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Thread: Ibuprofen Can Stop Your Heart (31% Increase In Cardiac Arrest Risk)

  1. #1

    Ibuprofen Can Stop Your Heart (31% Increase In Cardiac Arrest Risk)

    Ibuprofen Can Stop Your Heart (31% Increase In Cardiac Arrest Risk)

    By: Sayer Ji

    A new study reveals that a commonly consumed painkiller, wrongly considered "harmless" by millions, is probably causing thousands of deaths from cardiac arrest each year.

    According to the Sudden Cardiac Arrest Foundation, sudden cardiac arrest (SCA) is a leading cause of death among adults over 40 in the United States and other countries, with about 326,200 people experiencing an out-of-hospital SCA each year in the US alone; nine of 10 victims of SCA will die.1

    Suprisingly, however, the causes of SCA are still widely considered unknown. Instead, the medical profession opts for pointing the finger at vague risk factors, such as family history, previous heart problems, or elevated LDL cholesterol (a long debunked surrogate marker for heart disease].

    But what if something so obvious and preventable as the consumption of NSAID drugs could be contributing to this health epidemic?



    New Study Reveals Heart-Stopping Side Effects of NSAIDs
    In a concerning press release issued by the European Society of Cardiology entitled, “‘HARMLESS’ PAINKILLERS ASSOCIATED WITH INCREASED RISK OF CARDIAC ARREST,”2 researchers warn that painkillers considered harmless by the general public are associated with a significantly increased risk of cardiac arrest.

    The report was based on a study entitled, “Non-Steroidal Anti-Inflammatory Drug Use Is Associated With Increased Risk of Out-Of-Hospital Cardiac Arrest: A Nationwide Case-Time-Control Study,” published in the March issue of European Heart Journal - Cardiovascular Pharmacology.

    Professor Gunnar H. Gisalson, one of the lead researchers explained in interview:

    “Allowing these drugs to be purchased without a prescription, and without any advice or restrictions, sends a message to the public that they must be safe.”

    “Previous studies have shown that NSAIDs are related to increased cardiovascular risk which is a concern because they are widely used.”
    The study looked at a total of 28,947 patients who experienced an out-of-hospital cardiac arrest in Denmark over the course of a decade. Heart attack differs from cardiac arrest in that the former involves damage to the heart when the blood supply stops (usually through obstruction of circulation), whereas the latter involves damage from the heart itself stopping. 3,376 of these were treated with an non-steroidal anti-inflammatory drug (NSAIDs) up to 30 days before the event. The most common NSAIDs used were ibuprofen (51%) and diclofenac (22%).

    The study results revealed that NSAID use was associated with a 31% increased risk of cardiac arrest. Ibuprofen and diclofenac increased the risk by 31% and 50%, respectively. Naproxen, celecoxib and rofecoxib were not associated with increased cardiac arrest.

    Gunnar remarked on these findings:

    “The findings are a stark reminder that NSAIDs are not harmless. Diclofenac and ibuprofen, both commonly used drugs, were associated with significantly increased risk of cardiac arrest. NSAIDs should be used with caution and for a valid indication. They should probably be avoided in patients with cardiovascular disease or many cardiovascular risk factors.”
    This is not the first time that ibuprofen’s profound cardiotoxicity has come to light. We reported on the subject five years ago in an article entitled, Ibuprofen Kills Thousands Each Year, So What Is The Alternative?

    We strongly agree with Gunnar’s closing interview remarks when he says:

    “The current message being sent to the public about NSAIDs is wrong. If you can buy these drugs in a convenience store then you probably think ‘they must be safe for me’. Our study adds to the evidence about the adverse cardiovascular effects of NSAIDs and confirms that they should be taken seriously, and used only after consulting a healthcare professional.”
    Keep in mind that other common pain-killers, such as aspirin and acetaminophen (Tylenol), also have devastating side effects that are commonly underreported or minimized. You can read our previous writings on the topic:

    Tylenol Kills Emotions As Well As Pain, Study Reveals
    Surprising Side Effects of Tylenol
    The Dangers of Tylenol: Is it Time for the FDA to
    The Evidence Against Aspirin And For Natural
    Natural Alternatives That Don't Have Killer Side Effects Exist
    Given the clear evidence that pharmaceutical pain-killers have profound, even life-threatening side effects, natural alternatives should be researched and implemented. At GreenMedInfo.com we have a number of database sections that should help move the paradigm forward.

    Natural Pain Reducers

    Natural Anti-Inflammatory Agents

    Natural Analgesics

    NSAID Toxicity

    Ibuprofen Alternatives

    Aspirin Alternatives

    Tyelonol Toxicity

    Aspirin Toxicity

    Ibuprofen Toxicity
    References

    1 http://www.sca-aware.org/about-sca

    2 http://www.escardio.org/The-ESC/Pres...cardiac-arrest
    http://www.greenmedinfo.com/blog/ibu...ac-arrest-risk
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner



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  3. #2
    natural alternatives should be researched and implemented
    Opium!

  4. #3
    For anybody that wants to read the study for themselves.
    K.B. Sondergaard et al – Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study (2016): https://academic.oup.com/ehjcvp/arti...ry-drug-use-is


    Here’s the figure that shows the increased risk of a heart attack caused by Ibuprofen and Diclofenac.
    Last edited by Firestarter; 06-28-2017 at 03:08 AM. Reason: Fixed picture (third time)

  5. #4
    Turmeric for the win!

    Turmeric Beats Ibuprofen for Arthritis of the Knee
    http://www.greenmedinfo.com/blog/tur...arthritis-knee


    2231 Abstracts with Curcumin Research
    http://www.greenmedinfo.com/substance/curcumin
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  6. #5
    I should be dead. Used it a lot with my 3 bouts of strep throat recently. Off of it now.

  7. #6
    Quote Originally Posted by Carlybee View Post
    I should be dead. Used it a lot with my 3 bouts of strep throat recently. Off of it now.
    My sister used it for a year and it wound up perforating her stomach and putting her in the hospital for nearly a month.

    Effective Strep Throat Home Remedies

    Martin’s holistic strep throat treatment consisted of the following ingredients which he consumed at a rate of ½ teaspoon every 30 minutes to an hour.
    Use a mortar & pestle to mash up 3 cloves of fresh garlic (sources).
    Mix in half a teaspoon of cayenne pepper (sources).
    Mix in raw honey (manuka honey is best) to taste which has healing properties of its own (sources).
    Martin also gargled with raw apple cider vinegar diluted with some water 3x per day (sources). Below is his daily journal logging his progress to a cure.
    http://www.thehealthyhomeeconomist.c...t-antibiotics/
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  8. #7
    Sex can also stop your heart.

    Not gonna stop doing it
    It's all about taking action and not being lazy. So you do the work, whether it's fitness or whatever. It's about getting up, motivating yourself and just doing it.
    - Kim Kardashian

    Donald Trump / Crenshaw 2024!!!!

    My pronouns are he/him/his

  9. #8
    Quote Originally Posted by TheTexan View Post
    Sex can also stop your heart.

    Not gonna stop doing it
    Actually sex is good exercise for your heart.
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner



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  11. #9
    Quote Originally Posted by tod evans View Post
    Opium!
    that only works if you're not one of the people who's throat tries to close - also I become a whimpering cluster of hives while waiting for the benedryl/epinephrine
    Disclaimer: any post made after midnight and before 8AM is made before the coffee dip stick has come up to optomim level - expect some level of silliness,

    The problems we face today exist because the people who work for a living are out numbered by those who vote for a living !!!!!!!

  12. #10
    Quote Originally Posted by opal View Post
    that only works if you're not one of the people who's throat tries to close - also I become a whimpering cluster of hives while waiting for the benedryl/epinephrine
    Sucks to be you....

    Me too though..........Opium was easier to get in the 70's than now....

    Does weed help?

    Or any other 'naturals' ?

  13. #11
    Quote Originally Posted by donnay View Post
    Turmeric for the win!

    Turmeric Beats Ibuprofen for Arthritis of the Knee
    http://www.greenmedinfo.com/blog/tur...arthritis-knee


    2231 Abstracts with Curcumin Research
    http://www.greenmedinfo.com/substance/curcumin
    Cayenne stops heart attacks immediately; I've seen it in action.
    There is no spoon.

  14. #12
    Quote Originally Posted by Ender View Post
    Cayenne stops heart attacks immediately; I've seen it in action.
    Yes, Cayenne is great. However, Turmeric works everyday to help prevent a heart attack.

    Turmeric's Cardiovascular Benefits Found To Be As Powerful As Exercise
    http://www.greenmedinfo.com/blog/tur...ful-exercise-a


    Turmeric: Better Than Aspirin For Heart Disease Prevention?
    http://www.greenmedinfo.com/blog/tur...-your-arteries
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  15. #13
    Quote Originally Posted by donnay View Post
    My sister used it for a year and it wound up perforating her stomach and putting her in the hospital for nearly a month.


    http://www.thehealthyhomeeconomist.c...t-antibiotics/

    I did use manuka. Ultimately had to get a z pak. Apparently reinfected myself with my toothbrush.

  16. #14
    Quote Originally Posted by Carlybee View Post
    I did use manuka. Ultimately had to get a z pak. Apparently reinfected myself with my toothbrush.
    Aw gees, sorry to hear that. Colloidal silver in a little spray bottle works great on toothbrushes. Manuka is great stuff, no doubt.
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  17. #15
    Quote Originally Posted by tod evans View Post
    Sucks to be you....

    Me too though..........Opium was easier to get in the 70's than now....

    Does weed help?

    Or any other 'naturals' ?
    kinda depends on the weed.. not a big indica fan - vertigo in a big way. Sativa distracts me enough to not think about pain sometimes - I'm working on getting enough tumeric in me to make a difference. I kind of prefer a light sedative to make me care less.. mothers little helper comes to mind
    Disclaimer: any post made after midnight and before 8AM is made before the coffee dip stick has come up to optomim level - expect some level of silliness,

    The problems we face today exist because the people who work for a living are out numbered by those who vote for a living !!!!!!!

  18. #16
    'Heart attack risk' for common painkillers

    By Smitha Mundasad

    A fresh study suggests there may be a link between taking high doses of common anti-inflammatory painkillers - such as ibuprofen - and heart attacks.

    The paper, published in The BMJ, builds on a previous body of work linking these drugs to heart problems.

    This research suggests the risk could be greatest in the first 30 days of taking the drugs.

    But scientists say the findings are not clear cut. They say other factors - not just the pills - could be involved.

    In the study an international team of scientists analysed data from 446,763 people to try to understand when heart problems might arise.

    They focused on people prescribed non-steroidal anti-inflammatory drugs (such as ibuprofen, diclofenac, celecoxib and naproxen) by doctors rather than those who bought the painkillers over the counter.

    'Raise awareness'

    Studying the data from Canada, Finland and the UK, researchers suggest taking these Nsaid painkillers to treat pain and inflammation could raise the risk of heart attacks even in the first week of use.

    And the risk was seen especially in the first month when people were taking high doses (for example more than 1200mg of ibuprofen a day) .

    But scientists say there are a number of factors that make it difficult to be absolutely certain of the link.

    Are the painkillers definitely to blame?

    Kevin McConway, emeritus professor of statistics at The Open University, said the paper threw some light on possible relationships between Nsaid painkillers and heart attacks.

    But he added: "Despite the large number of patients involved, some aspects do still remain pretty unclear.

    "It remains possible that the painkillers aren't actually the cause of the extra heart attacks."

    He said if, for example, someone was prescribed a high dose of a painkiller because of severe pain, and then had a heart attack in the following week, it would be "pretty hard" to tell whether the heart attack had been caused by the painkiller or by whatever was the reason for prescribing it in the first place,

    It could even be down to something else entirely, he said.

    Prof McConway also pointed out that other influences on heart health - such as smoking and obesity - could not be taken into account fully and could be partly to blame.

    What should patients do?

    Doctors are already aware from previous studies that non-steroidal anti-inflammatory drugs could increase the risk of heart problems and strokes.

    And current UK guidelines state that Nsaids must be used carefully in people with heart problems and in some cases (such as very severe heart failure) they should not be used at all.

    Dr Mike Knapton of the British Heart Foundation, suggests patients and doctors weigh up the risks and benefits of taking high doses of these common painkillers, particularly if they have survived a heart attack or are at higher risk.

    Meanwhile, GP leader Prof Helen Stokes-Lampard said it was important that any decision to prescribe was based on a patient's individual circumstances and medical history, and was regularly reviewed.

    She said that as new research was published, it was important that it was taken on board to help inform guidelines.

    But she added: "The use of Nsaids in general practice to treat patients with chronic pain is reducing, and some of the drugs in this study are no longer routinely prescribed in the UK, such as coxibs, as we know that long-term use can lead to serious side-effects for some patients."


    What about over-the-counter use?

    This paper looks at patients prescribed painkillers rather than people buying them in a shop or taking them without medical advice.

    And it suggests higher doses than those often recommended for one-off use (for example more than 1200mg of ibuprofen a day) carry some of the greatest risks.

    But Prof Helen Stokes-Lampard said the study should also raise awareness among patients who self-medicated with Nsaids to treat their pain.

    According to NHS advice, people should generally take the lowest dose of Nsaids for the shortest time possible.

    And if people find they need to take Nsaids very often or are taking higher doses than recommended, medical advice should be sought.

    How big are the risks?

    Independent researchers say one of the main pitfalls of the study is it does not clearly spell out what the absolute risk - or the baseline risk of people having a heart attacks - is.

    And they say without an understanding of the baseline, it is then hard to judge the impact of any possible increase in risk.

    Meanwhile, Prof Stephen Evans, of the London School of Hygiene and Tropical Medicine, said though the study indicated that even a few days' use was associated with an increased risk, it might not be as clear as the authors suggested.

    He added: "The two main issues are that the risks are relatively small, and for most people who are not at high risk of a heart attack, these findings have minimal implications."
    http://www.bbc.com/news/health-39858179
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner



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  20. #17
    Piece also notes:

    But he added: "Despite the large number of patients involved, some aspects do still remain pretty unclear.

    "It remains possible that the painkillers aren't actually the cause of the extra heart attacks."

    He said if, for example, someone was prescribed a high dose of a painkiller because of severe pain, and then had a heart attack in the following week, it would be "pretty hard" to tell whether the heart attack had been caused by the painkiller or by whatever was the reason for prescribing it in the first place,

    It could even be down to something else entirely, he said.

    Prof McConway also pointed out that other influences on heart health - such as smoking and obesity - could not be taken into account fully and could be partly to blame.

  21. #18
    Ibuprofen Kills Thousands Each Year, So What Is The Alternative?

    By: Sayer Ji

    A recent Reuters' article opened with the following stunning sentence:

    "Long-term high-dose use of painkillers such as ibuprofen or diclofenac is 'equally hazardous' in terms of heart attack risk as use of the drug Vioxx, which was withdrawn due to its potential dangers, researchers said."

    The 2004 Vioxx recall, as you may remember, was spurred by the nearly 30,000 excess cases of heart attacks and sudden cardiac deaths caused by the drug between 1999-2003. Despite the fact that scientific research had accumulated as early as 2000 linking Vioxx to increased heart attacks and strokes, the drug's manufacturer Merck, and the FDA, remained silent as the death toll steadily increased.

    The Reuters report focused on new research published in Lancet indicating the risk of heart attack increases as much as a third and the risk of heart failure doubles among heavier users of NSAID drugs.

    INFLAMED: Our Default Bodily State
    Why are so many folks taking NSAID drugs like ibuprofen anyway?

    Pain and unhealthy levels of inflammation are fast becoming default bodily states in the industrialized world. While in most cases we can adjust the underlying pro-inflammatory conditions by altering our diet, and reducing stress and environmental chemical exposures, these approaches take time, discipline and energy, and sometimes we just want the pain to stop now. In those often compulsive moments we find ourselves popping an over-the-counter pill to kill the pain.

    The problem with this approach is that, if we do it often enough, we may kill ourselves along with the pain...

    Ibuprofen really is a perfect example of this. As mentioned above, this petrochemical-derivative has been linked to significantly increased risk of heart attack and increased cardiac and all-cause mortality (when combined with aspirin), with over two dozen serious adverse health effects, including:

    Anemia[1]
    DNA Damage[2]
    Hearing Loss[3]
    Hypertension[4]
    Influenza Mortality[5]
    Miscarriage[6]

    Ibuprofen is, in fact, not unique in elevating cardiovascular disease risk and/or mortality. The entire category of non-steroidal anti-inflammatory drugs (NSAIDs) appears to have this under-recognized dark side; cardiovascular disease and cardiac mortality score highest on the list of over 100 unintended adverse health effects associated with their use. See also our analysis of the rarely acknowledged dark side to aspirin: The Evidence Against Aspirin And For Natural Alternatives.

    So, what does one do? Pain is pain. Whether it happens to you, or you witness it in another (which can be worse), finding relief is a top priority.



    Research on Natural Alternatives To Ibuprofen

    Here is some evidence-based research on alternatives to ibuprofen, sourced from the National Library of Medicine:

    Ginger – A 2009 study found that ginger capsules (250 mg, four times daily) were as effective as the drugs mefenamic acid and ibuprofen for relieving pain in women associated with their menstrual cycle (primary dysmenorrhea). [7]

    Topical Arnica – A 2007 human study found that topical treatment with arnica was as effective as ibuprofen for hand osteoarthritis, but with lower incidence of side effects.[8]

    Combination: Astaxanthin, Ginkgo biloba and Vitamin C - A 2011 animal study found this combination to be equal to or better than ibuprofen for reducing asthma-associated respiratory inflammation.[9]

    Chinese Skullcap (baicalin) – A 2003 animal study found that a compound in Chinese skullcap known as baicalin was equipotent to ibuprofen in reducing pain.[10]

    Omega-3 fatty acids: A 2006 human study found that omega-3 fatty acids (between 1200-2400 mg daily) were as effective as ibuprofen in reducing arthritis pain, but with the added benefit of having less side effects.[11]

    Panax Ginseng – A 2008 animal study found that panax ginseng had analgesic and anti-inflammatory activity similar to ibuprofen, indicating its possible anti-rheumatoid arthritis properties.[12]

    St. John's Wort – A 2004 animal study found that St. John's wort was twice as effective as ibuprofen as a pain-killer.[13]

    Anthrocyanins from Sweet Cherries & Raspberries – A 2001 study cell study found that anthrocyanins extracted from raspberries and sweet cherries were as effective as ibuprofen and naproxen at suppressing the inflammation-associated enzyme known as cyclooxygenase-1 and 2.[14]

    Holy Basil – A 2000 study found that holy basil contains compounds with anti-inflammatory activity comparable to ibuprofen, naproxen and aspirin.[15]

    Olive Oil (oleocanthal) – a compound found within olive oil known as oleocanthal has been shown to have anti-inflammatory properties similar to ibuprofen.[16]

    There are, of course, hundreds of additional substances which have been studied for their pain-killing and/or anti-inflammatory effects, and there are also aromatherapeutic approaches that do not require the ingestion of anything at all, but there is also a danger here. When we think of taking an alternative pain-killer to ibuprofen, we are still thinking within the palliative, allopathic medical model: suppress the symptom, and go on about our business. It would behoove us to look deeper into what is causing our pain. And when possible, remove the cause(s). And that often requires a dramatic dietary shift away from pro-inflammatory foods, many of which most Westerners still consider absolutely delightful, e.g. wheat, dairy, nighshade vegetables and even wheat-free grains, etc.

    [1] Direct cytotoxicity of non-steroidal anti-inflammatory drugs in acidic media: model study on human erythrocytes with DIDS-inhibited anion exchanger. Pharmazie. 2002 Dec;57(12):848-51. PMID: 12561250

    [2] Genotoxicity of ibuprofen in mouse bone marrow cells in vivo. Drug Chem Toxicol. 2012 Jan 27. Epub 2012 Jan 27. PMID: 22283434

    [3] Analgesic use and the risk of hearing loss in men. Am J Med. 2010 Mar;123(3):231-7. PMID: 20193831

    [4] Effect on blood pressure of lumiracoxib versus ibuprofen in patients with osteoarthritis and controlled hypertension: a randomized trial. J Hypertens. 2008 Aug;26(8):1695-702. PMID: 18622250

    [5] The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analysis. J R Soc Med. 2010 Oct;103(10):403-11. PMID: 20929891

    [6] Taking non-aspirin NSAIDs in early pregnancy doubles risk of miscarriage, study shows. BMJ. 2011 ;343:d5769. Epub 2011 Sep 9. PMID: 21908536

    [7] Comparison of effects of ginger, mefenamic acid, and ibuprofen on pain in women with primary dysmenorrhea. J Altern Complement Med. 2009 Feb 13. PMID: 19216660

    [8] Choosing between NSAID and arnica for topical treatment of hand osteoarthritis in a randomised, double-blind study. Rheumatol Int. 2007 Apr;27(6):585-91. Epub 2007 Feb 22. PMID: 17318618

    [9] Summative interaction between astaxanthin, Ginkgo biloba extract (EGb761) and vitamin C in suppression of respiratory inflammation: a comparison with ibuprofen. Phytother Res. 2011 Jan;25(1):128-36. PMID: 20632299

    [10] The antiinflammatory and analgesic effects of baicalin in carrageenan-evoked thermal hyperalgesia. Anesth Analg. 2003 Dec;97(6):1724-9. PMID: 14633550

    [11] Omega-3 fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain. Surg Neurol. 2006 Apr;65(4):326-31. PMID: 16531187

    [12] Potential analgesic and anti-inflammatory activities of Panax ginseng head butanolic fraction in animals. Food Chem Toxicol. 2008 Dec;46(12):3749-52. Epub 2008 Oct 1. PMID: 18930781

    [13] Antinociceptive activity of methanolic extracts of St. John's Wort (Hypericum perforatum) preparation. Pak J Pharm Sci. 2004 Jul;17(2):13-9. PMID: 16414593

    [14] Cyclooxygenase inhibitory and antioxidant cyanidin glycosides in cherries and berries. Phytomedicine. 2001 Sep;8(5):362-9. PMID: 11695879

    [15] Antioxidant and cyclooxygenase inhibitory phenolic compounds from Ocimum sanctum Linn. Phytomedicine. 2000 Mar;7(1):7-13. PMID: 10782484

    [16] Molecular mechanisms of inflammation. Anti-inflammatory benefits of virgin olive oil and the phenolic compound oleocanthal. Curr Pharm Des. 2011 ;17(8):754-68. PMID: 21443487
    http://www.greenmedinfo.com/blog/ibu...t-alternatives
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  22. #19
    Quote Originally Posted by Firestarter View Post
    K.B. Sondergaard et al – Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study (2016): https://academic.oup.com/ehjcvp/arti...ry-drug-use-is


    Here’s the figure that shows the increased risk of a heart attack caused by Ibuprofen and Diclofenac.
    Since the last post of Donnnay, I checked this thread 4 times, every time the picture in post #3 was missing in action which I then inserted again. Here's a picture of post #3 including the figure...
    Do NOT ever read my posts. Google and Yahoo wouldn’t block them without a very good reason: Google-censors-the-world/page3

    The Order of the Garter rules the world: Order of the Garter and the Carolingian dynasty

  23. #20
    Quote Originally Posted by Zippyjuan View Post
    Piece also notes:

    It remains possible that the painkillers aren't actually the cause of the extra heart attacks."
    Yes, that was in the article for all to read. Nice try being contrary as usual.

    Science like this is interested in the probabilities; hence, the article reads, "a commonly consumed painkiller, wrongly considered "harmless" by millions, is probably causing thousands of deaths from cardiac arrest each year. [emphasis mine]."


    Yes, many things are possible. It is possible that the sky will fall tomorrow, but I would say that is not probable. The word "possible" is often included as a standard caveat in research. It is also included and even emphasized when the researchers' findings are opposite their expectations. Researchers also like caveats when they just don't like the results.
    Last edited by NorthCarolinaLiberty; 06-29-2017 at 03:59 PM.
    Quote Originally Posted by TheCount View Post
    ...I believe that when the government is capable of doing a thing, it will.
    Quote Originally Posted by Influenza View Post
    which one of yall fuckers wrote the "ron paul" racist news letters
    Quote Originally Posted by Dforkus View Post
    Zippy's posts are a great contribution.




    Disrupt, Deny, Deflate. Read the RPF trolls' playbook here (post #3): http://www.ronpaulforums.com/showthr...eptive-members

  24. #21
    Is Ibuprofen As Deadly As Vioxx?

    Saturday, July 1st 2017 at 4:15 am
    Written By: GreenMedInfo Research Group



    Our medicalized approach to pain may be putting us in harms way. However, there are safe, natural approaches that can ease painful conditions.

    How Coxibs Killed Tens of Thousands

    Non-steroidal anti-inflammatory drugs (NSAIDs), which include over-the-counter pharmaceuticals such as ibuprofen, naproxen, and aspirin, rank among the most widely used pharmaceuticals worldwide. Their chief mechanism of action is inhibition of two forms of cyclo-oxygenase (COX), namely COX-1 and COX-2 (1). Also known as prostaglandin-endoperoxide synthase (PTGS), COX is responsible for the production of downstream mediators of pain and inflammation, such as thromboxane and prostaglandins. Due to their suppression of prostaglandins, which exert protective roles in the gastrointestinal tract, one of the most frequent adverse effects of NSAIDs is irritation of the gastric mucosa.

    Thus, newer generation selective COX-2 drugs, known as the coxibs, were introduced in the 1990s to mitigate the risk of peptic ulceration that results from COX-1 suppression. By 2004, coxibs had dominated the prescription drug market for NSAIDs, with worldwide sales of approximately $10 billion (2). Their development was based on the premise that COX-1 was the source of the cytoprotective prostaglandins in the gastric epithelium, whereas COX-2 was the source of the inflammatory mediators, prostaglandins E2 and I2 (2). However, as early as 1999, scientists had reported that coxibs inhibit generation of prostaglandin I2, the primary product of COX in the endothelium, responsible for reducing platelet aggregation and proliferation of vascular smooth muscle cells and for inducing vascular vasodilation (2).

    Traditional NSAIDs inhibit both prostaglandin I2 and the major COX-1 product of platelets, thromboxane A2. Thromboxane A2 opposes the actions of prostaglandin I2, causing vasoconstriction, coagulation, and vascular proliferation (2). Thus, unlike traditional NSAIDs, coxibs leave thromboxane A2 production unopposed, such that,

    “Suppression of the COX-2-dependent formation of prostaglandin I2 by coxibs might predispose patients to myocardial infarction or thrombotic stroke…depression of prostaglandin I2 formation might be expected to elevate blood pressure, accelerate atherogenesis, and predispose patients receiving coxibs to an exaggerated thrombotic response or to the rupture of an atherosclerotic plaque” (2, p. 1709).
    Other researchers echoed these warnings, stating, “By decreasing vasodilatory and antiaggregatory prostacyclin production, COX-2 antagonists may lead to increased prothrombotic activity” and consequently raise risk for thrombotic cardiovascular events (4). This mechanism of action panned out in placebo-controlled trials, which unequivocally revealed that despite their lower gastrointestinal toxicity, coxibs were correlated with an increased risk of atherothrombotic vascular events (3).

    In fact, the multi-center, randomized, placebo-controlled, double-blind trial that led Merck to withdraw Vioxx from the market demonstrated that thromboembolitic event rates were double for the coxib rofecoxib, also known as Vioxx, compared to placebo (5). However, the incidence of myocardial infarction observed in those receiving Vioxx was increased by a factor of five (2). The safety of Vioxx was had been called into question ever since data from the Vioxx gastrointestinal outcomes research (VIGOR) study, submitted by Merck to the US Food and Drug Administration (FDA) in 2000, was re-analyzed. Mukherjee et al. (2001) found that Vioxx increased the risk of developing a myocardial infarction, cardiac thrombus, unstable angina, resuscitated cardiac arrest, ischemic stroke, transient ischemic attack, or sudden and unexplained death, by 2.38 times compared to a non-selective NSAID, Naproxen (4). Rather than attributing enhanced cardiac risk to Vioxx, Merck maintained that Naproxen was cardioprotective to explain the disparity in cardiac events, a claim which remained to be proven.

    Even after Dr. Eric Topol, chairman of the Cleveland Clinic’s department of cardiovascular medicine and co-author of the aforementioned study, called for trials to ascertain whether Vioxx and other coxibs increased cardiovascular risk, Merck and Pfizer, the latter of which manufacturers Celebrex, rejected their requests (6). In an interview, Dr. Topol asserts that industry scientists even paid him a visit in attempts to persuade him not to publish his findings (6). Thousands of internal industry documents revealed that Merck “misrepresented study results and used ghostwriters to prepare manuscripts for journal publication,” and that they shelved unfavorable company-funded studies that revealed cardiac risk (7, 8). Most damning was a study at Kaiser Permanente underwritten by the FDA, which revealed that high doses of Vioxx increased the risk of heart disease by 3.7 times (6).

    As a result of criminal malfeasance, in 2011, the pharmaceutical company Merck was ordered to pay $950 million over Vioxx, including $202 million to state Medicaid agencies and $426 million to the federal government to settle civil suits contending that its illegal marketing tactics convinced physicians to prescribe Vioxx and bill the government (9). Also part of that figure was the $321 million in criminal fines that Merck was ordered to pay resulting from their guilty plea to illegally introducing the drug into interstate commerce (9). These figures were in addition to the $2.85 billion Merck paid in 2007 to settle 27,000 lawsuits by patients, survivors, and their relatives who suffered injury or mortality after taking Vioxx (9). Further, Merck was also held culpable in a class-action securities lawsuit by investors who claimed they were defrauded by the drug maker and lost tens of billions of dollars in shareholder value when the drug was withdrawn (10). Altogether, over 20 million Americans took Vioxx, and conservative estimates by the FDA attest that the drug caused more than 27,000 deaths and heart attacks between 1999 and 2003 (6, 11).

    Are Traditional NSAIDs Any Safer?

    As a consequence, traditional non-selective NSAIDs (tNSAIDs) came to be perceived as safer in terms of cardiovascular effects than coxibs. However, this superior safety is an illusion, since meta-analyses of observational studies and randomized trials have underscored that both coxibs and tNSAIDs are associated with enhanced cardiovascular risk as well as gastrointestinal problems (12, 13, 14).

    A previous meta-analysis of placebo-controlled trials illuminated that tNSAIDs might predispose individuals to atherothrombotic events, depending on the extent and duration of suppression of platelet COX-1 inhibition (12). Other than Naproxen, high-dose tNSAID regimens that elicited transient effects on platelet COX-1 have been associated with statistically significant increases in vascular hazard (12). In addition, in a meta-analysis of 31 trials including 116,429 subjects, Trelle et al. (2011) found that both selective and non-selective NSAIDs significantly increased risk of heart attack, stroke, and cardiovascular death (14). As a result of these findings, the FDA required that all NSAIDs carry a black box warning of cardiovascular disease risk (3).

    Although the European Medicines Agency’s Committee for Medicinal Products for Human Use (CHMP) declared that coxibs are contraindicated for patients with pre-existing stroke, coronary heart disease, or risk factors for these conditions, they have not made the same decree regarding tNSAIDs (3). Because of biases inherent in some of the correlational studies, “There has been uncertainty about the nature and magnitude of these risks, and the relative safety of different NSAID regimens, especially in those at increased risk of coronary heart disease” (3, p. 775). Therefore, in order to quantify the cardiovascular and gastrointestinal risks of NSAID regimens, a recent meta-analysis examined individual participant and tabular data from randomized trials of NSAIDs (3).

    Researchers undertook a meta-analysis of 280 trials of tNSAIDs use versus placebo, consisting of 124,513 subjects and 68,342 person-years, and 474 trials comparing one NSAID regimen to another, comprised of 229,296 participants and a total of 165,456 person-years (3). The end-points analyzed were major coronary events, including non-fatal myocardial infarction or coronary death, and major vascular events, including non-fatal myocardial infarctions, non-fatal strokes, or vascular deaths (3). Researchers also examined other cardiovascular outcomes, including stroke, congestive heart failure, and mortality, as well as upper gastrointestinal complications including bleeds, obstructions, and perforations (3). The authors mention that the vast majority primary outcomes occurred in trials that used either a coxib or a high-dose NSAID, such as 1000 mg a day of naproxen, 150 mg a day of diclofenac, or 2400 mg a day of ibuprofen (3).

    Compared to controls, risk of major vascular event was increased by approximately one-third in subjects randomized to receive a coxib or the tNSAID diclofenac, owing mainly to a three-quarters increased risk in major coronary events (3). More surprising, however, was that Ibuprofen, which is still perceived as relatively benign by most health care providers, significantly increased incidence of major coronary events (3). Moreover, although tNSAIDs did not significantly increase risk of stroke, “The risk of hospitalization due to heart failure was roughly doubled by all tNSAID regimens studied,” with Ibuprofen posing the highest risk (3, p. 773).

    Further, both coxibs and diclofenac significantly increased risk of vascular death, whereas the increased risk of vascular death due to Ibuprofen did not reach statistical significance (3). Risk of overall mortality was increased by 25% for those administered a coxib; however, “Despite a clear excess of vascular deaths the corresponding excess was not significant for diclofenac,” or for ibuprofen or naproxen (3). In addition, although coxibs are advertised as posing less gastrointestinal risk, the meta-analysis showed that they increased risk of gastrointestinal complications, primarily bleeds, with higher doses yielding larger proportional excesses in risk of ulceration (3). As expected, the tNSAIDs diclofenac, ibuprofen, and naproxen exhibited the highest risk of gastrointestinal tract complications, doubling to quadrupling risk of upper gastrointestinal complications (3). Unambiguous evidence appeared that tNSAID use leads to higher rates of early risk of upper gastrointestinal complications as well (3).

    The study authors conclude that tNSAIDs such as high-dose diclofenac, and possibly ibuprofen, exert vascular risks comparable to coxibs such as celecoxib, or Celebrex, and rofecoxib, or Vioxx, etoricoxib, or Arcoxia, and lumiracoxib, or Prexige (3). Importantly, researchers state that, although limited data existed for subjects with a history of atherosclerosis, “The proportional effects of coxibs and tNSAIDs seemed similar irrespective of baseline characteristics, and in particular were similar at all levels of risk of major vascular events” (3, p. 777).

    Naproxen was the only tNSAID that did not increase risk of major vascular or coronary events, although it did almost double risk of hospitalization due to heart failure along with every other NSAID regimen (3). The authors attribute this possible advantage to the prolonged and intense COX-1 inhibition by naproxen, which is sufficient in magnitude to restrict platelet thromboxane biosynthesis, thus resulting in platelet inhibition, which mitigates vascular risks of COX-2 inhibition in some individuals (47). However, they still caution that this supposed advantage of naproxen may not persist with long-term use, and note that naproxen dramatically increases incidence of upper gastrointestinal complications (3, p. 777).

    Detriment to the Gut Barrier: Another Reason to Avoid NSAIDs

    If the cardiac risks were not enough to put the NSAIDs-are-safe myth to bed for good, even low-dose, short-term administration of NSAIDs adversely affects the small intestine, culminating in enhanced gut inflammation, intestinal permeability, ulcerations, and mucosal erosions (15). Endoscopic examinations have revealed that NSAIDs produce mucosal lesions along every segment of the gastrointestinal tract, especially the stomach and small intestine (16). After just two week courses of slow-release diclofenac or naproxen, small-bowel mucosal injuries were present in 68% to 75% of patients and in 55% of patients, respectively (17, 18). Similarly, large lesions and erosions appeared in 60% of healthy young individuals taking enteric-coated aspirin for only 7 days (19). Worse yet, small intestinal lesions often remain after NSAID discontinuation (20).

    Although the effects of NSAID-inflicted small intestinal damage remains to be determined, possible implications include dyspepsia or irritable bowel syndrome, inflammatory bowel diseases including Crohn’s disease or ulcerative colitis, diverticulitis, exacerbation of pre-existing chronic liver and kidney diseases, and occult gastrointestinal bleeding and resultant microcytic anemia (16).

    NSAID enteropathy is mediated by changes in the microbiota and pathophysiological mechanisms involving innate inflammatory cascades, as illustrated by studies that show 100% protection from indomethacin-induced ulcerations in germ-free animals or animals pretreated with antibiotics (21, 22). As elucidated by Marlicz and colleagues (2014), “It is possible that NSAID-induced mucosal damage allows for deeper microbial penetration and subsequent interaction with components of the innate immune system through activation of the Toll-like receptor 4 intestinal pathways” (16). These pathophysiological changes lead to mast cell degranuation, neutrophil recruitment, and release of pro-inflammatory cytokines such as tumor-necrosis factor-alpha (TNF-α ) and monocyte chemoattractant protein-1 (MCP-1) (23).

    Notably, NSAIDs have been observed to induce pathologic paracellular intestinal permeability, or leaky gut syndrome (16). According to the work of Dr. Alessio Fasano, intestinal permeability is prerequisite for the development of autoimmune disease, along with genetic predisposition and an environmental trigger (24). Breach of the mucosal barrier enables undigested food proteins, bacterial byproducts, and toxicants to traverse the gut lining and incite an inflammatory response that can result in the immune system becoming misdirected against self (24).

    When combined with proton pump inhibitors (PPIs) such as Prilosec or Prevacid, even low-dose NSAIDs can cause gut mucosal injury as well as bleeding and anemia (16). Marlicz and colleagues (2014) state that the use of PPIs should be conceived as an independent risk factor for NSAID-associated enteropathy, and discuss that, “The frequent use of PPIs can exacerbate NSAID-induced small intestinal injury by altering intestinal microbiota” (16, p. 1699). This is alarming in light of the recommendations by professional societies of gastroenterology, rheumatology, and cardiology, all of which promote the co-administration of NSAIDs with PPIs to minimize NSAID-related gastrointestinal complications (25, 26, 27). By altering the small intestinal microbiome, PPIs may accelerate the injurious effects of NSAIDs on the intestinal mucosa and lead to complications such as anemia (28, 29).

    NSAIDs likewise have been observed to decrease concentrations of beneficial commensal flora in our gut, including bifidobacteria and lactobacilli populations (30, 31). In addition, NSAIDs increase concentrations of gram-negative bacteria, which generate an endotoxin known as lipopolysaccharide (LPS) that can translocate across the gut barrier and generate a pro-inflammatory metabolic milieu (16). According to Marlicz and colleagues, “There is mounting evidence that disturbances in the interplay between bacteria and host at the mucosal level in the gut affect the gut-liver axis and contribute to the development of low-grade inflammation, metabolic endotoxemia, obesity, metabolic liver disorders (nonalcoholic fatty liver disease [NAFLD] and nonalcoholic steatohepatitis), and some cancers” (16, p. 1700). Metabolic endotoxemia is likewise associated with coronary heart disease, carotid atherosclerosis, fibrogenesis, adverse neurocognitive changes, increased mortality in chronic kidney disease, enhanced vulnerability to infection, and altered pain perception (16).

    Natural Alternatives to Dangerous NSAIDs

    As extensively catalogued in GreenMedInfo’s databases, there are a plethora of nontoxic substances with analgesic properties that can be used in place of NSAIDs for natural pain management.

    Dysmenorrhea

    For menstrual pain, 250 mg capsules of ginger rhizome powder taken four times a day was found to be as effective as 250 mg mefenamic acid or 400 mg ibuprofen capsules, in relieving menstrual pain (32). Another study demonstrated that 25 drops of thyme vulgaris essential oil given every six hours was as effective as 200 mg of ibuprofen administered at the same dosing frequency (33). Thyme contains active constituents such as thymol and carvacrol which have anti-spasmodic properties that improve menstrual cramping (33).

    Osteoarthritis

    A combination of two flavonoids, baicalin from Chinese skullcap and catechin from green tea, was found to be as effective as naproxen for osteoarthritis of the knee in a randomized, double-blind pilot study, without the edema and non-specific musculoskeletal discomfort that accompanied naproxen administration (34). In another multi-center, prospective, open-label study, osteoarthritis patients were given 1300 mg capsules of bromelain, a proteolytic enzyme from pineapple stems, combined with devil’s claw and turmeric, two to three times a day depending on pain severity (35). Both acute and chronic pain patients experienced statistically significant improvements in pain after fifteen or sixty days of follow-up, respectively (35). In fact, the researchers suggest this formula of plant extracts as a safe alternative to NSAIDs for patients suffering from degenerative joint diseases (35).

    Migraines

    Patients with migraine disorders have been shown to be magnesium deficient. A meta-analysis of 21 randomized controlled trials concluded that intravenous magnesium infusion reduces migraine attacks, whereas oral magnesium alleviates the frequency and intensity of migraines (36). Further, feverfew extract, which contains compounds called parthenolides which exert anti-migraine effects, has been shown to significantly reduce migraine frequency from 4.76 to 1.9 migraine attacks per month (37). Another herb effective in migraine prophylaxis is butterbur, which elicited a 48% decrease in migraine frequency when subjects received 75 mg twice a day for four months, compared to an only 26% decrease in the control group (38).

    Back Pain

    White willow bark, the botanical from which aspirin was originally derived, has anti-inflammatory, anti-pyretic, and analgesic qualities, owing to active constituents such as salicin, polyphenols, and flavonoids (39). In particular, the anti-inflammatory mechanism of willow bark extract occurs via down-regulation of inflammatory mediators TNF-α and nuclear factor-kappa B (NFkB) (39). A systematic review demonstrated that white willow bark exerts a dose-dependent analgesic effect that is not inferior to rofecoxib for low back pain (40).

    Functional Foods

    Wild lettuce of the Lactuca virosa and Cichorium intybus species, as well as other members of the family Asteraceae such as chicory root, can be incorporated into a food-as-medicine approach to pain management. These wild lettuce varieties contain guaiane-type sesquiterpene lactones including lactucin and its ester derivative, lactucopicrin (41). According to Wesolowska et al. (2006), “The latex released from damaged lactifers of leaves or stems of the flowering plants, when left in the open, dries into a brown gummy product, known as lactucarium or lettuce opium,” which exhibits antitussive, sedative, and analgesic properties (41, p. 254). These compounds, which have an extensive history of use in traditional Ayurvedic and Unani medical systems, induce pain-relieving effects comparable to ibuprofen in animal models (41, 42). Probable mechanisms include inhibition of NFkB, prostaglandin E2, and COX-2 expression (41).

    Lastly, tart cherry anthocyanins, administered at 400 mg/kg, suppressed inflammation as effectively as the NSAID indomethacin in an animal model (43). Moreover, an in vitro study found that anthocyanins from sweet cherries and raspberries were as effective as naproxen and ibuprofen at inhibiting COX-1 and COX-2 enzymes (44). Another randomized, double-blind, placebo-controlled trial of healthy runners found that ingesting 355 mL bottles of tart cherry juice twice daily for seven days preceding a strenuous running event and on the day of the event minimized post-race muscle pain (45). According to researchers, “These data suggest that tart cherry anthocyanins may have a beneficial role in the treatment of inflammatory pain” (43, p. 181).

    Practice Root Cause Resolution Medicine

    According to philosopher Ivan Illich, we have become divorced from the metaphysical meaning of pain as an inevitable component of the subjective human experience and instead seek to artificially anesthetize ourselves against its presence (46). Pain has become medicalized within our cultural landscape, such that pain is perceived as an emergent contingency requiring heroic measures to be annihilated (46). The social determinants of pain, as well as the value of pain as an intrinsic and intimate facet of human life, go unrecognized, as “medical civilization focuses primarily on pain as a systemic reaction that can be verified, measured, and regulated” (46).

    Instead of seeking to extinguish pain whenever it manifests, we should search for the meaning in the pain, and the message that our physical, psychic and social body is attempting to communicate (46). We would be better served by unearthing the root causes of our physical pain—whether they be micronutrient deficiencies, toxicant burden, or deviance from the ancestral lifestyles to which we are evolutionary accustomed—and by adopting the ancient wisdom of traditional cultures (46). According to Illich, pain is made tolerable by its integration into a meaningful context: “Traditional cultures confront pain, impairment, and death by interpreting them as challenges soliciting a response from the individual under stress” (46).

    References
    1. Fitzgerald, G.A. (2001). The coxibs, selective inhibitors of cyclooxygenase-2. New England Journal of Medicine, 345, 433-442.

    2. Fitzgerald, G.A. (2004). Coxibs and cardiovascular disease. The New England Journal of Medicine, 351(17), 1709-1711.

    3. Coxib and traditional NSAID Trialists’ (CNT) Collaboration et al. (2013). Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. Lancet, 382(9849), 769-779. doi: 10.1016/S0140-6736(13)60900-9

    4. Mukherjee, D., Nissen, S.E., & Topol, E.J. (2001). Risk of Cardiovascular Events Associated With Selective COX-2 Inhibitors. Journal of the American Medical Association, 286(8), 954-959. doi:10.1001/jama.286.8.954doi:10.1001/jama.286.8.954

    5. Singh, D. (2004). Merck withdraws arthritis drug worldwide. The British Medical Journal, 329. doi: https://doi-org.uws.idm.oclc.org/10.1136

    6. Berenson et al. (2004). Despite Warnings, Drug Giant Took Long Path to Vioxx Recall. The New York Times. Retrieved from http://www.nytimes.com/2004/11/14/bu...xx-recall.html

    7. Tanne, J.H. (2008). Merck used ghostwriters and selective data in Vioxx publications, JAMA says. British Medical Journal, 336(849). doi: https://doi.org/10.1136/bmj.39553.344965.DB

    8. Steenhuysen, J. (2009). Vioxx risks could have been detected earlier: study. Reuters. Retrieved from http://www.reuters.com/article/us-vi...5AM4MV20091123

    9. Willson, D. (2011). Merck to Pay $950 Million Over Vioxx. The New York Times. Retrieved from http://www.nytimes.com/2011/11/23/bu...ioxx-case.html

    10. The Associated Press. (2010). Supreme Court Allows Investors to Sue Merck Over Vioxx. The New York Times. Retrieved from http://www.nytimes.com/2010/04/28/bu...8bizcourt.html

    11. ConsumerAffairs. (2004). The Food and Drug Administration (FDA) estimates that Vioxx may have contributed to 27,785 heart attacks. Retrieved from https://www.consumeraffairs.com/news...estimates.html

    12. Kearney et al. (2006). Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drug increase the risk of atherothrombosis? Meta-analysis of randomised trials. British Medical Journal, 332, 1302-1308.

    13. McGettigan, P., & Henry, D. (2011). Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Medicine, 8, e1001098.

    14. Trelle et al. (2011). Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. British Medical Journal, 342, c7086.

    15. Sostres, C., Gargallo, C.J., & Lanas, A. (2013). Nonsteroidal anti-inflammatory drugs and upper and lower gastrointestinal mucosal damage. Arthritis Research Therapies, 15(Suppl 3), S3.

    16. Marlicz et al. (2014). Nonsteroidal anti-inflammatory drugs, proton pump inhibitors, and gastrointestinal injury: contrasting interactions in the stomach and small intestine. Mayo Clinic Proceedings, 89(12), 1699-1709.

    17. Maiden et al. (2005). A quantitative analysis of NSAID-induced small bowel pathology by capsule endoscopy. Gastroenterology, 128(5), 1172-1178.

    18. Goldstein et al. (2005). Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole and placebo. Clinical Gastroenterology and Hepatology, 3(2), 133-141.

    19. Shiotani et al. (2010). Randomized, double-blind pilot study of gnarly geranylacetone versus placebo in patients taking low dose enteric-coated aspirin: low-dose aspirin-induced small bowel damage. Scandinavian Journal of Gastroenterology, 45(3), 292-298.

    20. Caunedo-Alvarez et al. (2010). Macroscopic small bowel mucosal injury caused by chronic non steroidal anti-inflammatory drugs (NSAIDs) use as assessed by capsule endoscopy. Rev Esp Enferm Dig, 102(2), 80-85.

    21. Kent, T.H., Cardelli, R.M., & Stamler, F.W. (1969). Small intestinal ulcers and intestinal flora in rats given indomethacin. American Journal of Pathology, 54(2), 237-249.

    22. Uejima et al. (1996). Role of intestinal bacteria in ileal ulcer formation in rats treated with a non steroidal anti-inflammatory drug. Microbiology and Immunology, 40(8), 553-560.

    23. Watanbe et al. (2008). Non-steroidal anti-inflammatory drug-induced intestinal damage is Toll like 4 receptor dependent. Gut, 57(2), 181-187.

    24. Fasano, A. (2012). Leaky gut and autoimmune disease. Clinical Reviews in Allergy and Immunology, 42(1), 71-78.

    25. Lanza, F.L., Chan, F.K., & Quigley, E.M. (2009). Practice parameters committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. American Journal of Gastroenterology, 104(2), 728-238.

    26. Bhatt et al. (2008). ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of anti platelet therapy and NSAID use: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. Circulation, 118(18), 1894-1909.

    27. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis and Rheumatology, 46(2), 328-346.

    28. Wallace et al. (2011). Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Gastroenterology, 141(4), 1314-1322.

    29. Endo et al. (2011). Efficacy of Lactobacillus casei treatment on small bowel injury in chronic low-dose aspirin users: a pilot randomized controlled study. Journal of Gastroenterology, 46(7), 894-905.

    30. Bhala et al. (2013). Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. The Lancet, 382(9894), 769-779.

    31. Montenegro et al. (2014). Non steroidal anti-inflammatory drug induced damage on lower gastro-intestinal tract: is there an involvement of microbiota? Current Drug Safety, 9(3), 196-204.

    32. Ozgoli, G., Goli, M., & Moattar, F. (2009). Comparison of effects of ginger, mefenamic acid, and ibuprofen on pain in women with primary dysmenorrhea. Journal of Alternative and Complementary Medicine, 15(2), 129-132. doi: 10.1089/acm.2008.0311.

    33. Salmalian et al. (2014). Comparative effect of thymus vulgaris and ibuprofen on primary dysmenorrhea: A triple-blind clinical study. Caspian Journal of Internal Medicine, 5(2), 82-88.

    34. Levy et al. (2009). Flavocoxid is as effective as naproxen for managing the signs and symptoms of osteoarthritis of the knee in humans: a short-term randomized, double-blind pilot study. Nutrition Research, 29(5), 298-304. doi: 10.1016/j.nutres.2009.04.003.

    35. Conrozier et al. (2014). A Complex of Three Natural Anti-inflammatory Agents Provides Relief of Osteoarthritis Pain. Alternative Therapies in Health and Medicine, 20(Suppl 1), 32-37.

    36. Chiu et al. (2016). Effects of Intravenous and Oral Magnesium on Reducing Migraine: A Meta-analysis of Randomized Controlled Trials. Pain Physician, 19(1), E97-E112.

    37. Diener et al. (2005). Efficacy and safety of 6.25 mg tid feverfew CO2‐extract (MIG‐99) in migraine prevention—a randomized, double‐blind, multicentre, Placebo‐controlled study. Cephalalgia, 25(11), 1031–1041.

    38. Lipton et al. (2004). Petasites hybridus root (butterbur) is an effective preventive treatment for migraine. Neurology, 63(12), 2240-2244.

    39. Shara, M., & Stohs, S.J. (2015). Efficacy and Safety of White Willow Bark (Salix alba) Extracts. Physiotherapy Research, 29(8), 1112-1116. doi: 10.1002/ptr.5377.

    40. Vlachojannis, J.E., Cameron, M., & Chrubasik, S. (2009). A systematic review on the effectiveness of willow bark for musculoskeletal pain. Phytotherapy Research, 23(7), 897-900. doi: 10.1002/ptr.2747.

    41. Wesolowska et al. (2006). Analgesic and sedative activities of lactucin and some lactucin-like guaianolides in mice. Journal of Ethnopharmacology, 107, 254-258.

    42. Gupta, S.K., & Ansari, S.H. (2005). Review on phytochemical and pharmacological aspects of Cichorium intybus L. Asian Journal of Chemistry, 17, 33-36.

    43. Tall et al. (2004). Tart cherry anthocyanins suppress inflammation-induced pain behavior in rat. Brain and Behavior Research, 153(1), 181-188.

    44. Seeram et al. (2001). Cyclooxygenase inhibitory and antioxidant cyanidin glycosides in cherries and berries. Phytomedicine, 8(5), 362-369.

    45. Kuehl et al. (2010). Efficacy of tart cherry juice in reducing muscle pain during running: a randomized controlled trial. Journal of International Society of Sports Nutrition, 7, 17. doi: 10.1186/1550-2783-7-17.

    46. Illich, I. (1974). Medical Nemesis: The Expropriation of Health. New York: Pantheon Books.

    47. Capone et al. (2004). Clinical pharmacology of platelet, monocyte, and vascular cyclooxygenase inhibition by naproxen and low-dose aspirin in healthy subjects. Circulation, 109, 1468-1471.
    http://www.greenmedinfo.com/blog/ibuprofen-deadly-vioxx
    Last edited by donnay; 07-01-2017 at 09:58 AM.
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner

  25. #22
    i choose tumeric since this will help your heart and blood relax i drink tumeric mostly every day
    taste like ginger with honey but it help my cholesterol go down

  26. #23
    Quote Originally Posted by Thakildis View Post
    i choose tumeric since this will help your heart and blood relax i drink tumeric mostly every day
    taste like ginger with honey but it help my cholesterol go down
    Yes I have seen proof of that as well.
    “The spirits of darkness are now among us. We have to be on guard so that we may realize what is happening when we encounter them and gain a real idea of where they are to be found. The most dangerous thing you can do in the immediate future will be to give yourself up unconsciously to the influences which are definitely present.” ~ Rudolf Steiner



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