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Is Copd Respiratory Acidosis?

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Respiratory acidosis #sign and symptoms of Respiratory acidosis Respiratory acidosis ABGs Analyse https://youtu.be/L5MWy1iHacI Plz share n subscribe my chanel is a condition that occurs when the lungs cant remove enough of the Suctioning https://youtu.be/hMJGkxvXTW0 carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45).Rinku Chaudhary NSG officer AMU ALIGARH https://www.facebook.com/rinkutch/ Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Suctioning https://youtu.be/hMJGkxvXTW0 Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs cant remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: asthma COPD pneumonia sleep apnea TYPES Forms of respiratory acidosis There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. Its a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesnt cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. SYMPTOMS Symptoms of respiratory acidosis Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: https://www.healthline.com/health/res... sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of respiratory acidosis doesnt typically cause any noticeable symptoms. Signs are subtle and nonspecific and may include: memory loss sleep disturbances personality changes CAUSES Common causes of respiratory acidosis The lungs and the kidneys are the major organs that help regulate your bloods pH. The lungs remove acid by exhaling CO2, and the kidneys excrete acids through the urine. The kidneys also regulate your bloods concentration of bicarbonate (a base). Respiratory acidosis is usually caused by a lung disease or condition that affects normal breathing or impairs the lungs ability to remove CO2. Some common causes of the chronic form are: asthma chronic obstructive pulmonary disease (COPD) acute pulmonary edema severe obesity (which can interfere with expansion of the lungs) neuromuscular disorders (such as multiple sclerosis or muscular dystrophy) scoliosis Some common causes of the acute form are: lung disorders (COPD, emphysema, asthma, pneumonia) conditions that affect the rate of breathing muscle weakness that affects breathing or taking a deep breath obstructed airways (due to choking or other causes) sedative overdose cardiac arrest DIAGNOSIS How is respiratory acidosis diagnosed? The goal of diagnostic tests for respiratory acidosis is to look for any pH imbalance, to determine the severity of the imbalance, and to determine the condition causing the imbalance. Several tools can help doctors diagnose respiratory acidosis. Blood gas measurement Blood gas is a series of tests used to measure oxygen and CO2 in the blood. A healthcare provider will take a sample of blood from your artery. High levels of CO2 can indicate acidosis.

Respiratory Acidosis

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Respiratory acidosis is primary increase in carbon dioxide partial pressure (Pco2) with or without compensatory increase in bicarbonate (HCO3); pH is usually low but may be near normal. Cause is a decrease in respiratory rate and/or volume (hypoventilation), typically due to CNS, pulmonary, or iatrogenic conditions. Respiratory acidosis can be acute or chronic; the chronic form is asymptomatic, but the acute, or worsening, form causes headache, confusion, and drowsiness. Signs include tremor, myoclonic jerks, and asterixis. Diagnosis is clinical and with ABG and serum electrolyte measurements. The cause is treated; oxygen (O2) and mechanical ventilation are often required. Respiratory acidosis is carbon dioxide (CO2) accumulation (hypercapnia) due to a decrease in respiratory rate and/or respiratory volume (hypoventilation). Causes of hypoventilation (discussed under Ventilatory Failure ) include Conditions that impair CNS respiratory drive Conditions that impair neuromuscular transmission and other Continue reading >>

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  1. Gemmablower

    So my daughter fasts for 12 hours at night and I have noticed that when her basal is flat at night just a couple mmol drop then her ketones can be low at the beginning of the night but reach 0.7-0.9 in the morning even with a bed glucose reading of 8mmol and waking on 6mmol.
    When I increase her basal by half unit they diminish to 0.4 but in turn the higher basal creates a huge drop at night meaning going to bed on 11mmol means a waking glucose of 4mmol so the result is having to send my daughters sugars up to compensate for extra basal.
    My questions is what level of ketones is ok in the morning after fasting for 12 hours? I would prefer to send her to bed in range but more ketones are being produced so it worries me?
    What level of starvation ketones would you expect after 12 hours of fasting? X

  2. novorapidboi26

    significant ketones that would need attention is anything over 1.5mmol/l.........
    now I say significant, but this is me talking about a sick day scenario as opposed to fasting ketones......
    but its still a good guide......
    the levels you have posted are normal I would say.......

  3. teacher123

    Those ketone levels are completely fine.
    The danger is when glucose levels are high (13 mmol/l +) and ketones are high and rising. It indicates a lack of insulin in the body so action needs to be taken immediately otherwise diabetic ketoacidosis will ensue. If you want more clarification, I'll tag @LucySW who knows more about this topic than me

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A short hand-drawn tutorial to explain the basic mechanisms behind simple respiratory acidosis/alkalosis, and the compensatory mechanisms that can be used to correct them

Acid-base Disturbance In Copd

Summarized from Bruno M, Valenti M. Acid-base disorders in patients with chronic obstructive pulmonary disease: A pathophysiological review. J Bomedicine and Biotechnology (2012) Article ID 915150 8 pages ( available at :) Arterial blood gases are frequently useful in the clinical management of patients with chronic obstructive pulmonary disease (COPD) to assess both oxygenation and acid-base status. A recent review article focuses on disturbance of acid-base in these patients, which occurs in advanced disease when pulmonary gas exchange is so compromised that the rate of carbon dioxide production in the tissues exceeds the rate of carbon dioxide elimination by the lungs. The article begins with an explanation of how the resulting carbon dioxide accumulation in blood leads to respiratory acidosis, the acid-base disturbance that commonly occurs in advanced COPD. An important distinction is made between acute and chronic respiratory acidosis; compensation is less effective in the former. Then follows a detailed description of the several renal mechanisms involved in the compensatory response to chronic respiratory acidosis. Although this mitigates the acidosis to a considerable exte Continue reading >>

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  1. humbled

    This just begs to be in a table.
    Red Wine
    Varietal Calories Carbs

    Merlot
    120
    3.7
    Pinot Noir
    121
    3.4
    Cabernet
    120
    3.8
    White Wine
    Varietal Calories Carbs

    Chardonnay
    118
    3.7
    Pinot Gris/Grigio
    122
    3.2
    Riesling
    118
    5.5
    Champagne/Sparkling whites
    96
    1.5
    Beer
    Beer Calories Carbs

    Bud Select 55
    55
    1.9
    MGD 64
    64
    2.4
    Rolling Rock Green Light
    92
    2.4
    Michelob Ultra
    95
    2.6
    Bud Select
    99
    3.1
    Miller Lite
    96
    3.2
    Natural Light
    95
    3.2
    Michelob Ultra Amber
    114
    3.7
    Coors Light
    102
    5
    Amstel Light
    95
    5
    Bud Light
    110
    6.6

  2. xtrumpclimbs

    Great!!!
    Please, post it in the FAQ.

  3. schmearcampain

    Also important in the light beer conversation is the amount of alcohol in them. Many times to cut calories, they reduce alcohol content as well as carbs. link

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Chronic Obstructive Pulmonary Disease (COPD) and Respiratory Acidosis Why is it related to respiratory acidosis? 1. Progression of the disease will make the patient breath harder (hypoventilation) which makes them hold on to carbon dioxide resulting to respiratory acidosis ----------------------------------------------------------------------------------------- What is ABG? https://www.youtube.com/watch?v=88fGs... ----------------------------------------------------------------------------------------- 1. Respiratory Acidosis and Chronic Obstruction Pulmonary Disorder (COPD) 1. What? 1. Is a breathing disorder that progresses over time. 2. Why is it related to respiratory acidosis? 1. Progression of the disease will make the patient breath harder (hypoventilation) which makes them hold on to carbon dioxide resulting to respiratory acidosis 3. Who is at risk? 1. Smokers 2. Toxic environment exposure 4. Signs and Symptoms 1. Barrel Chest 2. Fatigue 3. Confusion 4. Cyanotic 5. Wheezing and Crackles 6. Oxygen saturation normally in the 80s percentage 7. Cough 8. Sputum production 5. Intervention 1. Elevate the head of the bed 30 45 degrees 2. Pursed lip breathing 3. Tripod positioning 4. Oxygen as prescribed 5. Administer medication 6. Treatment 1. Stop smoking 2. Pneumonia vaccine 3. Yearly flu vaccine 4. Physical therapy 5. Oxygen therapy 6. Surgery 7. Medications 1. Short Acting Bronchodilators 1. B2 adrenergic agonist a) Albuterol i) Smooth muscle relaxation b) Theophylline (Short and Long acting) i) Adult Normal level 5 - 15 mcg/dL ii) Children 5 - 10 mcg/dL iii) More than 20 is toxic! iv) Treat emphysema and chronic bronchitis 2. Anticholinergic Bronchodilators 1. Atrovent a) Inhaler and nebulizer solution 3. Inhaled Corticosteroid 1. Used for moderate to severe 2. Not for long term use a) Combined Fluticasone/salmeterol (Advair) i) Fluticasone One. To stop chest tightness ii) Salmeterol (long acting bronchodilator) . To open up the airways Personal Item I used: These links will direct you to amazon at no cost to you. If you buy from my link, I will be getting few pennies worth. Thank you! YouTube plugin: https://www.tubebuddy.com/redhawk Saunders Book 7th Ed NCLEX-RN: http://amzn.to/2iG6YHS Saunders Drug Book 2017: http://amzn.to/2jXuZuZ Saunders Nursing Today 8th Ed: http://amzn.to/2jXpqNj blender bottle: http://amzn.to/2jFn3hP Weightlifting belt: http://amzn.to/2ippd4f shoes: http://amzn.to/2il8QKC Camera Setup Canon t6: http://amzn.to/2jFmogp waterproof vlogging camera: http://amzn.to/2jXpLPV vlogging tripod: http://amzn.to/2jwZcnF 5 Life saving nursing kit clinical items must have: https://youtu.be/6smxIZAcLQE Learn about blood pressure at http://abnormalbloodpressure.com/ Top 5 Books to Lower High Blood Pressure without Medication http://wp.me/P864rR-9H Top 5 Wrist Blood Pressure Monitor http://wp.me/P864rR-9e Top 3 Upper Arm Blood Pressure Monitor http://wp.me/P864rR-9q Top 5 Fitbit Wristband Fitness Tracker http://wp.me/P864rR-a2 Top 5 Weighing Scale http://wp.me/P864rR-aC come join me and become a member: https://www.goherbalife.com/jbegdamin step 1: click the link above step 2: register step 3: sign in step 4: choose your product of choice step 5: checkout step 6: let's do it together! #nursing #nursingschool #nursingstudents #studentmursejb #stundentnurse #murse Disclaimer: This video is for educational purposes only. If you are experiencing the same signs and symptoms, please do not diagnose yourself. Call your primary provider immediately. -~-~~-~~~-~~-~- #1 Best Selling Camera: "Canon EOS Rebel T6 Full Accessory Bundle | What Comes with it for Paying $469.95?" https://www.youtube.com/watch?v=MhSnU... -~-~~-~~~-~~-~-

Acid Base Status In Chronic Obstructive Pulmonary Disease Patients

Acid base status in chronic obstructive pulmonary disease patients 348 patients of chronic obstructive pulmonary diseases (COPD) were studied for their acid base profile using ABL-3 blood gas analyser (Radiometer, copenhagan). 185 patients (53.1%) had simple disorders (respiratory acidosis53%, respiratory alkalosis25.4%, metabolic acidosis11.3%, metabolic alkalosis10.2%). Mixed disorders were present in 131 patients (34.9%) (respiratory acidosis and metabolic acidosis75.2%, respiratory acidosis and metabolic acidosis14%, metabolic acidosis and metabolic alkalosis5.7%, metabolic alkalosis and respiratory alkalosis4.9%). Hypoxemia without other acid base abnormalities was observed in early patients of GOPD (42 patients12%). Chronic respiratory acidosis was the most common finding in advanced cases of COPD (98%). An almost equal number of such patients had a mixed disorder of respiratory acidosis with metabolic alkalosis (91%). Salt restriction, prolonged use of steriods and hypokalemia were often related to metabolic alkalosis in such patients. Chronic Obstructive Pulmonary DiseaseChronic Obstructive Pulmonary Disease PatientMetabolic AcidosisHypokalemiaAcid Base These keywords were Continue reading >>

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  1. Ash Simmonds

    As usual the conventional wisdom is arse-about with cause/effect, gout etc isn't primarily caused by purine rich or high protein foods upping uric acid, it's the inability to effectively clear out uric acid which eventually form crystals in the joints and stones in the kidneys - which is from a feedback loop of inflammation, and usually there's a catalyst feature which induces it.
    If you are newish to low carb/keto and wondering about the dangers, then uric acid levels can rise substantially in the first 2-4 weeks, but they level out after 6-8 weeks. This is explained in the literature later in this thread, basically what happens is ketones compete for excretion with uric acid, but as you keto-adapt this is no longer a problem.
    The worst thing you can do is go back and forth between keto/carbs whilst you are still adapting. Either stick to it religiously for at least 2 months and adapt properly, or don't bother and save yourself some possible flare-ups.

  2. AshSimmonds

    From ZIOH back in 2008:
    http://forum.zeroinginonhealth.com/showthread.php?tid=1994&page=2
    Quote from: Charles
    I received the following from Gary Taubes:
    Hi Charles,
    My apologies for not getting back to you on your last e-mail. Life has been crazier than usual lately. Anyway, I've attached the section on gout that I cut from GCBC. It's a little rough -- unedited, not fact-checked, etc -- but should give you the general idea. It has some references in it, in the footnotes, but I didn't look to see what form they're in. It should help, though. Meanwhile, Loren Cordain has also written some on gout on his paleolithic diet website. You might look into that. If you post any of this, please credit it appropriately as unpublished from GCBC.
    Here you go,
    Best,
    gt (Emphasis Mine)
    Gout and the condition known technically as hyperuricemia, or elevated levels of uric acid, are the most recent examples of this kind of institutional neglect of the potential health effects of fructose, and how pervasive it can be. Gout itself is an interesting example because it is a disease that has gone out of fashion in the last century and yet the latest reports suggest it is not only as prevalent as ever, but becoming more so. Recent surveys suggest that nearly 6 percent of all American men in their fifties suffer from gout, and over ten percent in their seventies. The proportion of women afflicted is considerably less at younger ages but still rises over 3 percent by age 60. Moreover, the prevalence of gout seems to have doubled over the last quarter century, coincident (perhaps not coincidentally) with the reported increase in obesity, and it may have increased five- or even six-fold since the 1950s, although a large portion of that increase may be due to the aging of the population. CKTK
    Until the late 17th century, when the spread of gout reached almost epidemic proportions in Britain, the disease afflicted almost exclusively the nobility, the rich and the educated, and so those who could afford to indulge an excessive appetite for food and alcohol. This made gout the original example of a disease linked to diet and over-consumption, and so, in effect, the original disease of civilization. But once gout became easily treatable, in the early 1960s, with the discovery of the drug allopuranol, clinical investigators and researchers began to lose interest. And the pathology of gout has been understood since the British physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent; the idea being that uric acid accumulates in the circulation to the point that it falls out of solution, as a chemist would put it, and so crystallizes into needle-sharp urate crystals. These crystals then lodge in the soft tissues and in the joints of the extremities - classically, the big toe -- and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one's eyeballs. Because uric acid itself is a breakdown product of protein compounds known as purines - the building blocks of amino acids - and because purines are at their highest concentration in meat, it has been assumed for the past 130-odd years that the primary dietary means of elevating uric acid levels in the blood, and so causing first hyperuricemia and then gout, is an excess of meat consumption.
    The actual evidence, however, has always been less-than-compelling: Just as low cholesterol diets have only a trivial effect on serum cholesterol levels, for instance, and low-salt diets have a clinically insignificant effect on blood pressure, low-purine diets have a negligible effect on uric acid levels. A nearly vegetarian diet, for instance, is likely to drop serum uric acid levels by 10 to 15% percent CKTK compared to a typical American diet, but that's rarely sufficient to return high uric acid levels to normality, and there is little evidence that such diets reliably reduce the incidence of gouty attacks in those afflicted. Thus, purine-free diets are no longer prescribed for the treatment of gout, as the gout specialist Irving Fox noted in 1984, "because of their ineffectiveness" and their "minor influence" on uric acid levels. Moreover, the incident of gout in vegetarians, or mostly vegetarians, has always been significant and "much higher than is generally assumed." (One mid-century estimate, for instance, put the incidence of gout in India among "largely vegetarians and teetotalers" at 7%.) Finally, there's the repeated observation that eating more protein increases the excretion of uric acid from the kidney and, by doing so, decreases the level of uric acid in the blood. This implies that the meat-gout hypothesis is at best debatable; the high protein content of meats should be beneficial, even if the purines are not.
    The alternative hypothesis is suggested by the association between gout and the entire spectrum of diseases of civilization, and between hyperuricemia and the metabolic abnormalities of syndrome x. In the past century, gout has manifested all of the now-familiar patterns, chronologically and geographically, of diseases of civilization, and so those diseases associated with western diets. European physicians in World War I, for instance, reported a reduced incidence of gout in countries undergoing food shortages. In primitive populations eating traditional diets, gout was virtually unknown or at least went virtually unreported (with the conspicuous exception of Albert Schweitzer who says he saw it with surprising frequency.) The earliest documented cases reported in Asia and Africa were in the late 1940s. And even in the 1960s, hospital records from Kenya and Uganda suggested an incidence of gout lower than one in a thousand among the native Africans. Nonetheless, by the late 1970s, uric acid levels in Africa were increasing with westernization and urbanization, while the incidence of both hyperuricemia and gout among South Pacific islanders was reportedly sky-rocketing. By 1975, the New Zealand rheumatologist B.S. Rose, a colleague of Ian Prior's, was describing the native populations of the South Pacific as "one large gouty family."?
    Gout has also been linked to obesity since the Hippocratic era, CKTK and this association is the origin of the assumption that high-living and excessive appetites are the cause. Gouty men have long been reported to suffer higher rates of atherosclerosis and hypertension, while stroke and coronary heart disease are common causes of death. Diabetes is also commonly associated with gout. In 1951, Menard Gertler, working with Paul Dudley White's Coronary Research Project at Harvard, reported that serum uric acid levels rose with weight, and that men who suffered heart attacks were four times as likely to be hyperuricemic as healthy controls. This led to a series of studies in the 1960s, as clinical investigators first linked hyperuricemia to glucose intolerance and high triglycerides, and then later to high insulin levels and insulin resistance. By the 1990s, Gerald Reaven, among others, was reporting that insulin resistance and hyperinsulinemia raised uric acid levels, apparently by decreasing uric acid excretion by the kidney, just as they raised blood pressure by decreasing sodium excretion. "It appears that modulation of serum uric concentration by insulin resistance is exerted at the level of the kidney," Reaven wrote, "the more insulin-resistant an individual, the higher the serum uric acid concentration."
    These observations would suggest that anything that raised insulin levels would in turn raise uric acid levels and might cause gout, which would implicate any high carbohydrate diet with sufficient calories. But this neglects the unique contribution of fructose. The evidence arguing for sugar or fructose as the primary cause of gout is two-fold. First, the distribution of gout in western populations has paralleled the availability of sugar for centuries, and not all refined carbohydrates in this case. It was in the mid-17th century, that gout went from being exclusively a disease of the rich and the nobility to spread downward and outward through British society, reaching near epidemic proportions by the 18th century. Historians refer to this as the "gout wave," and it coincides precisely with the birth and explosive growth of the British sugar industry and the transformation of sugar, in the words of the anthropologist Sydney Mintz, from "a luxury of kings into the kingly luxury of commoners." British per capita sugar consumption in the 17th century was remarkably low by modern standards, a few pounds per capita per year at the turn of the century, but the change in consumption over the next century and a half was unprecedented: between 1650 and 1800, following the British acquisition of Barbados, Jamaica and other "sugar islands", total sugar consumption in England and Wales increased 20- to 25-fold.?
    The second piece of evidence is much less circumstantial: simply put, fructose increases serum levels of uric acid. The "striking increase" in uric acid levels with an infusion of fructose was first reported in the Lancet in the late 1960s by clinicians from Helsinki, Finland, who referred to it as fructose-induced hyperuricemia. This was followed by a series of studies through the late 1980s confirming the existence of the effect and reporting on the variety of mechanisms by which it came about. Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid. Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it. Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism.
    These mechanistic explanations of how fructose raises uric acid levels were then supported by a genetic connection between fructose metabolism and gout itself. Gout often runs in families, so much so that those clinicians studying gout have always assumed the disease has a strong hereditary component. In 1990, Edwin Seegmiller, one of the few veteran gout researchers in the U.S., and the British geneticist George Radda, who would go onto become director of the Medical Research Counsel, reported that the explanation for this familial association seemed to be a very specific defect in the genes that regulate fructose metabolism. Thus, individuals who inherit this defect will have trouble metabolizing fructose and so will be born with a predisposition to gout. This suggested the possibility, Seegmiller and Radda concluded, that this defect in fructose metabolism was "a fairly common cause of gout."
    As these observations appeared in the literature, the relevant investigators were reasonably clear about the implications: "since serum-uric-acid levels are critical in individuals with gout, fructose might deserve consideration in their diet," noted the Helsinki clinicians in The Lancet in 1967, and so the chronic consequences of high-fructose diets on healthy individuals required further evaluation. Gouty patients should avoid high-fructose or high-sucrose diets, explained Irving Fox in 1984, because "fructose can accelerate rates of uric acid synthesis as well as lead to increased triglyceride production." Although none of these investigators seemed willing to define what precisely constituted a high-fructose or a high-sucrose diet. Was it 50 pounds of sugar a year? 100 pounds? 150 pounds? 300 pounds? And would high-fructose diets induce gout in healthy individuals or would they only exacerbate the problem in those already afflicted? In 1993, the British biochemist Peter Mayes published an article on fructose metabolism in the American Journal of Clinical Nutrition that is now considered the seminal article in the field. (This was in the special issue of the AJCN dedicated to the health effects of fructose.) Mayes reviewed the literature and concluded that high-fructose diets in healthy individuals were indeed likely to cause hyperuricemia, and he implied that gout could be a result, as well, but the studies to address that possibility had simply never been done. "It is clear," Mayes concluded, "that systematic
    investigations in humans are needed to ascertain the precise amounts, both of fructose consumption and of its concentration in the blood, at which deleterious effects such as hyperlipidemia and hyperuricemia occur." Add to this Reaven's research reporting that high insulin levels and insulin resistance will increase uric acid levels, and it suggests, as Mayes had remarked about triglycerides, that sugar (sucrose) and high fructose corn syrup would constitute the worst of all carbohydrates when it comes to uric acid and gout. The fructose would increase uric acid production and decrease uric acid excretion, while the glucose, though its effect on insulin, would also decrease uric acid excretion. Thus, it would be reasonable to assume or at least to speculate that sugar is a likely cause of gout, and that the patterns of sugar consumption explain the appearance and distribution of the disease.
    Maybe so, but this hypothesis has never been seriously considered. Those investigators interested in gout have focused almost exclusively on alcohol and meat consumption, in part because these have historical precedents and because the implication that gouty individuals and particularly obese gouty individuals shy away from meat and alcohol fit in well with the dietary prescriptions of the 1970s onward.
    More than anything, however, this sugar/fructose hypothesis was ignored, once again, because of bad timing. With the discovery and clinical application of allopurinol in the 1960s, those clinical investigators whose laboratories were devoted to studying the mechanisms of gout and purine metabolism - James Wyngaarden's, for instance, at Duke and Edwin Seegmiller's at NIH - began focusing their efforts either on working out the nuances of allipuranol therapy, or to applying the new techniques of molecular biology to the genetics of gout and rare disorders of hyperuricemia or purine metabolism. Nutritional studies were simply not considered worthy of their time, if for no other reason than that allopuranol allowed gout suffers to eat or drink whatever they wanted. "We didn't care so much whether some particular food might do something," says William Kelley, who is a co-author with Wyngaarden of the 1976 textbook, Gout and Hyperuricemia and who started his career in Seegmiller's lab at NIH. "We could take care of the disease."
    This exodus, however, coincided with the emergence of research on fructose-induced hyperuricemia. By the 1980s, when the ability of fructose and sucrose consumption to raise uric acid levels in human subjects was demonstrated repeatedly, the era of basic research on gout had come to an end. The major players had left the field and NIH funding on the subject had dwindled to a trickle. Wyngaarden published his last research paper in 1977 and spent the years 1982 to 1989 as director of the National Institutes of Health. Kelley published his last papers on the genetics of gout in 1989, when he became dean of medicine at the University of Pennsylvania. Irving Fox, who did much of the basic research on fructose- and alcohol-induced hyperuricemia in Kelley's lab, went to work in the biotechnology industry in the early 1990s. Only Edwin Seegmiller remained interested in the etiology of gout, and Seegmiller says that when he applied to the NIH for funding to study the relationship between fructose and gout, after elucidating the genetic connection with Radda in 1990, his grant proposals were rejected on the basis that he was too old and, as an emeritus professor, technically retired. "In the 1950s and 1960s, we had the greatest clinical scientists in the world working on this disease," says Kelley. "By the 1980s and 1990s, there was no one left."
    Meanwhile, the medical journals would occasionally run articles on the clinical management of the gout, but these would concentrate almost exclusively on drug therapy. Discussions of diet would be short, perhaps a few sentences, and confused about the science. On those occasions when the authors would suggest that gouty individuals might benefit from low-purine diets, they would invariably include "sugars" and "sweets" as among the recommended foods with low-purine contents. In a few cases - a 1996 article in the New England Journal of Medicine, for instance -- the articles would also note that fructose consumption would raise uric acid levels, suggesting only that the authors had been unaware of the role of fructose in "sugars" and "sweets." Even when the New England Journal published a report from Walter Willett and his Harvard colleagues in March 2004, this same kind of nutritional illiteracy manifested itself. Willett's article had reported that men with gout seemed to eat more meat than healthy men. But Willett, who by this time was arguably the nation's most influential nutritional epidemiologist, later explained that they had never considered sugar consumption in their analysis because neither he nor his collaborators had been aware of the hyperuricemic effect of fructose. Willett's co-author, Gary Curhan, a nephrologist and gout specialist with a doctorate in epidemiology, said he might have once known that fructose raised uric acid levels, but it had slipped his mind. "My memory is not what it used to be," he said. He also acknowledged, in any case, that he never knew sucrose was half fructose.
    The addenda to this fructose-induced hyperuricemia story may be even more important. When the New England Journal of Medicine published Willett's gout study, it ran an editorial to accompany it written by the University of Florida nephrologist Richard Johnson. Over the past decade, Johnson's research has supported the hypothesis that elevating the uric acid concentration in the circulation also damages the blood vessels leading into the kidneys in such a way as to raise blood pressure directly, and so suggests that fructose consumption will raise blood pressure.
    This is another potentially harmful effect of fructose that post-dates the official reports exonerating sugar in the diet. And it is yet another mechanism by which sugar and high fructose corn syrup could be a particularly unhealthy combination. The glucose in these sugars would raise insulin levels, which in turn would raise blood pressure by inhibiting the kidney's secretion of sodium and by stimulating the sympathetic nervous system, as we discussed in an earlier chapter, and the fructose would do it independently by raising uric acid levels and so damaging the kidney directly. If this were the case, which has never been tested, it would potentially explain the common association of gout and hypertension and even of diabetes and hypertension. Johnson is only now looking into this possibility, however. Unlike Willett and his colleagues, Johnson had long been aware of the ability of fructose to raise uric acid levels, and so was studying that phenomenon in his laboratory. But it was only in the summer of 2004, he explained, three months after his NEJM editorial was published, that he realized that sucrose was half fructose and that his research of the past years was even relevant to sugar.
    ? A decade later, Thomas Benedek described the epidemiology of gout in The Cambridge World History of Human Disease this way: "Worldwide the severity and prevalence of gout have changed paradoxically since the 1940s. In the highly developed countries, as a result of the advent of effective prophylactic drug therapy, the disease is now rarely disabling. Elsewhere, however, it has become more prevalent, predominantly as a result of `improved diets.'"
    ? The economist and historian Ralph Davis estimates that the supply of sugar from the Caribbean into Britain rose from three or four thousand tons a year in the late fifteenth century to over two hundred thousand tons by the 1770s, or an increase of over fifty-fold. (davis r, the rise of the atlantic economies, cornell university press, 1973, p. 251, 255)
    Kramer hm, curhan g, the association between gotu and nephrolithiasis: the national health and nutrition examination survey III. 1988-1994. Am J Kidney Dis 2002;40:37-42
    Arromdee E, Michet CJ, Crowson CS, O'Fallon WM, Gabriel SE. Epidemiology of gout: is the incidence rising? J Rheumatol. 2002 Nov;29(11):2403-6.
    Interview with choi, sept 16, 2004
    Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, Heyse SP, Hirsch R, Hochberg MC, Hunder GG, Liang MH, Pillemer SR, Steen VD, Wolfe F. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States.
    Arthritis Rheum. 1998 May;41(5):778-99.
    gout, the patrician disease, p. 3
    hydrick and fox, p. 748-749.
    Duncan's diseases of metabolism, p. 632.
    Hydrick cr and fox ih, nutrition and gout, in present knowledge in nutrition, fifth edition, the nutrition foundation, Washington dc, 1984, p. 743
    duncans diseases of metabolism, p. 638
    Traut ef, rheumatic diseases, diagnosis and treatment, the C.V. Mosby Company, St. Louis, 1952 p. 303.
    benedek, in Cambridge history of diseases
    Trowel hc, a case of gout in a ruanda African, the east African medical journal, oct. 1947, p. 346-348
    Beighton p et al, 1977, rheumatic disorders in th south African negro, part IV. Gout and hyperuricemia. South Af Med J. 51(26):969-72
    Gout in the Maoris, B.S. Rose, Seminars in Arthritis and Rheumatism. Vol. 5, no. 2, (November) 1975, pg. 121-145.
    duncan's diseases of metabolism, 1947, p. 631
    gertler mm, et al, erum uric acid in relation to age and physique in health andin coronary ehart disease, Ann Intern Med. 1951 Jun;34(6):1421-31. Reiser S, Uric Acid and Lactic Acid, in REISER S AND HALLFRISCH J, METABOLIC EFFECTS OF FRUCTOSE, crc press, boca raton fl, 1987 p. 113-134
    duncan's diseases of metabolism, p. 631
    reaven gm, The Kidney: An Unwilling Accomplice in Syndrome X, Am J Kid Dis, Vol. 30, n0 6, December, 1997: pp. 928-931.
    Facchini F et al, Relationship Between Resistance to Insulin-Mediated Glucose Uptake, Urinary Uric Acid Clearance, and Plasma Uric Acid Concentration, JAMA, December 4, 1991, vol. 266, no. 21, 3008-3011
    Wyngaarden and Kelley p. ix
    mintz
    Sydney Mintz, Sweetness and Power, The Place of Sugar in Modern History, penguin books, ny 1985 p. 96.
    mintz p. 64, 66
    perheentupa j raivio k, fructose-induced hyperuricaemia, lancet, September 9, 1967, p.528531
    emmerson bt, getting rid of gout
    mayes pa, metabolism of fructose, ajcn, 1993
    hydrick c fox i, nutrition and gout, in modern reviews of nutrition
    Seegmiller JE, Dixon RM, Kemp GJ, Angus PW, McAlindon TE, Dieppe P, Rajagopalan B, Radda GK. Fructose-induced aberration of metabolism in familial gout identified by 31P magnetic resonance spectroscopy.
    Proc Natl Acad Sci U S A. 1990 Nov;87(21):8326-30
    peerheentupa ibid
    hydrick and fox, p. 748-749.
    Mayes pa, metabolism of fructose, ajcn 1993
    Kelley interview
    seegmiller interview
    See for instance, fam ag, gout, diet and the insulin resistance syndrome, j. rheum. 2002;29, 1350-55
    Emmerson BT. The management of gout.
    N Engl J Med. 1996 Feb 15;334(7):445-51
    get citation from Richard Johnson articles on uric acid and hypertension.
    Johnson interview, june 3, 2004
    UNPUBLISHED MATERIAL FROM THE BOOK, GOOD CALORIES, BAD CALORIES BY GARY TAUBES
    The Gary Taubes half-finished article was later published to Tim Ferriss's site:
    http://www.fourhourworkweek.com/blog/2009/10/05/gout/
    Included some recent commentary that I'd not heard of before:
    Quote from: Burton Abrams
    Your gout article rightfully refers to the work of Dr. Richard Johnson, who has moved from U. Fla to U. Col in Denver. His work clearly shows that dietary fructose is processed in the body to produce uric acid, and hence raises the level of uric acid in the blood.
    But there is more to the question of why the high concentration of serum uric acid precipitates as the crystals of monosodium urate (MSU) which cause gout. Consider that most gout attacks originate while the individual is sleeping. Why? The answer is sleep apnea, which is the frequent cessation of breathing for many seconds at a time during sleep. The resulting reduction of oxygen in the blood has three effects, each of which can make MSU precipitation more likely. The first is cell catabolism, in which ATP undergoes a chain of chemical transitions which culminates in the cellular generation of excess uric acid fed into the blood. The second is that the reduced oxygen in the blood makes the blood more acidic (lower pH) so it can hold less uric acid in solution. These two effects are transient, so blood tests taken after awakening misses their peaks. The third effect is long term. Over time the chronic intermittent reduction in oxygen causes gradual reduction of kidney function, so uric acid is removed from the blood more slowly.
    So fructose ingestion raises the uric acid baseline, but sleep apnea causes it to reach an abrupt tipping point which leads to gout. I've told hundreds of gout experts about this physiology, and the only one who already knew about it was Dr. Johnson. Unfortunately, he thought it was common knowledge.
    Dr. Johnson's recent book The Fat Switch is written for general readership. It describes how fructose activates a biological switch in the body to cause it to store fat rather than burn fat. It is an excellent companion to The Four Hour Body.
    Quote from: Burton Adams
    My experience was that when I completely overcame my sleep apnea, my gout attacks ceased immediately and completely. If your Mom's CPAP machine is properly adjusted for her, and if she always uses it whenever she sleeps, I expect that her gout attacks would be greatly mitigated. Unfortunately, many sleep physicians don't recommend total adherence to CPAP usage. I think that is a big disservice to the patient.
    MSU crystals form quickly (minutes), but then dissolve very slowly (months).
    Most gout attacks last for about a week because the immune system places a protein sheath around the crystals so that they are no longer sensed by other immune system cells which activate the gout pain and inflammation. (A gout attack is initiated by the immune system chemically sensing the presence of these crystals, not by the physical fact that these crystals are needle shaped.) So a gout attack can be initiated if the sheath is ruptured, either chemically by an uricosic drug such as allopurinol or physically by undue stress on the affected joint. Sleep apnea may be the reason why the crystals are formed in the first place, but once formed they may initiate multiple gout attacks by these other means.

  3. Burton Abrams

    So went and found more stuff by him:
    http://www.beatinggout.com/2009/04/gout-and-the-sleep-apnea-connection/
    Quote
    Gout and the Sleep Apnea Connection
    There is a frequently overlooked factor that can cause an acute increase in the concentration of uric acid in the blood as well as increased likelihood of its precipitation as MSU (monosodium urate or uric acid crystals. See, Gout Basics for background). That factor is the reduction of the concentration of oxygen in the blood, which occurs in an individual suffering from sleep apnea.
    Sleep apnea is the repeated cessation of breathing for many seconds at a time during sleep, when the muscles lining the airway relax enough to allow it to close, until the brain jolts them to reopen. The resulting reduction of oxygen in the blood causes the cells in the body to undergo a process of disintegration, which leads to their generation of excess uric acid. Once the uric acid is formed, the process is irreversible, even when breathing restarts. With each apneic period, more and more uric acid is fed into the blood, faster than the kidneys can dispose of it. Furthermore, the increased ratio of carbon dioxide to oxygen in the blood makes the blood more acidic, so that its ability to hold uric acid in solution is reduced and MSU is more likely to precipitate. These processes were described in medical journal literature about twenty years ago, and subsequent literature has confirmed that sleep apnea leads to excess uric acid in the blood and in the urine.
    Thus, sleep apnea hits gout attacks with a double whammy. It feeds more uric acid into the blood plus it reduces the ability of the blood to hold the uric acid in solution so that MSU precipitates. The result is a gout attack that develops while sleeping.
    This dysfunctional blood chemistry begins to resolve after the sleeper awakens, when the apneic periods cease and the kidneys have time to catch up in their removal of uric acid from the blood. Thus, a blood test of uric acid taken several hours after awakening will often measure as normal. The excess uric acid occurs as a flare that the belated blood test never detects.
    The factors for increased risk of developing gout - heredity, overweight, alcohol use, middle or elderly age, male gender, female gender past menopause - are all the same increased risk factors for developing sleep apnea. But those who do not fall into these categories can develop either condition. It's just less likely. I am not overweight, and I never was. Yet I developed both in middle age. Now I have neither.
    Where Are The Data?
    One would think that in the twenty-year period since these physiologic processes were described, gout researchers would have conducted studies to determine what percentage of gout sufferers also have sleep apnea, and in what percentage of those does resolving the sleep apnea cure their gout. It hasn't happened. One can only speculate as to why, and some speculated conclusions may have a very cynical view of gout experts. What has been reported recently is a long list of serious diseases that have been found to have a strong association with elevated uric acid, but with no recognition given that all these diseases have previously been shown to be consequences of sleep apnea.
    I realized the sleep apnea/gout connection over five years ago when resolving my sleep apnea resulted in the complete cessation of my gout attacks. And I know that I am not the only one who has observed that result. Based on my information, my primary care physician has been screening all his gout patients for sleep apnea. He has found that a large majority of them have sleep apnea, when neither he nor they would have otherwise suspected it.
    Why This Is So Important
    The results found by my literature search and by my primary care physician have convinced me the sleep apnea is a major cause of gout attacks. I have the view that all gout sufferers should assume they have sleep apnea as the underlying cause of gout until proven otherwise. That means that all gout sufferers should be screened for sleep apnea, not only to cure their gout, but more importantly to prevent the development of much more serious diseases.
    Resolving gout is important. Even more important is diagnosing and resolving sleep apnea. Gout is very painful, but by itself it is not life threatening. If left untreated, sleep apnea is known to have numerous consequences that are life threatening - heart attack, heart arrhythmias, heart failure, stroke, diabetes, depression, kidney disease, and many other maladies. It is no wonder that this list matches closely the list of associations with hyperuricemia presented in the Is Gout Dangerous? posting on this website, because hyperuricemia is a direct consequence of sleep apnea. A fourteen-year study in Australia of people with sleep apnea who refused treatment concluded that the life expectancy of these people was 18 years shorter that of the general population, a conclusion that stunned even the study's researchers.
    Unfortunately, palliating your gout by using NSAIDs or prescription drugs does nothing to overcome your sleep apnea. It just masks the warning until one or more of the dire consequences of sleep apnea smacks you. In my case it was a transient ischemic attack (ministroke), atrial fibrillation heart arrhythmia, and diabetes, all of which I have recovered from. I was lucky that my sleep apnea consequences turned out to be reversible, but I have to maintain a strict diet to prevent the return of my diabetes.
    There are about 80 times as many people with sleep apnea as there are with gout. Ironically, those of us with gout may be the fortunate ones because we have an early warning of our sleep apnea, but only if we and our doctors know about the connection.
    Written by
    Burton Abrams
    Author of, The Perils of Sleep Apnea - An Undiagnosed Epidemic
    Update (August 1, 2009):
    A recent study performed in Australia of the medical records of over 16,000 patients diagnosed with obstructive sleep apnea found that gout was present in about 5% of them. Other sources estimate that the prevalence of gout in Australia is .27% of the population. That means that in Australia the likelihood of gout is 19 times higher in people with sleep apnea vs. the general population. Statistics for other first world countries are probably very similar.
    -Burton Abrams

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