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Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More
Posted by Jackie
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Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 07, 2012 11:26AM |
Registered: 6 years ago Posts: 18,881 |
Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More
Because of the hypercoagulation risk, afibbers learn quickly about concerns to keep blood thin and flowing. Various influences add to clotting risks and many are the result of Silent Inflammation (SI). This report is an update of the original 2005 post by the same title.
Additionally, two very exciting natural therapies for extinguishing those smoldering fires add new and significant dimensions to standard protocols for managing Afib; namely, tissue alkalinization and grounding or Earthing.
The beneficial effects of alkaline tissue pH and grounding are cutting edge natural therapy, yet not ‘new’ by any means. As you read, hold in your mind the concept of how simply drinking alkaline, magnesium bicarbonate water (WW) and walking barefoot might go a very long way toward reversing your atrial fibrillation and many other health woes-- simplistically and inexpensively.
A review of the basics is, of necessity, lengthy due to the vast scope of variables for each contributing factor in SI, but it lays the groundwork for understanding the risks and dangers of Silent Inflammation. Many natural remedies have proven useful and are listed.
It is often suggested that a definition of health is…. the absence of inflammation.
Is your body smoldering?
Do you know your Inflammatory Risk Profile?
If not, why not?
This review identifies and outlines areas of concern, risk-marker testing and some of many remedies for either preventing the occurrence of or reducing elevated levels of SI. An abundance of reliable reference information and outstanding web links is easily accessible for continuing study. It is especially important to recognize the various factors that produce silent inflammation (SI) and the corresponding risk-marker tests.
Notable for everyone (especially afibbers) is the SI connection to increased blood viscosity.
Thick blood is inflamed blood. Thick blood invites adverse clotting. Acidic blood promotes clotting.
Sinatra, Metabolic Cardiology, 2011
Thick blood has toxic blood components. Some toxic blood components have a genetic link. We know we can influence genetic expression if we are aware we need that focus. Awareness about toxic-blood components, pro-inflammatory messengers called cytokines and leukotrienes along with intermediary substances and thick, acidic blood is the absolute #1 most important thing you can study to avoid cardiovascular (CV) consequences and more.
Chronic, systemic inflammation is often said to be the Trojan Horse of most age-related disease. The increasing recognition and prevalence of inflammation as causative in so many adverse health conditions has spawned a new word…Inflamm-aging. Yet, you don’t have to be elderly to host SI, but an inflamed body does age faster.
Although the risk of cardiovascular events such as stroke or heart attack is low in the Lone Atrial Fibrillation population, it is smart to know all your risk marker levels and act accordingly if any numbers are elevated. Prevention always makes sense.
Quite often, new afibbers are placed on anticoagulants as a precaution against adverse clotting. But, also quite often, the relevant marker evaluations are not ordered concurrently by the patient’s physician. Unfortunately, it is not unusual that patients must insist strongly to have these tests ordered as they are not yet considered ‘routine’ in many medical practices. Don’t give up. These tests could save your life. Even if your doctor doesn’t think so, a large body of science supports the need to control and protect against systemic, chronic inflammation. When testing is not available, following the recommendations for reducing SI will certainly be beneficial. Checking your urine pH at home is easy.
I’ve begun with the basics and included details on a few of the most commonly-troublesome risk indicators. If all you read is Dr. Sinatra’s, “Fire in the Heart” chapter, you will be well on your way toward becoming informed enough to manage your own Inflammatory Risk Profile assessment. The referenced Life Extension articles are easy to understand. Overall, there is no shortage of supporting data, Web articles, newsletters, reports, studies and many books that provide resources for your personal study so you can monitor your inflammatory status, remain healthy and help to prevent a disaster caused by Silent Inflammation.. Empower yourself.
Once you’ve done your research and if there is enough interest, we can open this up for a Conference Room Session discussion.
The bottom line is…your risk markers for Silent Inflammation must be within the safe limits. A variety of options follows including the easiest, most convenient, least expensive—WW and Earthing….It’s working well for me.
Healthy regards,
Jackie Burgess
CONTENTS
I. Introduction
What is silent inflammation?
Conditions related to SI
Causes of SI
Risk Marker Testing
Drugless Anti-inflammatories
II. C-reactive Protein
Causes of elevated CRP
Measurement of CRP – Blood test
Remedies for elevated CRP
III. Blood Viscosity
Alkaline pH
Natural Blood Thinning-Earthing
Measuring Viscosity – Hemathix
Fibrinogen
Natural Remedies
Nanobacteria – MesoSilver
IV. Homocysteine
V. Interleukin 6
VI. Lipoprotein (a)
VII. Ferritin
VIII. Forum Resource Links
IX. References
I. INTRODUCTION
The inflammatory response is an acute and immediate, natural defense mechanism to a physical trauma or repeated irritation and is a protective mechanism that typically resolves rather quickly. We all know the symptoms of pain, redness, swelling that occur when we smash a finger or from a blister caused by an ill-fitting shoe. This type of inflammation is essential for survival and is not the topic of this report.
The concern is about ongoing, systemic, internal, chronic inflammation that brews in the body, smoldering silently, until a chronic disease manifests as a result… or worse, an acute symptom such as heart attack or stroke results. Chronic inflammation is known to be at the core of Coronary Artery Disease (CAD). Heart attacks (MI) result from many years of chronic cycles of arterial inflammation, injury, repair and re-injury on the inside of blood vessels. Over decades, the injuries compound. The process that leads to CAD has been in place long before there are symptoms.
In the early stages of chronic inflammation, it can be suppressed with a variety of interventions such as lifestyle changes, nutrients and sometimes drugs. Once systemic inflammation takes hold, however, immune cells release damaging cytokines that destroy tissues throughout the body. And in response to tissue destruction, even more inflammatory cytokines such as Interleukin 6 are produced continually because the body thinks it is under attack. Quenching the Flames of Inflammation, Cunningham, LEF 2004
Quoting from the chapter, Fire in the Heart:
We now know that SI also plays a central role in the chronic illness that remains our number 1 killer: coronary artery disease. In fact, elevated markers of silent inflammation: such as homocysteine, C-reactive protein (CRP), Lipoprotein a (Lp(a), and interleukin-6 (IL-6), have been found to be more predictive of heart disease than traditional risk factors such as elevated cholesterol levels. In fact, 50% of patients hospitalized for heart disease have normal cholesterol levels.
A landmark study showed that people with high levels of CRP, one of the cardinal markers of inflammation, were over four times more likely to have heart attacks than those with low levels of CRP. Researchers then began to link CRP, along with other markers of inflammation, to a wide range of chronic diseases including Alzheimer’s, arthritis, Parkinson’, and even cancer.
It is now accepted that chronic SI is a warning that something is drastically out of balance with one’s overall health
Fire in the Heart, Ch 4 – Sinatra/Simpson Anti-Aging Therapies 2004
(Clips from Dr. Sinatra’s Cardiologist’s Guide)
Silent inflammation is different from classical inflammation in that it is below the threshold of perceived pain. As a result, no action is taken to stop it and so it lingers for years, if not decades, causing continued insults on the heart, the immune system and the brain and can result in heart disease, Alzheimer’s and cancer.
In many ways, SI can be considered “silent pain” in that the immune system continues to attack at the cellular level but without the perception of pain. Like free radicals, the existence of SI is not a disease, only an indication that potential medical problems lie ahead.
An inflammation is ultimately driven by a group of hormones known as eicosanoids. These hormones are derived from long-chain essential fatty acids and can be altered by dietary interventions. Although the search for anti-inflammatory medications to shut down the generation of inflammatory pain ahs been the goal of medicine since recorded history, very little progress has been made in measuring the extent of other types of inflammation other than asking a patient how much it hurts.
Thus, for years, it was impossible to even discuss SI let alone how to reverse it until suitable clinical markers were established. The first, was high sensitivity C-reactive protein (hs-CRP). This is a relatively non-specific marker of chronic low-level inflammation since it can dramatically increase with any type of infection. However, an increase in hs-CRP only indicates that the low level inflammation has already started. The actual silent inflammation occurs well before the appearance of the C-reactive protein. Thus, it is critical to stop silent inflammation at the cellular level.
To measure this type of SI, a more powerful clinical marker of SI has been developed. This includes the ratio of long-chain omega 6 fatty acid – arachidonic acid (AA) to the long-chain omega 3 fatty acid eicosapentaenoic acid ((EPA) in the isolated plasma phospholipids. The AA/EPA ratio in blood gives a precise insight into the balance of the precursors of pro-inflammatory eicosanoids (derived from AA) and the anti-inflammatory eicosanoids (derived from EPA) in each of the 60 trillion cells in the body. It is this the balance of these eicosanoids precursors that determine the actual extent of silent inflammation in the body.
When using this more sophisticated marker (the AA/EPA ratio), more than 75% of Americans have high levels of silent inflammation including millions of children. (End notes from Sinatra)
An often-forgotten consequence of silent inflammation is fibrosis – of interest to afibbers. A fibrotic response is the result of inflammation and fibrosis is not limited to blood vessels. (Fibrosis – The Enemy of Life – William Wong, PhD) Conference Room Session 24, Cardiac Fibrotic Remodeling should be reviewed in conjunction with this SI report.
CONDITIONS RELATED TO CHRONIC INFLAMMATION
Atrial fibrillation was not on this published LEF list, but since we know the influence of inflammation on the myocytes (heart cells) and the vagus nerve, it definitely should be included. A Google search on heart arrhythmia and inflammation yields 4 million hits.
•Arrhythmia
•Allergy
•Alzheimer’s
•Anemia
•Aortic valve stenosis/damage
•Cancer
•Congestive heart failure
•Diabetes
•Fibromyalgia
•Fibrosis
•Heart attack
•Kidney failure
•Lupus
•Pancreatitis
•Psoriasis
•Stroke
Chronic Inflammation LEF, July 2004
Not included but should be
•Arthritic conditions resulting from acidic tissue pH
CAUSES OF SILENT INFLAMMATION
•Poor dietary choices
•Poor lifestyle habits
•Acidic tissue pH
•Hi temp cooking/grilling →glycotoxins→ inflammation
•Stress – physical and emotional
•Excess blood insulin levels
•Obesity – especially abdominal fat
•Hydrogenated fats & oils
•Elevated levels of Arachidonic Acid
•Cigarette smoking (raises fibrinogen)
•Radiation
•Environmental pollutants/ toxins, air, food, water
•Mercury-amalgam fillings and other heavy metals
•Oxidative stress from free radicals
•Bacterial and viral infection,. nanobacteria, H.pylori, cytomegalovirus, spirochetes such as Lyme’s Borrelia burgdorferi, Chlamydia pneumoniae
•Periodontal (gum) disease
•Some pharmacological drugs
•Lack of sleep increases inflammatory cytokines
•Leaky Gut Syndrome
•Food sensitivities
•Low vitamin D levels
RISK MARKER TESTING
•C-reactive protein hs-CRP
•Homocysteine HCY
•AA/EPA eicosanoid testing
•Ferritin
•Fibrinogen/ blood viscosity
•Hemoglobin A1C
•Insulin & Glucose - fasting
•Oxidized LDL foam cells secrete inflammatory cytokines
•Lipoprotein(a) Lp(a) (statins increase Lp(a)
•Interleukin 6 IL6
•Tumor Necrosis Factor - Alpha
•Tissue pH (urine testing with pH strips)
•Mercury challenge with DMSA
•Food sensitivities
•H.pylori
•Intestinal Permeability -Leaky Gut Syndrome
DRUGLESS ANTI-INFLAMMATORIES
There are many natural anti-inflammatories rather than aspirin, NSAIDS and statins and some work better for specific targets depending on the symptom or marker levels.
A few of many popular choices
•Magnesium Bicarbonate water, aka WW offers inflammation reduction by means of alkalizing tissue.
•Vitamin C – consensus is that generous dosing is highly beneficial
•Magnesium has anti-inflammatory effects and decreases serum CRP Townsend Letter Oct 2011
•Systemic Enzymes lower fibrous inflammation –(not to be confused with digestive enzymes) such as Serrato peptidase (Serrapeptase- silk worm enzyme) or Boluoke (lumbrokinase – earthworm enzyme).
•Astaxanthin
•Curcumin – the highly absorbable C3 complex
•Pterostilbene
•Omega 3 Essential Fatty Acids
•High DHA Omega 3
•Krill Oil
•Pine Bark Extract – Pycnogenol – inhibits NF kB and decreases pro-inflammatory mediators.
•Vitamin D3
•MesoSilver for various pathogens
•Overall detoxification program
A variety of Anti-inflammatory botanicals blends often include
Curmin, Rosemary, Holy Basil, Green Tea, Ginger, and Ginger tea, Coptis, Barberry, Skull cap, Polygonium, Quercetin, Nettles, all of which collectively protect and support. Actions:
Modulates activity of NF-kB and pro-inflammatory cytokines
Reduces inflammatory arachidonic acid metabolites
Helps balance COX and LOX enzymes
Boost antioxidant defenses against free radical damage.
Supplements to reduce pro-inflammatory cytokines include DHA from fish oil suppresses TNF-a, IL6, IL1b, and Il-8. DHEA, vitamin K, GLA and nettle leaf extract also lower cytokines. Antioxidants vitamin C and E, N-acetylcysteine and green tea extract may lower inflammatory cytokines and protect against toxic effects.
II. C-REACTIVE PROTEIN (CRP)
CRP normally functions as the first line of immune system defense to eliminate invading pathogens via the inflammatory response. Many studies show CRP to be much more than that.
CRP is an acute-phase protein produced in the liver and released into the blood stream as a defense mechanism to a wide range of stimuli but primarily in response to Interleukin 6 (IL-6) which is both a pro- and anti-inflammatory cytokine.
In healthy individuals, CRP circulates in fairly low levels and amounts increase dramatically in response to infections, inflammation, injury, common colds and in autoimmune disorders such as rheumatoid arthritis.
CRP was discovered nearly 75 years ago. The High Sensitivity CRP (hs-CRP) has become a standard, predictive marker for cardiovascular (CV) coronary artery disease (CAD) risk assessment and it is an even stronger predictor of CV status than LDL cholesterol. In 1942, Dr. Oswald Avery who discovered CRP suggested that “it closely parallels the clinical course of disease.”
Quenching the Flames - Cunningham– LEF, July 2004
CRP is an indicator or a predictor of atherosclerotic events – not causative, so the search to determine the source of chronic inflammation becomes significantly important when your tests indicate consistently-elevated level.
People with CRP levels lower than 0.5mg/L rarely have heart attacks.
A 2008 study showed 572% more heart attacks in patients with C-reactive protein levels above 3.0mg/L – or triple the risk of MI.
Those with elevated CRP have 2 to 3 times greater risk of stroke. In those who have already suffered a major stroke, elevated CRP is predictive of another stroke, MI or dying within the following year.
In 28,263 healthy postmenopausal women, elevated CRP was the most significant of the 12 markers as a predictor of future cardiac events and was the strongest risk factor associated with an acute coronary event such as plaque rupture and myocardial infarction.
A connection between CVD and inflammation was noted in the ‘90’s but didn’t get much validation until what is known as the landmark study by Paul M. Ridker in 2000 that placed the spotlight on Inflammation, CRP and CV disease.
As quoted in Metabolic Cardiology, Ridker’s findings show:
People with the highest blood levels of CRP had five times the risk of developing cardiovascular disease and four times the risk of heart attack or stroke compared to individuals with the lowest levels. Dr. Ridker says, “We have to think of heart disease as an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease.
A Google search for “Paul M. Ridker_CRP” yields 159,000 hits. Dr. Ridker (MD, MPH, FACC, FAHA), directs the Center for Cardiovascular Disease Prevention, a translational research unit at Brigham & Women’s Hospital in Boston, Mass. that focuses on molecular and genetic epidemiology of cardiovascular disease. Because of his research sponsored by Crestor (statin), controversy rages on the implications. While his work supports the use of statins, other medical professionals have chosen this opportunity to fight and reduce inflammation by natural means which include food choices, weight loss, lifestyle changes and many botanicals with anti-inflammatory and anti-oxidant properties rather than subject patients to the risks of using statin drugs.
Two excerpts from a Medscape interview with Dr. Ridker in 2005 on the Inflammatory Marker – C-Reactive Protein and More in Cardiovascular Disease are worth noting as is the entire interview.
•Dr. Ridker’s work on inflammation and CRP led to the first set of federal guidelines advocating CRP evaluation as new method for cardiovascular disease detection.
•What’s evolving more recently is that CRP may be more than just a marker and may be directly involved in the atherothrombotic process itself.
The Crestor study found that those with baseline CRP blood levels of 4.25 mg/L placed them at greater risk for age-related diseases including cancer, diabetes, dementia, Alzheimer’s, heart attack and stroke. Additionally, many other studies add visual disorders including ARMD, arthritis, and liver failure caused by elevated CRP.
CAUSES OF ELEVATED CRP
•Food choices
•response to insulin – as insulin rises, so does CRP
•diet high in saturated fat
•low fiber intake
•low testosterone levels and increased estrogen (estradiol) levels in males
•overweight – abdominal adiposity
•increased levels of Interleukin 6 (IL6)
•CRP is synthesized by the liver in response to factors released by fat cells
•Elevated uric acid in gouty arthritis..
•Nanobacteria, viruses, Candida/fungal infections
•Periodontal disease
•CRP is elevated in Systemic Lupus Erythematosus
“Regardless of the presence or absence of symptoms, an elevated CRP level is clinically significant and should not be ignored,” says Dean S. Cunningham, MD, PhD, Quenching the Flames of Inflammation
Measurement of hs-CRP – blood test
Some doctors fail to order the “high sensitivity” C-reactive protein test.
The standard test used by many labs does not measure the minute levels of CRP necessary to determine cardiovascular risk.
Dr. Sinatra says optimal CRP level is less than 0.8 mg/dL.
Life Extension Foundation says optimal levels are below .55mg/L for men and 1.5mg/L for women.
Others say as close to zero as possible is optimal.
Once CRP levels fall to the safe ranges, it indicates the underlying inflammatory fire has been extinguished.
REMEDIES
•Proper dietary choices
•Reducing Homocysteine levels
•Exercise
•Weight loss– especially abdominal obesity/fat cells which produces the CRP.
•Moderating alcohol intake
•Systemic enzymes – not to be confused with digestive enzymes lower CRP…dramatically in some cases.
•Drugs – statins, aspirin, ibuprofen, insulin sensitizers, ACE inhibitors, beta blockers
•A consensus indicates that ample daily vitamin C is a core supplement… for both antioxidant and anti-inflammatory benefits.
•MesoSilver for Candida, pathogens and nanobacteria
Dr. Sinatra’s recommendations - Nutritional remedies that suppress inflammation
At least 1000 mg vitamin C daily
Mediterranean diet
High fiber supported by studies
Low saturated fat diet
Restore sex hormone profile
Males – optimize testosterone levels and lower estradiol levels- Check DHEA
Women – low DHEA increases inflammation
Supplements
Magnesium supplements reduce CRP
Curcumin
Irgvingia
Vitamin K
Leutolin
Omega 3 Fish oil - Krill oil
Borage Oil
Acetyl L-Carnitine
Theaflavin
Soluble Fiber
CoQ10
Isoflavones
Chronic Inflammation LEF 2004
Here’s where Astaxanthin comes in as well… along with Resveratrol… as potent antioxidants.
Two newer natural products offer exciting options to help reduce silent inflammation…
A Life Extension article says Krill oil slashed CRP activity in half after just one month dosing at.300 mg/day.
Works in synergy with other Omega 3’s.
Astaxanthin, relatively new on the scene. It is a naturally-occurring carotenoid pigment found abundantly in ocean-dwelling algae. It is both a powerful antioxidant and natural anti-inflammatory agent. Widely studied for beneficial effects on chronic inflammatory conditions such as arthritis, Astaxanthin acts by at least four direct mechanisms
1. reduces oxidant-provoked cell death and mitochondrial dysfunction – two basic triggers of inflammation
2. enhances natural cellular antioxidant function and decreases formation of reactive oxygen species (ROS) and their lipid
oxidation byproducts which are both additional inflammation triggers
3. suppresses activity of caspase-3, a protein needed to produce the cell death by apoptosis
4. reduces release of inflammatory cytokines such as IL 1, IL6 and TNF-alpha.
Astaxanthin:
• Reduces levels of tissue oxidation that lead to inflammation.
• Down-regulates production and activity of enzymes that produce pro-inflammatory cytokines
• Inhibits apoptosis (programmed cell death)
LEF Nov/Dec 2011
III. BLOOD VISCOSITY
Afibbers have the edge on concern over blood stickiness or platelet aggregation since whenever our hearts churn in chaotic dysrhythmia, we can be at risk for clot formation so we need to be especially aware that our blood viscosity markers are at safe levels.
Dr. Sinatra frequently writes about the risks of pumping blood that is sludge and compares some blood viscosity to the consistency of catsup when it should flow like wine.
Thick blood is inflamed blood. Thick blood invites adverse clotting. Acidic blood promotes clotting.
As Dr. Sinatra warns, SI affects blood viscosity. He says 95% of chronically sick patients are hypercoagulable and suffer from “Toxic Blood Syndrome” characterized by elevated levels of oxidized LDL, CRP, Fibrinogen, HCY, Lp(a) and Ferritin.
Dietary intake Omega 3’s and 6’s which are essential, need to be in appropriate ratios. More 3’s, less 6’s. These essential fatty acids metabolize and produce eicosanoids hormones which can have either good or bad effects. The good effects from Omega 3’s are anti-inflammatory and the bad eicosanoids (arachidonic acid – or AA) is a precursor and pro-inflammatory.
AA causes platelet aggregation by triggering release of thromboxane A2 which irritates endothelial cells (that line blood vessels) and sets the stage for chronic SI while promoting blood clotting at the same time.
Too much insulin in the body increases AA production and then catalyzes inflammation. Excess insulin production accelerates inflammation, heart disease, obesity, and Type II diabetes.
High levels of EPA essential fatty acids (fish oils) counteract AA and control inflammation. The ideal AA/EPA ratio is 1.5
Fire in the Heart – Sinatra/ Simons
Alkaline pH
Acidosis refers to low pH in tissue.
Acidemia refers to low blood pH.
In medicine, metabolic acidosis is a condition that occurs when the body produces too much acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney.
(Wikipedia)
This discussion focuses on low tissue pH.
An acid-ash-producing diet causes inflammation if care is not taken to include an abundance of alkaline-ash producing foods. The pH balancing experts say a diet should be 80% alkaline-ash producing foods with 20% acid ash. This makes Paleo and Keto eating a challenge to maintain alkaline tissue pH as well as those diets high carb/grain and sugar.
Excess acid causes thick blood. Acidosis means less oxygen in the blood.
All drugs accumulate as acid waste in the body.
Overwork, stress, anger, fear, jealousy… all produce an acidic tissue pH
Alkalize or Die, Baroody
Daily consumption of alkalizing water, the magnesium bicarbonate water we refer to as WW and make at home, is an easy, inexpensive means of maintaining alkaline tissue pH. See references for links details.
Natural Blood Thinning – Earthing or Grounding
In both Metabolic Cardiology and Earthing, Dr. Sinatra devotes a segment to observing the effects of grounding on blood viscosity and shows darkfield microscopy images of blood platelets before and after Earthing and the amazing improvement. He calls it “Nature’s most abundant anti-inflammatory.” Earthing alters and normalizes blood voltage rapidly, improving the zeta potential and viscosity. (p 223)
He discusses using the zeta potential of blood as a new gold standard for measuring blood viscosity. He notes that cardiologists are mostly unfamiliar with the bioelectrical nature of blood and is actively working on larger studies.
Refer to the book, Earthing – The Most Important Health Discovery – Ever?.
Dr. Sinatra says putting the fire out with Earthing is the Barefoot Revolution.
Measuring Blood Viscosity
Blood viscosity is the common factor tying cardiovascular disease together with nearly 300 independent risk factors. As reported in the article by Drs Larsen and Holsworth in the January 2012 Townsend Letter. Measuring Blood Viscosity to Improve Patient Outcomes. They explain that blood viscosity, the measurement of thickness and stickiness, is either a contributor or an effect.
The key points of Blood Viscosity Physics are described
•Blood is not the same thickness or stickiness at all times.
•Blood thickens as flow slows down
•During diastole, slower moving red blood cells clump more easily and can form rouleaux (microscopically looks like a stack of coins)
•Slow flow allows for intermolecular reactions between plasma and cellular components which increases viscosity
•During systole, more active dispersion and decreased viscosity.
Blood viscosity fluctuates constantly with every heartbeat – greater to lesser and at diastole, can be from 5 to 20 times more viscous than at systole.
Thick or viscous blood causes atherosclerotic plaque at bifurcations in large arteries of neck, around heart and large leg arteries.
These junctions are the source of turbulence or eddies that cause abrasion damage called shear stress. Plaque forms as a protective mechanism.
The importance of keeping blood viscosity low can not be over-emphasized. Monitoring fibrinogen levels is important – and lowering elevated fibrinogen is crucial. High fibrinogen promotes spontaneous formation of fibrin clots and increases the risk of heart disease.
Fibrinogen is an inflammatory protein produced by the liver. Increased levels are a strong mortality predictor.
Nattokinase prevents adverse coagulation of blood clots and dissolves existing thrombus. Efficacy and prolonged action of NK can be determined by measuring levels of EFA (euglobulin fibrinolytic activity) and FDP(fibrin degradation product) which become elevated as fibrin is dissolved.
Testing Viscosity
Three types of testing. Serum or plasma viscosity – single measurement with narrow clinical utility that does not account for hematocrit, blood cell deformability or factors increasing RBC aggregation. Whole blood viscosity, available from a few labs, does include these contributing factors. WBV is generally done with a Brookfield viscometer, older technology designed for measuring the viscosity of house paint or engine oil. It yields a single measurement that is roughly equivalent to the viscosity of blood at systolic pressures, when it is the most fluid and least sticky.
The newest and most advanced testing uses a Hemathix SCV-200 automated scanning capillary tube viscometer (formerly Rheolog) capable of measure viscosity over the complete range of physiologic values experienced in a cardiac cycle (10,000 shear rates) with a single continuous measurement. January 2012 Townsend – Measuring Viscosity - Details at Meridian Labs website – references.
Fibrinogen levels
215 mg/dl to 300 mg/dl considered acceptable.
Lower is better than higher in the range.
Levels greater than 360mg/dl are associated with coronary calcification.
Natural remedies
Dr. Sinatra suggests Fish oils, garlic, bromelain and natural Cox 2 inhibitors such as ginger and green tea to lower fibrinogen levels. Pycnogenol or pine bark extract reduces inflammation. Vitamin C helps normalize fibrinogen levels. (I drink a lot of ginger tea…hot or iced)
Optimizing magnesium helps reduce platelet aggregation.
Review Conference Rooms sessions 39 and 40 on Nattokinase.
Ginkgo biloba
Ginkgo biloba taken at a higher dosage, is equal to taking one or two aspirin a day in terms of anti-coagulation. Retired neurosurgeon, Russell L Blaylock says :“This makes it excellent in preventing heart attacks and strokes.”
“Ginkgo biloba is a wonderful example. It contains numerous powerful antioxidants as well as special compounds that increase blood flow through numerous arteries, including those in the brain. It also improves glucose uptake by brain cells and shown impressive results in Alzheimer’s disease patients. Reports of hemorrhages associated with Ginkgo should be taken with a healthy portion of salt. Most are single anecdotal reports that in no way make a scientific link to Ginkgo biloba. Hemorrhages that have been reported occurred in elderly patients due to atrophied brains with thinned and fragile blood vessels. Certain blood vessels pass through the skull and enter the surface of the brain, virtually suspended in space – it does take much to rupture one of these vessels in a damaged brain.
He says, I find it strange that, despite the much larger reports of brain hemorrhages in elderly people who take aspirin every day, evidence-based doctors do not hesitate to put their patients on such a ridiculous treatment. No matter how many come in with brain hemorrhages, the connection is simply ignored. Ginkgo biloba does not reduce platelet adhesiveness any more than one aspirin a day.
I would much rather have my elderly patients take Ginkgo biloba every day than aspirin. Unlike aspirin, Ginkgo biloba will not erode holes in the stomach or result in GI bleeding. Also, it improves memory in the elderly, protects the brain against the effects of aging and may play a major role in preventing degenerative brain disorders.” (Blaylock Wellness Report July 2006)
Nanobacteria and other pathogens cause thick blood
Nanobacteria are particularly troublesome. They are 1/1000th the size of normal bacteria that hide inside calcified shells. Since the body sees it as calcium and not a foreign invader, they are free to proliferate, unchecked.
While these bugs, themselves, cause damage, more is caused by the body’s reaction to them. The body hurts itself with a defense trigger which show up in the risk markers.. such as C-reactive protein This helps explain why elevated levels such as CRP is a major harbinger of coronary artery disease.
ETDA chelation therapy works well to break up mineral deposits and pull away from the cardiovascular system. Used with tetracycline, it is successful in killing nanobacteria and may help to eliminate the need for patients to have coronary bypass surgery.
For other types of pathogenic bacteria, the use of the nanoparticle, MesoSilver avoids Rx drugs and adverse effects and is highly successful.
Useful for Candida, leaky gut to stop inflammation of gut lining. See resource links for extensive info on the use of nano-particle silver.
There is thought that the use of sulfides to break down or dissolve nanobacteria calcifications combined with MesoSilver pure colloids would work well. As with the use of MesoSilver for Lyme’s disease, we should do more research to confirm the efficacy. It would be a very inexpensive and safe way to avoid clear out blood vessels and avoid blockages and surgery.
IV. HOMOCYSTEINE
Homocysteine (HCY) is an amino acid by-product of protein metabolism. Too much causes (free radical) oxidative damage to the endothelium and other body tissues. High HCY makes blood platelets more sticky. There are no drugs or medications that effectively reduce HCY levels.
Elevated levels of homocysteine (hyperhomocysteinemia) are directly toxic to blood vessels in the brain and heart. It is not only a risk factor for CVD, but is also implicated in
-Increase in clotting factors
-diabetes
-osteoporosis,
-low birth weight,
-neural tube deficits,
-certain cancers,
-cognitive decline and Alzheimer’s disease
-causes oxidative stress
-endothelial dysfunction
-neuronal DNA damage
-mitochondrial membrane weakening
-High HCY levels cause cerebral microangiopathy and apoptosis of neural cells.
Elevated levels of homocysteine double the risk of Alzheimer’s disease.
Levels over 14 umol/L and above double the risk of Alzheimer’s
For every 5 umol/L increase, the risk of developing Alzheimer’s rises by 40%.
The correlation between homocysteine levels and Alzheimer’s was independent of age, gender and APOE genotype.
Homocysteine is produced during the metabolism of the amino acid, methionine. In a healthy body, homocysteine is either recycled back into methionine or altered to another harmless substance in a process called methylation.
However, if there are insufficient B vitamins for the recycling process (methylation), it converts methionine (amino acid in red meat) into homocysteine instead of a usable form. Elevated levels of homocysteine contribute, big-time, to inflammation in the linings of blood vessels and the heart. Endothelial inflammation is a risk factor for afib. Cholesterol deposits amass to fill in the area damaged by inflammation-- setting the stage for heart attack or stroke.
About 40% of the population has genetic polymorphisms of 5,10-methyltetrahydrafolate reductase (MTHFR) and cannot properly metabolize synthetic folic acid and are not helped by the standard B supplements and natural methylators. These people with hyperhomocysteinemia who are resistant to B vitamins must use the special, highly available form of methyltetrahydrofolate (L-5 MTHF) that readily crosses the blood brain barrier and is a form more effective than other forms of folic acid or folate.
High HCY levels when accompanied by elevated Lp(a) are especially dangerous because together they can induce binding of Lp(a) to fibrin, the clot-promoting mechanism.
HCY Levels
Acceptable levels
Less than 7 umol/L is ideal
Over 10 – unacceptable
Dr. Sinatra in a 2011 interview on homocysteine said this about levels:
people think homocysteine is like cholesterol…you want it lower and lower … but people who have HCY around 7 have an over-expression of cystathione synthethase which means they are metabolizing HCY at a rapid rate which means when they are doing that there is a block in their methylation pathway. People with low HCY around 7, 6 or 5 have an over-expression of sulfate and sulfite in the urine and this is as bad as people with HCY of 11, 12, 13 and 14 and 15. Homocysteine has a sweet spot. And lower is not necessarily better
(post from General Health Forum)
If you can’t methylate properly, that’s where the trouble starts. Food alone is not enough. Important factors in lowering HCY is the use of supplemental B vitamins… including natural folates, B6 and the P 5-P form of B6, folinic acid, B12 as methylcobalamin, Zinc, Magnesium, trimethylglycine (TMG), choline and serine. Garlic, beets, broccoli and SAMe are potent methyl donors that help reverse toxic homocysteine back to harmless methionine. 10-15% of people are B-vitamin resistant, but respond to supplemental trimethylglycine (TMG) – 500 – 1000 mg. a day and recheck levels in 3 – 4 months.
Metfolin (Pure Prescriptions)
L-5-MTHF- by Thorne, Designs for Health
Homocysteine Supreme, Designs for Health
Daily important dietary inclusions with normal HCY levels
B vitamins are important and easy to get from food – leafy green veggies, beans, legumes, freshly squeezed OJ, limit red meat to twice a week. Eliminate processed and packaged foods.
Note: Niacin raises homocysteine as does theophylline, methotrexate and L-dopa. If you have a family history of heart disease, or are hypothyroid, have lupus or kidney disease, check your levels.
Important reading on Homocysteine
The major work by Kilmer S. McCully, MD, The Homocysteine Revolution is a must read. It’s been known since 1960 that homocysteine was linked to cardiovascular diseases, but the research community leaned toward the importance of “the cholesterol theory of heart disease” until about year 2000 when national news officially recognized that vitamins B6 B12 and folate can prevent heart disease… thereby validating the significance of a nutritional approach to treatment. The B vitamins, folate, trimethylglycine and choline neutralize this dangerous compound.
Methyl Magic by Craig Cooney, Ph.D. who says:
"Methylation helps give life, and it can take it away. In fact, without methylation there would be no life at all." "In our bodies, methylation takes place more than a billion times a second.
V. INTERLEUKIN 6
Identified as one of the most dangerous inflammatory cytokines that increases with age is IL-6 and is markedly reduced with caloric restriction which also slows aging.
IL-6 is the only non-cellular mediator that induces synthesis of all the liver’s inflammatory proteins (most notably C-reactive protein and fibrinogen). IL-6 is of paramount importance to Cardiovascular homeostasis as it is the principle initiator of the inflammatory response.
In cases of overweight and obese people or those with metabolic syndrome, they can secrete enough to mimic a low-grade systemic inflammatory disorder complete with an elevated CRP marker. IL-6 levels increase with age and contribute to muscle protein degradation, increased breakdown of fats and fatigue, poor quality sleep or sleep deprivation.
Research as firmly established that high levels of CRP, IL-6 and other inflammatory cytokines indicate significantly greater risks heart attack, stroke and Alzheimer’s. Chronic Inflammation - Faloon
In the healthy elderly, higher IL 6 levels were associated with a two-fold greater risk of death. CRP to a lesser extent. Subjects with both elevated CRP and IL 6 were 2.6 times more likely to die during follow-up that those with low levels of both. Chronic inflammation - Faloon
Excess IL-6 and other inflammatory cytokines attack bone and promote the formation of fibrinogen which can induce heart attack or stroke.
VI. LIPOPROTEIN(a)
Elevated Lp(a) is called the `killer` component of Low Density Lipoprotein (LDL) plus a protein (apoprotein a) and is a very strong risk factor for heart disease. This has been well established, yet few physicians check for it.
It is 10 times more atherogenic than LDL on a mg/dL basis leading to heart attack and stroke.
Lp(a) is a cholesterol particle with a disulfide bridge that is highly inflammatory and thrombotic. An adhesive protein coating gives it sticky properties that causes inflammation and clogging of blood vessels because of its repair properties.
In a 10-year follow-up of 5200 myocardial infarction patients, those with the highest Lp(a) had a 70% increased incidence of MI.
Dr Sinatra says in the Fire chapter:
“For the clinical cardiologist, Lp(a) is probably the most difficult risk factor to neutralize. Statin therapy is known to increase Lp(a), so it is important to track Lp(a) levels when using statin treatment.
What should your Lp(a) level be?
<10 mg/dL - acceptable
11-24 mg/dL -borderline high
>25 mg/dL - very high
NOTE: If your Lp (a) level is over 10 mg per deciliter (dL) of blood, you need to take action at once.
Lp(a) is entirely hereditary. Studies indicate people with the highest levels have 70% more heart attacks than with lower levels.
Modifying Lp(a) is very difficult but can be modified some with the following protocol – which should ONLY be followed by those who have tested out high… as the doses of the supplements are high.
Vit. C 2- 4 grams
Q10 120 mg.
L-Carnitine 1 – 2 grams
Omega 3’s 1 – 2 grams
L-lysine 500-1000 mg
L-proline 500-1000 mg.
No flush niacin – niacinamide 1 – 2 grams.
Eat fresh fish, reduce saturated fats, eliminate all hydrogenated fats; avoid soy products;
Exercise regularly.
Nutraceuticals, especially liver-supporting nutrients and: CoQ10, Omega 3’s, in combination with niacin and/or Niaspan often neutralize the toxic effects of Lp(a).(Sinatra -Heart Sense 12/00)
Dr. Mercola’s comment:
Elevated levels of Lp(a) are frequently overlooked by traditional medicine as a cause of heart disease. Part of the reason why it is not looked for by traditional medicine is that they really do not have a good way to treat it. They have not discovered any drugs to lower Lp(a). The only thing that appears to work is the specific type of pharmacological nutrient manipulation discussed by Pauling. (www.mercola.com)
Garry F. Gordon, MD, DO, MD(H)
Lp(a) is synergistically bad with elevated homocysteine so measure and control that variable with adequate B12, Folate, B6, TMG, etc. Be aware that niacin can also raise homocysteine so everything needs to be balanced carefully. To further help prevent the artherosclerosis, make sure vit D 25-OH levels are high-normal and take vit K in form of MK-7 to minimize arterial calcification. Consider IV glutathione, leucovorin and Lipostabile to help reverse the ASCVD.
Other supplements that can lower Lp(a) are Co Q10, vitamin C, proline and lysine. Required niacin doses can be several grams/day if tolerated (build up very gradually). CoQ10 at several hundred mgs/day, Vit C to bowel tolerance and proline and lysine also 2 grams each/ day. Since Lp(a) causes it's problems by increasing risk of clots, nattokinase is a good choice
The Niacin/Niacinamide controversy
If your Lp(a) tests high, do plenty of research before you decide to treat with either niacin or niacinamide as there is a lot of controversy over efficacy and some concern that it can affect the liver and raise liver enzymes. Dr. Garry Gordon writes at his website that it is safe in the standard doses. Many people do not tolerate the flushing effects from niacin.
VII. FERRITIN
Serum Ferritin reflects iron stored in the body – excess iron is toxic and can injure every part of the body including the heart and brain.. and cause or contribute to arrhythmias.
Lab ranges 10-191 ng/ml. with a preferable below 100. (some reports now say 50)
High levels of stored iron can oxidize LDL cholesterol. If iron overload or Hereditary Hemochromatosis is present, use caution with high-dose vitamin C as doses over 500 mg daily enhance iron absorption from the diet.
Natural remedies are easy – just donate blood regularly and keep checking the levels until within a normal range. Avoid supplements and foods containing added iron and limit intake of red meat.
Men over 18 should not take MultiVitamins with added iron unless instructed to do so by a physician.
High serum ferritin levels may be associated with inflammation, liver disease, megaloblastic anemia, hemolytic anemia, sideroblastic anemia, thalassemia, iron overload (hemochromatosis, hemosiderosis), malignant diseases including leukemia and malignant lymphoma.
Very high levels indicate iron overload. Ferritin levels in hemochromatosis may be >1000 ng/mL. Increased serum ferritin may be a risk factor in primary hepatocellular carcinoma.
Serum ferritin levels, however, can be nonspecifically elevated in patients with inflammation and or liver disease, regardless of iron stores. This is attributed to hepatocellular leakage of ferritin from damaged cells.
Joint pain is the most common complaint of people with iron overload
Other common symptoms include fatigue, lack of energy, abdominal pain, loss of sex drive, and heart problems. Symptoms tend to occur in men between the ages of 30 and 50 and in women over age 50. However, many people have no symptoms when they are diagnosed.
If the disease is not detected early and treated, iron may accumulate in body tissues and may eventually lead to serious problems such as
arthritis
•liver disease, including an enlarged liver, cirrhosis, cancer, and liver failure
•damage to the pancreas, possibly causing diabetes
•heart abnormalities, such as irregular heart rhythms or congestive heart failure
•impotence
•early menopause
•abnormal pigmentation of the skin, making it look gray or bronze
•thyroid deficiency
•damage to the adrenal gland
Hemochromatosis is often undiagnosed and untreated. It is considered rare and doctors may not think to test for it. The initial symptoms can be diverse and vague and can mimic the symptoms of many other diseases.
Also, doctors may focus on the conditions caused by hemochromatosis-arthritis, liver disease, heart disease, or diabetes--rather than on the underlying iron overload. However, if the iron overload caused by hemochromatosis is diagnosed and treated before organ damage has occurred, a person can live a normal, healthy life.
End
This concludes the outline for a few of the markers identifying Silent Inflammation. There is much more detail for these as well as the ones listed but not addressed.
Following are Resource References and links from clips used in the report.
You’ll probably want to read this segmentally because of the vast scope of implications.
Take this information ‘to heart’ as a very important Awareness Alert.
Happy reading!
Jackie
AFIB FORUM RESOURCES
The very excellent chapter on Inflammation in the book, Lone Atrial Fibrillation – Toward a Cure (Larsen) details specific points on this topic. Be sure you add that to your reading list. Page 130.
Silent Inflammation –Risk Marker for Stroke & Heart Attack- The original July, 2005
Nattokinase and systemic enzymes.
SESSION 39: Nattokinase - Interim Survey (March 10 - April 25, 2005)
SESSION 40: Nattokinase: Update and Summary (April 27 - May 15, 2005)
MesoSilver to Destroy Pathogens
[www.afibbers.org]
[www.afibbers.org]
UNIQUE WATER AND WALLER WATER
From UW to WW with Love [www.afibbers.org]
WW recipe [www.afibbers.org]
RESOURCES
The Sinatra Solution - Metabolic Cardiology
Stephen T. Sinatra, MD, FACC, FACN, CNS
Introduction by James C Roberts, MD, FACC
2011 edition; Paperback
[www.amazon.com]
A Cardiologist’s Guide to Total Wellness – Special Report
Stephen T. Sinatra, © 2005 Heart Health and Nutrition
www.drsinatra.com
Quenching the Flames of Inflammation
Dean S. Cunningham, MD, PhD
Life Extension July 2004 p 27
Fire in the Heart – New Developments in Diagnosis, Prognosis and Treatment of Cardiovascular Disease Chapter 4
Stephen T. Sinatra, MD, FACC, FACN, CNS, CBT and Graham Simpson, MD. [tinyurl.com]
Published in Anti-Aging Therapeutics – 2004
Ronald Klatz, Robert Goldman
Cardiac Fibrotic Remodelling
[www.afibbers.org]
Fibrosis – The Enemy of Life
William Wong, PhD www.totalityofbeing.com
C-Reactive Protein—Inflammatory Marker and More in Cardiovascular Disease: An Expert Interview with Paul M. Ridker, MD, MPH, FACC, FAA
[www.medscape.org]
Ridker controversy – Crestor, CRP
Breaking News: The Crestor Controversy
April 1, 2010 [www.clinicalcorrelations.org]
Chronic Inflammation
Life Extension July 2004 William Faloon
[www.lifeextensionvitamins.com]
No More Heart Attacks
Life Extension Editorial - William Faloon May 2009
[www.lef.org]
How to Circumvent 17 Independent Heart Attack Risk Factors
[www.lef.org]
The Fires Within
Time Magazine 2004 – Reprinted by Life Extension w/permission
[www.lef.org]
July 2004 p 47
Drugless Prescriptions for Inflammation
Townsend Letter Aug/Sept 2011
C-reactive protein and homocysteine risk factors
Jaroz, A, Nowicka Prezeg; Lek, 2008;65(6):268-72
Current Opinion in Rheumatology
Uric Acid in Heart Disease - A New C-reactive Protein?
Eswar Krishnan; Jeremy Sokolove
Curr Opin Rheumatol. 2011;23(2):174-177
[www.medscape.com]
(article on Krill and Astaxanthin)
Krill Oil Optimizes Multimodel Arthritis Control
Life Extension November/December 2011
[www.lef.org]
Beyond Eye Health, How Astazanthin Combats Degenerative Disease
[www.lef.org]
Astaxanthin – This “Miracle” Antioxidant Could Be 10x More Powerful Than Resveratrol
[www.liveinthenow.com]
Alkalize or Die – Superior Health Through Proper Alkaline-Acid Balance
Theodore A. Baroody, MA, DC, ND, L.M.T., Ph.D (Nutrition), Dipl. Acupuncture (I.A.M.A.), Fellow (A.S.A.)
[www.amazon.com]
Measuring Blood Viscosity to Improve Patient Outcomes
by Pushpa Larsen, ND, and Ralph Holsworth, DO
[www.townsendletter.com]
Townsend Letter for Doctors & Patients
January 2012
Blood Viscosity The Common Denominator for Cardiovascular Risk
by Ralph E Holsworth, DO
Meridian Valley Labs/ Tahoma Clinic Dispensary
MeridianValleyLab.com
Earthing - Ober, Sinatra, Zucker
[www.amazon.com]
Boosting Heart Health Through Earthing - Sinatra
[www.drsinatra.com]
Putting the Fire out -Grounding/Earthing – Sinatra
U-Tube [www.youtube.com]
Homocysteine
Dr. Kilmer McCully was a highly regarded physician at Harvard and the Massachusetts General Hospital until his controversial theories on heart disease cost him his research funding and his job. He continued his work at a VA Hospital in Providence, Rhode Island. At long last, his theories are now widely accepted by the medical and scientific community. His coauthor, daughter, Martha McCully, is the beauty director at Allure magazine
The Heart Revolution: The B Vitamin Breakthrough That Lowers Homocysteine, Cuts Your Risk of Heart Disease, and Protects Your Health
Kilmer S. McCully, MD, Martha McCully
1999
[www.amazon.com]
The Homocysteine Revolution
Kilmer S. McCully, MD ©1997
[www.amazon.com]
Methyl Magic: Maximum Health Through Methylation
A preview article by biochemist, Craig Cooney, PhD can be reviewed at [www.lef.org]
[www.amazon.com]
The Fire Within. How to Halt and Reverse Silent Inflammation NOW…
[www.drsinatra.com]
Garry F. Gordon, MD, DO, MD(H)
[www.gordonresearch.com]
The Anti-Inflammation Zone: Reversing the Silent Epidemic That's Destroying Our Health
Barry Sears, PhD.
[www.amazon.com]
Combat silent inflammation -- the most serious health threat you never heard of
Heart disease is the #1 killer of Americans.
Cancer is the #1 fear of Americans.
Dementia is the #1 concern of Americans.
What do these devastating illnesses have in common? All three have been linked to silent inflammation, a condition that occurs when the body's natural immune response goes awry. Silent inflammation attacks the heart, arteries, and even the brain -- and you will not even know it. Obesity is the primary cause of silent inflammation and excess body fat is causing today's epidemic rise in countless health threats.
Dr. Barry Sears shows you how to combat silent inflammation in this comprehensive guide.
Inflammation Rx: learn why inflammation is called the silent killer—and how you can reverse it
Most researchers agree that the ideal relationship of omega-6s (proinflammatory fatty acids) to omega-3s (anti-inflammatory fatty acids) is about 1:1--the exact ratio you find in the diets of hunter-gatherer societies, which were so remarkably free of the diseases of aging. This ratio keeps the eicosanoid production factories in harmony, with the body producing a nice balance of inflammatory and anti-inflammatory chemicals. The ratio of proinflammatory fats to anti-inflammatory fats in the typical Western diet is 15:1.
Think it doesn't matter? Think again. The importance of this balance to health and anti-aging can't be overstated. "A high omega-6/omega-3 ratio promotes the pathogenesis of many diseases, including cardiovascular disease, cancer, osteoporosis, and inflammatory and autoimmune diseases," says Artemis P. Simopoulos, MD, of the Center for Genetics, Nutrition and Health in Washington. "A lower ratio of omega-6/omega-3 fatty acids is needed for the prevention and management of chronic diseasesBetter Nutrition / March, 2009
by Jonny Bowden PhD, CNS
[findarticles.com]
Potentiation of nociceptive responses to low pH injections in humans by prostaglandin E2.
Rukwied R, Chizh BA, Lorenz U, Obreja O, Margarit S, Schley M, Schmelz M.
J Pain. 2007 May;8(5):443-51. Epub 2007 Mar 6.
Abstract
Inflammation and trauma lead to tissue acidification and release of inflammatory mediators, including prostaglandin E2 (PGE2). Protons can evoke pain through acid-sensing ion channels (ASICs) and TRPV1 receptors. In this study, we examined whether PGE2 can potentiate proton-induced nociception in humans on injection into skin and muscle. Psychophysical and vascular responses to microinjections of protons (pH 6.0 and 6.5), PGE2 (10-6 and 10-7 M) and their combinations into forearm skin (30 microL) or anterior tibial muscle (50 microL) were assessed in 16 male subjects. Pain intensity, axon reflex erythema, and heat pain thresholds were recorded after skin challenge; pain intensity and thresholds for pressure-evoked pain were recorded after intramuscular injections. Intradermal or intramuscular injections of PGE2 induced very low levels of pain similar to saline. Administration of low pH caused moderate pain within 5 seconds that declined rapidly over 15 to 20 seconds. In comparison, coinjection of low pH with PGE2 led to a biphasic profile of the pain response. Combined pH + PGE2 stimulation provoked significantly increased pain in the second phase after injections (20 to 100 seconds) both in skin and muscle, whereas the initial injection pain was not enhanced. Heat pain thresholds were reduced after PGE2 and combined pH + PGE2, whereas flare responses were rather attenuated on coadministration of low pH with PGE2. Intriguingly, when compared with skin, muscle pain was significantly lower in the initial phase (0 to 15 seconds) but significantly higher in the second phase (20 to 100 seconds after injection). PERSPECTIVE: PGE2 can potentiate nociceptor activation by protons in human skin and muscle, indicated by increased sustained pain ratings. This can be best explained by TRPV1 sensitization in the presence of PGE2, a mechanism potentially relevant for inflammatory and injury-induced pain.
PMID:17337250[PubMed - indexed for MEDLINE]
[www.ncbi.nlm.nih.gov]
PPAR Promotes Monocyte/Macrophage Differentiation and Uptake of Oxidized LDL
The formation of foam cells from macrophages in the arterial wall is characterized by dramatic changes in lipid metabolism, including increased expression of scavenger receptors and the uptake of oxidized low-density lipoprotein (oxLDL). We demonstrate here that the nuclear receptor PPAR is induced in human monocytes following exposure to oxLDL and is expressed at high levels in the foam cells of atherosclerotic lesions. Ligand activation of the PPAR:RXRα heterodimer in myelomonocytic cell lines induces changes characteristic of monocytic differentiation and promotes uptake of oxLDL through transcriptional induction of the scavenger receptor CD36. These results reveal a novel signaling pathway controlling differentiation and lipid metabolism in monocytic cells, and suggest that endogenous PPAR ligands may be important regulators of gene expression during atherogenesis.
[www.cell.com]
Because of the hypercoagulation risk, afibbers learn quickly about concerns to keep blood thin and flowing. Various influences add to clotting risks and many are the result of Silent Inflammation (SI). This report is an update of the original 2005 post by the same title.
Additionally, two very exciting natural therapies for extinguishing those smoldering fires add new and significant dimensions to standard protocols for managing Afib; namely, tissue alkalinization and grounding or Earthing.
The beneficial effects of alkaline tissue pH and grounding are cutting edge natural therapy, yet not ‘new’ by any means. As you read, hold in your mind the concept of how simply drinking alkaline, magnesium bicarbonate water (WW) and walking barefoot might go a very long way toward reversing your atrial fibrillation and many other health woes-- simplistically and inexpensively.
A review of the basics is, of necessity, lengthy due to the vast scope of variables for each contributing factor in SI, but it lays the groundwork for understanding the risks and dangers of Silent Inflammation. Many natural remedies have proven useful and are listed.
It is often suggested that a definition of health is…. the absence of inflammation.
Is your body smoldering?
Do you know your Inflammatory Risk Profile?
If not, why not?
This review identifies and outlines areas of concern, risk-marker testing and some of many remedies for either preventing the occurrence of or reducing elevated levels of SI. An abundance of reliable reference information and outstanding web links is easily accessible for continuing study. It is especially important to recognize the various factors that produce silent inflammation (SI) and the corresponding risk-marker tests.
Notable for everyone (especially afibbers) is the SI connection to increased blood viscosity.
Thick blood is inflamed blood. Thick blood invites adverse clotting. Acidic blood promotes clotting.
Sinatra, Metabolic Cardiology, 2011
Thick blood has toxic blood components. Some toxic blood components have a genetic link. We know we can influence genetic expression if we are aware we need that focus. Awareness about toxic-blood components, pro-inflammatory messengers called cytokines and leukotrienes along with intermediary substances and thick, acidic blood is the absolute #1 most important thing you can study to avoid cardiovascular (CV) consequences and more.
Chronic, systemic inflammation is often said to be the Trojan Horse of most age-related disease. The increasing recognition and prevalence of inflammation as causative in so many adverse health conditions has spawned a new word…Inflamm-aging. Yet, you don’t have to be elderly to host SI, but an inflamed body does age faster.
Although the risk of cardiovascular events such as stroke or heart attack is low in the Lone Atrial Fibrillation population, it is smart to know all your risk marker levels and act accordingly if any numbers are elevated. Prevention always makes sense.
Quite often, new afibbers are placed on anticoagulants as a precaution against adverse clotting. But, also quite often, the relevant marker evaluations are not ordered concurrently by the patient’s physician. Unfortunately, it is not unusual that patients must insist strongly to have these tests ordered as they are not yet considered ‘routine’ in many medical practices. Don’t give up. These tests could save your life. Even if your doctor doesn’t think so, a large body of science supports the need to control and protect against systemic, chronic inflammation. When testing is not available, following the recommendations for reducing SI will certainly be beneficial. Checking your urine pH at home is easy.
I’ve begun with the basics and included details on a few of the most commonly-troublesome risk indicators. If all you read is Dr. Sinatra’s, “Fire in the Heart” chapter, you will be well on your way toward becoming informed enough to manage your own Inflammatory Risk Profile assessment. The referenced Life Extension articles are easy to understand. Overall, there is no shortage of supporting data, Web articles, newsletters, reports, studies and many books that provide resources for your personal study so you can monitor your inflammatory status, remain healthy and help to prevent a disaster caused by Silent Inflammation.. Empower yourself.
Once you’ve done your research and if there is enough interest, we can open this up for a Conference Room Session discussion.
The bottom line is…your risk markers for Silent Inflammation must be within the safe limits. A variety of options follows including the easiest, most convenient, least expensive—WW and Earthing….It’s working well for me.
Healthy regards,
Jackie Burgess
CONTENTS
I. Introduction
What is silent inflammation?
Conditions related to SI
Causes of SI
Risk Marker Testing
Drugless Anti-inflammatories
II. C-reactive Protein
Causes of elevated CRP
Measurement of CRP – Blood test
Remedies for elevated CRP
III. Blood Viscosity
Alkaline pH
Natural Blood Thinning-Earthing
Measuring Viscosity – Hemathix
Fibrinogen
Natural Remedies
Nanobacteria – MesoSilver
IV. Homocysteine
V. Interleukin 6
VI. Lipoprotein (a)
VII. Ferritin
VIII. Forum Resource Links
IX. References
I. INTRODUCTION
The inflammatory response is an acute and immediate, natural defense mechanism to a physical trauma or repeated irritation and is a protective mechanism that typically resolves rather quickly. We all know the symptoms of pain, redness, swelling that occur when we smash a finger or from a blister caused by an ill-fitting shoe. This type of inflammation is essential for survival and is not the topic of this report.
The concern is about ongoing, systemic, internal, chronic inflammation that brews in the body, smoldering silently, until a chronic disease manifests as a result… or worse, an acute symptom such as heart attack or stroke results. Chronic inflammation is known to be at the core of Coronary Artery Disease (CAD). Heart attacks (MI) result from many years of chronic cycles of arterial inflammation, injury, repair and re-injury on the inside of blood vessels. Over decades, the injuries compound. The process that leads to CAD has been in place long before there are symptoms.
In the early stages of chronic inflammation, it can be suppressed with a variety of interventions such as lifestyle changes, nutrients and sometimes drugs. Once systemic inflammation takes hold, however, immune cells release damaging cytokines that destroy tissues throughout the body. And in response to tissue destruction, even more inflammatory cytokines such as Interleukin 6 are produced continually because the body thinks it is under attack. Quenching the Flames of Inflammation, Cunningham, LEF 2004
Quoting from the chapter, Fire in the Heart:
We now know that SI also plays a central role in the chronic illness that remains our number 1 killer: coronary artery disease. In fact, elevated markers of silent inflammation: such as homocysteine, C-reactive protein (CRP), Lipoprotein a (Lp(a), and interleukin-6 (IL-6), have been found to be more predictive of heart disease than traditional risk factors such as elevated cholesterol levels. In fact, 50% of patients hospitalized for heart disease have normal cholesterol levels.
A landmark study showed that people with high levels of CRP, one of the cardinal markers of inflammation, were over four times more likely to have heart attacks than those with low levels of CRP. Researchers then began to link CRP, along with other markers of inflammation, to a wide range of chronic diseases including Alzheimer’s, arthritis, Parkinson’, and even cancer.
It is now accepted that chronic SI is a warning that something is drastically out of balance with one’s overall health
Fire in the Heart, Ch 4 – Sinatra/Simpson Anti-Aging Therapies 2004
(Clips from Dr. Sinatra’s Cardiologist’s Guide)
Silent inflammation is different from classical inflammation in that it is below the threshold of perceived pain. As a result, no action is taken to stop it and so it lingers for years, if not decades, causing continued insults on the heart, the immune system and the brain and can result in heart disease, Alzheimer’s and cancer.
In many ways, SI can be considered “silent pain” in that the immune system continues to attack at the cellular level but without the perception of pain. Like free radicals, the existence of SI is not a disease, only an indication that potential medical problems lie ahead.
An inflammation is ultimately driven by a group of hormones known as eicosanoids. These hormones are derived from long-chain essential fatty acids and can be altered by dietary interventions. Although the search for anti-inflammatory medications to shut down the generation of inflammatory pain ahs been the goal of medicine since recorded history, very little progress has been made in measuring the extent of other types of inflammation other than asking a patient how much it hurts.
Thus, for years, it was impossible to even discuss SI let alone how to reverse it until suitable clinical markers were established. The first, was high sensitivity C-reactive protein (hs-CRP). This is a relatively non-specific marker of chronic low-level inflammation since it can dramatically increase with any type of infection. However, an increase in hs-CRP only indicates that the low level inflammation has already started. The actual silent inflammation occurs well before the appearance of the C-reactive protein. Thus, it is critical to stop silent inflammation at the cellular level.
To measure this type of SI, a more powerful clinical marker of SI has been developed. This includes the ratio of long-chain omega 6 fatty acid – arachidonic acid (AA) to the long-chain omega 3 fatty acid eicosapentaenoic acid ((EPA) in the isolated plasma phospholipids. The AA/EPA ratio in blood gives a precise insight into the balance of the precursors of pro-inflammatory eicosanoids (derived from AA) and the anti-inflammatory eicosanoids (derived from EPA) in each of the 60 trillion cells in the body. It is this the balance of these eicosanoids precursors that determine the actual extent of silent inflammation in the body.
When using this more sophisticated marker (the AA/EPA ratio), more than 75% of Americans have high levels of silent inflammation including millions of children. (End notes from Sinatra)
An often-forgotten consequence of silent inflammation is fibrosis – of interest to afibbers. A fibrotic response is the result of inflammation and fibrosis is not limited to blood vessels. (Fibrosis – The Enemy of Life – William Wong, PhD) Conference Room Session 24, Cardiac Fibrotic Remodeling should be reviewed in conjunction with this SI report.
CONDITIONS RELATED TO CHRONIC INFLAMMATION
Atrial fibrillation was not on this published LEF list, but since we know the influence of inflammation on the myocytes (heart cells) and the vagus nerve, it definitely should be included. A Google search on heart arrhythmia and inflammation yields 4 million hits.
•Arrhythmia
•Allergy
•Alzheimer’s
•Anemia
•Aortic valve stenosis/damage
•Cancer
•Congestive heart failure
•Diabetes
•Fibromyalgia
•Fibrosis
•Heart attack
•Kidney failure
•Lupus
•Pancreatitis
•Psoriasis
•Stroke
Chronic Inflammation LEF, July 2004
Not included but should be
•Arthritic conditions resulting from acidic tissue pH
CAUSES OF SILENT INFLAMMATION
•Poor dietary choices
•Poor lifestyle habits
•Acidic tissue pH
•Hi temp cooking/grilling →glycotoxins→ inflammation
•Stress – physical and emotional
•Excess blood insulin levels
•Obesity – especially abdominal fat
•Hydrogenated fats & oils
•Elevated levels of Arachidonic Acid
•Cigarette smoking (raises fibrinogen)
•Radiation
•Environmental pollutants/ toxins, air, food, water
•Mercury-amalgam fillings and other heavy metals
•Oxidative stress from free radicals
•Bacterial and viral infection,. nanobacteria, H.pylori, cytomegalovirus, spirochetes such as Lyme’s Borrelia burgdorferi, Chlamydia pneumoniae
•Periodontal (gum) disease
•Some pharmacological drugs
•Lack of sleep increases inflammatory cytokines
•Leaky Gut Syndrome
•Food sensitivities
•Low vitamin D levels
RISK MARKER TESTING
•C-reactive protein hs-CRP
•Homocysteine HCY
•AA/EPA eicosanoid testing
•Ferritin
•Fibrinogen/ blood viscosity
•Hemoglobin A1C
•Insulin & Glucose - fasting
•Oxidized LDL foam cells secrete inflammatory cytokines
•Lipoprotein(a) Lp(a) (statins increase Lp(a)
•Interleukin 6 IL6
•Tumor Necrosis Factor - Alpha
•Tissue pH (urine testing with pH strips)
•Mercury challenge with DMSA
•Food sensitivities
•H.pylori
•Intestinal Permeability -Leaky Gut Syndrome
DRUGLESS ANTI-INFLAMMATORIES
There are many natural anti-inflammatories rather than aspirin, NSAIDS and statins and some work better for specific targets depending on the symptom or marker levels.
A few of many popular choices
•Magnesium Bicarbonate water, aka WW offers inflammation reduction by means of alkalizing tissue.
•Vitamin C – consensus is that generous dosing is highly beneficial
•Magnesium has anti-inflammatory effects and decreases serum CRP Townsend Letter Oct 2011
•Systemic Enzymes lower fibrous inflammation –(not to be confused with digestive enzymes) such as Serrato peptidase (Serrapeptase- silk worm enzyme) or Boluoke (lumbrokinase – earthworm enzyme).
•Astaxanthin
•Curcumin – the highly absorbable C3 complex
•Pterostilbene
•Omega 3 Essential Fatty Acids
•High DHA Omega 3
•Krill Oil
•Pine Bark Extract – Pycnogenol – inhibits NF kB and decreases pro-inflammatory mediators.
•Vitamin D3
•MesoSilver for various pathogens
•Overall detoxification program
A variety of Anti-inflammatory botanicals blends often include
Curmin, Rosemary, Holy Basil, Green Tea, Ginger, and Ginger tea, Coptis, Barberry, Skull cap, Polygonium, Quercetin, Nettles, all of which collectively protect and support. Actions:
Modulates activity of NF-kB and pro-inflammatory cytokines
Reduces inflammatory arachidonic acid metabolites
Helps balance COX and LOX enzymes
Boost antioxidant defenses against free radical damage.
Supplements to reduce pro-inflammatory cytokines include DHA from fish oil suppresses TNF-a, IL6, IL1b, and Il-8. DHEA, vitamin K, GLA and nettle leaf extract also lower cytokines. Antioxidants vitamin C and E, N-acetylcysteine and green tea extract may lower inflammatory cytokines and protect against toxic effects.
II. C-REACTIVE PROTEIN (CRP)
CRP normally functions as the first line of immune system defense to eliminate invading pathogens via the inflammatory response. Many studies show CRP to be much more than that.
CRP is an acute-phase protein produced in the liver and released into the blood stream as a defense mechanism to a wide range of stimuli but primarily in response to Interleukin 6 (IL-6) which is both a pro- and anti-inflammatory cytokine.
In healthy individuals, CRP circulates in fairly low levels and amounts increase dramatically in response to infections, inflammation, injury, common colds and in autoimmune disorders such as rheumatoid arthritis.
CRP was discovered nearly 75 years ago. The High Sensitivity CRP (hs-CRP) has become a standard, predictive marker for cardiovascular (CV) coronary artery disease (CAD) risk assessment and it is an even stronger predictor of CV status than LDL cholesterol. In 1942, Dr. Oswald Avery who discovered CRP suggested that “it closely parallels the clinical course of disease.”
Quenching the Flames - Cunningham– LEF, July 2004
CRP is an indicator or a predictor of atherosclerotic events – not causative, so the search to determine the source of chronic inflammation becomes significantly important when your tests indicate consistently-elevated level.
People with CRP levels lower than 0.5mg/L rarely have heart attacks.
A 2008 study showed 572% more heart attacks in patients with C-reactive protein levels above 3.0mg/L – or triple the risk of MI.
Those with elevated CRP have 2 to 3 times greater risk of stroke. In those who have already suffered a major stroke, elevated CRP is predictive of another stroke, MI or dying within the following year.
In 28,263 healthy postmenopausal women, elevated CRP was the most significant of the 12 markers as a predictor of future cardiac events and was the strongest risk factor associated with an acute coronary event such as plaque rupture and myocardial infarction.
A connection between CVD and inflammation was noted in the ‘90’s but didn’t get much validation until what is known as the landmark study by Paul M. Ridker in 2000 that placed the spotlight on Inflammation, CRP and CV disease.
As quoted in Metabolic Cardiology, Ridker’s findings show:
People with the highest blood levels of CRP had five times the risk of developing cardiovascular disease and four times the risk of heart attack or stroke compared to individuals with the lowest levels. Dr. Ridker says, “We have to think of heart disease as an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease.
A Google search for “Paul M. Ridker_CRP” yields 159,000 hits. Dr. Ridker (MD, MPH, FACC, FAHA), directs the Center for Cardiovascular Disease Prevention, a translational research unit at Brigham & Women’s Hospital in Boston, Mass. that focuses on molecular and genetic epidemiology of cardiovascular disease. Because of his research sponsored by Crestor (statin), controversy rages on the implications. While his work supports the use of statins, other medical professionals have chosen this opportunity to fight and reduce inflammation by natural means which include food choices, weight loss, lifestyle changes and many botanicals with anti-inflammatory and anti-oxidant properties rather than subject patients to the risks of using statin drugs.
Two excerpts from a Medscape interview with Dr. Ridker in 2005 on the Inflammatory Marker – C-Reactive Protein and More in Cardiovascular Disease are worth noting as is the entire interview.
•Dr. Ridker’s work on inflammation and CRP led to the first set of federal guidelines advocating CRP evaluation as new method for cardiovascular disease detection.
•What’s evolving more recently is that CRP may be more than just a marker and may be directly involved in the atherothrombotic process itself.
The Crestor study found that those with baseline CRP blood levels of 4.25 mg/L placed them at greater risk for age-related diseases including cancer, diabetes, dementia, Alzheimer’s, heart attack and stroke. Additionally, many other studies add visual disorders including ARMD, arthritis, and liver failure caused by elevated CRP.
CAUSES OF ELEVATED CRP
•Food choices
•response to insulin – as insulin rises, so does CRP
•diet high in saturated fat
•low fiber intake
•low testosterone levels and increased estrogen (estradiol) levels in males
•overweight – abdominal adiposity
•increased levels of Interleukin 6 (IL6)
•CRP is synthesized by the liver in response to factors released by fat cells
•Elevated uric acid in gouty arthritis..
•Nanobacteria, viruses, Candida/fungal infections
•Periodontal disease
•CRP is elevated in Systemic Lupus Erythematosus
“Regardless of the presence or absence of symptoms, an elevated CRP level is clinically significant and should not be ignored,” says Dean S. Cunningham, MD, PhD, Quenching the Flames of Inflammation
Measurement of hs-CRP – blood test
Some doctors fail to order the “high sensitivity” C-reactive protein test.
The standard test used by many labs does not measure the minute levels of CRP necessary to determine cardiovascular risk.
Dr. Sinatra says optimal CRP level is less than 0.8 mg/dL.
Life Extension Foundation says optimal levels are below .55mg/L for men and 1.5mg/L for women.
Others say as close to zero as possible is optimal.
Once CRP levels fall to the safe ranges, it indicates the underlying inflammatory fire has been extinguished.
REMEDIES
•Proper dietary choices
•Reducing Homocysteine levels
•Exercise
•Weight loss– especially abdominal obesity/fat cells which produces the CRP.
•Moderating alcohol intake
•Systemic enzymes – not to be confused with digestive enzymes lower CRP…dramatically in some cases.
•Drugs – statins, aspirin, ibuprofen, insulin sensitizers, ACE inhibitors, beta blockers
•A consensus indicates that ample daily vitamin C is a core supplement… for both antioxidant and anti-inflammatory benefits.
•MesoSilver for Candida, pathogens and nanobacteria
Dr. Sinatra’s recommendations - Nutritional remedies that suppress inflammation
At least 1000 mg vitamin C daily
Mediterranean diet
High fiber supported by studies
Low saturated fat diet
Restore sex hormone profile
Males – optimize testosterone levels and lower estradiol levels- Check DHEA
Women – low DHEA increases inflammation
Supplements
Magnesium supplements reduce CRP
Curcumin
Irgvingia
Vitamin K
Leutolin
Omega 3 Fish oil - Krill oil
Borage Oil
Acetyl L-Carnitine
Theaflavin
Soluble Fiber
CoQ10
Isoflavones
Chronic Inflammation LEF 2004
Here’s where Astaxanthin comes in as well… along with Resveratrol… as potent antioxidants.
Two newer natural products offer exciting options to help reduce silent inflammation…
A Life Extension article says Krill oil slashed CRP activity in half after just one month dosing at.300 mg/day.
Works in synergy with other Omega 3’s.
Astaxanthin, relatively new on the scene. It is a naturally-occurring carotenoid pigment found abundantly in ocean-dwelling algae. It is both a powerful antioxidant and natural anti-inflammatory agent. Widely studied for beneficial effects on chronic inflammatory conditions such as arthritis, Astaxanthin acts by at least four direct mechanisms
1. reduces oxidant-provoked cell death and mitochondrial dysfunction – two basic triggers of inflammation
2. enhances natural cellular antioxidant function and decreases formation of reactive oxygen species (ROS) and their lipid
oxidation byproducts which are both additional inflammation triggers
3. suppresses activity of caspase-3, a protein needed to produce the cell death by apoptosis
4. reduces release of inflammatory cytokines such as IL 1, IL6 and TNF-alpha.
Astaxanthin:
• Reduces levels of tissue oxidation that lead to inflammation.
• Down-regulates production and activity of enzymes that produce pro-inflammatory cytokines
• Inhibits apoptosis (programmed cell death)
LEF Nov/Dec 2011
III. BLOOD VISCOSITY
Afibbers have the edge on concern over blood stickiness or platelet aggregation since whenever our hearts churn in chaotic dysrhythmia, we can be at risk for clot formation so we need to be especially aware that our blood viscosity markers are at safe levels.
Dr. Sinatra frequently writes about the risks of pumping blood that is sludge and compares some blood viscosity to the consistency of catsup when it should flow like wine.
Thick blood is inflamed blood. Thick blood invites adverse clotting. Acidic blood promotes clotting.
As Dr. Sinatra warns, SI affects blood viscosity. He says 95% of chronically sick patients are hypercoagulable and suffer from “Toxic Blood Syndrome” characterized by elevated levels of oxidized LDL, CRP, Fibrinogen, HCY, Lp(a) and Ferritin.
Dietary intake Omega 3’s and 6’s which are essential, need to be in appropriate ratios. More 3’s, less 6’s. These essential fatty acids metabolize and produce eicosanoids hormones which can have either good or bad effects. The good effects from Omega 3’s are anti-inflammatory and the bad eicosanoids (arachidonic acid – or AA) is a precursor and pro-inflammatory.
AA causes platelet aggregation by triggering release of thromboxane A2 which irritates endothelial cells (that line blood vessels) and sets the stage for chronic SI while promoting blood clotting at the same time.
Too much insulin in the body increases AA production and then catalyzes inflammation. Excess insulin production accelerates inflammation, heart disease, obesity, and Type II diabetes.
High levels of EPA essential fatty acids (fish oils) counteract AA and control inflammation. The ideal AA/EPA ratio is 1.5
Fire in the Heart – Sinatra/ Simons
Alkaline pH
Acidosis refers to low pH in tissue.
Acidemia refers to low blood pH.
In medicine, metabolic acidosis is a condition that occurs when the body produces too much acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney.
(Wikipedia)
This discussion focuses on low tissue pH.
An acid-ash-producing diet causes inflammation if care is not taken to include an abundance of alkaline-ash producing foods. The pH balancing experts say a diet should be 80% alkaline-ash producing foods with 20% acid ash. This makes Paleo and Keto eating a challenge to maintain alkaline tissue pH as well as those diets high carb/grain and sugar.
Excess acid causes thick blood. Acidosis means less oxygen in the blood.
All drugs accumulate as acid waste in the body.
Overwork, stress, anger, fear, jealousy… all produce an acidic tissue pH
Alkalize or Die, Baroody
Daily consumption of alkalizing water, the magnesium bicarbonate water we refer to as WW and make at home, is an easy, inexpensive means of maintaining alkaline tissue pH. See references for links details.
Natural Blood Thinning – Earthing or Grounding
In both Metabolic Cardiology and Earthing, Dr. Sinatra devotes a segment to observing the effects of grounding on blood viscosity and shows darkfield microscopy images of blood platelets before and after Earthing and the amazing improvement. He calls it “Nature’s most abundant anti-inflammatory.” Earthing alters and normalizes blood voltage rapidly, improving the zeta potential and viscosity. (p 223)
He discusses using the zeta potential of blood as a new gold standard for measuring blood viscosity. He notes that cardiologists are mostly unfamiliar with the bioelectrical nature of blood and is actively working on larger studies.
Refer to the book, Earthing – The Most Important Health Discovery – Ever?.
Dr. Sinatra says putting the fire out with Earthing is the Barefoot Revolution.
Measuring Blood Viscosity
Blood viscosity is the common factor tying cardiovascular disease together with nearly 300 independent risk factors. As reported in the article by Drs Larsen and Holsworth in the January 2012 Townsend Letter. Measuring Blood Viscosity to Improve Patient Outcomes. They explain that blood viscosity, the measurement of thickness and stickiness, is either a contributor or an effect.
The key points of Blood Viscosity Physics are described
•Blood is not the same thickness or stickiness at all times.
•Blood thickens as flow slows down
•During diastole, slower moving red blood cells clump more easily and can form rouleaux (microscopically looks like a stack of coins)
•Slow flow allows for intermolecular reactions between plasma and cellular components which increases viscosity
•During systole, more active dispersion and decreased viscosity.
Blood viscosity fluctuates constantly with every heartbeat – greater to lesser and at diastole, can be from 5 to 20 times more viscous than at systole.
Thick or viscous blood causes atherosclerotic plaque at bifurcations in large arteries of neck, around heart and large leg arteries.
These junctions are the source of turbulence or eddies that cause abrasion damage called shear stress. Plaque forms as a protective mechanism.
The importance of keeping blood viscosity low can not be over-emphasized. Monitoring fibrinogen levels is important – and lowering elevated fibrinogen is crucial. High fibrinogen promotes spontaneous formation of fibrin clots and increases the risk of heart disease.
Fibrinogen is an inflammatory protein produced by the liver. Increased levels are a strong mortality predictor.
Nattokinase prevents adverse coagulation of blood clots and dissolves existing thrombus. Efficacy and prolonged action of NK can be determined by measuring levels of EFA (euglobulin fibrinolytic activity) and FDP(fibrin degradation product) which become elevated as fibrin is dissolved.
Testing Viscosity
Three types of testing. Serum or plasma viscosity – single measurement with narrow clinical utility that does not account for hematocrit, blood cell deformability or factors increasing RBC aggregation. Whole blood viscosity, available from a few labs, does include these contributing factors. WBV is generally done with a Brookfield viscometer, older technology designed for measuring the viscosity of house paint or engine oil. It yields a single measurement that is roughly equivalent to the viscosity of blood at systolic pressures, when it is the most fluid and least sticky.
The newest and most advanced testing uses a Hemathix SCV-200 automated scanning capillary tube viscometer (formerly Rheolog) capable of measure viscosity over the complete range of physiologic values experienced in a cardiac cycle (10,000 shear rates) with a single continuous measurement. January 2012 Townsend – Measuring Viscosity - Details at Meridian Labs website – references.
Fibrinogen levels
215 mg/dl to 300 mg/dl considered acceptable.
Lower is better than higher in the range.
Levels greater than 360mg/dl are associated with coronary calcification.
Natural remedies
Dr. Sinatra suggests Fish oils, garlic, bromelain and natural Cox 2 inhibitors such as ginger and green tea to lower fibrinogen levels. Pycnogenol or pine bark extract reduces inflammation. Vitamin C helps normalize fibrinogen levels. (I drink a lot of ginger tea…hot or iced)
Optimizing magnesium helps reduce platelet aggregation.
Review Conference Rooms sessions 39 and 40 on Nattokinase.
Ginkgo biloba
Ginkgo biloba taken at a higher dosage, is equal to taking one or two aspirin a day in terms of anti-coagulation. Retired neurosurgeon, Russell L Blaylock says :“This makes it excellent in preventing heart attacks and strokes.”
“Ginkgo biloba is a wonderful example. It contains numerous powerful antioxidants as well as special compounds that increase blood flow through numerous arteries, including those in the brain. It also improves glucose uptake by brain cells and shown impressive results in Alzheimer’s disease patients. Reports of hemorrhages associated with Ginkgo should be taken with a healthy portion of salt. Most are single anecdotal reports that in no way make a scientific link to Ginkgo biloba. Hemorrhages that have been reported occurred in elderly patients due to atrophied brains with thinned and fragile blood vessels. Certain blood vessels pass through the skull and enter the surface of the brain, virtually suspended in space – it does take much to rupture one of these vessels in a damaged brain.
He says, I find it strange that, despite the much larger reports of brain hemorrhages in elderly people who take aspirin every day, evidence-based doctors do not hesitate to put their patients on such a ridiculous treatment. No matter how many come in with brain hemorrhages, the connection is simply ignored. Ginkgo biloba does not reduce platelet adhesiveness any more than one aspirin a day.
I would much rather have my elderly patients take Ginkgo biloba every day than aspirin. Unlike aspirin, Ginkgo biloba will not erode holes in the stomach or result in GI bleeding. Also, it improves memory in the elderly, protects the brain against the effects of aging and may play a major role in preventing degenerative brain disorders.” (Blaylock Wellness Report July 2006)
Nanobacteria and other pathogens cause thick blood
Nanobacteria are particularly troublesome. They are 1/1000th the size of normal bacteria that hide inside calcified shells. Since the body sees it as calcium and not a foreign invader, they are free to proliferate, unchecked.
While these bugs, themselves, cause damage, more is caused by the body’s reaction to them. The body hurts itself with a defense trigger which show up in the risk markers.. such as C-reactive protein This helps explain why elevated levels such as CRP is a major harbinger of coronary artery disease.
ETDA chelation therapy works well to break up mineral deposits and pull away from the cardiovascular system. Used with tetracycline, it is successful in killing nanobacteria and may help to eliminate the need for patients to have coronary bypass surgery.
For other types of pathogenic bacteria, the use of the nanoparticle, MesoSilver avoids Rx drugs and adverse effects and is highly successful.
Useful for Candida, leaky gut to stop inflammation of gut lining. See resource links for extensive info on the use of nano-particle silver.
There is thought that the use of sulfides to break down or dissolve nanobacteria calcifications combined with MesoSilver pure colloids would work well. As with the use of MesoSilver for Lyme’s disease, we should do more research to confirm the efficacy. It would be a very inexpensive and safe way to avoid clear out blood vessels and avoid blockages and surgery.
IV. HOMOCYSTEINE
Homocysteine (HCY) is an amino acid by-product of protein metabolism. Too much causes (free radical) oxidative damage to the endothelium and other body tissues. High HCY makes blood platelets more sticky. There are no drugs or medications that effectively reduce HCY levels.
Elevated levels of homocysteine (hyperhomocysteinemia) are directly toxic to blood vessels in the brain and heart. It is not only a risk factor for CVD, but is also implicated in
-Increase in clotting factors
-diabetes
-osteoporosis,
-low birth weight,
-neural tube deficits,
-certain cancers,
-cognitive decline and Alzheimer’s disease
-causes oxidative stress
-endothelial dysfunction
-neuronal DNA damage
-mitochondrial membrane weakening
-High HCY levels cause cerebral microangiopathy and apoptosis of neural cells.
Elevated levels of homocysteine double the risk of Alzheimer’s disease.
Levels over 14 umol/L and above double the risk of Alzheimer’s
For every 5 umol/L increase, the risk of developing Alzheimer’s rises by 40%.
The correlation between homocysteine levels and Alzheimer’s was independent of age, gender and APOE genotype.
Homocysteine is produced during the metabolism of the amino acid, methionine. In a healthy body, homocysteine is either recycled back into methionine or altered to another harmless substance in a process called methylation.
However, if there are insufficient B vitamins for the recycling process (methylation), it converts methionine (amino acid in red meat) into homocysteine instead of a usable form. Elevated levels of homocysteine contribute, big-time, to inflammation in the linings of blood vessels and the heart. Endothelial inflammation is a risk factor for afib. Cholesterol deposits amass to fill in the area damaged by inflammation-- setting the stage for heart attack or stroke.
About 40% of the population has genetic polymorphisms of 5,10-methyltetrahydrafolate reductase (MTHFR) and cannot properly metabolize synthetic folic acid and are not helped by the standard B supplements and natural methylators. These people with hyperhomocysteinemia who are resistant to B vitamins must use the special, highly available form of methyltetrahydrofolate (L-5 MTHF) that readily crosses the blood brain barrier and is a form more effective than other forms of folic acid or folate.
High HCY levels when accompanied by elevated Lp(a) are especially dangerous because together they can induce binding of Lp(a) to fibrin, the clot-promoting mechanism.
HCY Levels
Acceptable levels
Less than 7 umol/L is ideal
Over 10 – unacceptable
Dr. Sinatra in a 2011 interview on homocysteine said this about levels:
people think homocysteine is like cholesterol…you want it lower and lower … but people who have HCY around 7 have an over-expression of cystathione synthethase which means they are metabolizing HCY at a rapid rate which means when they are doing that there is a block in their methylation pathway. People with low HCY around 7, 6 or 5 have an over-expression of sulfate and sulfite in the urine and this is as bad as people with HCY of 11, 12, 13 and 14 and 15. Homocysteine has a sweet spot. And lower is not necessarily better
(post from General Health Forum)
If you can’t methylate properly, that’s where the trouble starts. Food alone is not enough. Important factors in lowering HCY is the use of supplemental B vitamins… including natural folates, B6 and the P 5-P form of B6, folinic acid, B12 as methylcobalamin, Zinc, Magnesium, trimethylglycine (TMG), choline and serine. Garlic, beets, broccoli and SAMe are potent methyl donors that help reverse toxic homocysteine back to harmless methionine. 10-15% of people are B-vitamin resistant, but respond to supplemental trimethylglycine (TMG) – 500 – 1000 mg. a day and recheck levels in 3 – 4 months.
Metfolin (Pure Prescriptions)
L-5-MTHF- by Thorne, Designs for Health
Homocysteine Supreme, Designs for Health
Daily important dietary inclusions with normal HCY levels
B vitamins are important and easy to get from food – leafy green veggies, beans, legumes, freshly squeezed OJ, limit red meat to twice a week. Eliminate processed and packaged foods.
Note: Niacin raises homocysteine as does theophylline, methotrexate and L-dopa. If you have a family history of heart disease, or are hypothyroid, have lupus or kidney disease, check your levels.
Important reading on Homocysteine
The major work by Kilmer S. McCully, MD, The Homocysteine Revolution is a must read. It’s been known since 1960 that homocysteine was linked to cardiovascular diseases, but the research community leaned toward the importance of “the cholesterol theory of heart disease” until about year 2000 when national news officially recognized that vitamins B6 B12 and folate can prevent heart disease… thereby validating the significance of a nutritional approach to treatment. The B vitamins, folate, trimethylglycine and choline neutralize this dangerous compound.
Methyl Magic by Craig Cooney, Ph.D. who says:
"Methylation helps give life, and it can take it away. In fact, without methylation there would be no life at all." "In our bodies, methylation takes place more than a billion times a second.
V. INTERLEUKIN 6
Identified as one of the most dangerous inflammatory cytokines that increases with age is IL-6 and is markedly reduced with caloric restriction which also slows aging.
IL-6 is the only non-cellular mediator that induces synthesis of all the liver’s inflammatory proteins (most notably C-reactive protein and fibrinogen). IL-6 is of paramount importance to Cardiovascular homeostasis as it is the principle initiator of the inflammatory response.
In cases of overweight and obese people or those with metabolic syndrome, they can secrete enough to mimic a low-grade systemic inflammatory disorder complete with an elevated CRP marker. IL-6 levels increase with age and contribute to muscle protein degradation, increased breakdown of fats and fatigue, poor quality sleep or sleep deprivation.
Research as firmly established that high levels of CRP, IL-6 and other inflammatory cytokines indicate significantly greater risks heart attack, stroke and Alzheimer’s. Chronic Inflammation - Faloon
In the healthy elderly, higher IL 6 levels were associated with a two-fold greater risk of death. CRP to a lesser extent. Subjects with both elevated CRP and IL 6 were 2.6 times more likely to die during follow-up that those with low levels of both. Chronic inflammation - Faloon
Excess IL-6 and other inflammatory cytokines attack bone and promote the formation of fibrinogen which can induce heart attack or stroke.
VI. LIPOPROTEIN(a)
Elevated Lp(a) is called the `killer` component of Low Density Lipoprotein (LDL) plus a protein (apoprotein a) and is a very strong risk factor for heart disease. This has been well established, yet few physicians check for it.
It is 10 times more atherogenic than LDL on a mg/dL basis leading to heart attack and stroke.
Lp(a) is a cholesterol particle with a disulfide bridge that is highly inflammatory and thrombotic. An adhesive protein coating gives it sticky properties that causes inflammation and clogging of blood vessels because of its repair properties.
In a 10-year follow-up of 5200 myocardial infarction patients, those with the highest Lp(a) had a 70% increased incidence of MI.
Dr Sinatra says in the Fire chapter:
“For the clinical cardiologist, Lp(a) is probably the most difficult risk factor to neutralize. Statin therapy is known to increase Lp(a), so it is important to track Lp(a) levels when using statin treatment.
What should your Lp(a) level be?
<10 mg/dL - acceptable
11-24 mg/dL -borderline high
>25 mg/dL - very high
NOTE: If your Lp (a) level is over 10 mg per deciliter (dL) of blood, you need to take action at once.
Lp(a) is entirely hereditary. Studies indicate people with the highest levels have 70% more heart attacks than with lower levels.
Modifying Lp(a) is very difficult but can be modified some with the following protocol – which should ONLY be followed by those who have tested out high… as the doses of the supplements are high.
Vit. C 2- 4 grams
Q10 120 mg.
L-Carnitine 1 – 2 grams
Omega 3’s 1 – 2 grams
L-lysine 500-1000 mg
L-proline 500-1000 mg.
No flush niacin – niacinamide 1 – 2 grams.
Eat fresh fish, reduce saturated fats, eliminate all hydrogenated fats; avoid soy products;
Exercise regularly.
Nutraceuticals, especially liver-supporting nutrients and: CoQ10, Omega 3’s, in combination with niacin and/or Niaspan often neutralize the toxic effects of Lp(a).(Sinatra -Heart Sense 12/00)
Dr. Mercola’s comment:
Elevated levels of Lp(a) are frequently overlooked by traditional medicine as a cause of heart disease. Part of the reason why it is not looked for by traditional medicine is that they really do not have a good way to treat it. They have not discovered any drugs to lower Lp(a). The only thing that appears to work is the specific type of pharmacological nutrient manipulation discussed by Pauling. (www.mercola.com)
Garry F. Gordon, MD, DO, MD(H)
Lp(a) is synergistically bad with elevated homocysteine so measure and control that variable with adequate B12, Folate, B6, TMG, etc. Be aware that niacin can also raise homocysteine so everything needs to be balanced carefully. To further help prevent the artherosclerosis, make sure vit D 25-OH levels are high-normal and take vit K in form of MK-7 to minimize arterial calcification. Consider IV glutathione, leucovorin and Lipostabile to help reverse the ASCVD.
Other supplements that can lower Lp(a) are Co Q10, vitamin C, proline and lysine. Required niacin doses can be several grams/day if tolerated (build up very gradually). CoQ10 at several hundred mgs/day, Vit C to bowel tolerance and proline and lysine also 2 grams each/ day. Since Lp(a) causes it's problems by increasing risk of clots, nattokinase is a good choice
The Niacin/Niacinamide controversy
If your Lp(a) tests high, do plenty of research before you decide to treat with either niacin or niacinamide as there is a lot of controversy over efficacy and some concern that it can affect the liver and raise liver enzymes. Dr. Garry Gordon writes at his website that it is safe in the standard doses. Many people do not tolerate the flushing effects from niacin.
VII. FERRITIN
Serum Ferritin reflects iron stored in the body – excess iron is toxic and can injure every part of the body including the heart and brain.. and cause or contribute to arrhythmias.
Lab ranges 10-191 ng/ml. with a preferable below 100. (some reports now say 50)
High levels of stored iron can oxidize LDL cholesterol. If iron overload or Hereditary Hemochromatosis is present, use caution with high-dose vitamin C as doses over 500 mg daily enhance iron absorption from the diet.
Natural remedies are easy – just donate blood regularly and keep checking the levels until within a normal range. Avoid supplements and foods containing added iron and limit intake of red meat.
Men over 18 should not take MultiVitamins with added iron unless instructed to do so by a physician.
High serum ferritin levels may be associated with inflammation, liver disease, megaloblastic anemia, hemolytic anemia, sideroblastic anemia, thalassemia, iron overload (hemochromatosis, hemosiderosis), malignant diseases including leukemia and malignant lymphoma.
Very high levels indicate iron overload. Ferritin levels in hemochromatosis may be >1000 ng/mL. Increased serum ferritin may be a risk factor in primary hepatocellular carcinoma.
Serum ferritin levels, however, can be nonspecifically elevated in patients with inflammation and or liver disease, regardless of iron stores. This is attributed to hepatocellular leakage of ferritin from damaged cells.
Joint pain is the most common complaint of people with iron overload
Other common symptoms include fatigue, lack of energy, abdominal pain, loss of sex drive, and heart problems. Symptoms tend to occur in men between the ages of 30 and 50 and in women over age 50. However, many people have no symptoms when they are diagnosed.
If the disease is not detected early and treated, iron may accumulate in body tissues and may eventually lead to serious problems such as
arthritis
•liver disease, including an enlarged liver, cirrhosis, cancer, and liver failure
•damage to the pancreas, possibly causing diabetes
•heart abnormalities, such as irregular heart rhythms or congestive heart failure
•impotence
•early menopause
•abnormal pigmentation of the skin, making it look gray or bronze
•thyroid deficiency
•damage to the adrenal gland
Hemochromatosis is often undiagnosed and untreated. It is considered rare and doctors may not think to test for it. The initial symptoms can be diverse and vague and can mimic the symptoms of many other diseases.
Also, doctors may focus on the conditions caused by hemochromatosis-arthritis, liver disease, heart disease, or diabetes--rather than on the underlying iron overload. However, if the iron overload caused by hemochromatosis is diagnosed and treated before organ damage has occurred, a person can live a normal, healthy life.
End
This concludes the outline for a few of the markers identifying Silent Inflammation. There is much more detail for these as well as the ones listed but not addressed.
Following are Resource References and links from clips used in the report.
You’ll probably want to read this segmentally because of the vast scope of implications.
Take this information ‘to heart’ as a very important Awareness Alert.
Happy reading!
Jackie
AFIB FORUM RESOURCES
The very excellent chapter on Inflammation in the book, Lone Atrial Fibrillation – Toward a Cure (Larsen) details specific points on this topic. Be sure you add that to your reading list. Page 130.
Silent Inflammation –Risk Marker for Stroke & Heart Attack- The original July, 2005
Nattokinase and systemic enzymes.
SESSION 39: Nattokinase - Interim Survey (March 10 - April 25, 2005)
SESSION 40: Nattokinase: Update and Summary (April 27 - May 15, 2005)
MesoSilver to Destroy Pathogens
[www.afibbers.org]
[www.afibbers.org]
UNIQUE WATER AND WALLER WATER
From UW to WW with Love [www.afibbers.org]
WW recipe [www.afibbers.org]
RESOURCES
The Sinatra Solution - Metabolic Cardiology
Stephen T. Sinatra, MD, FACC, FACN, CNS
Introduction by James C Roberts, MD, FACC
2011 edition; Paperback
[www.amazon.com]
A Cardiologist’s Guide to Total Wellness – Special Report
Stephen T. Sinatra, © 2005 Heart Health and Nutrition
www.drsinatra.com
Quenching the Flames of Inflammation
Dean S. Cunningham, MD, PhD
Life Extension July 2004 p 27
Fire in the Heart – New Developments in Diagnosis, Prognosis and Treatment of Cardiovascular Disease Chapter 4
Stephen T. Sinatra, MD, FACC, FACN, CNS, CBT and Graham Simpson, MD. [tinyurl.com]
Published in Anti-Aging Therapeutics – 2004
Ronald Klatz, Robert Goldman
Cardiac Fibrotic Remodelling
[www.afibbers.org]
Fibrosis – The Enemy of Life
William Wong, PhD www.totalityofbeing.com
C-Reactive Protein—Inflammatory Marker and More in Cardiovascular Disease: An Expert Interview with Paul M. Ridker, MD, MPH, FACC, FAA
[www.medscape.org]
Ridker controversy – Crestor, CRP
Breaking News: The Crestor Controversy
April 1, 2010 [www.clinicalcorrelations.org]
Chronic Inflammation
Life Extension July 2004 William Faloon
[www.lifeextensionvitamins.com]
No More Heart Attacks
Life Extension Editorial - William Faloon May 2009
[www.lef.org]
How to Circumvent 17 Independent Heart Attack Risk Factors
[www.lef.org]
The Fires Within
Time Magazine 2004 – Reprinted by Life Extension w/permission
[www.lef.org]
July 2004 p 47
Drugless Prescriptions for Inflammation
Townsend Letter Aug/Sept 2011
C-reactive protein and homocysteine risk factors
Jaroz, A, Nowicka Prezeg; Lek, 2008;65(6):268-72
Current Opinion in Rheumatology
Uric Acid in Heart Disease - A New C-reactive Protein?
Eswar Krishnan; Jeremy Sokolove
Curr Opin Rheumatol. 2011;23(2):174-177
[www.medscape.com]
(article on Krill and Astaxanthin)
Krill Oil Optimizes Multimodel Arthritis Control
Life Extension November/December 2011
[www.lef.org]
Beyond Eye Health, How Astazanthin Combats Degenerative Disease
[www.lef.org]
Astaxanthin – This “Miracle” Antioxidant Could Be 10x More Powerful Than Resveratrol
[www.liveinthenow.com]
Alkalize or Die – Superior Health Through Proper Alkaline-Acid Balance
Theodore A. Baroody, MA, DC, ND, L.M.T., Ph.D (Nutrition), Dipl. Acupuncture (I.A.M.A.), Fellow (A.S.A.)
[www.amazon.com]
Measuring Blood Viscosity to Improve Patient Outcomes
by Pushpa Larsen, ND, and Ralph Holsworth, DO
[www.townsendletter.com]
Townsend Letter for Doctors & Patients
January 2012
Blood Viscosity The Common Denominator for Cardiovascular Risk
by Ralph E Holsworth, DO
Meridian Valley Labs/ Tahoma Clinic Dispensary
MeridianValleyLab.com
Earthing - Ober, Sinatra, Zucker
[www.amazon.com]
Boosting Heart Health Through Earthing - Sinatra
[www.drsinatra.com]
Putting the Fire out -Grounding/Earthing – Sinatra
U-Tube [www.youtube.com]
Homocysteine
Dr. Kilmer McCully was a highly regarded physician at Harvard and the Massachusetts General Hospital until his controversial theories on heart disease cost him his research funding and his job. He continued his work at a VA Hospital in Providence, Rhode Island. At long last, his theories are now widely accepted by the medical and scientific community. His coauthor, daughter, Martha McCully, is the beauty director at Allure magazine
The Heart Revolution: The B Vitamin Breakthrough That Lowers Homocysteine, Cuts Your Risk of Heart Disease, and Protects Your Health
Kilmer S. McCully, MD, Martha McCully
1999
[www.amazon.com]
The Homocysteine Revolution
Kilmer S. McCully, MD ©1997
[www.amazon.com]
Methyl Magic: Maximum Health Through Methylation
A preview article by biochemist, Craig Cooney, PhD can be reviewed at [www.lef.org]
[www.amazon.com]
The Fire Within. How to Halt and Reverse Silent Inflammation NOW…
[www.drsinatra.com]
Garry F. Gordon, MD, DO, MD(H)
[www.gordonresearch.com]
The Anti-Inflammation Zone: Reversing the Silent Epidemic That's Destroying Our Health
Barry Sears, PhD.
[www.amazon.com]
Combat silent inflammation -- the most serious health threat you never heard of
Heart disease is the #1 killer of Americans.
Cancer is the #1 fear of Americans.
Dementia is the #1 concern of Americans.
What do these devastating illnesses have in common? All three have been linked to silent inflammation, a condition that occurs when the body's natural immune response goes awry. Silent inflammation attacks the heart, arteries, and even the brain -- and you will not even know it. Obesity is the primary cause of silent inflammation and excess body fat is causing today's epidemic rise in countless health threats.
Dr. Barry Sears shows you how to combat silent inflammation in this comprehensive guide.
Inflammation Rx: learn why inflammation is called the silent killer—and how you can reverse it
Most researchers agree that the ideal relationship of omega-6s (proinflammatory fatty acids) to omega-3s (anti-inflammatory fatty acids) is about 1:1--the exact ratio you find in the diets of hunter-gatherer societies, which were so remarkably free of the diseases of aging. This ratio keeps the eicosanoid production factories in harmony, with the body producing a nice balance of inflammatory and anti-inflammatory chemicals. The ratio of proinflammatory fats to anti-inflammatory fats in the typical Western diet is 15:1.
Think it doesn't matter? Think again. The importance of this balance to health and anti-aging can't be overstated. "A high omega-6/omega-3 ratio promotes the pathogenesis of many diseases, including cardiovascular disease, cancer, osteoporosis, and inflammatory and autoimmune diseases," says Artemis P. Simopoulos, MD, of the Center for Genetics, Nutrition and Health in Washington. "A lower ratio of omega-6/omega-3 fatty acids is needed for the prevention and management of chronic diseasesBetter Nutrition / March, 2009
by Jonny Bowden PhD, CNS
[findarticles.com]
Potentiation of nociceptive responses to low pH injections in humans by prostaglandin E2.
Rukwied R, Chizh BA, Lorenz U, Obreja O, Margarit S, Schley M, Schmelz M.
J Pain. 2007 May;8(5):443-51. Epub 2007 Mar 6.
Abstract
Inflammation and trauma lead to tissue acidification and release of inflammatory mediators, including prostaglandin E2 (PGE2). Protons can evoke pain through acid-sensing ion channels (ASICs) and TRPV1 receptors. In this study, we examined whether PGE2 can potentiate proton-induced nociception in humans on injection into skin and muscle. Psychophysical and vascular responses to microinjections of protons (pH 6.0 and 6.5), PGE2 (10-6 and 10-7 M) and their combinations into forearm skin (30 microL) or anterior tibial muscle (50 microL) were assessed in 16 male subjects. Pain intensity, axon reflex erythema, and heat pain thresholds were recorded after skin challenge; pain intensity and thresholds for pressure-evoked pain were recorded after intramuscular injections. Intradermal or intramuscular injections of PGE2 induced very low levels of pain similar to saline. Administration of low pH caused moderate pain within 5 seconds that declined rapidly over 15 to 20 seconds. In comparison, coinjection of low pH with PGE2 led to a biphasic profile of the pain response. Combined pH + PGE2 stimulation provoked significantly increased pain in the second phase after injections (20 to 100 seconds) both in skin and muscle, whereas the initial injection pain was not enhanced. Heat pain thresholds were reduced after PGE2 and combined pH + PGE2, whereas flare responses were rather attenuated on coadministration of low pH with PGE2. Intriguingly, when compared with skin, muscle pain was significantly lower in the initial phase (0 to 15 seconds) but significantly higher in the second phase (20 to 100 seconds after injection). PERSPECTIVE: PGE2 can potentiate nociceptor activation by protons in human skin and muscle, indicated by increased sustained pain ratings. This can be best explained by TRPV1 sensitization in the presence of PGE2, a mechanism potentially relevant for inflammatory and injury-induced pain.
PMID:17337250[PubMed - indexed for MEDLINE]
[www.ncbi.nlm.nih.gov]
PPAR Promotes Monocyte/Macrophage Differentiation and Uptake of Oxidized LDL
The formation of foam cells from macrophages in the arterial wall is characterized by dramatic changes in lipid metabolism, including increased expression of scavenger receptors and the uptake of oxidized low-density lipoprotein (oxLDL). We demonstrate here that the nuclear receptor PPAR is induced in human monocytes following exposure to oxLDL and is expressed at high levels in the foam cells of atherosclerotic lesions. Ligand activation of the PPAR:RXRα heterodimer in myelomonocytic cell lines induces changes characteristic of monocytic differentiation and promotes uptake of oxLDL through transcriptional induction of the scavenger receptor CD36. These results reveal a novel signaling pathway controlling differentiation and lipid metabolism in monocytic cells, and suggest that endogenous PPAR ligands may be important regulators of gene expression during atherogenesis.
[www.cell.com]
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Anonymous User
Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 07, 2012 03:34PM |
Thank you Jackie - excellent work, important for us to read and understand. Going through it quickly (careful reading comes later) it reminded me of an article in Life Extension Magazine some years ago (July '04) with a memorable cover shouting The Aging Body ON FIRE [www.lef.org]
The Fires Within
Inflammation is the body's first defense against infection, but when it goes awry,
it can lead to heart attacks, colon cancer, Alzheimer's and a host of other diseases.
By Christine Gorman and Alice Park
© 2004 TIME, Inc. Reprinted with permission.
(full article at [www.lef.org] )
=============================
Erling.
The Fires Within
Inflammation is the body's first defense against infection, but when it goes awry,
it can lead to heart attacks, colon cancer, Alzheimer's and a host of other diseases.
By Christine Gorman and Alice Park
© 2004 TIME, Inc. Reprinted with permission.
(full article at [www.lef.org] )
=============================
Erling.
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 10:00AM |
Registered: 6 years ago Posts: 18,881 |
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 10:01AM |
Registered: 6 years ago Posts: 18,881 |
Magnesium deficiency (MgD) fits in with this discussion... Important to keep endothelial cells healthy.
MgD may be an initiating factor in the evolution of endothelial dysfunction.
Dysfunction in the endothelium, the thin layer of cells that line blood vessels,
is part of the disease process that can lead to the development of atherosclerosis.
Sources:
Clin Sci (Lond). 2012 May;122(9):397-407.
Endothelial cells and magnesium: implications in atherosclerosis.
Maier JA.Dipartimento di Scienze Cliniche L. Sacco, Università di Milano, Via G.B. Grassi 74, Milano, Italy. jeanette.maier@unimi.it
Abstract
There is no doubt that the functional and structural integrity of the endothelium is critical in maintaining vascular homoeostasis and in preventing atherosclerosis. In the light of epidemiological and experimental studies, magnesium deficiency is emerging as an inducer of endothelial dysfunction. In particular, data on the effects of low extracellular magnesium on cultured endothelial cells reinforce the idea that correcting magnesium homoeostasis might be a helpful and inexpensive intervention to prevent and treat endothelial dysfunction and, consequently, atherosclerosis.
PMID: 22248353
[www.ncbi.nlm.nih.gov]
Clin Interv Aging. 2012; 7: 51–54.
Published online 2012 February 16. doi: 10.2147/CIA.S28768 PMCID: PMC3287408
Copyright © 2012 Rowe, publisher and licensee Dove Medical Press Ltd.
Correcting magnesium deficiencies may prolong life
William J Rowe
Former Assistant Clinical Professor of Medicine, Medical University of Ohio at Toledo, Ohio, USA
Correspondence: William J Rowe, 1485 Bremerton La, Keswick, VA 22947, Virginia, USA, Email rowerun@aol.com
This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
Abstract
The International Space Station provides an extraordinary facility to study the accelerated aging process in microgravity, which could be triggered by significant reductions in magnesium (Mg) ion levels with, in turn, elevations of catecholamines and vicious cycles between the two. With space flight there are significant reductions of serum Mg (P < 0.0001) that have been shown in large studies of astronauts and cosmonauts. The loss of the functional capacity of the cardiovascular system with space flight is over ten times faster than the course of aging on Earth. Mg is an antioxidant and calcium blocker and in space there is oxidative stress, insulin resistance, and inflammatory conditions with evidence in experimental animals of significant endothelial injuries and damage to mitochondria. The aging process is associated with progressive shortening of telomeres, repetitive DNA sequences, and proteins that cap and protect the ends of chromosomes. Telomerase can elongate pre-existing telomeres to maintain length and chromosome stability. Low telomerase triggers increased catecholamines while the sensitivity of telomere synthesis to Mg ions is primarily seen for the longer elongation products. Mg stabilizes DNA and promotes DNA replication and transcription, whereas low Mg might accelerate cellular senescence by reducing DNA stability, protein synthesis, and function of mitochondria. Telomerase, in binding to short DNAs, is Mg dependent. On Earth, in humans, a year might be required to detect changes in telomeres, but in space there is a predictably much shorter duration required for detection, which is therefore more reasonable in time and cost. Before and after a space mission, telomere lengths and telomerase enzyme activity can be determined and compared with age-matched control rats on Earth. The effect of Mg supplementation, both on maintaining telomere length and extending the life span, can be evaluated. Similar studies in astronauts would be fruitful.
[www.ncbi.nlm.nih.gov]
MgD may be an initiating factor in the evolution of endothelial dysfunction.
Dysfunction in the endothelium, the thin layer of cells that line blood vessels,
is part of the disease process that can lead to the development of atherosclerosis.
Sources:
Clin Sci (Lond). 2012 May;122(9):397-407.
Endothelial cells and magnesium: implications in atherosclerosis.
Maier JA.Dipartimento di Scienze Cliniche L. Sacco, Università di Milano, Via G.B. Grassi 74, Milano, Italy. jeanette.maier@unimi.it
Abstract
There is no doubt that the functional and structural integrity of the endothelium is critical in maintaining vascular homoeostasis and in preventing atherosclerosis. In the light of epidemiological and experimental studies, magnesium deficiency is emerging as an inducer of endothelial dysfunction. In particular, data on the effects of low extracellular magnesium on cultured endothelial cells reinforce the idea that correcting magnesium homoeostasis might be a helpful and inexpensive intervention to prevent and treat endothelial dysfunction and, consequently, atherosclerosis.
PMID: 22248353
[www.ncbi.nlm.nih.gov]
Clin Interv Aging. 2012; 7: 51–54.
Published online 2012 February 16. doi: 10.2147/CIA.S28768 PMCID: PMC3287408
Copyright © 2012 Rowe, publisher and licensee Dove Medical Press Ltd.
Correcting magnesium deficiencies may prolong life
William J Rowe
Former Assistant Clinical Professor of Medicine, Medical University of Ohio at Toledo, Ohio, USA
Correspondence: William J Rowe, 1485 Bremerton La, Keswick, VA 22947, Virginia, USA, Email rowerun@aol.com
This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
Abstract
The International Space Station provides an extraordinary facility to study the accelerated aging process in microgravity, which could be triggered by significant reductions in magnesium (Mg) ion levels with, in turn, elevations of catecholamines and vicious cycles between the two. With space flight there are significant reductions of serum Mg (P < 0.0001) that have been shown in large studies of astronauts and cosmonauts. The loss of the functional capacity of the cardiovascular system with space flight is over ten times faster than the course of aging on Earth. Mg is an antioxidant and calcium blocker and in space there is oxidative stress, insulin resistance, and inflammatory conditions with evidence in experimental animals of significant endothelial injuries and damage to mitochondria. The aging process is associated with progressive shortening of telomeres, repetitive DNA sequences, and proteins that cap and protect the ends of chromosomes. Telomerase can elongate pre-existing telomeres to maintain length and chromosome stability. Low telomerase triggers increased catecholamines while the sensitivity of telomere synthesis to Mg ions is primarily seen for the longer elongation products. Mg stabilizes DNA and promotes DNA replication and transcription, whereas low Mg might accelerate cellular senescence by reducing DNA stability, protein synthesis, and function of mitochondria. Telomerase, in binding to short DNAs, is Mg dependent. On Earth, in humans, a year might be required to detect changes in telomeres, but in space there is a predictably much shorter duration required for detection, which is therefore more reasonable in time and cost. Before and after a space mission, telomere lengths and telomerase enzyme activity can be determined and compared with age-matched control rats on Earth. The effect of Mg supplementation, both on maintaining telomere length and extending the life span, can be evaluated. Similar studies in astronauts would be fruitful.
[www.ncbi.nlm.nih.gov]
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Howie
Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 10:13AM |
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Dee
Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 10:39AM |
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 11:08AM |
Registered: 12 years ago Posts: 84 |
All I can say is "wow!". You have outdone yourself, Jackie. This is very important information, and I appreciate the huge amount of work it took to create this document. It's a good thing school is on Spring Break next week, I think it will take me that long to read, along with the important references.
Gratefully, Louise
Gratefully, Louise
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 11:43AM |
Registered: 12 years ago Posts: 66 |
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Mike Harris
Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 01:00PM |
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More April 08, 2012 09:14PM |
Admin Registered: 12 years ago Posts: 761 |
Hello Jackie,
Thank you for compiling this amazing amount of essential information. A "keeper" well worth the wait!!
You mentioned the section on inflammation from my first book Lone Atrial Fibrillation: Toward a Cure. As not everyone has my book I have made the section available at: [www.afibbers.org]. More recent information about the inflammation/LAF connection can be found in the afibbers.com database at [www.afibbers.com].
Hans
Thank you for compiling this amazing amount of essential information. A "keeper" well worth the wait!!
You mentioned the section on inflammation from my first book Lone Atrial Fibrillation: Toward a Cure. As not everyone has my book I have made the section available at: [www.afibbers.org]. More recent information about the inflammation/LAF connection can be found in the afibbers.com database at [www.afibbers.com].
Hans
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More November 21, 2019 11:48PM |
Registered: 7 years ago Posts: 9 |
Hi Jackie,
I'd like to pass on my experience coming from my recent visit to the cardiologist who had been assigned to me during my one-day stay at a hospital about 10 days ago. Because I was careless and unknowingly imbibed some energy tea containing a perfect storm of afib triggers, I developed a scary tachycardia with a pulse of 126, I spent about 7 hours overnight in the ER. I was offered heart rate control drugs and shock therapy, to which I said no thanks, but settled on a simple saline IV drip which allowed me to go back into sinus rhythm some hours later. Before I left the hospital the above-mentioned cardiologist informed me that medical protocol states that the proper thing for me to do would be to take Eliquis, "probably the best option for my condition."
I was not impressed, especially after reading about this drug's many adverse effects, and I am still resisting this advice.
During my followup visit with the same cardiologist today which showed good heart and circulatory function, she did not press me about taking this drug, but merely said that I might change my mind if my afib frequency increases (I had not had an episode for over four years before the last one occurred), and said to come back in a year. Before I left her office, I asked her about having some blood tests that would check the SI markers that you have talked about in your many interesting articles.She said (and I am paraphrasing), "No, no, paroxysmal afib is a mechanical/electrical issue and would not be helped or informed in any way from such tests! The blood in your left atrial appendage (LAA) during an afib episode would turn its contained blood into a sort of viscous mud, even if you had very good cardiovascular health! The muddy blood in your LAA during an afib attack would readily eject a clot, an embolus, into your brain or eye and could lead to a serious stroke. Proteolytic enzymes would not be potent enough to dissolve a rapidly forming massive embolus."
Regardless, I am still optimistic that taking nattokinase at a total combined daily dose of 8000 FU (fibrotic units), morning and night (at 12-hour intervals), would offer sufficient protection to keep my blood (even in the LAA) sufficiently primed to continually clear my blood of incipient clots and avoid the" muddy" state described by my cardiologist.
What do you think of my cardiologist's characterization of tests for SI and about my confidence in the effectiveness of nattokinase for averting strokes during a prolonged afib episode?
I'd like to pass on my experience coming from my recent visit to the cardiologist who had been assigned to me during my one-day stay at a hospital about 10 days ago. Because I was careless and unknowingly imbibed some energy tea containing a perfect storm of afib triggers, I developed a scary tachycardia with a pulse of 126, I spent about 7 hours overnight in the ER. I was offered heart rate control drugs and shock therapy, to which I said no thanks, but settled on a simple saline IV drip which allowed me to go back into sinus rhythm some hours later. Before I left the hospital the above-mentioned cardiologist informed me that medical protocol states that the proper thing for me to do would be to take Eliquis, "probably the best option for my condition."
I was not impressed, especially after reading about this drug's many adverse effects, and I am still resisting this advice.
During my followup visit with the same cardiologist today which showed good heart and circulatory function, she did not press me about taking this drug, but merely said that I might change my mind if my afib frequency increases (I had not had an episode for over four years before the last one occurred), and said to come back in a year. Before I left her office, I asked her about having some blood tests that would check the SI markers that you have talked about in your many interesting articles.She said (and I am paraphrasing), "No, no, paroxysmal afib is a mechanical/electrical issue and would not be helped or informed in any way from such tests! The blood in your left atrial appendage (LAA) during an afib episode would turn its contained blood into a sort of viscous mud, even if you had very good cardiovascular health! The muddy blood in your LAA during an afib attack would readily eject a clot, an embolus, into your brain or eye and could lead to a serious stroke. Proteolytic enzymes would not be potent enough to dissolve a rapidly forming massive embolus."
Regardless, I am still optimistic that taking nattokinase at a total combined daily dose of 8000 FU (fibrotic units), morning and night (at 12-hour intervals), would offer sufficient protection to keep my blood (even in the LAA) sufficiently primed to continually clear my blood of incipient clots and avoid the" muddy" state described by my cardiologist.
What do you think of my cardiologist's characterization of tests for SI and about my confidence in the effectiveness of nattokinase for averting strokes during a prolonged afib episode?
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Re: Silent Inflammation – Risk Marker for Stroke, Heart Attack & Much More November 24, 2019 09:12PM |
Registered: 7 years ago Posts: 9 |
Sorry, only registered users may post in this forum.