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EDITORIAL
Hans Larsen |
Evaluation of Survey Results
Demographics
Present Age
The difference in present age between the paroxysmal group and the permanent group was statistically significant as was the difference in age between vagal and permanent afibbers.
Age at Diagnosis
There were no statistically significant differences in age at diagnosis. The finding that the average age at diagnosis among 341 lone afibbers is 47 years (median 48 years) should hopefully put a serious dent in the myth that lone atrial fibrillation is an "old age" disease. It clearly is not – quite the contrary, it tends to strike men and women at their most productive age. As a matter of fact, well over 50% of all afibbers were between the ages of 40 and 55 years when first diagnosed and over 16% were at or below the age of 35 when first diagnosed. Only 6.5% were 65 years of age or older when first diagnosed.
Years of Afib
Although the years of afib and the present age of respondents are not really that indicative of anything other than as a measure of how long the afibber had suffered with afib before finding www.afibbers.org and participating in the survey, it is interesting to note that it is indeed possible to live with LAF for a very long time – up to 40 years for paroxysmal afibbers and 65 years for permanent. As a matter of fact, 25% of paroxysmal afibbers had lived with afib for 10 years or more. I am not sure whether this is good news or bad. Living with this condition for 65 years sure seems like a very, very long time indeed! But, unless we come up with a solution that is exactly what some of us may just have to do.
Number of Episodes During First Year
Clearly there is a vast variation in the number of episodes during the first year of afib. However, 50% of all afibbers experienced 3 or fewer episodes during the first year while 68% had 6 or fewer. There was no statistically significant difference between the number of first-year episodes for the various types of afib. There was, however, a very significant correlation between the number of episodes experienced during the first year and the use of pharmaceutical drugs during the first year. Sixty-seven respondents (49%) had not taken any drugs (antiarrhythmics or beta-blockers) while the remaining 71 respondents (51%) had taken drugs. The non-drug takers experienced an average (mean) number of episodes of 4.7 during the year (median =2) while drug takers experienced an average (mean) number of episodes of 13.9 (median =6). This difference was highly significant (p<0.0001). The detrimental effects of drugs applied to all types of paroxysmal afib. There were too few permanent responses to draw a valid conclusion.
All the differences in episode frequency between drug and non-drug users were statistically highly significant. It is clear that taking antiarrhythmics or beta-blockers during the first year of afib is detrimental. This could well be because the first choice in drugs is often digoxin or sotalol or a beta-blocker. All are directly detrimental to vagal afibbers and of dubious, if any, value for mixed and adrenergic afibbers. So based on this statistically highly significant finding the conclusion is to stay away from antiarrhythmics and beta-blockers for at least the first year of your afib career unless your heart rate goes so high during an episode that you need to slow it down by taking a calcium channel blocker or a beta-blocker during the actual episode only.
Conversion to Permanent Afib
Gender Differences
Only the 8-year difference in median age at diagnosis between male and female vagal afibbers was statistically significant (p<0.02). Is it possible that the delay in females developing vagal afib could be due to a protective effect of estrogen? Tantalizing possibility, but as far as I know, pure speculation on my part.
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Magnesium & Potassium in Lone Atrial Fibrillation – Part IIby Patrick Chambers, MD
Cyclic AMP/cGMP and Taurine Interestingly, hyperinsulinism tends to maintain this reduction in cAMP(13). Jean Durlach, M.D., Editor-in-Chief, Magnesium Research, President of the International Society for the Development of Research on Magnesium, and author of Magnesium in Clinical Practice, suggests that taurine may affect this turnaround (less cGMP and more cAMP). Catecholamines and insulin favor cellular influx of taurine. Taurine is a powerful membrane stabilizer. It also chelates Ca, a Mg antagonist, facilitates maintenance of intracellular K and opposes the undesirable cellular effects of insulin and catecholamines(13). Taurine plays an important role in Mg deficiency. Ingestion of monosodium glutamate (MSG) can lead to taurine deficiency, since glutamate competes with cysteine (required to make taurine) for cellular uptake(46).
Glutamate and Aspartate
Autonomic Nervous System Catecholamine-O-methyltransferase (COMT) and monoamine oxidase (MAO) catabolize (break down) norepinephrine (NE), the neurotransmitter for the rest of the SNS. However, unlike acetylcholine but like glutamate, neuronal reuptake of discharged norepinephrine is a major mechanism for terminating sympathetic neurotransmission (see glutamate discussion above). MAO catabolizes this NE, while COMT is more active in catabolizing extracellular circulating (humoral) catecholamines secreted by the adrenal gland(30). Both are part of the SNS. COMT requires Mg as a cofactor(28,29). Neuronal reuptake also requires ATP (and Mg). Low Mg translates to higher sympathetic tone(105). These enzymatic shortfalls might produce an exaggerated response of either the PNS or the SNS at transition or crossover points, a time when many VMAF episodes arise, e.g., lying down or bending over. The neurotransmitter substance or hormone secreted on each occasion is not degraded or removed, resulting in a prolonged over response. For example, cocaine blocks dopamine reuptake, leaving more dopamine in the synaptic cleft, which results in over stimulation of the D2 receptors (causing schizophrenic episodes)(106). Sexual activity triggers some episodes for many afibbers(72). In addition to MAO breakdown of dopamine within neurons (neuronal reuptake) COMT breaks down circulating dopamine, an important hormone produced at this time. The dopamine no doubt triggers automaticity (associated with beta-1 receptors) in ectopic foci with a resulting increase in PACs (see EP discussion below)(107). The over responding vagus causes a shortening of the AERP. Mg deficiency in this scenario (independent of K) may be causative in bedtime episodes and even some more typically adrenergic episodes.
GERD
Dysinsulinism There is an epidemic of overweight/obesity in the Western world, especially here in America. Syndrome X (or Metabolic Syndrome = includes high blood pressure, obesity, diabetes, high blood insulin and triglyceride levels) represents the far end of the spectrum of this disorder of carbohydrate metabolism. Useful laboratory tests include serum hemoglobin A1C, which will detect large swings in blood glucose levels over the preceding three months. Fasting blood glucose and then an OGTT (oral glucose tolerance test) are the best tests to diagnose impaired glucose tolerance and diabetes mellitus. Mg deficiency plays an important role in this process (see insulin section above). Postprandial (after a meal) reactive hypoglycemia (PRH) is defined as low blood sugar (less than 3.3 mmol = 60 gm/dl) concurrent with symptoms (dizziness, depression, sweating, weakness, hunger, anxiety)(82,83,89). LAF has recently been added to this list(84,85,86). Although the oral glucose tolerance test (OGTT) is not abnormal (88,89), a characteristic pattern is often seen in PRH. The release of insulin is sluggish and the insulin peak delayed with respect to the peak value for blood glucose(72,98,99). These flat curves are associated with excessive vagal tone(29,72,100). Instead of insulin resistance, as seen in diabetes, there is insulin hypersensitivity in 50 to 70% of those with PRH. In addition to insulin the body secretes other hormones, such as glucagon like peptide (GLP), from GI tract endocrine cells that stimulate insulin synthesis and secretion(96). GLP-1 levels in those with PRH average 10 times those of normals(89) and it is this hormone that is felt to be responsible for this insulin hypersensitivity. However, this alone is insufficient for a diagnosis of PRH(89). Glucagon dysfunction is a necessary ingredient(97,98). Mg deficiency and its negative effect on gluconeogenesis (glucagon dysfunction) in combination with insulin hypersensitivity may well explain postprandial reactive hypoglycemia in some individuals (see glucagon section above). Furthermore, many with PRH are very lean or women with moderate lower body weight(89) with increased HDL cholesterol. These lean individuals with excessive vagal tone are precisely those that pursue endurance activities. VMAF is increased in endurance athletes (101). Studies comparing the effect of blood glucose on right and left atrial refractory periods reveal these to be shortest under hypoglycemia in the left atrium and longest under normo or hyperglycemia in the right atrium(102) (see EP discussion below). Triggering PACs in LAF typically arise in the left atrium(72,75). Magnesium deficiency also causes release of catecholamines(12). Perhaps this is partially because Mg deficiency causes glucagon dysfunction, which stimulates catecholamine release to cover the glucose shortfall(89). Catecholamines stimulate release of fatty acids that complex with blood Mg, further aggravating the Mg shortfall(60,62,63). Insulin and catecholamines both cause intracellular migration of K and decrease serum K(12). Consequently, catecholamines (and insulin) cause a greater gradient, not only promoting steady leakage of cardiac muscle cell K to blood but also facilitating renal K excretion. Increased K within renal tubule cells stimulates more secretion of K into urine. Hypokalemia, hypoglycemia induced or otherwise, is highly arrhythmogenic.
Hyperthyroidism
Dehydration
Left-Handedness
*****For references please see Part 1*****
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Digestive Wellness – What You Need to Knowby Jackie Burgess, RDH It is well recognized by holistic physicians that proper digestion, absorption, assimilation, and elimination of foods is the key to health. No matter how good, pure, or complete the foods and nutrients consumed are, unless they are broken down so the body can absorb and assimilate them into cells, a person will suffer from malnutrition and enjoy less than optimal health. So says Dr. Jeffrey Bland, noted lecturer and author on health and nutrition. Over 20 million Americans suffer from various digestive disorders which impair their nutrition, he reports[1]. Cardiologist, Stephen Sinatra says, "Sad but true, there are millions of people out there—many of them healthcare providers—who don't fully appreciate the impact that digestive problems can have on the major diseases that afflict us today. Mainstream medicine, in fact, is ten years behind the times when it comes to understanding how interrelated the body's organs and functions really are." Poor digestion can set you up for many diseases. Says Dr. Sinatra, "Indigestion is a little recognized symptom of impending heart problems. One of its symptoms, excessive gas, causes bowel distension which presses against organs that have a direct connection with your heart. A heavy meal may shunt so much blood over to the stomach that a person with coronary blockages can be more prone to angina following such a digestive overload[2]." A thorough understanding of the functional aspects of digestion is best accomplished by reading any of the several referenced books because the topic is so extensive. This article discusses less than optimal digestive functioning and points out its symptoms and consequences. Its goal is to heighten awareness that many chronic conditions or diseases have origins in faulty digestion, absorption and, ultimately, elimination of toxic waste. Scientific evidence exists to support that allergies, all types of arthritis, asthma, chronic fatigue, irritable bowel syndrome, eczema, psoriasis, and migraines, to name a few, have origins in digestive disorders[3,4]. In children, the digestive abuses frequently manifest as allergies and conditions such as colic and ear infections. As we mature, our body adapts and does the best it can with the lifestyle choices we give it. Eventually, when poor choices are made over cumulative years, conditions develop for which mainstream medicine has little to offer in the way of cure or reversal, but rather we are placated with masking drugs— inhalers for asthma, antihistamines for allergies and steroids and antibiotics when all else fails. These remedies are only cover-ups; they are seldom a cure. Major contributing factors to digestive ailments are:
"Leaky Gut" Syndrome The immune system identifies these large particles as "foreign invaders" and signals for the manufacture of antibodies to the invader-antigens. Over time, repeated "leaking" of the same food molecule through the intestinal wall causes an allergic reaction often manifesting as sneezing, flushing, coughing, hives, and headache. This is termed the "leaky gut syndrome." People commonly have these reactions to many foods but fail to make the connection. It's interesting to observe the frequency of people in restaurants having reactions like coughing, sneezing and wiping eyes after or during a meal. The problem is exacerbated by habitually eating the same foods daily, weekly, yearly. In children, food sensitivity can be signaled by ADD (attention deficit disorder), behavior problems and recurring ear problems[6]. The path to digestive wellness begins with thorough chewing followed by adequate stomach acid production along with enzymes required to breakdown protein, fat and starch, and abundant "good" intestinal bacteria.
Digestive Enzyme Deficiency Our lifestyles of eating too many cooked, microwaved and irradiated foods kill live enzymes essential to health. Most everyone can benefit from supplemental enzymes; and, especially those over age 50, since this is about the time digestive systems begin to fail to some degree. Supplementation helps spare the pancreas from overwork. Some reliable brands to take at the beginning of each meal include[7]:
There is some indication that pancreatic enzymes (especially amylase) work better if the content of the capsule is sprinkled on the food prior to eating rather than swallowing the capsule whole.
Adequate Stomach Acid
An adequate level of stomach acid (gastric acid or hydrochloric acid [HCl]) is essential. The digestive enzyme, pepsin, is activated by HCl. Pepsin breaks down proteins and thereby releases vitamins, minerals and other nutrients into a "digestive soup" which eventually will be absorbed into the blood stream. Gastric acid (HCl) is a barrier against infection. Bacteria, viruses and fungi inhaled or ingested are normally destroyed in the stomach. It is the first line of defense against food poisoning. Low stomach acid allows bad bacteria to flourish and interfere with nutrient absorption[8]. With all the ads we see on TV promoting antacids to "neutralize excess stomach acid," it may seem hard to believe that too little acid may be as big a problem as too much. But, symptoms of hypo-acidity often mimic hyper-acidity. Often, the very problem we try to correct, gas and bloating after meals is actually the result of too little HCl and is compounded by what we do—take antacids[9]. Disease conditions caused by low stomach acid include asthma, chronic hepatitis, diabetes, eczema, osteoporosis, thyroid disorders, gallbladder disease, vitiligo, various rheumatic conditions including rheumatoid, lupus, Sjögren's and weak adrenals[10]. The negative effects of low stomach acid production can be ameliorated by taking betaine hydrochloride capsules with each meal. Interesting dental note: Hypochlorhydria (low stomach acid) may result in reduced absorption of calcium, magnesium, copper, folic acid and other nutrients related to osteoporosis prevention. Stomach acid production was measured in 79 people aged 16 to 53 years. Those with evidence of alveolar bone loss produced less than half as much HCl as those without alveolar bone loss[11].
Imbalance of Intestinal Flora Some cause acute or chronic illness and others offer protective and nutritive properties. The latter, the friendly bacteria, are known as intestinal flora or "probiotics" meaning "healthful to life." It is these bacteria we want to nurture because they, in turn help keep us well[12]. Over-consumption of colas, coffee and alcohol disturbs the acid-base relationship in the bowel and this can also lead to an overgrowth of bad bacteria. Bad bacteria discharge nasty toxins, many of which are carcinogenic. A toxic bowel can initiate a chain of reactions resulting in digestive problems which ultimately lead to immune dysfunction, allergies, skin rashes, osteoporosis, high cholesterol, chronic fatigue, vitamin deficiencies, bad breath and cancer of the colon[13]. Good bacteria help with the absorption of nutrients and are involved in the manufacture of several vitamins. The balance is disrupted by processed foods, excess sugar and carbohydrates, and flour products along with a diet heavy in red meat and saturated fats. Too much animal protein putrefies in the bowel. It actually breaks down into carcinogens inducing the worst cancer-producing chemicals around—phenolic compounds[14]. Antibiotics wipe out all intestinal bacteria—good and bad—and allow an overgrowth of the yeast, Candida. Steroids (like Prednisone), birth control pills and chlorinated water seriously impact the friendly bacteria in a negative manner[15].
Probiotic Supplements Some reliable brands are:
Take them upon arising and between meals so they aren't subjected to excessive acidity from meal activity. It is wise, also, to take probiotics whenever taking antibiotics is unavoidable. Obviously, take at different times from the antibiotic. In cases of diarrhea, it is also helpful to take additional doses of probiotics. Friendly bacteria label names include: for infants and toddlers, bifido bacteria infantis; for children and adults— lactobacillus acidophilus, bifido bacterium bifidus longum, lactobacillus bulgaricus in a base of FOS (fructo- oligosaccharides) a carbohydrate to support bacterial proliferation. FOS is a prebiotic that fertilizes probiotics. Food prebiotics are in barley, wheat, rye, tomato, garlic, onion, bananas and whey. Just think of gardening. Adding pre-and probiotics to your diet is just fertilizing the good bacteria so they grow healthy and crowd out the bad....just as in fertilizing the lawn to crowd out weeds.
Inadequate Dietary Fiber People on good diets with plenty of water have one to two bowel movements a day; and the transit time (from when first swallowed to exit) should be from 18 to 36 hours. The book, "Digestive Wellness", by Elizabeth Lipski, describes how to check transit time and offers remedies for improvement[3]. The recommended daily intake of dietary fiber is between 25 and 30 grams. Pearled barley, beans, oat bran, prunes, tomatoes, and raspberries are good sources of dietary fiber. However, it can be difficult to reach the recommended daily intake through diet alone so a fiber supplement may be necessary. An economical fiber, such as plain whole psyllium husk sold in bulk quantities in health food stores for about $8 for 12 ounces, mixes easily into water, soup or juice. Follow the directions and add to the diet very gradually to become accustomed to the effects. Remember, soluble fiber such as found in oat bran and psyllium binds up cholesterol and sweeps it out of the body.
Conclusion
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The AFIB REPORT is published monthly by Hans R. Larsen MSc ChE 1320 Point Street Victoria, BC, Canada V8S 1A5 Phone: (250) 384-2524 E-mail: [email protected] URL: http://www.afibbers.org Copyright © 2003 by Hans R. Larsen The AFIB REPORT does not provide medical advice. Do not attempt self- diagnosis or self-medication based on our reports. Please consult your health-care provider if you wish to follow up on the information presented. |