and then into aspirin. Thanks though, I'll try it alone on an empty stomach a few days to see if it is aggravating, like aspirin.

[maxwatt]

Thee is also a genetic factor. Many people have an SNP which inhibits the effectiveness of an enzyme that metabolizes aspirin, so it stays around longer, and they need half the dose of aspirin and other NSAIDS that others do. As for bleeding, I've read that whether you have symptoms or not, the standard 200 mg aspirin dose will cause two or three teaspoons of blood to leak into the intestines. The COX inhibition resulting in reduced generation of prostaglandins can be compensated with EPA supplements, or eating high omega-3 fish two or three times a week.

A question: does taking vitamin K2 as MK7 make up for the increased risk of bleeding from aspirin and fish oil? I suspect it does by decreasing clotting time.

That's a lot of occult blood; is that supposed to be a daily amount? The usual aspirin doses are 81mg (baby aspirin) and 650mg, the latter being two 325mg tablets; the famed 'take two aspirin and call me in the morning' dose. Seems like too much blood to not notice.

This is the first I've heard of fish oil being helpful. Is it on the pathway for whichever prostaglandin is protective? All I ever hear is that since they are both "blood thinners", you should be careful when mixing.

Vitamin K beyond normal requirements doesn't help; it is involved in the clotting cascade, but once there is enough, my understanding is that that's it; more K doesn't make you clot more because all of the GLA proteins are already carboxylated. If you had a deficiency, it would be a different story, as your clotting would be compromised. Warfarin works by inducing a vitamin K deficiency, so K is considered an antidote to it.

Thanks. My bad on the doses; by "usual" dose, I meant the proverbial doctor's advice: "take two aspirin and call me in the morning". Still it's 325 mg, not 100 mg. I was thinking of 5 grains of aspirin, and did the conversion wrong.

As I understand it: Aspirin inhibits COX-2 and COX-1 and maybe COX-3 (reducing pain by inhibiting formation of inflammatory, pain and fever producing prostaglandins such as PGE₂ and TXA₂ ) but it also inhibits the production of delta-5 desaturase, needed to elongate omega-3 molecules into EPA and DHA, which in turn are needed to make the omega-3 derived prostaglandins (PGG₃, PGH₃, PGI₃, TXA₃ which are mostly anti-inflammatory). Fish oil contains EPA and DHA; In that regard taking an EPA or fish oil supplement bypasses the conversion making up for the effect of aspirin at inhibiting it, so you can get the good effects of aspirin without some of the undesired side effects associated with too little of the beneficial prostaglandins.

[brunotto]

Management of NSAID/Aspirin-Induced Small Intestinal Damage by GI-Sparing NSAIDs, Anti-Ulcer Drugs and Food Constituents
pp.82-89 (8) Authors: H. Satoh, K. Takeuchi

Abstract

Recent advances in endoscopic techniques such as capsule endoscopy have revealed that aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) often cause mucosal lesions not only in the upper gastrointestinal tract, but also in the small intestine in humans.

Gastric and duodenal lesions caused by NSAIDs can be treated with anti-secretory agents such as proton pump inhibitors or histamine H2-receptor antagonists; however, these drugs are ineffective in treating NSAID-induced lesions in the small intestine. Furthermore, there are few effective agents for the treatment of small intestinal lesions. Therefore, identification of effective therapies for the treatment of NSAID/aspirin-induced small intestinal lesions remains an urgent priority. In the present review, we focus on novel pharmacological treatments to prevent or reduce NSAID-induced intestinal lesions, i.e.,

1) GI-sparing NSAIDs (NO- or H2S-NSAIDs, NSAIDs mixed with phosphatidylcholine);
2) anti-ulcer drugs such as mucosal protective agents (misoprostol, rebamipide, teprenone, etc.) and anti-secretory agents (lansoprazole, etc.);
3) antibiotics (metronidazole) and probiotics (Lactobacillus sp.); and
4) food constituents (lactoferrin and soluble dietary fibers).

We surveyed data from clinical trials evaluating these novel treatments. Also reviewed herein were the pros and cons of the novel protective methods from the standpoint of safety, efficacy, convenience, and cost.

http://www.benthamdi...00001/0012C.SGM

[brunotto]

Phosphatidylcholine-associated nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit DNA synthesis and the growth of colon cancer cells in vitro

In an attempt to improve the GI safety of traditional NSAIDs, a new class of NSAIDs has been developed in which the drug has been associated (non-covalently) with a phosphatidylcholine (PC) molecule. This results in an ‘‘NSAID–PC’’ with little or no associated GI erosions and/or bleeding in both rodents and clinical trials [1, 15]. In addition, NSAID–PCs have the same or greater efficacy to relieve pain, fever and inflammation than unmodified NSAIDs

http://www.plxpharma...ory%20drugs.pdf

Edited by brunotto, 07 April 2012 - 11:18 AM.