Non-steroidal anti-inflammatory drugs and the risk of atrial fibrillation: A population-based follow-up study British Medical Journal Open April 8, 2014; Vol. 4; No. 4;
Non-steroidal anti-inflammatory drugs and the risk of atrial fibrillation: A population-based follow-up study British Medical Journal Open April 8, 2014; Vol. 4; No. 4;
From the Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands
1) Atrial fibrillation (AF) is a common cardiac arrhythmia, which is associated with increased morbidities (stroke and heart failure), increased mortality and reduced life expectancy.
2) “Several drugs have been associated with an increased risk of AF including nonsteroidal anti-inflammatory drugs.” [NSAIDs]
3) NSAIDs are inhibitors of cyclooxygenase, and are widely used to treat inflammatory conditions and pain. [They block the conversion of the omega-6 fatty acid arachidonic acid into the inflammatory eicosanoid prostaglandin-E2 (PGE2)].
4) Use of NSAIDs is associated with a higher risk of myocardial infarction, stroke and heart failure.
5) The objective of this study was to investigate the association of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of atrial fibrillation in a prospective community based population. The study involved 8,423 participants without atrial fibrillation at baseline. The mean baseline age of the study population was 68.5 years. Follow-up averaged 12.9 years.
6) Current use of NSAIDs increased the risk of atrial fibrillation by 76% compared with never-use.
7) Recent use (within 30 days after discontinuation of NSAIDs) was associated with an increased risk of atrial fibrillation by 84% compared with never-use.
8) “In this study, use of NSAIDs was associated with an increased risk of atrial fibrillation.”
9) Higher dosages of NSAIDs appeared to be associated with a higher risk of atrial fibrillation.
10) “Our results suggest that NSAID use is associated with a higher risk of AF. Current use and recent past use were associated with a higher risk of AF, adjusted for age, sex and cardiovascular risk factors.”
11) The risk of AF was strongest for COX-2 inhibitors. [Celebrex] 1
12) NSAIDs damage the kidneys, increasing blood pressure and thus increasing risk of AF.
13) “In conclusion, we found that use of NSAIDs is associated with an increased risk of AF. Current use and recent past use were especially associated with a higher risk of AF, adjusted for age, sex and cardiovascular risk factors.”
COMMENTS FROM DAN MURPHY: Over the years we have reviewed a number of studies showing adverse effects to NSAID pain medications, including these:
KIDNEY DAMAGE Article Review #50-10 Risk of Kidney Failure Associated with the Use of Acetaminophen, Aspirin, and Nonsteroidal Antiinflammatory Drugs New England Journal of Medicine, December 22, 1994 GASTROINTESTINAL BLEEDING Article Review #33-1999
GASTROINTESTINAL TOXICITY OF NONSTEROIDAL ANTIINFLAMMATORY DRUGS The New England Journal of Medicine, June 17, 1999 Article Review #21-06 Omega-3 Fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti- inflammatory drugs for discogenic pain Surgical Neurology, April 2006
HEART ATTACK / STROKE Article #30-06 NSAID use and the risk of hospitalization for first myocardial infarction in the general population European Heart Journal, May 26, 2006 Article Review #13-12 Cardiovascular safety of non-steroidal anti-inflammatory drugs British Medical Journal, January 11, 2011 Article Review #33-12 Duration of Treatment With Nonsteroidal Anti-Inflammatory Drugs and Impact on Risk of Death and Recurrent Myocardial Infarction in Patients With Prior Myocardial Infarction Circulation; May 21, 2011
DEMENTIA / ALZHEIMER’S Article Review #29-10 Risk of dementia and AD with prior exposure to NSAIDs Neurology, April 22, 2009
HEARING LOSS Article Review #5-12 Analgesic Use and the Risk of Hearing Loss in Men The American Journal of Medicine; March 2010
ERECTILE DYSFUNCTION Article Review #17-12 Regular Nonsteroidal Anti-Inflammatory Drug Use and Erectile Dysfunction Journal of Urology; April 2011 2
Gregg F. Moses DC
1800 Forest Hill Blvd
Ste A 8 – A 10
West Palm Beach, FL 33406
This article adds to the evidence that acetaminophen in Great article reporting that Tylenol and other products are detrimental to the developing fetal brain.
Acetaminophen Use During Pregnancy, Behavioral Problems, and Hyperkinetic Disorders
Journal of the American Medical Association, Pediatrics February 24, 2014
Zeyan Liew, MPH; Beate Ritz, MD, PhD; Cristina Rebordosa, MD, PhD; Pei-Chen Lee, PhD; Jørn Olsen, MD, PhD The primary authors are from the University of California, Los Angeles (UCLA).
KEY POINTS FROM THIS ARTICLE:
These authors evaluated whether prenatal exposure to acetaminophen increases the risk for developing attention-deficit/hyperactivity disorder (ADHD)–like behavioral problems or hyperkinetic disorders (HKDs) in children. Hyperkinetic disorder (HKD) is a particularly severe form of ADHD.
They evaluated 64,322 live- born children and mothers enrolled in the Danish National Birth Cohort.
1) Acetaminophen (paracetamol) [the active ingredient in Tylenol] is the most commonly used medication for pain and fever during pregnancy in many countries.
2) “Acetaminophen (paracetamol) is the most commonly used OTC pain and fever medication, with more than 50% of pregnant women reporting use in the United States and Denmark.”
3) “Acetaminophen is a hormone disruptor, and abnormal hormonal exposures in pregnancy may influence fetal brain development.” “Acetaminophen has endocrine- disrupting properties. Prenatal exposure to endocrine disruptors may affect neurodevelopment and cause behavioral dysfunction.”
4) “Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurobehavioral disorders worldwide, characterized by inattention, hyperactivity, increased impulsivity, and motivational/emotional dysregulation.”
5) There is a rapid increase in childhood neurodevelopmental disorders, including ADHD, over the past decades. Part of the neuropathology of ADHD may already be present at birth, potentially as a consequence of exposures during pregnancy and/or infancy.
6) Maternal acetaminophen use during pregnancy is associated with a higher risk for HKDs and ADHD-like behaviors in children: A)) Hyperkinetic disorders (HKD) by 37% B)) ADHD by 29%
These associations became stronger with increased use of acetaminophen.
17) Acetaminophen is increasingly used as a perceived safe OTC drug during pregnancy.
8) “When women reported having used acetaminophen for 20 or more weeks during pregnancy, the risk for HKD diagnosis in children almost doubled [84%], and the risk for receiving ADHD medication increased by 50% [53%]”
9) “In this large pregnancy cohort with prospective data, children born to mothers who used acetaminophen during pregnancy were at higher risk for receiving a hospital diagnosis of HKD, ADHD medications, or having ADHD-like behaviors during follow-up.”
10) “Acetaminophen can cross the placental barrier and recent studies suggested that maternal use of acetaminophen increases the risk for cryptorchidism (undescended testis) in boys due to its endocrine-disrupting properties.”
11) “Maternal hormones, such as sex hormones and thyroid hormones, play critical roles in regulating fetal brain development, and it is possible that acetaminophen may interrupt brain development by interfering with maternal hormones or via neurotoxicity such as the induction of oxidative stress that can cause neuronal death.”
12) “Maternal infections or immunological factors have previously been linked to childhood ADHD. Acetaminophen is often used by mothers to relieve symptoms due to infections, which may induce confounding by indication in our study.”
13) “Using prospective data from a well-designed large cohort of pregnant women with a long duration of follow-up and registry based outcome assessment, we found that prenatal exposures to acetaminophen may increase the risk in children of receiving a hospital diagnosis of HKD or ADHD medication and of exhibiting ADHD- like behaviors, with higher use frequency increasing risk in an exposure-response manner.”
14) “If these results reflect causal associations, acetaminophen should no longer be considered a safe drug for use in pregnancy.”
Is Vitamin D Deficiency associated with Non Specific Musculoskeletal Pain?
Global Journal of Health Science
Vol. 5, No. 1; 2013; pp. 107-111
Mahnaz Abbasi, Sima Hashemipour, Fatemeh Hajmanuchehri, Amir Mohammad Kazemifar From the Metabolic Diseases Research Center, Qazvin University of Medical Science, Iran. This study evaluated 65 adult patients living in Iran.
The aim of this study is evaluation of the association of musculoskeletal pain with vitamin D deficiency and the response of the patients to vitamin D supplementation.
KEY POINTS FROM THIS STUDY: 1) Vitamin D deficiency is common worldwide. 2) Vitamin D deficiency is associated with non-specific musculoskeletal pain.
3) “Treatment with vitamin D can relieve the pain in a majority of the patients with vitamin D deficiency. Lack of response can be due to an insufficient increase in serum vitamin D concentration.”
4) There are physiologic differences in the intestinal absorption of vitamin D.
5) “Calcium absorption from the GI is reduced in vitamin D deficiency.”
6) “Mild vitamin D deficiency may produce a variety of musculoskeletal pains such as fibromyalgia-like pain, low back pain, and arthralgia.” [Key Point]
7) Those with vitamin D deficiency were treated with 50,000 oral units of vitamin D3 per week [averaging 7,143 IU/day] for 12 weeks and 1,000 mg/day elemental calcium. Three months after end of the treatment they were reassessed for response of their pain to the treatment using the Visual Assessment Score (VAS).
8) 95.4% of the patients had vitamin D deficiency (serum 25 (OH) D concentration less than 50 nmol/l). [50 nmol/l = 20 ng/ml]
9) In 85.5% of those with vitamin D deficiency, supplementation reduced their VAS scores more than 60%.
10) In 75.8% of those with vitamin D deficiency, supplementation completely eliminated their pain.
111) Supplementing with vitamin D significantly raised the serum concentrations of 25(OH)D, and especially in those who responded favorably to the intervention. [This suggests that vitamin D supplementation in higher doses or for longer periods may improve musculoskeletal pain in the poorer responders].
“In patients who respond to vitamin D supplementation, more notable rise in serum concentrations of 25(OH)D was detected.”
12) These authors review literature showing: • 2003: 93% of patients with musculoskeletal pain have vitamin D deficiency. • 2003: 83% of patients with low back pain have vitamin D deficiency. • 2010: 63% of patients with musculoskeletal pain have vitamin D deficiency.
13) Dr. Michael Hollick, MD, [the discoverer of the active form of vitamin D] proposes the following biological mechanism:
• Low vitamin D causes low GI absorption of calcium. • Low calcium increases secretion of parathyroid hormone (PTH). • Increased PTH increases bone osteoclast activity. • Increased osteoclast activity causes lower bone matrix mineralization. • Lower bone matrix mineralization absorbs water. • Bone water absorption causes subperiosteal space edema. • Subperiosteal space edema produces bone pain.
14) This study “confirmed that vitamin D supplementation can relieve the pain in majority of the patients” with musculoskeletal pain.
15) The rise in serum 25 (OH) D concentrations after vitamin D supplementation is variable between patients. Therefore, when musculoskeletal pain patients do not respond to vitamin D supplementation, their serum levels should be retested to assess their effectiveness of that level of supplementation for that individual.
16) It is suggested that the pain associated with vitamin D deficiency is usually sensed on the bone or muscle; bone tenderness is noted at the sternum, tibia, radius or ulna. Low back, thoracic, shoulder, ribs and pelvic pain is also common in those with vitamin D deficiency.
17) The findings of present the study show that vitamin D deficiency is widespread and associated with musculoskeletal pain which is relieve with vitamin D supplementation; “in pain nonresponders reassessment of serum 25(OH) D concentrations is recommended.”
Aluminum Induced Immunoexcitotoxicity in Neurodevelopmental and Neurodegenerative Disorders
Current Inorganic Chemistry 2012, Vol. 2, No. 1
Russell L. Blaylock, MD This article has 85 references
An interesting published article about aluminum and toxicity and autism.
1) Aluminum is a neurotoxin that disrupts cellular function.
2) Aluminum and aluminofluoride compounds activate the brain’s innate immune system (microglia) releasing neurotoxic concentrations of excitotoxins [glutamate / aspartate] and pro-inflammatory cytokines, chemokines and immune mediators. This damages the brain.
3) Excitotoxicity [release of glutamate / aspartate, amino acids that function as excitatory neurotransmitters and in excess kill brain neurons] plays a significant role in the neurotoxic action of a number of metals including aluminum.
4) Metal ions, including aluminum drive crosstalk between cytokine (immune) receptors and glutamate (excitatory) receptors, called immunoexcitotoxicity.
5) Aluminum is the third most abundant metal on earth.
6) Aluminum “is a major neurotoxin and disrupter of neurological function.”
7) Aluminum “is not essential to human metabolism at any concentration.”
8) When humans are exposed to aluminum through the gut (from foods, industrial exposures, drinking water, and drugs), they are very poorly absorbed.
9) When humans are exposed to aluminum via parenteral fluids and/or vaccines, it is “completely absorbed and distributed throughout the body.”[Very Important]
10) Microglia make up 5-15% of the cells in the central nervous system (CNS). When activated, microglia can secrete pro-inflammatory cytokines and excitotoxins. Microglia are activated by trauma, metal toxins, and immune system activation.
11) In neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s, Pick’s, HIV dementia, multiple sclerosis and amyotrophic lateral sclerosis, activated microglia are present in large numbers.
12) Because of its receptors, microglia function as the nervous system’s resident immune cells.
113) Activated microglia release excitatory amino acids, particularly glutamate. Excess glutamate drives excitotoxicity. It is the excitotoxicity that “is the main pathological mechanism for actual damage to neurons and their processes.”
14) The excitotoxic cascade can be triggered by an excessive release of glutamate from microglia and/or astrocytes.
15) “Under conditions of reduced energy [ATP] production, even low levels of glutamate can become excitotoxic.” [Very important: insulin resistance is epidemic in the US, and insulin resistance reduces ATP production]
16) Neurodegeneration is a self-perpetuating chronic cycle: Glutamate activates microglia. Activated microglia produce and release inflammatory cytokines. Inflammatory cytokines stimulate the release of glutamate.
This glutamate activates the microglia.
17) “Microglia and astrocytes are sites of preferential aluminum accumulation and toxic action.” [Aluminum kills microglia and astrocytes, dumping their glutamate]
18) The release of glutamate from dying astrocytes is the main neurotoxic mechanism. [Key Point]
19) There is “indisputable evidence that aluminum can increase the levels of both pro-inflammatory cytokines and glutamate in the brain.”
20) TNF-alpha [a cytokine] is elevated with aluminum exposure and triggers release of glutamate from microglia.
21) The “long-term persistence of aluminum [vaccine] adjuvants in humans results in cognitive dysfunction, affecting visual and verbal memory, as well as executive functions such as attention, working memory and planning.”
22) “The greatest aluminum exposure from vaccines occurs during initial vaccinations soon after birth and during early childhood. Should a child follow the recommended vaccine schedule for the United States, they will receive a total of 5 mg of aluminum by 2 years of age from a total of 17 aluminum-adjuvanted pediatric vaccines. Such repetitive and continuous exposure to aluminum from vaccines could induce prolonged activation of microglia and subsequent release of glutamate and pro-inflammatory cytokines.”
23) Adjuvant-aluminum in vaccines can accumulate in the brain, which “can be extremely detrimental to normal brain development.” [Important]
24) Aluminum exposure from vaccines can directly activate both microglia and astrocytes causing immunoexcitotoxicity.
25) Aluminum in water causes systemic exposure to aluminum causing brain inflammation. “Even very small amounts of aluminum can activate microglia in a pro-inflammatory mode.”
26) Aluminum in combination with copper additively increases brain inflammation.
[Excessive copper is found in 80% of US household water]
27) Aluminum, mercury, lead and manganese all promote inflammation and oxidative stress in the brain.
28) “Aluminum preferentially accumulates in the mitochondria and cell nucleus, which makes this metal very resistant to removal by chelation.”“The difficulty of removing brain intracellular aluminum will lead to its progressive accumulation over a lifetime, eventually reaching a neurotoxic threshold sufficient to trigger neurodegenerative disease processes.”
29) Aluminum accumulates in the mitochondria and disrupts mitochondrial functions leading to energy deficits, increasing the sensitivity of neurons to excitotoxicity, accelerating neuronal damage.
30) Fluoride has a high affinity for aluminum, creating aluminofluoride. Exposure to aluminofluoride complexes has profound detrimental consequences on brain functions, especially as related to glutamate neurotransmission. [Fluoride is found in a lot of US water supplies and tooth paste]
31) Aluminum enhances excitotoxicity by inducing apoptosis of astrocytes. 32) Aluminum dramatically lowers neuronal glutathione levels.
33) “Two forms of aluminum are of special concern: aluminum-L-glutamate and nanoscaled aluminum, both of which have high absorption from the gut and passage into the brain, as well as higher toxicity profiles than aluminum alone.”
34) Aluminum-L-glutamate is capable of crossing the blood brain barrier.
35) Nanoscaled aluminum, used in a growing number of products and vaccines, has higher absorption rates than naturally found aluminum.
36) Immune stimulation by vaccine aluminum adjuvants result in adverse neurological outcomes via activation of microglia, which are the brain’s resident immune cells. “Once activated, microglia become the main source of both pro- inflammatory immune cytokines and excitotoxins such as glutamate. It is the interaction of cytokines and glutamate receptors that leads to immunoexcitotoxicity.”
37) “In the immature and developing brain, immunoexcitotoxicity might lead to a number of neurodevelopmental conditions, such as autism spectrum disorders and seizures. In the mature, and especially the aging brain, these mechanisms can lead to progressive neurodegeneration, as seen with Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis.”
38) “The presence of aluminum deposits within the neurons and glial cells could act as a continuous stimulus for immunoexcitotoxicity.”
39) “There is now sufficient evidence from a great number of studies to call for a re-evaluation of the use of aluminum additives for human consumption or as immune adjuvants.”
COMMENTS FROM DAN MURPHY
Aluminum is never beneficial for biological systems; it is always toxic. It is especially toxic to the brain, and especially for the developing brain. Incredibly, aluminum is commonly used as an adjuvant in vaccines (see Article Review #38- 13: Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure), and this aluminum is “completely absorbed and distributed throughout the body.” Because the blood brain barrier is incomplete until after the second year of life, this aluminum gets into the brain. As noted, US children receive 17 aluminum-adjuvanted pediatric vaccines containing a total of 5 mg of aluminum by 2 years of age. This is unconscionable and crazy, and the official incidence of autism in US children now stands at 1 in 50.
Brain aluminum kills microglia and astrocytes, dumping their glutamate. The glutamate causes excitotoxic damage and death of neurons.
Brain aluminum also damages the neuron’s mitochondria, reducing its ability to produce ATP for energy use. Yet, ATP is required to pump excessive glutamate into the astrocytes where it is held inactive. Consequently, more excitotoxic neuronal damage occurs.
I believe that one should not vaccinate with aluminum adjuvants and that aluminum should be removed from all vaccinations.
Other noted sources for human exposure to aluminum include drinking water (which uses aluminum sulfate [alum]), antiperspirants, aluminum cans, and aluminum cookware.
The bottom line is to understand these concepts, do what we can to avoid aluminum exposure, and increase glutathione production for detoxification purposes.
So the other day a patient and I are talking about getting old and I discussed how free radicals can produce inflammation and how inflammation subsequently causes pain. Then I was asked to explain what are free radicals? I then remembered this book which helped me understand free radicals…..so I share with you…..
The Better Brain Book
David Perlmutter, MD Board-Certified Neurologist
Riverhead Books 2004 pp. 21-23
“The same forces that are aging your body are aging your brain, only they hit your brain earlier and harder.”
“These culprits are at the core of virtually all brain problems, from mild memory issues to brain fog to severe Alzheimer’s disease. They are:
1) The proliferation in the brain of destructive chemicals called free radicals. 2) The decline in the ability of the brain cells to make energy.”
The brain is the most metabolically active organ of the body; it uses 20% of consumed oxygen to make the energy to fuel all of its activities.
“Energy is made in the specialized parts of the cell called the mitochondria.”
“There is a price to pay for making all this energy. Every time a cell makes energy— any cell, in any part of your body—it also produces toxic substances call free radicals.”
Free radicals are unstable, and bond with molecules in healthy cells, damaging tissues and organs, such as the heart, joints, skin, and the fats of ones brain.
Over time, free radicals can destroy substantial amounts of the brain and nerve tissue through this process of oxidation.
“When the mitochondria of your brain cells are injured, they become less efficient, produce less energy, and increase free radical production.”
“Free radicals can inhibit the brain’s ability to produce neurotransmitters, which have a profound impact on memory, learning, mood, and even balance and hand- eye coordination.”
“Free radicals pose another potentially deadly problem for the brain—they promote inflammation.”
Inflammation is linked to nearly all chronic brain diseases, including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and dementia.
Please leave comments or ask questions:
Dr. Gregg F. Moses
Smoking Is An Influence on Pain and Back Pain Specifically
About 1 in 5 Americans smoke (4), so West Palm Beach is likely to have smokers like anywhere else. Smoking is a leading preventable cause of disease and death in the US, resulting in 438,000 deaths annually. (5) Smoking’s influence on low back pain, reported level of pain and recovery from low back is a popular field of study. For the most part, smoking’s influence on back pain is sizeable enough to quit smoking or not start.
In a large scale review of 81 studies and 40 studies analyzed on the topic of smoking and back pain, the association between smoking and back pain prevalence is reported as modest. However, it was found that both current and former smokers have a higher prevalence and incidence of low back pain than non-smokers. This association is even stronger in adolescent smokers than adult smokers. (6)
Since chronic low back pain is one of the main causes of disability in the community, likely even low back pain in West Palm Beach, researchers studied 73,507 Canadians (aged 20 to 59 years) to report on their chronic low back pain status as well as other factors like smoking. Daily smokers have a prevalence of 23.3% for chronic low back pain versus only 15.37% in non-smokers. Occasional smokers were found to have only a slightly increased change of having chronic low back pain. Daily smoking increases the risk of low back pain in young adults. (7)
Another Canadian study reports that persons with chronic low back pain were more likely to smoke than those without chronic low back pain or arthritis. (8)
A significant association between tobacco smoke and pain is reported in smokers and non-smokers exposed to environmental smoke. This study done in Denmark compared active and passive smoking and the frequency of pain due to the exposure. Daily smokers reported significantly more frequent pain than never smokers. The younger the smoker started smoking increases the probability of frequent pain in daily smokers. (9)
Does Stress and Smoking Influence on Back Pain?
Certainly. A study of 571 individuals who experienced onset of low back pain at 32 and 33 years of age and 5210 individuals who were pain free at that age were compared for risk facts (smoking, psychological distress at 23 years of age, social class, childhood emotional status, body mass index, job satisfaction). Psychological stress more than doubles later risk of low back pain, and smoking modestly influences it. The other factors did not significantly influence low back pain onset. (10) Smoking influences back pain in West Palm Beach.
Smoking and Exercise in Low Back Pain Patients
The smoking habits and exercise habits of 50 low back pain or leg pain sufferers were compared to 50 asymptomatic persons.
- 33% of low back or leg pain sufferers smoked.
- 14% of those without pain smoked.
- 47% of low back or leg pain sufferers exercised
- 86% of those without pain exercised.
It is suggested, therefore, that the level of physical activity and general exercise improves strength, mobility and endurance, possibly enough to prevent future back injury. (11)
Research reports the negative health effects of smoking like poor physical fitness and reduced muscle strength. Smokers are found to have reduced muscle strength and fatigability of the lumbar spine extensor muscles, making them possibly more vulnerable to back injuries. This study does report that weakness is reversible with rigorous exercise. (12)
In closing, not smoking is a healthier lifestyle choice than smoking. The evidence that smoking may well negatively impact the incidence of back pain and recovery from low back pain makes not smoking or stopping smoking a worthy goal. Smoker or not, your back pain can be controlled, and we at Moses Chiropractic appreciate the opportunity to help you.
Dr. Gregg F. Moses
1800 Forest Hill Blvd. Ste. A8-10
West Palm Beach, FL 33406
JOURNAL OF BONE & JOINT SURGERY (AMERICAN VOLUME). 1991 Jan;73(1):124-128