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An Overview of Hypoglycemia


US Pharm. 2012;37(6):50-56.

Hypoglycemia is a low concentration of glucose in the blood, but no specific plasma glucose level defines the condition.1 Rather, hypoglycemia is best described as a plasma glucose concentration sufficiently low to elicit signs and/or symptoms.1 In healthy individuals, the glycemic threshold for symptoms is 50 to 55 mg/dL, although plasma glucose levels under 70 mg/dL signal impending hypoglycemia.2 Symptoms can occur at higher concentrations in patients with poorly controlled diabetes, and at lower levels in those with tight glycemic control or recent hypoglycemic exposure.2 Most hypoglycemia is iatrogenic and associated with drug-treated diabetes mellitus.1 Other causes of hypoglycemia, rare in individuals older than 10 years of age, will be briefly discussed later.

Glucose supplies immediate energy needs and fuels metabolic functions between meals. If it is not needed for immediate use, glucose is stored as glycogen in the liver and muscles, or else as fat.3 Glucose is a requisite metabolic fuel for brain cells. Because the brain can neither synthesize glucose nor store more than a few minutes’ supply in the form of glycogen, it is critically important that a steady glucose supply be available to brain cells via the circulation.2

In healthy individuals, a finely choreographed interaction between insulin and several counterregulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone, ensures that blood glucose concentrations are maintained within the physiological range. This process is called glucose counterregulation. As plasma glucose concentrations drop below physiological range, insulin secretion decreases and ultimately ceases. Glucagon and epinephrine concentrations increase concurrently to produce a rapid rise in plasma glucose, thus averting or swiftly correcting hypoglycemia.2 Glucagon stimulates glycogenolysis (the breakdown of glycogen into glucose) in the liver, as well as hepatic gluconeogenesis (the formation of glucose from noncarbohydrate substrates). Epinephrine promotes hepatic glycogenolysis and hepatic and renal gluconeogenesis. Cortisol and growth hormone work slowly over hours to defend against prolonged hypoglycemia, but they play a minimal role in reversing hypoglycemia.1

The goal of diabetes management is a lifetime of euglycemia without hypoglycemia.4 Hypoglycemia constitutes a significant roadblock to achieving both short-term and long-term glycemic control, which may lead to the development of long-term complications of diabetes.2 It is estimated that, on average, individuals with type 1 diabetes mellitus (T1DM) experience two symptomatic episodes of hypoglycemia weekly and one severe event annually. With declining pancreatic function, the incidence of hypoglycemia increases in type 2 diabetes mellitus (T2DM).2 The negative effects of hypoglycemia include psychological morbidity, physical morbidity, and mortality. In patients with diabetes, the fear of hypoglycemia exceeds the fear of long-term complications.2

Pathophysiology

In T1DM and advanced T2DM, glucose counterregulation is compromised by the impaired secretion of insulin, glucagon, and epinephrine, breaching three physiological defenses against hypoglycemia. First, falling plasma glucose concentrations fail to elicit a corresponding decrease in insulin secretion in patients taking insulin or insulin secretagogues. With absolute or relative exogenous insulin excess, insulin activity is dictated by the pharmacokinetic characteristics of the drug. Second, hypoglycemia does not trigger glucagon secretion. Third, a lower plasma glucose concentration is required to stimulate an epinephrine response.2

Hypoglycemia Unawareness

Some patients with T1DM or advanced T2DM lose the neurogenic warning symptoms that herald impending hypoglycemia. This state, hypoglycemia unawareness, is likely the result of repeated iatrogenic hypoglycemia episodes that lead to impaired epinephrine response and diminished neurogenic symptoms.2 The weakened counterregulatory response, hypoglycemia-associated autonomic failure (HAAF), puts the patient at high risk for severe hypoglycemia. Fortunately, a 2- to 3-week period of strict avoidance of hypoglycemia appears to improve the epinephrine response and restore hypoglycemia awareness.2,3

Causes and Risk Factors

Iatrogenic hypoglycemia results from therapy that raises insulin concentrations and lowers plasma glucose concentrations.1 Agents include insulin and insulin secretagogues. Other diabetes drugs may cause hypoglycemia when combined with insulin or insulin secretagogues (TABLE 1).

Conventional risk factors for iatrogenic hypoglycemia relate to relative or absolute insulin excess (FIGURE 1). As discussed previously, HAAF is associated with a high risk of hypoglycemia. Risk factors include an absolute deficiency of endogenous insulin; a history of severe hypoglycemia and/or hypoglycemia unawareness, as well as recent hypoglycemia, prior exercise, and sleep; and intensive glycemic therapy as evidenced by lower glycosylated hemoglobin concentrations and/or lower glycemic goals.1

Symptoms of Hypoglycemia

A reduction in blood glucose initiates an autonomic nervous system response, resulting in neurogenic signs and symptoms (categorized as adrenergic or cholinergic) that alert the patient to a hypoglycemic episode (TABLE 2). Each patient’s array of symptoms is unique and may vary in magnitude over time. However, signs and symptoms often present in diabetes are also frequently associated with other disease states, and hypoglycemia does not necessarily elicit these signs and symptoms. Thus, hypoglycemia is best confirmed by Whipple’s triad: symptoms consistent with hypoglycemia, a low plasma glucose concentration, and symptom relief when the glucose concentration is raised.4 Optimally, the presence of signs and symptoms during mild hypoglycemia prompts the patient to ingest carbohydrates, thereby enabling blood glucose concentrations to normalize. If the episode progresses, the deficiency of glucose in brain cells results in neuroglycopenic symptoms. Lack of attention to mild symptoms or compromised autonomic response signals may preclude recognition of a hypoglycemic event. The pharmacist should counsel the patient to be attentive to symptoms, self-monitor blood glucose (SMBG) whenever suspicious, and treat for hypoglycemia if monitoring is not available.2

It is estimated that more than 50% of hypoglycemic episodes occur during sleep, and the sufferer usually is unaware of them.4 An individual might assume the occurrence of hypoglycemia if he or she awakens with bedclothes damp with sweat and is confused, irritated, or tired, or was calling out or having nightmares during sleep.3 In such cases, periodic 3-AM SMBG is recommended to determine whether hypoglycemia is occurring overnight. Nighttime hypoglycemia is suspected of causing arrhythmias that lead to unforeseen death, or dead-in-bed syndrome.1

Treatment of Mild-to-Moderate Hypoglycemia

When hypoglycemia is suspected, SMBG should be performed if a meter is available. A reading below 70 mg/dL indicates the need for immediate consumption of 15 to 20 g of simple carbohydrates, preferably glucose.5 If testing is not possible, remember: “When in doubt, treat.” Untreated hypoglycemia presents a greater risk than that posed by an episode of hyperglycemia. Severe and protracted neuroglycopenia, although rare, may lead to permanent brain damage and even death.2 Recommended carbohydrates include 3 to 4 glucose tablets (5 g each); 1 tube of glucose gel; 4 oz. fruit juice or soft drink (not sugar free); 8 oz. milk (low-fat preferred); 4 to 6 pieces of hard candy (not sugar free); or 1 tbsp. sugar, honey, or corn syrup. Protein does not impair the desired glycemic response, but fat does. Therefore, chocolate candy is not recommended unless no other simple carbohydrate is available.

Blood glucose should be rechecked at 15-minute intervals, and treatment repeated if glucose remains below 70 mg/dL. Once blood glucose is at or above 70 mg/dL, the patient should eat a snack or meal to maintain euglycemia.3

Treatment of Severe Hypoglycemia

Neuroglycopenia can impair an individual to the extent that someone else must administer treatment. If the patient can safely swallow, glucose gel, honey, jelly, or syrup should be placed inside the cheek for absorption. If the patient is unable to swallow or is unconscious, a glucagon injection is required to rapidly elevate the serum glucose level.3 IV dextrose is the preferred treatment for hospitalized patients. Once conscious, the patient should drink a carbohydrate-rich fluid, followed by a snack once he or she is no longer nauseated. Medical supervision is indicated until the risk of recurrent hypoglycemia has passed.2

A prudent pharmacist counsels patients with diabetes on hypoglycemia avoidance during each contact.1 Patients should follow a diabetes management plan that includes blood glucose monitoring (with scrupulous monitoring when ill), a medication protocol, meal and snack planning, management of activity and exercise, and moderate alcohol ingestion.3

The patient should be reminded that diabetes medication may need to be adjusted to respond to changes in food ingestion and physical activity. The pharmacist should ascertain that the patient knows how to use his or her meter, and should suggest alternative solutions if medications or meter supplies are a financial hardship. Information on medications that are more likely to cause hypoglycemia should be provided, and patients taking acarbose or miglitol should be cautioned that only dextrose will raise blood glucose during a hypoglycemic episode.3 The pharmacist should offer glucagon emergency kit training to the patient’s family members. The patient should be reminded to carry a simple carbohydrate source—preferably glucose tablets—at all times and to avoid the accidental consumption of sugar-free candy or soft drinks in the treatment of hypoglycemia. The patient should be advised to perform SMBG before driving if he or she is at risk for hypoglycemia, to test often during long driving trips, and to refrain from driving until blood glucose is at least 70 mg/dL.3 The pharmacist must recognize that information and willingness to follow a diabetes management plan are essential for enabling a patient to avoid hypoglycemia and live successfully with diabetes.2

Hypoglycemia can occur in those not being treated for diabetes. Organizations such as the National Institutes of Health and the National Diabetes Information Clearinghouse note the existence of several types of noniatrogenic hypoglycemia.

Reactive (Postprandial) Hypoglycemia

Reactive hypoglycemia occurs within 4 hours after a meal is consumed,with diagnosis based on documentation of Whipple’s triad.1,3 Several causes have been proposed but are unsubstantiated, including excessive release of insulin following high sugar intake, enhanced sensitivity to the normal secretion of epinephrine and its attendant hypoglycemic symptoms, and deficient glucagon secretion.3

Gastrointestinal surgery can cause hypoglycemia if food passes into the small intestine too quickly, but this is uncommon. Rare hereditary enzyme deficiencies can lead to fructose intolerance and reactive hypoglycemia.3

Fasting (Postabsorptive) Hypoglycemia

This condition may be diagnosed when the serum glucose concentration is below 50 mg/dL after overnight fasting, between meals, or following physical activity.3 Several underlying conditions can contribute to fasting hypoglycemia, including the consumption of medications other than those used to treat diabetes (TABLE 3). Alcohol consumption, especially binge drinking, can cause severe or even fatal hypoglycemia by halting gluconeogenesis and depleting hepatic glycogen.6 Critical illnesses affecting the liver, heart, or kidneys can contribute to fasting hypoglycemia.3 Sepsis can deplete hepatic glycogen stores and impair gluconeogenesis.7 Disorders involving renal insufficiency can decrease drug elimination and affect serum glucose concentration.8 Starvation conditions (e.g., anorexia nervosa) can deplete glycogen and fat stores used for energy between meals, as well as substrates used in gluconeogenesis.

Treatment of the underlying cause will help resolve hypoglycemia. Deficiencies of glucagon, epinephrine, cortisol, and growth hormone, which are rare, are usually corrected by exogenous hormone supplementation.3Such conditions are more common in very young children than in adults. Insulinomas—rare, usually benign pancreatic tumors that secrete excessive amounts of insulin—can cause hypoglycemia.1,3 Surgical removal of the insulinoma is preferred, but pharmacologic agents such as diazoxide or octreotide also may be used to lower serum insulin concentrations.

CONCLUSION

Hypoglycemic episodes compromise wellness in all who experience them. In diabetic patients, the risk of hypoglycemia may limit the potential for lifelong euglycemia.2,4 Pharmacists who offer education and support afford their patients the opportunity to better understand and follow their disease-management plans and to enjoy better health.

REFERENCES

1. Cryer PE, Axelrod L, Grossman AB, et al. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2009;94:709-728.
2. Cryer PE, Davis SN, Shamoon H. Hypoglycemia in diabetes. Diabetes Care. 2003;26:1902-1912.
3. National Diabetes Information Clearinghouse. Hypoglycemia. http://diabetes.niddk.nih.gov/dm/pubs/hypoglycemia/#nodiabetes. Accessed October 6, 2011.
4. American Diabetes Association. Defining and reporting hypoglycemia in diabetes: a report from the American Diabetes Association Workgroup on Hypoglycemia. Diabetes Care. 2005;28:1245-1249.
5. American Diabetes Association. Executive summary: standards of medical care in diabetes—2012. Diabetes Care. 2012;35(suppl 1):S11-S63.
6. Masharani U. Diabetes mellitus and hypoglycemia. In: McPhee SJ, Papadakis MA, Rabow MW, eds. CURRENT Medical Diagnosis and Treatment 2012. 51st ed. New York, NY: McGraw-Hill Medical; 2011.
7. Miller SI, Wallace RJ Jr, Musher DM, et al. Hypoglycemia as a manifestation of sepsis. Am J Med. 1980;68:649-654.
8. Mayo Clinic. Hypoglycemia. Causes. www.mayoclinic.com/health/hypoglycemia/DS00198/DSECTION=causes. Accessed March 27, 2012.
9. Thomson Reuters Micromedex 2.0. www.micromedex.com. Accessed March 25, 2012.
10. Vue MH, Setter SM. Drug-induced glucose alterations part 1: drug-induced hypoglycemia. Diabetes Spectrum. 2011;24:171-177.
11. MedlinePlus. Drug-induced hypoglycemia. www.nlm.nih.gov/medlineplus/ency/article/000310.htm. Accessed March 25, 2012.
12. CDC. Treatment of malaria (guidelines for clinicians). www.cdc.gov/malaria/resources/pdf/clinicalguidance.pdf. Accessed May 1, 2012.
13. Kojak G Jr, Barry MJ Jr, Gastineau CF. Severe hypoglycemic reaction with haloperidol: report of a case. Am J Psychiatry. 1969;126:573-576.
14. Walter RB, Hoofnagle AN, Lanum SA, Collins SJ. Acute, life-threatening hypoglycemia associated with haloperidol in a hematopoietic stem cell transplant recipient [letter]. Bone Marrow Transplant. 2006;37:109-110.

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Metabolic Syndrome: Risk Factors and Recommendations


ABSTRACT: Metabolic syndrome comprises many risk factors, including—but not limited to—high blood sugar, hypertension, and dyslipidemia, the incidences of which are continuing to rise in the United States. It is important for pharmacists to be familiar with the various components of metabolic syndrome so that they can perform appropriate screenings in at-risk patients and encourage therapeutic lifestyle changes. Pharmacists can also make drug-therapy recommendations to help prevent further complications associated with metabolic syndrome.

Metabolic syndrome is a collection of co-occurring disorders that increase the risk of heart disease, stroke, and diabetes mellitus (DM). Metabolic risk factors such as elevated plasma glucose, high blood pressure (BP), and dyslipidemia contribute to atherosclerosis, as well as to a prothrombotic and proinflammatory state.1,2 Additional risk factors include abdominal obesity, physical inactivity, insulin resistance, cigarette smoking, and family history of premature coronary heart disease (CHD).2 Compared with patients who do not have metabolic syndrome, those with metabolic syndrome are twice as likely to develop CHD and five times more likely to develop DM.1-3 While the pathophysiology of metabolic syndrome is multifactorial, one component is the proinflammatory state, as denoted by an elevated level of C-reactive protein. In obesity, cytokine release from the adipose tissue causes inflammation, which leads to the development of dyslipidemia and increasing waist circumference.2,4

In the United States, metabolic syndrome affects approximately 35% of adults, of whom 85% also have DM.2,3 Prevalence, which varies by sex with respect to race and ethnicity, increases with age. Compared with non-Hispanic white males, non-Hispanic black males have a lower incidence of metabolic syndrome (37% vs. 25%). Non-Hispanic black and Mexican-American females are nearly 1.5 times more likely than non-Hispanic white females to have metabolic syndrome.5 Forty-one percent of males and 37% of females aged 40 to 59 years and 52% of males and 54% of females older than 60 years meet diagnostic criteria for metabolic syndrome.5

Diagnosis and Treatment

The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) outlines diagnostic criteria for metabolic syndrome (TABLE 1).6 Treatment for metabolic syndrome focuses on modification of these criteria. The primary treatment approach is nonpharmacologic, including weight reduction, dietary changes, physical activity, and smoking cessation.6 In addition to therapeutic lifestyle changes (TLC), patients may consider adjunct treatment with a weight-loss agent.

Weight-Loss Management

Medications such as Xenical or Alli (orlistat) or one of two recently approved weight-loss agents, Belviq (lorcaserin) and Qsymia (phentermine-topiramate extended-release), may be used adjunctively to manage weight loss. TABLE 2 presents these agents in greater detail.

Orlistat: Xenical and Alli are indicated for weight loss and maintenance in obese patients and to reduce the risk of weight gain following a substantial weight loss. Orlistat exerts its effect on weight as a reversible inhibitor of gastrointestinal (GI) lipase enzymes. Since this drug acts locally within the GI tract, common side effects are GI in nature.7

Lorcaserin:Belviq is indicated as adjunct treatment in obese or overweight patients with comorbid conditions including hypertension, dyslipidemia, and type 2 DM (DM2). The CDC defines obesity as a BMI of ≥30.0 kg/m2 and overweight as a BMI of 25.0 to 29.9 kg/m2. Lorcaserin, an agonist of the serotonin 2C receptor, promotes satiety and decreases food consumption. Dosing is 10 mg twice daily. Side effects are minimal; however, patients with DM are more susceptible to hypoglycemia. If ≥5% weight loss is not achieved after 12 weeks, therapy should be discontinued. Lorcaserin is a Class IV controlled substance because of its potential for abuse. Patients should be advised to take this drug only as prescribed and never to share it.8

Three phase III clinical trials (BLOOM, BLOOM-DM, and BLOSSOM) investigated the safety and efficacy of lorcaserin in nondiabetic and diabetic subjects.9-11 The primary outcome was the percentage of subjects achieving ≥5% weight loss from baseline to week 52. In BLOOM, lorcaserin 10 mg twice daily was compared with placebo twice daily. The primary outcome was achieved in 47.5% of the lorcaserin group and 20.3% of the placebo group, respectively (P <.0001).9 BLOOM-DM compared both of these treatment modalities, plus lorcaserin 10 mg once daily. The once-daily group also received a placebo dose nightly for blinding purposes. The primary outcome was achieved in 37.5%, 44.7%, and 16.1% of the lorcaserin twice-daily, lorcaserin once-daily, and placebo groups, respectively (P <.001).10 BLOSSOM evaluated the same treatment modalities as BLOOM-DM. Higher percentages of subjects in the lorcaserin twice-daily (47.2%) and once-daily (40.2%) groups met the primary outcome, versus 25% of the placebo group (P <.0001).11

Phentermine/Topiramate Extended-Release: Although the exact mechanism of action of Qsymia is unknown, its components—a sympathomimetic and an extended-release antiepileptic—are thought to augment chronic weight management by increasing satiety and decreasing appetite. The indications are the same as those for lorcaserin. Dose titration is required upon initiation and discontinuation to prevent seizure occurrence. Dosing is 3.75/23 mg daily for 14 days, then 7.5/46 mg daily as maintenance. If 3% weight loss is not achieved after 12 weeks, therapy may be discontinued, or the dosage may be deescalated or increased to 11.25/69 mg daily for 14 days before being increased to a maximum of 15/92 mg daily. If 5% weight loss is not achieved after 12 weeks on the maximum dosage, therapy should be gradually discontinued. This product is available only through pharmacies enrolled in the Qsymia Certified Pharmacy Network.12

The safety and efficacy of phentermine/topiramate extended-release were evaluated in three phase III clinical trials (EQUIP, CONQUER, and SEQUEL).13-15 Over 52 weeks, EQUIP assessed severely obese subjects (BMI ≥35 kg/m2) and CONQUER studied overweight and obese subjects (BMI ≥27 to ≤45 kg/m2) with two or more comorbidities, such as hypertension, hyperlipidemia, DM, or increased waist circumference (women, ≥88 cm; men, ≥102 cm). The endpoint was ≥5% weight loss by trial completion. In EQUIP, subjects taking 3.75/23 mg and those taking 15/92 mg achieved an overall weight loss of 5.1% and 10.9%, respectively, versus 1.6% for the placebo group (P <.0001). In CONQUER, subjects taking 7.5/46 mg and those taking 15/92 mg achieved an overall loss of 7.8% and 9.8%, respectively, versus an overall loss of 1.2% in the placebo group (P <.0001).13,14 SEQUEL, a 52-week CONQUER extension study, evaluated long-term results of drug therapy, focusing on weight-loss maintenance during year 2. From baseline, 9.3% and 10.5% of subjects taking 7.5/36 mg and 15/92 mg, respectively, experienced weight-loss maintenance (P <.001).15

Management of Other Risk Factors

In addition to weight loss and/or maintenance, the other components of metabolic syndrome must be managed. In treating dyslipidemia, the primary goal is to lower LDL cholesterol (LDL-C). The target LDL-C depends upon the presence of CHD, risk equivalents, or risk factors. The ATP III LDL-C goal—as well as optional goals described in the 2004 update to the NCEP’s clinical practice guidelines—for each risk category appears in TABLE 3.6,16To achieve goal LDL-C, TLC—a multifaceted lifestyle approach—must be implemented. In addition, drug therapy may be required to achieve the desired LDL-C. An HMG-CoA (statin) is recommended, not only for its LDL-C reduction potential, but also for its primary prevention of cardiovascular disease in high-risk patients and secondary prevention in patients with CHD.6

According to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), a number of TLC are warranted for BP reduction. These include the Dietary Approaches to Stop Hypertension (DASH) eating plan (emphasizing consumption of fruits, vegetables, fat-free or low-fat milk/dairy products, and whole grains); sodium restriction (≤2.4 g/day); weight reduction (to maintain BMI of 18.5-24.9 kg/m2); physical activity (regular aerobic activity for 30 minutes/day most days of week); moderate alcohol consumption (men, ≤2 drinks/day; women, ≤1 drink/day); and smoking cessation.17

The JNC 7’s target BP goal for patients with chronic kidney disease or DM is <130/80 mmHg; for all others, it is <140/90 mmHg.17 The American Heart Association provides hypertension guidelines and goals for other categories. Target BP for patients with coronary artery disease (CAD) or CAD risk equivalents (carotid artery disease, peripheral artery disease, abdominal aortic aneurysm), as well as those at high risk for CAD (DM, chronic renal disease, or 10-year Framingham risk score ≥10%), is <130/80 mmHg. For ventricular dysfunction, the target BP goal is <120/80 mmHg.18 According to theJNC 7, drug-therapy selection is based upon compelling indications (TABLE 4).17

The 2013 American Diabetes Association guidelines recommend lifestyle modifications (similar to those in JNC 7) to reduce blood glucose (BG) and prevent DM2. Metformin also may be considered to treat elevated BG. Without a diagnosis of DM, the fasting BG goal is <100 mg/dL.19

Finally, since a proinflammatory state exists in metabolic syndrome, the use of aspirin should be considered. Aspirin 81 mg daily should be considered in patients with a 10-year risk ≥10%. Aspirin 81 to 325 mg daily should be used for secondary prevention in patients with a history of CHD.1

Pharmacist Interventions

Since most components of metabolic syndrome do not have associated symptoms, patients may not be concerned about risk. Pharmacists can host educational and screening programs to foster awareness of metabolic syndrome and identify at-risk patients who are candidates for therapy. Upon identification, patients should schedule a primary care appointment for further assessment and pharmacologic therapy.

Pharmacists can intervene further by setting measurable and achievable goals; assessing adherence; identifying barriers to treatment; emphasizing the role of nonpharmacologic therapy; supporting patients engaged in lifestyle modifications; and educating patients about safe medication use, risk-factor modification, diagnosis of metabolic syndrome, device use (glucometer or BP cuff), and lifestyle interventions. Pharmacists are in an ideal position to assess patients’ self-monitoring of weight, BG, and BP and help them develop care plans. As another component of the medication-therapy process, pharmacists can help patients develop and update a personal medication record.20 No matter which aspect is addressed, it is essential to engage patients during all encounters.

NOTE: Subsequent to the writing of this paper, new guidelines were issued by the Eighth Joint National Committee (2014), American Diabetes Association (2014), American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines [cholesterol treatment] (2013), and ACC/AHA/The Obesity Society [overweight/obesity management] (2013).

REFERENCES

1. Grundy SM, Cleeman JI, Daniels SR, et al; American Heart Association; National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005;112:2735-2752.
2. Grundy SM, Brewer HB Jr, Cleeman JI, et al; American Heart Association; National Heart, Lung, and Blood Institute. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004;109:433-438.
3. Fowler MJ. Microvascular and macrovascular complications of diabetes. Clin Diabetes. 2008;26:77-82.
4. Reilly MP, Rader DJ. The metabolic syndrome: more than the sum of its parts? Circulation. 2003;108:1546-1551.
5. CDC. NHANES III. 2009. www.cdc.gov/nchs/nhanes/nh3data.htm. Accessed August 30, 2013.
6. National Heart, Lung, and Blood Institute. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. NIH Publication No. 02-5215. September 2002. www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf. Accessed September 5, 2013.
7. Xenical (orlistat) product information. South San Francisco, CA: Genentech USA, Inc; December 2013.
8. Belviq (lorcaserin) product information. Woodcliff Lake, NJ: Eisai Inc; August 2012.
9. Smith SR, Weissman NJ, Anderson CM, et al; Behavioral Modification and Lorcaserin for Overweight and Obesity Management (BLOOM) Study Group. Multicenter, placebo-controlled trial of lorcaserin for weight management. N Engl J Med. 2010;363:245-256.
10. O’Neil PM, Smith SR, Weissman NJ, et al. Randomized placebo-controlled clinical trial of lorcaserin for weight loss in type 2 diabetes mellitus: the BLOOM-DM study. Obesity (Silver Spring). 2012;20:1426-1436.
11. Fidler MC, Sanchez M, Raether B, et al; BLOSSOM Clinical Trial Group. A one-year randomized trial of lorcaserin for weight loss in obese and overweight adults: the BLOSSOM trial. J Clin Endocrinol Metab. 2011;96:3067-3077.
12. Qsymia (phentermine and topiramate extended-release) product information. Mountain View, CA: Vivus, Inc; September 2013.
13. Allison DB, Gadde KM, Garvey WT, et al. Controlled-release phentermine/topiramate in severely obese adults: a randomized controlled trial (EQUIP). Obesity (Silver Spring). 2012;20:330-342.
14. Gadde KM, Allison DB, Ryan DH, et al. Effects of low-dose, controlled-release, phentermine plus topiramate combination on weight and associated comorbidities in overweight and obese adults (CONQUER): a randomised, placebo-controlled, phase 3 trial. Lancet. 2011;377:1341-1352.
15. Garvey WT, Ryan DH, Look M, et al. Two-year sustained weight loss and metabolic benefits with controlled-release phentermine/topiramate in obese and overweight adults (SEQUEL): a randomized, placebo-controlled, phase 3 extension study. Am J Clin Nutr. 2012;95:297-308.
16. Grundy SM, Cleeman JI, Merz CN, et al; Coordinating Committee of the National Cholesterol Education Program. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110:227-239.
17. Chobanian AV, Bakris GL, Black HR, et al; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42:1206-1252.
18. Rosendorff C, Black HR, Cannon CP, et al; American Heart Association (AHA) Council for High Blood Pressure Research; AHA Council on Clinical Cardiology; AHA Council on Epidemiology and Prevention. Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention. Circulation. 2007;115:2761-2788.
19.American Diabetes Association. Standards of medical care in diabetes—2013. Diabetes Care. 2013;36(suppl 1):S11-S66.
20. American Pharmacists Association and the National Association of Chain Drug Stores Foundation. Medication Therapy Management in Pharmacy Practice: Core Elements of an MTM Service Model. Version 2.0. www.pharmacist.com/MTM/CoreElements2. Accessed August 30, 2013.
21. Last AR, Ference JD, Falleroni J.Pharmacologic treatment of hyperlipidemia. Am Fam Physician. 2011;84:551-558.

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Abstract

Indian traditional medicine, Ayurveda has a great history. Researchers in India have tried to corroborate ancient wisdom with the modern scientific practices. Tailabindu pariksha is a diagnostic tool of urine examination developed by the medieval Ayurvedic scholars, and also throws a light on the prognosis of the disease condition. This study aims at using this ancient wisdom to diagnose the medical conditions and to study about their prognosis, and studying about how it can be applied to modern medical practice and its limitations. For the purpose of the study, 30 volunteers were divided into 3 groups. Group I consisting of healthy volunteers, group II of those patients who suffer from curable conditions and group III consisting of patients suffering from chronic diseases which can be regarded as incurable. The urine collection, oil drop instillation and evaluation, were all done according to the guidelines laid down in Ayurvedic practices. Upon the evaluation of the color, appearance, consistency and pattern of oil drop spreading in different patients of different groups, it could be seen that the data could be correlated to what has been provided in the literature in majority of the cases. In today’s modern medical practices, there is a plethora of urine diagnostic examinations available. These act as an added financial burden to the patients. In the midst of this, making use of Tailabindu pariksha for urine examination, will not only prove economical, but also is a time-tested and scientifically proven method. More in-depth studies on larger groups of patients, suffering from various diseases need to be done to standardize the procedure and make it scientifically more acceptable.

Keywords: Ayurveda, Basavarajeeyam, Nidana, Mutra Pariksha, Tailabindu Pariksha, Yogaratnakara

Introduction

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Object name is Ayu-32-76-g015.jpg

Rogamadou pariksheta tatoanantaramoushadham” (Charaka sutrasthana 20/20)[1]

Ayurvedic texts suggest to diagnose the disease first and then to think over the treatment. For proper diagnosis of the disease and disease condition, patient’s different patho-physiological conditions are examined under the broad heading Ashtavidha pariksha (8 types of investigations).

Ashtavidha pariksha include the following:

  1. Nadi/Pulse
  2. Mutra/Urine
  3. Malam/Stool
  4. Jihwa/Tongue
  5. Shabda/Speech
  6. Sparsha/Touch
  7. Drik/Eye
  8. Akrti/shape

Among the above mentioned diagnostic procedures, Mutra pariksha, (examination of urine) has been given special attention to in some of the medieval texts like Yogaratnakar, Basavarajiyam, Chikitsasara etc. Along with the examination of color, appearance and consistency of urine, a special technique for the examination of the Mutra, Tailabindu pariksha, was developed to diagnose disease conditions and to find out about their prognosis. For this, the patient’s early morning (around 5 o’clock) urine sample is to be collected either in clean oval shaped open earthen pot ora clean glass vessel. This should be maintained in a stable condition and closely and carefully examined during sunrise. For this, one drop of Tila taila (sesame oil) is slowly dropped over the surface of urine with out causing disturbance under sunlight. The patterns’ and the distribution of the oil drop on the urine are then considered to determine the diagnosis and prognostic features of the disease.

Review of Literature

Diagnosis of the disease by the examination of urine

By appearance of urine

  1. Diagnosis of Dosha involvement
    1. In “Vata” aggravated diseases, urine of the patient appears as Pandu varna (whitish) or slightly ‘Nilam’ (Bluish).
    2. In Kapha dominated conditions urine becomes “Phenayukta”, i.e., frothy or Snigdha (cloudy).
    3. In Pitta aggravation urine appears yellowish or Rakta varna (reddish).
    4. In case of rakta-aggravation urine become Snigdha, Ushna (hot) and resembles blood.
    5. In Dwandaja, i.e., a state of combined Dosha aggravation, mixed colours are seen in the appearance of the urine as per the Dosha involved in the diseases causation.
    6. In Sannipata state urine becomes Krishna varna (blackish).[24]
  2. Diagnosis of disease involvement[2]
    1. In the case of diseases related to ‘Ajirna’ (indigestion), urine appears like Tandulodaka (rice water).
    2. In Navina Jwara (acute fever) urine appears ‘Smoky” and the affected passes more urine (Bahu Mutrata)
    3. In Vata-Pitta jwara – urine is smoky, watery and hot.
    4. In Vata Shlesmajwara – urine is whitish with air bubbles.
    5. In Shlesma-Pitta jwara – urine is polluted and is mixed with blood.
    6. In Jirna (Chronic) jwara – urine becomes yellowish and red.
    7. In Sannipata jwara – urine appears in mixed shades depending on the Dosha involvement.[2]

Also, it is said that if urine is placed in a glass jar and appears reddish in the bottom, the patient is suffering from Atisara(diarrhoea). If the urine has particles appearing like the droplets of ghee, it indicates Jalodara (Ascites). In Amavata (Rheumatoid arthritis), urine appears as Vasa (fat) or Takra (buttermilk). In Vata jvara, urine appears reddish or kunkuma (saffron) in colour, and in excessive passage of stools’, urine becomes yellowish.[5]

By shape of the spread oil drop

  1. Diagnosis of Dosha involvement
    1. If Tailabindu takes a snake like image in the urine, it is Vata roga.
    2. If urine takes an “Umbrella” shape it is Pittaja roga.
    3. If urine spreads like Pearl (Mukta) it is Kaphaja roga.[2]
    Also, it is said that if the Vata is predominant, then the Taila attains Mandala (circular shape); in Pitta diseases it attains Budbuda (bubbles) shape; in Kapha diseases it becomes Bindu (globule or droplet) and in the Sannipata the Taila sinks in the urine.[35]
  2. Diagnosis of disease involvement
    1. If the dropped Taila bindu takes a Chalini (sieve) shape in the urine sample and then spreads, it is a definite indication of ‘Kuladosha” (genetic disorder).
    2. If the dropped Taila bindu takes the image of human being (narakaram) or skull it indicates ‘Bhutadosha’ and is treated accordingly.[2]

Prognosis of disease by the examination of urine

By spreading nature of the oil

  1. If inserted oil spreads quickly over the surface of urine, that disease is Sadhya (curable or manageable).
  2. If the oil does not spread it is considered as Kashta sadhya or difficult to treat.
  3. If the dropped oil directly goes inside and touches the bottom of the vessel, then it is regarded as Asadhya or incurable.[2] Also, in another text it is mentioned that if the oil does not spread and remains as a droplet in the middle of the urine the disease is considered incurable.[5]

By spreading direction of the oil

  1. If the oil spreads in the direction of Purva (east) the patient gets relief.
  2. If the oil spreads in the south direction, the individual will suffer from jwara (fever) and gradually recovers.
  3. If the oil spreads in the northern direction, the patient will definitely be cured and become healthy.
  4. If the oil spreads towards the west, he will attain Sukha and Arogya i.e. happy and healthy.
  5. If the oil spreads towards the Ishanya (Northeast), the patient is bound to die in a month’s time; similarly, if the oil spreads into Agneya (Southeast) or Nairutya (Southwest) directions, or when the instilled oil drop splits, the patient is bound to die.
  6. If the oil spreads on to Vayavya (Northwest) direction, he is going to die any way.[2]

By spreading shapes of the oil

  1. It is a good prognosis if the oil creates the images of Hamsa (swan), lotus, Chamara (chowri composed of the tail of Yak), Torana (arch), Parvata (mountain) elephant, camel, tree, umbrella and house.[2,5]
  2. If the taila attains the shape of a fish, then the patient is free of dosha and the disease can be treated easily.
  3. If the drop of the taila attains the shape of Valli (creeper), Mrdanga (a kind of drum), Manushya (human being), Bhanda (pot), Chakra (wheel) or Mriga (deer) then the disease is considered as the Kashtasadhya (difficultly curable).[5]
  4. If the spreading oil creates the shapes of tortoise, buffalo, honey-bee, bird, headless human body, astra (instrument used in surgery, like knife etc), Khanda (piece of body material) physician should not treat that patient as that disease is incurable.[2]
  5. If the shape of the drop of taila is seen as four-legged, three-legged, two-legged that patient will die soon.[5]
  6. If the shape of the drop of taila is seen in the shape of Shastra (sharp instruments), Khadga (sword), Dhanus (bow), Trishulam (type of weapon with three sharp edges) Musalayudham (pestle), Shrugala (jackal), Sarpa (snake), Vrishchika (scorpion), Mushika (rat), Marjara (cat), arrow, Vyaghra (tiger), Markata (monkey) or Simha (lion), then it is understood that the patient will die soon.[5]

Materials and Methods

  • Bottle with lid to collect urine
  • Round large mouthed glass bowl measuring around 4-5 inches in diameter and 1.5 inches deep.
  • Dropper
  • Urine of the patient
  • Tila taila (Sesame oil)

To maintain uniformity, every patient was advised to sleep early (before 9 PM) with usual intake (2 to 3 glasses) of water during the dinner. Before sunrise, around 5 AM, patients were asked to collect the mid stream urine of the first urination of the day in a clean and neat bottle. Urine thus collected was poured in a round wide mouthed glass bowl (4-5 inches in diameter and 1.5 inch depth), kept on a flat surface and is allowed to settle. After ascertaining that the urine was stable and devoid of wave or ripples or other influence of the wind, the urine was examined in day light at 6.30 AM. Tila taila was then taken in a dropper and one drop of the taila (approximately 1/20 ml) was dropped over the surface of urine slowly (keeping a distance of 1 mm from the surface of the urine to the lower end of the oil drop) without disturbing/touching the surface. It was then left for a few minutes, and the oil drop pattern in the urine was observed. The inferences were then recorded.

Precautions

  1. Mid stream of the day’s first urine should be considered for the test.
  2. Bowl in which the urine is kept should be kept on a flat surface and must be devoid of external influences like wind.
  3. Oil must be dropped only when the urine becomes stable without any movement.
  4. Oil drop must be dropped from a very low height (1 mm height from the lower end point of the oil drop) without touching the urine with the dropper, because this can disturb the urine and give false results.

Selection of patients

Subjects of either sex between 20 to 60 years of age were selected for the study. In Group I, 10 healthy volunteers without any known chronic or acute ailments were taken. In Group II, 10 patients with curable diseases like Jvara (viral fever), Ajirna (indigestion), Atisara (diarrhea), Kamala (Hepatitis-A), Pandu (anemia), Kaphaja Kasa (Productive cough), Amlapitta (Gastritis) were taken. In Group III, 10 patients suffering from chronic disease conditions like Madhumeha (Diabetes), Tamaka Swasa (Bronchial asthma) and Amavata (Rheumatoid arthritis) were taken.

Observations

Total 30 Subjects were selected for the study and were divided into three groups (10 subjects in each group) as explained below:

Group I: In this group, 10 patients not suffering from any disease were considered.

Group II: In this group, patients suffering from curable diseases like Jvara (Viral fever), Ajirna (Indigestion) or Atisara (Diarrhoea) were taken [Table 1].

Table 1

Distribution of subjects in group II according to the disease condition

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Object name is Ayu-32-76-g001.jpg

Group III: In this group, patients suffering from incurable diseases like Madhumeha (Diabetes), Tamaka Shwasa (Bronchial asthma), Amavata (Rheumatoid arthritis) were taken [Table 2].

Table 2

Distribution of subjects in group III according to the disease condition

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Object name is Ayu-32-76-g002.jpg

Demographic pattern

Among the groups created, maximum number of patients were seen in the age group of 41 to 50 years (13(43.33%) [Table 3]. 15 male and 15 female patients were selected for the study. In Group I and Group II females were more in number and in Group III males were more [Table 4].

Table 3

Distribution of subjects in groups I, II and III according to the age for the study

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Object name is Ayu-32-76-g003.jpg

Table 4

Distribution of subjects in group I, II and III according to the sex for the study

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Object name is Ayu-32-76-g004.jpg

Results

In group I

Out of the 10 samples, 8 samples were Pandu varna (whitish) and 2 samples were slightly yellowish in colour. In all these samples, the oil drop was seen to spread quickly over the surface of urine. The 9 samples out of 10, did not show any specific shape which could be compared to the literature. In one sample, the spread oil showed the shape of a swan [Figures ​1 and ​2].

Spreading of oil with out any specific pattern in group I of patients consisting of healthy volunteers

Swan shape of oil spreading in the urine sample of one of the healthy volunteers’ of group I during the study

In group II

The 8 out of 10 samples were Pandu varna (whitish), one sample of Kamala (Hepatitis-A) was slight yellowish in color, and another sample of Kamala (Hepatitis-A) was reddish yellow in color, in which taila bindu showed the shape of demon/Vyaghra (tiger) [Figure 3]. In all these samples, the oil drop was seen to spread quickly over the surface of urine. One of the samples, of a patient with viral fever showed the spread oil drop in the shape of a snake, [Figure 4] and another one was in the shape of Bindus (globule or droplet) [Figure 5]. The sample of a patient suffering from Pandu (anemia) was in the shape of a ring [Figure 6]. Another patient suffering from Kaphaja Kasa (Productive cough) showed the oil drop taking a shape of Mukta (pearls) [Figure 7]. Patients of Atisara and Ajirna did not show any specific shape.

Reddish yellow tinged urine of Kamala (Hepatitis-A) patient, with demon or tiger shaped pattern of oil spread in the urine sample of a volunteer in group II which consisted of patients suffering from curable diseases

A sample of a group II patient (which consisted of patients’ suffering from curable diseases) suffering from viral fever with the oil spread pattern in the shape of snake

Budbuda (bubbles) shape of oil spread in a Viral fever patient belonging to group II of the study which consisted of patients suffering from curable diseases

Ring shape oil spread in the urine sample of a patient suffering from Pandu (Anemia) and belonging to group II in the study which consisted of patients suffering from curable diseases

Mukta (pearls) shape of oil spread in a patient belonging to group II which consisted of patients suffering from curable diseases in the study and suffering from Kaphaja Kasa (Productive cough)

In group III

All the samples were Pandu varna (whitish). Out of these 10 samples, the inserted oil drop was seen to spread quickly over the urine surface in around 8 samples, whereas in 2 of the Madhumeha (Diabetes) samples’, the oil was seen to spread slowly. In one sample of Amavata (Rheumatoid arthritis) oil was seen to spread in the shape of a “sieve”, [Figure 8] and in another in the shape of a skull [Figure 9]. In one of the Madhumeha (Diabetes) samples, the spreading of the oil drop was seen in the shape of an Owl [Figure 10] and in the remaining Amavata, Madhumeha and Tamaka Shwasa patients, the spreading of oil did not show specific shapes.

Sieve shape of oil spread in a Amavata (Rheumatoid arthritis) patient belonging to group III in the study which consisted of patients’ suffering from incurable diseases

Skull shape of oil spread in a Amavata (Rheumatoid arthritis) patient belonging to group III in the study which consisted of patients’ suffering from incurable diseases

Owl bird shape of oil spread in a Madhumeha (Diabetes) patient belonging to group III in the study which consisted of patients’ suffering from incurable diseases

Discussion

Diagnosis of a disease involves clinical assessment of the patient and laboratory investigations. The latter, especially the examination of the excretory and secretary products of the body, has always been important for the diagnosis of the disease from the ancient to the modern day times. Now a day, with the advancement of modern technology, clinical assessment is clouded by the diagnostic tools, which have become a costly affair for the patients. So to minimize the cost of the diagnosis, age old practices like Tailabindu pariksha mentioned in the Ayurvedic classical texts can be employed.

Though Tailabindu pariksha seems to be a crude method, but it has its own importance in diagnosing the disease and prognosis of the patient’s condition. It may be an age-old method; however, it is time-tested and has been proved successful by the generations of Ayurvedic community. By corroborating the modern knowledge to this age-old method, its efficacy can be enhanced and new horizons can be explored.

Tailabindu pariksha, is based on the consistency, thickness, density of urine and by seeing the shape of a spread oil drop on the urine surface. These changes in the properties of the urine as compared to normal occur due to the release of various excretory substances in the urine in different disease conditions which can be assessed by the patterns’ formed by the oil drop during the Tailabindu pariksha, and thereby the diagnosis and prognosis can be assessed. According to Ayurveda, due to alteration of the body’s normal physiological functions during diseases and the production of Vata, Pitta and Kapha, the chemical composition of urine also changes which ultimately changes the pattern of Tailabindu pariksha.

In the present study, in Group-I in 9 healthy volunteers’ samples, oil did not show any specific shape and in 1 sample it showed the shape of a swan. In classical literature, the shape of a swan is the sign of good prognosis. In Group-II, the snake shape seen in the viral fever patient is a sign of poor prognosis, though viral fever is now a day manageable due to advances in medical sciences. Also, Bindus (globule or droplet) of another patient suffering from fever showed predominance of Pitta dosha; Ring or Mandalakara of PAndu patient showed the predominance of Vata and Mukta (pearls) shape of Kaphaja Kasa (Productive cough) patient showed predominance of Kapha dosha. In Group-III, sieve and skull shaped spread of oil in Amavata (Rheumatoid arthritis) patients’ was pointing towards a poor prognosis. Even today, treatment of Rheumatoid arthritis (RA) is very difficult and both patients’ were suffering from RA in multiple joints. Also the patients were in a miserable condition when their urine samples’ were collected. Though sieve shape has an inference of genetic involvement in the disease condition, no such involvement was seen here. In one of the Madhumeha (Diabetes) samples, the oil spread in the shape of bird owl which also indicates a poor prognosis.

Conclusion

Even though in the present study, the sample size of 30 was small, the findings with respect to the patterns created by the spread of oil drop in majority of the patients matched with the description given in literature. The present study is a basic step to know about the methods and techniques used in Tailabindu pariksha. The need for further research on a larger group of patients’ suffering from different disease conditions’ to arrive at more definite conclusions is being felt.

References

1. Acharya Yadavji Trikamji. Varanasi: Chaukhambha Sanskrit Sansthan; 2004. Charaka samhita; p. 115. [Google Scholar]

2. Babu Suresh. Vol. 1. Varanasi: Choukhamba Sanskrit Series Office; 2005. S. Yogaratnakara; pp. 16–9. [Google Scholar]

3. Chikitsasara. Chennai: Vavilla Ramaswamy Shastrulu and Sons; 1927. Puvvada Suryanarayana; pp. 9–10. [Google Scholar]

4. Anonymous. MSS Chikitsasara. NIIMH. p. 5. S-19-49-33.

5. Rangacharya V. New Delhi: CCRAS Publications; 2007. Basavarajeeyam; pp. 137–42. [Google Scholar]

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Acupuncture involves the stimulation of certain points on or near the skin by the insertion of needles or by other methods. It has been used as a treatment in Asia for several thousand years but has not been proven effective by modern standards.

Acupuncture is being promoted as both an “alternative” treatment and an adjunct to standard treatment. In China, it was banned in 1929 but underwent resurgence in the 1960s during the Cultural Revolution. In the United States, it is used mainly for pain relief. Some states permit only licensed physicians to perform acupuncture, while others license lay persons as well. While acupuncture organizations are trying to standardize training, researchers are still attempting to determine whether acupuncture is effective.

NCAHF believes:

  1. Acupuncture is an unproven modality of treatment;
  2. Its theory and practice are based on primitive and fanciful concepts of health and disease that bear no relationship to present scientific knowledge;
  3. Research during the past twenty years has failed to demonstrate that acupuncture is effective against any disease;
  4. Perceived effects of acupuncture are probably due to a combination of expectation, suggestion, counter- irritation, operant conditioning, and other psychological mechanisms;
  5. The use of acupuncture should be restricted to appropriate research settings;
  6. Insurance companies should not be required by law to cover acupuncture treatment; and
  7. Licensure of lay acupuncturists should be phased out.

Theory and Practices

Acupuncture is based on ancient Chinese medical philosophy, which views illness quite differently than does contemporary science [1]. In ancient China, diseases were not systematically described or classified [2]. Internal organs, which were felt to be intermediaries between the body and nature, were assigned qualities representing emotional states, colors, and seasons. Some organs, such as the “triple warmer,” were imaginary.  There were no concepts of modern physiology, biochemistry, nutrition or mechanisms of healing. There was no knowledge of the existence of cells, the circulation of the blood, the function of nerves, or the existence of hormones. Dissection of the human body was not done, so that even knowledge of anatomy was incomplete.

Diagnosis

Traditional Chinese diagnosis does not correlate with modern scientific concepts. An ill person was considered out of balance with nature and its two opposing forces, yin and yang. Yin represented the feminine, passive, or accepting qualities, and yang the masculine, aggressive, or forceful ones. Diseases were not described or named. Diagnoses were made by examining the pulse (of which there were supposedly six variations) and the tongue, which was said to vary in appearance with certain disease states. Today we know that there is only one pulse, which corresponds to the pumping action of the heart, and that the appearance of the tongue is seldom a clue to the diagnosis of disease in other parts of the body.

Traditional Chinese treatments were directed at reestablishing “balance” and “harmony,” which supposedly occur as symptoms improve. Since there was no formal study of diseases or description of their natural history, the ancient Chinese could rarely determine how an illness actually improved. Treatments were chosen by trial and error, and perpetuated by personal experience.  Since there were no scientific criteria for success or failure, the judgment that “healing” had taken place was based on the word of the therapist or the patient. The natural course of the disease usually took place unaltered by treatment.

Acupuncture points were assigned to “meridians” on the surface of the body. These supposedly represent channels through which flows the life force, “Ch’i” or “Qi..” Fourteen channels were said to permit maximal influence on the flow of Ch’i inside the body.  Insertion of needles at the designated points was said to increase or decrease the flow of  Ch’i to achieve a more normal and harmonious state. Originally there were 365 acupuncture points, corresponding to the days of the year, but the number identified by proponents during the past 2,000 years increased gradually to over 2,000. [3]

The life force, Ch’i, has no basis in human physiology. The meridians are imaginary; their locations do not relate to internal organs, and therefore do not relate to human anatomy. Acupuncture points are also imaginary.  (Various acupuncture charts give different locations for the points.)  These fanciful concepts continue to form the basis of modern acupuncture therapy even though extremely sophisticated methods are used to measure its reputed biochemical effects. Although scientific methods may be applied to biochemical studies, many published reports are based solely and uncritically on clinical anecdotes and tradition [4].

Acupuncture is not difficult to perform. It involves a variety of procedures performed at “acupuncture points” on the skin. The modalities include:

  • Insertion of needles. Fine stainless steel needles are inserted to varying depths with an in-and-out twirling motion until there is a local feeling of numbness (a temporary reaction to injury). They are left in place for about twenty minutes, then removed.
  • Burning of vegetable fibers (moxibustion). [5]
  • Suction by cups containing heated air (cupping)
  • Injected solutions
  • Low-voltage current applied to needles (electroacupuncture), a relatively recent development

Other variations and offshoots include:

  • Trigger point therapy. Some proponents claim that acupuncture points coincide with “trigger points’ – areas at which the injections of a local anesthetic can relieve regional pain.  However, trigger points are not anatomically demonstrable and vary from individual to individual.  Any effects from acupuncture are likely to be due to nonspecific mechanisms rather than location of the “points”.
  • Auriculotherapy.  This is based on the notion that the body and organs are represented on the ear [6].
  • Needles are placed in the imaginary points representing the diseased organs. There is no scientific evidence that these points exist or that auriculotherapy has any therapeutic value [7].
  • Staplepuncture. Staples are placed at acupuncture points on the ear, typically to aid smoking cessation or drug withdrawal.
  • Acupressure, firm digital pressure on trigger points or acupuncture points.
  • “Touch for Health,” developed by a chiropractor using acupressure points and an unreliable muscle-testing method (“applied kinesiology”). The therapist claims to diagnose nutritional and glandular “deficiencies” that are then “corrected” by manipulation or nutrition supplements.

Proposed Mechanisms of Action

The following mechanisms have been proposed to explain acupuncture’s presumed action on pain:

  • Release of endorphins (narcotic-like substances produced by the body). Naloxone, which reverses the effects of administered opiates, has been reported to reduce the analgesia produced by acupuncture.  However, some studies show no reversal. Even if endorphin release were a real mechanism for acupuncture action, there are simpler and non invasive ways to cause endorphin release.
  • The “gate theory.” This suggests that if pain fibers carry impulses from an acupuncture site, impulses from a painful body organ will be unable to reach the brain. However, there is no anatomical or physiological basis for this explanation.
  • Diversion.  Attention can be diverted from a symptom by stimulating or irritating another part of the body.
  • Psychological mechanisms. These include suggestion, operant conditioning and other psychological mechanisms, any of which may be involved in the placebo effect.

Current Use in China

Acupuncture anesthesia has been observed by Western anesthesiologists and other medical scientists. American interest was triggered in 1972 by a rumor that New York Times reporter James Reston had received acupuncture anesthesia for an appendectomy while visiting China. Actually, he had had standard anesthesia and received acupuncture for postoperative cramps.

Despite popular claims, acupuncture anesthesia is not used for emergency surgery. It is not used routinely, but only on the 10% to 15% of people who are suggestible and perhaps easily hypnotizable. It is seldom used for abdominal or chest surgery, in which muscle relaxation is necessary (general anesthesia as done in the West is used.)   Moreover, when acupuncture is used for surgery, the patient is usually medicated with narcotics and other standard drugs [8-10].

For other medical conditions, acupuncture and herbalism are regarded as elective procedures. Of the forty-six major medical journals published by the Chinese Medical Association, none is devoted to acupuncture, herbalism, and their variants. The great majority of papers are about scientific, rather than traditional Chinese methods. Few articles concern the integration of acupuncture with modern treatments. Reports of acupuncture successes are often not accompanied by reliable measurements.

Scientific Status

The World Health Organization has listed forty conditions for which claims of effectiveness have been made.  They include acute and chronic pain, rheumatoid and osteoarthritis, muscle and nerve “difficulties,” depression, smoking, eating disorders, drug “behavior problems,” migraine, acne, ulcers, cancer, and constipation.  Some chiropractors and psychologists have made unsubstantiated claims to improve dyslexia and learning disorders by acupressure.  However, scientific evidence supporting these claims is either inadequate or nonexistent.

Experimental Difficulties

The following should be considered when evaluating an acupuncture research paper:

  • Symptom relief is difficult to assess because there is no objective standard of measurement.
  • Double-blind studies comparing the insertion of needles at acupuncture points and at other points (“sham acupuncture”) are difficult to design.  If an experienced acupuncturist locates the points, the practitioner’s expectations may be transmitted to the patient.  If an inexperienced person inserts the points, misplaced needles may undermine the results. Moreover, practitioners may differ about the location of the points, and so many points have been postulated that it may be difficult to find a patch of skin that has not been labeled an “acupuncture point.”
  • Chronic pain is often cyclic, with periods of relief.  Since people often request help when their pain is most severe, spontaneous improvement may occur independent of the treatment [11].
  • Most acute (recent onset) pain improves with time and no intervention.  Thus, people may report improvement of symptoms from any intervention, even if the method has no effect.
  • There is general agreement that 30%  to 35% of subjects’ pain improves from suggestion or placebo effect alone.  Thus, measuring a small difference between placebo and acupuncture requires a large number of subjects (several hundred in each group) to show as little difference as 25%.
  • People who volunteer for acupuncture may have a conscious or unconscious bias toward the procedure and thus may be more prone to suggestion.
  • Proponents of a method tend to report trials showing positive effects, and not to report trials showing no effect or negative effects.

Despite these difficulties, well controlled trials can be carried out by using: 1) unbiased subjects, 2) random assignment of subjects into treatment and control groups, 3) blinding of both therapists and subjects, 4) blinded evaluations by separate observers, 5) a reliable diary or reporting system if symptom relief is the end point, 6) adequate period of follow-up past the time of treatment, 7) enough subjects to test the significance of any difference found.  Few studies have satisfied these requirements.

Scientific Reviews

Richardson and Vincent analyzed 28 studies of effect of acupuncture on pain, all published between 1973 and 1986 in English language peer-reviewed journals.  Fifteen showed no difference in effectiveness between acupuncture and control groups. Thirteen showed some effectiveness for acupuncture over control groups, but not all controls were the same. (Some were compared to sham acupuncture, some to medical therapy, etc.) Overall, the differences were small [12-13].

The NCAHF Task Force on Acupuncture evaluated the above studies, as well as more recent ones, and found that reported benefits varied inversely with quality of the experimental design.  The greater the benefit claimed, the worse the experimental design. Most studies that showed positive effects used too few subjects to be statistically significant.  The best designed experiments – those with the highest number of controls on variables – found no difference between acupuncture and control groups.

In 1989, three Dutch epidemiologists reported similar conclusions about 91 separate clinical trials of acupuncture for various disorders.  They also found that the stricter the controls, the smaller the difference between acupuncture and control groups [14].

Acupuncture is being used in drug and alcohol rehabilitation programs. Because there are serious flaws in the way studies on rehabilitation have been performed, the results cannot be considered valid.

A successful medical procedure should be consistently effective in a large majority of trials, and be repeatable in the hands of most therapists. Acupuncture does not satisfy these basic criteria.

The American Medical Association’s Council on Scientific Affairs stated in a 1981 report that since acupuncture is an experimental procedure, it should be performed only in research settings by licensed physicians or others under their direct supervision. The report urged state medical societies to seek appropriate laws to restrict the performance of acupuncture to research settings [15].

Acupuncture Training

Acupuncture is not part of the curriculum at most American medical schools. Nevertheless, proponents say that several thousand physicians in the U.S. and Canada use it in their practices. The American Academy of Medical Acupuncture of Berkeley, California, sponsors courses for physicians given under the auspices of medical schools, including UCLA, Jefferson Medical College, and Temple University. The University of Hawaii also sponsors a course. Tuition is as much as $3,600 for a one-week course.

Lay persons who perform acupuncture may use the following degrees and/or titles:

  • Certified Acupuncturist (C.A.): This title can be granted to lay persons by a state licensing board after qualifying examination.
  • Master Acupuncturist (M.A.): A title granted to some licensed acupuncturists in certain states.
  • Diplomate of Acupuncture (Dpl.Ac.):  Certified by an organization called the National Commission for the Certification of Acupuncturists (NCCA).
  • Oriental Medical Doctor (O.M.D. or M.O.D): This is not a recognized degree.
  • Doctor of Philosophy (Ph.D): No American school granting this degree for acupuncture is accredited. One such school is the Center for Chinese Medicine, Monterey Park, California. Its 250-hour course lasts about 30 days and costs $3,500.

Hazards

The frequency of complications of acupuncture needling is not known, since no survey has been done.  Nevertheless, serious complications occur even in experienced hands and are reported in medical journals.  These include fainting, local hematoma (bleeding from punctured blood vessel), pneumothorax (punctured lung), convulsions, local infections, hepatitis B (from unsterile needles), bacterial endocarditis, contact dermatitis, and nerve damage. The herbs used by acupuncture practitioners are not regulated for safety, potency or effectiveness. There is also the risk that a lay acupuncturist will fail to diagnose a dangerous condition.

Legal Status

All states permit acupuncture to be performed – some by physicians only, some by lay acupuncturists under medical supervision, and some by unsupervised lay persons. Seventeen states permit lay acupuncturists to practice without medical supervision. In 1990 the National Accreditation Commission for Schools and Colleges of Acupuncture and Oriental Medicine was recognized by the U.S. Secretary of Education as an accrediting agency. [Note: Such recognition is not based upon the scientific validity of what is taught but upon other criteria.]

Many insurance companies cover acupuncture treatment if performed by a licensed physician, but Medicare and Medicaid generally do not. Acupuncture needles are considered investigational (unapproved) devices by the U.S. Food and Drug Administration.

In California, where acupuncture is being offered for hypertension, obesity, heart failure, arthritis, and smoking and drug withdrawal, the acupuncture law permits acupuncturists to advertise treatment for any ailment except cancer, as long as a cure is not promised. Cancer treatment is prohibited by the California Cancer Law.

Every ethnic group has its own set of medical customs not supported by science. Some proponents argue that Asian populations should have access to their traditional remedies, however ineffective and unscientific they may be. This question is difficult to resolve because it conflicts with the modern principle of consumer protection based on reliability and fulfillment of promised claims. Cultural activities are generally tolerated provided that they do not conflict with laws for the general population and are not dangerous. Chaos would result if the populace could not be protected from misrepresentation, and if insurance companies were forced to pay for all traditional foreign methods.

NCAHF Recommendations

The National Council Against Health Fraud believes that after more than twenty years in the court of scientific opinion, acupuncture has not been demonstrated effective for any condition. We therefore advise the following:

To Physicians:

Note that the scientific literature provides no evidence that acupuncture can perform consistently better than a placebo in relieving pain or other symptoms for which it has been proposed.  Most reports claiming positive and statistically significant results for acupuncture are flawed by biased patient selection, poor controls, lack of blinding, or insufficient numbers.  There is no physiologic rationale for why acupuncture should work other than for its placebo or counter-irritant and distracting effects. For these reasons, acupuncture should not be offered without full informed consent, reminding patients that acupuncture is experimental, has not been proven more effective than a placebo, and has some risk of complications.

To Consumers:

Beware of misleading and untrue statements made for acupuncture.  Some states do not regulate such claims.  Because laws are political tools, not scientific ones, the political process often responds to pressures independent of scientific evidence. Acupuncture cures nothing.  It may relieve symptoms with the frequency of a placebo.   It may be harmful.  Consumers wishing to try acupuncture should discuss their situation with a knowledgeable physician who has no commercial interest.

To Legislators:

Acupuncture licensing should be abolished. Public display of unaccredited degrees by individuals offering any form of health care should be banned.  Insurance companies, HMOs and government insurance programs should not be forced to cover acupuncture unless scientific evidence demonstrates that it has value.

References

  1. Motokawa T. Sushi science and hamburger medicine. Perspect Biol Med 1989;32:489-504.
  2. Kaptchuk TJ. The web that has no weaver, understanding Chinese medicine. New York: Congden & Weed. 1983.
  3. Skrabanek P. Acupuncture: past, present, and future. In Stalker D and Glymour C: Examining Holistic Medicine. Buffalo, NY, 1985, Prometheus Books.
  4. Patel MS.Problems in the evaluation of alternative medicine. Soc Sci Med 1987;25:669-678.
  5. Stemfeld M et al. Cell membrane activities and regeneration mechanisms as therapy mediators in moxibustion and acupuncture treatments: theoretical considerations. Med Hypotheses 1990;31:227-231.
  6. Oleson TD, Kroening RI, Bresier DE. An experimental evaluation of auricular diagnosis: the somatic mapping of musculoskeletal pain at car acupuncture points. Pain 1980;8:217-229.
  7. Melzack R, Katz K. Auriculotherapy fails to relieve chronic pain: a controlled crossover study. JAMA 1984; 251:1041-1043.
  8. Bonica JI. Therapeutic acupuncture in the People’s Republic of China: implications for American Medicine. JAMA 1974;228:1544-1551.
  9. Kerr FML. Personal communication.
  10. Taub A. Quackupuncture? In Barrett S (ed). The Health Robbers. Philadelphia, George F Stickley Co., 1980:257-266.
  11. Malone RD, Strube MJ. Meta-analysis of nonmedical treatments for chronic pain. Pain 1988;34:231-244.
  12. Richardson PH, Vincent CA. The evaluation of therapeutic acupuncture: concepts and methods. Pain 24:1-13, 1986.
  13. Richardson PH, Vincent CA. Acupuncture for the treatment of pain. Pain 24:1540, 1986.
  14. Ter Riet G et al. The effectiveness of acupuncture. Huisarts Wet 32:170-175, 176-181, 308-312, 1989.
  15. AMA Council on Scientific Affairs. Reports of the Council on Scientific Affairs of the American Medical Association. 1981. Chicago, 1982, American Medical Association.

Approved by the NCAHF Board of Directors on September 16, 1990.
Copyright, NCAHF. Permission to reprint is granted with proper citation.
Please retain the following notice on any copies made of this position paper:

The National Council Against Health Fraud, Inc.

NCAHF is a private nonprofit, voluntary health agency that focuses upon health misinformation, fraud and quackery as public health problems. Its funding is derived primarily from membership dues, newsletter subscriptions, and consumer information services. NCAHF’s officers and board members serve without compensation. NCAHF unites consumers with health professionals, educators, researchers, attorneys, and others who believe that everyone has a stake in the quality of the health marketplace. NCAHF’s positions on consumer health issues are based upon principles of science that underlie consumer protection law. Required are: (1) adequate disclosure in labeling and other warranties to enable consumers to make proper choices; (2) premarketing proof of safety and efficacy for products and services that claim to prevent, alleviate, or cure any disease or disorder; and, (3) accountability for those who violate consumer laws

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What is Vata Dosha? Tips and diet for balancing vata

7-9 minutes


The word vata means to blow or move like the wind.

Consisting of the elements air and ether, it is the principle force of motion in the body and mind. When vata dosha is healthy, the movements of the body are graceful, unimpeded, and yet controlled. When out of balance, the movements become erratic, excessive, decreased, or blocked.

To understand the vata dosha, it is important to understand its qualities. Vata dosha is light, dry, mobile, cold, hard, rough, sharp, subtle, flowing, and clear. A body and mind in which the vata dosha predominates expresses or reflects these qualities.

Vata dosha is best understood in terms of its component parts, its subdoshas, which are the five types of vata or five types of movement. Each subdosha defines a direction of movement and governs specific actions in the body.

Prana Vayu: Prana vayu represents the force that draws sensory experience to us. It is the force of attraction and has a magnetic nature. The way it functions determines the types of impressions we expose ourselves to. Prana vayu resides in the head and heart (chest) where desire dwells, choices are made, and sensory experience is processed. When it is healthy, we are drawn toward that which is harmonious and which brings us health and well-being. When prana vayu is out of balance, we misuse our senses and bring inside of us that which will cause disease.

Samana Vayu: Whereas prana vayu represents the force of attraction, samana vayu represents the force of absorption, pulling the impressions we are drawn to toward the center of our being. For example, samana vayu carries nutrients from the intestines into the circulatory system, and the sensations of things we touch are carried from the skin to the central nervous system. When samana vayu is functioning properly, impressions are properly absorbed. When it is in a state of dysfunction, absorption becomes difficult, and malnourishment or numbness may occur.

Vyana Vayu: Once absorbed, an impression must be acted upon. This is the role of vyana vayu, which is the force that circulates the response, moving it from the center toward the periphery. Following our examples, in the digestive system blood carries the nutrients throughout the body so that each cell receives its proper supply. In the nervous system, a signal is sent from the central nervous system toward a muscle or organ.

Udana Vayu: Udana vayu is responsible for action and expression, which means putting the energy received to work. Cells take the energy received and perform their unique functions. Nutrients are used for cellular energy and for building proteins. The nerves instruct muscles and organs to act properly.

Apana Vayu: Cellular activity produces both work and waste. While udana vayu is responsible for the work, apana vayu is responsible for cleaning up the waste. Apana vayu eliminates waste primarily through the functions of urination, defecation, and menstruation. It is responsible for all the downward flowing energy of the body and as such is also responsible for the energy needed for carrying the child out of the womb and into the world.

The Qualities and Presentation of Vata Dosha

The natural expression of vata dosha in the constitutioni of the body and mind reflects the qualities inherent in the dosha. Examples of the way these qualities manifest are as follows:

Light: The bones of the body are narrow

Cold: A person tends to become chilled easier than others

Dry: The skin or eyes have a tendency to become dry

Mobile: A person moves quickly, often with a lack of focus

Subtle: The mind is open to new ideas, expansive, and interested in the esoteric

Hard: If the tissues of the body become dry, they will then become hard; this is easiest to see as an imbalance

Flowing: The mind flows easily from one idea to the next

Sharp: The bridge of the nose is thinner and sharper than in other constitutional types

Rough: As the skin becomes drier, it becomes rougher; which is easiest to see as an imbalance

Clear: The eyes are clear

When vata dosha is out of balance, there is an excess of the qualities that define the dosha. The specific symptoms produced as a result of the imbalance depend upon which srota (channel system) and which dhatu (tissue) inside that channel are affected. Generalized examples of excess vata qualities (imbalances) in the body are as follows:

Light: The body loses weight

Cold: A person feels chilled

Dry: The lips become chapped

Mobile: The voice becomes too quick and rambles

Subtle: A person is too easily affected by the feelings of others

Hard: The stools become hard and difficult to eliminate

Flowing: There is an inability of the mind to focus

Sharp: Pain in the body is sharp like the prick of a needle

Rough: The skin becomes rough

Clear: The eyes and the mind become vacant

Managing Vata Dosha

Ayurvedai offers many approaches to bringing vata dosha into balance. Whether the tools used are dietary, herbal, colors, aromas, mantras, massage oils, or lifestyle; the principles used to return to balance are the same. It is necessary to increase the qualities opposed to the imbalance. Where there is an excess of lightness, we increase heaviness; where there is an excess of coldness, we increase heat; where there is an excess of hardness, we increase softness; and so on. While each of the treatment tools noted above are valuable, by far the most important tool is lifestyle. Only through adopting an appropriate lifestyle can the vata dosha remain in balance and the cause of disease be removed.

One of the most important lifestyle tools for maintaining health and for supporting healing in the vata individual is the adoption of regular healthy routines that are in harmony with the rhythms of nature. Stability is greatly improved through eating and sleeping at the same times every day.

It is best to arise within a half hour of the sun rising. The morning routine should include time for self abhyanga (oil massage), meditation, and yoga asana practice in addition to proper daily hygiene. Meals should be taken regularly throughout the day; as many as five small meals per day taken every three hours would be appropriate. These meals should be taken at the same time each day. This increases both the heavy and stable qualities. The foods should be somewhat oily (moist), cooked when possible (warm), and moderately spiced (warm). Bed time should occur at about 9 or 10pm, though this depends somewhat on the rhythm of the sunset and varies season to season and by latitude. Waking and sleeping times should be consistent from day to day to increase stability.

Specific treatments are available for almost every known condition in the body, as such symptoms can be understood in terms of the ten pairs of opposite qualities. Once the qualities of the patient’s constitution and condition are known, the experienced practitioner, knowing the qualities of the remedies, is able to design a treatment program that brings these opposite qualities into harmony. These qualities provide the body with the fundamental energies and raw material needed to support the healing process.

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What is Dialysis?

8-10 minutes


Dialysis is a treatment that does some of the things done by healthy kidneys. It is needed when your own kidneys can no longer take care of your body’s needs.

When is dialysis needed?

You need dialysis when you develop end stage kidney failure –usually by the time you lose about 85 to 90 percent of your kidney function and have a GFR of <15. Click here to learn more about the stages of Chronic Kidney Disease and GFR.

What does dialysis do?

When your kidneys fail, dialysis keeps your body in balance by:

  • removing waste, salt and extra water to prevent them from building up in the body
  • keeping a safe level of certain chemicals in your blood, such as potassium, sodium and bicarbonate
  • helping to control blood pressure

Is kidney failure permanent?

Usually, but not always. Some kinds of acute kidney failure get better after treatment. In some cases of acute kidney failure, dialysis may only be needed for a short time until the kidneys get better.

In chronic or end stage kidney failure, your kidneys do not get better and you will need dialysis for the rest of your life. If your doctor says you are a candidate, you may choose to be placed on a waiting list for a new kidney.

Where is dialysis done?

Dialysis can be done in a hospital, in a dialysis unit that is not part of a hospital, or at home. You and your doctor will decide which place is best, based on your medical condition and your wishes.

Are there different types of dialysis?

Yes, there are two types of dialysis –hemodialysis and peritoneal dialysis.

What is hemodialysis?

In hemodialysis, an artificial kidney (hemodialyzer) is used to remove waste and extra chemicals and fluid from your blood. To get your blood into the artificial kidney, the doctor needs to make an access (entrance) into your blood vessels. This is done by minor surgery to your arm or leg.

Sometimes, an access is made by joining an artery to a vein under your skin to make a bigger blood vessel called a fistula.

However, if your blood vessels are not adequate for a fistula, the doctor may use a soft plastic tube to join an artery and a vein under your skin. This is called a graft.

Occasionally, an access is made by means of a narrow plastic tube, called a catheter, which is inserted into a large vein in your neck. This type of access may be temporary, but is sometimes used for long-term treatment.

Click here to learn more about hemodialysis

How long do hemodialysis treatments last?

The time needed for your dialysis depends on:

  • how well your kidneys work
  • how much fluid weight you gain between treatments
  • how much waste you have in your body
  • how big you are
  • the type of artificial kidney used

Usually, each hemodialysis treatment lasts about four hours and is done three times per week.

A type of hemodialysis called high-flux dialysis may take less time. You can speak to your doctor to see if this is an appropriate treatment for you.

What is peritoneal dialysis and how does it work?

In this type of dialysis, your blood is cleaned inside your body. The doctor will do surgery to place a plastic tube called a catheter into your abdomen (belly) to make an access. During the treatment, your abdominal area (called the peritoneal cavity) is slowly filled with dialysate through the catheter. The blood stays in the arteries and veins that line your peritoneal cavity. Extra fluid and waste products are drawn out of your blood and into the dialysate. There are two major kinds of peritoneal dialysis.

Click here to learn more about peritoneal dialysis

What are the different kinds of peritoneal dialysis and how do they work?

There are several kinds of peritoneal dialysis but two major ones are:
Continuous Ambulatory Peritoneal Dialysis (CAPD) and Automated Peritoneal Dialysis (APD).

Continuous Ambulatory Peritoneal Dialysis (CAPD) is the only type of peritoneal dialysis that is done without machines. You do this yourself, usually four or five times a day at home and/or at work. You put a bag of dialysate (about two quarts) into your peritoneal cavity through the catheter. The dialysate stays there for about four or five hours before it is drained back into the bag and thrown away. This is called an exchange. You use a new bag of dialysate each time you do an exchange. While the dialysate is in your peritoneal cavity, you can go about your usual activities at work, at school or at home.

Automated Peritoneal Dialysis (APD) usually is done at home using a special machine called a cycler. This is similar to CAPD except that a number of cycles (exchanges) occur. Each cycle usually lasts 1-1/2 hours and exchanges are done throughout the night while you sleep.

Will dialysis help cure the kidney disease?

No. Dialysis does some of the work of healthy kidneys, but it does not cure your kidney disease. You will need to have dialysis treatments for your whole life unless you are able to get a kidney transplant.

Is dialysis uncomfortable?

You may have some discomfort when the needles are put into your fistula or graft, but most patients have no other problems. The dialysis treatment itself is painless. However, some patients may have a drop in their blood pressure. If this happens, you may feel sick to your stomach, vomit, have a headache or cramps. With frequent treatments, those problems usually go away.

How long has dialysis been available?

Hemodialysis and peritoneal dialysis have been done since the mid 1940’s. Dialysis, as a regular treatment, was begun in 1960 and is now a standard treatment all around the world. CAPD began in 1976. Thousands of patients have been helped by these treatments.

How long can you live on dialysis?

If your kidneys have failed, you will need to have dialysis treatments for your whole life unless you are able to get a kidney transplant.  Life expectancy on dialysis can vary depending on your other medical conditions and how well you follow your treatment plan. Average life expectancy on dialysis is 5-10 years, however, many patients have lived well on dialysis for 20 or even 30 years. Talk to your healthcare team about how to take care of yourself and stay healthy on dialysis.

Is dialysis expensive?

Yes. Dialysis costs a lot of money. However, the federal government pays 80 percent of all dialysis costs for most patients. Private health insurance or state Medicaid programs also help with the costs.

Click here to learn more about insurance options

Do dialysis patients feel normal?

Many patients live normal lives except for the time needed for treatments. Dialysis usually makes you feel better because it helps many of the problems caused by kidney failure. You and your family will need time to get used to dialysis.

Do dialysis patients have to control their diets?

Yes. You may be on a special diet. You may not be able to eat everything you like, and you may need to limit how much you drink. Your diet may vary according to the type of dialysis.

Click here to learn more about diet for dialysis patients

Can dialysis patients travel?

Yes. Dialysis centers are located in every part of the United States and in many foreign countries. The treatment is standardized. You must make an appointment for dialysis treatments at another center before you go. The staff at your center may help you make the appointment.

Click here to learn more about traveling on dialysis

Can dialysis patients continue to work?

Many dialysis patients can go back to work after they have gotten used to dialysis. If your job has a lot of physical labor (heavy lifting, digging, etc. ), you may need to get a different job.

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covid-19

Intake and OutputKey Points:• Normal urine output for pediatric patient is at least 1mL/kg/hr.• If the child has diarrhea stool or vomits, stools and emesis must be replaced mL/mL or ½ mL/mL, follow MD’s orders.• Calculations for Maintenance FluidNewborn: up to 72 hrs after birth60-100mL/kg/dayUp to 10Kg100mL/kg/day11-20kg1000mL+50mL/kg/day21-30kg1500mL+25mL/kg/dayFor example:  15kg baby should receive 1250mL/day(1000mL+250=1250mL/day) • Use non-sucking or dominant hand.• Do not have an ID band on the IV hand. If the IV infiltrates the ID band may cut the circulation to the arm and hand.• Burretrols must be used when delivering IV fluids.• Do not fill the microdrip chamber with more than 2 hours worth of IV fluids.• Check the IV site every 1 – 2 hours.• Turn the control IV pump away from the child; children sometimes play with the dials.• If you suspect IV infiltration, assess for redness, edema, coolness, slow infusion. If the blood does not flow back it does not mean the IV is infiltrated. Sometimes the vein’s pressure is less then the IV fluid’s pressure

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Potassium and kidney is the key element

causes of high potassium include:

  • Dehydration
  • Some medicines
  • Uncontrolled diabetes
  • Injuries that cause severe bleeding
  • Some rare diseases

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www.kidneynest.com

A small crowd of villagers waits at a low-slung concrete school building in Pedda Srirampuram, a village in the southern Indian state of Andhra Pradesh. The early morning air is crisp and the men and women are dressed in light shawls and sweaters. Each holds two plastic bags—one with their medical records, the other with a clear plastic container of their urine. They line up to be seen by one of four young men at two large wooden tables.

A researcher named Srinivas Rao sits at the first table. “What’s your name?” he asks a short, wiry man who is next in line. “D. Kesava Rao,” the man replies, handing over his medical records. Rao, the researcher, flips through the pages, noting down details. “His kidneys are not functioning at all,” Rao remarks. “Both his kidneys.”

Kesava Rao, 45, has chronic kidney disease of unknown etiology (CKDu) and depends on dialysis to survive. “Every week I undergo dialysis, 4 weeks a month,” Rao says. A soft-spoken man with a ready smile, Rao has worked all his life on construction sites or coconut farms. He lived a healthy life and hardly ever saw a doctor, he says, until a fever led to an exam and his diagnosis. Rao didn’t have diabetes or, until his kidneys failed, hypertension, the two main causes of chronic kidney disease worldwide. Nor do most of the other villagers who have gathered here, all chronic kidney disease patients, waiting to get a free blood test for creatinine, a metabolite and a proxy for kidney function, and give samples of urine and blood for research.

This region in coastal Andhra Pradesh is at the heart of what local doctors and media are calling a CKDu epidemic. There is little rigorous prevalence data, but unpublished studies by Gangadhar Taduri, a nephrologist at the Nizam’s Institute of Medical Sciences in Hyderabad, in the neighboring state of Telangana, suggest the disease affects 15% to 18% of the population in this agricultural region, known for rice, cashews, and coconuts. Unlike the more common kind of CKD, seen mostly in the elderly in urban areas, CKDu appears to be a rural disease, affecting farm workers, the majority of them men between their 30s and 50s. “It is a problem of disadvantaged populations,” says Taduri, who is leading the team of researchers in the village.

Chronic kidney disease mainly strikes rural farm laborers, like these men husking coconuts in the hot south Indian sun.

A rash of similar outbreaks in other countries has underscored that it is a global problem. Some rice-growing regions of Sri Lanka have their own epidemic, and the disease is rampant in sugar-producing regions of Mexico and Central America (Science, 11 April 2014, p. 143). It has also been reported in Egypt. Just about everywhere, prevalence numbers are scarce and uncertain, but “there is a great deal of concern,” says Virginia Weaver, an epidemiologist at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland. “This is an illness that has substantial mortality. People who would [otherwise] be working, raising families, are dying. It’s quite extraordinary.”

Public health experts and researchers are alarmed and baffled. In Central America, which has been hit the hardest, the leading hypothesis is that this is an occupational disease, caused by chronic exposure to heat and dehydration in the cane fields. Here in Andhra Pradesh, Taduri and his colleagues think natural toxins in the drinking water—lithium, for example—could contribute. Using the blood and urine samples from Pedda Srirampuram, “we’re going to evaluate whether [trace elements] are really present in the body or not,” says C. Prabhakar Reddy, one of the researchers collecting the samples.

But in India, as in Sri Lanka and Central America, researchers trying to explain CKDu are pursuing a wide range of ideas, including excessive use of over-the- counter painkillers and exposure to pesticides. Nephrologist Ajay Singh of Harvard Medical School in Boston has found high levels of silica, present in some pesticides, in the region’s drinking water, and thinks it could be responsible. “There’s a smoking gun,” he says, though he concedes, “I don’t know whether the smoking gun is responsible.”

As the global scale of the disease becomes clear, the search for answers is accelerating. The beginnings of an international scientific network to study CKDu are taking shape, and researchers are working on simple, accurate diagnostics so that they can map incidence around the globe—and try to correlate it with potential causes.

Like most places where CKDu is rampant, India doesn’t have a good idea how many people have the disease (also known as CKDnT, for nontraditional causes). But the anecdotal evidence from Andhra Pradesh is sobering. We have “almost 126 widows” of men who have died from CKD, says Rajni Kumar Dolai, the chief of the village of Balliputtuga. The total population of his village is 3270, which implies that almost 4% of its inhabitants have died of the disease.

By screening village populations in a van equipped with an ultrasound machine and other diagnostic equipment, Taduri and his colleagues came up with their estimated incidence of 15% or more in this region. Most people diagnosed with CKDu “didn’t have any complaints that suggested a kidney problem,” Taduri says. “But … their creatinine was high.” Ultrasound exams revealed that they had “shrunken” kidneys.

In the village of Pedda Srirampuram, a mobile testing team interviews villagers and collects blood and urine samples to test their kidneys.

CKDu is so deadly in part because it is hard to detect. “It is a silent killer,” says A. K. Chakravarthy, a nephrologist in Nellore, Andhra Pradesh. In the disease’s early stages, people show no symptoms. “By the time they find out, it is too late,” he says. Their kidneys are already beyond repair, leading to high blood pressure, weakness, and other symptoms. Access to dialysis here remains limited, even though the state govern- ment of Andhra Pradesh has added facilities in recent years. For many patients, death comes not long after their diagnosis.

Those lucky enough to get dialysis survive for several years, but are unable to earn a living, pushing their families deeper into poverty. His strength and endurance sapped by the disease and dialysis, Kesava Rao can no longer provide for his family of five. His eldest son, now 20, has had to step into his father’s shoes. “He finished high school, and then stopped studying,” Rao says. “He’s the primary breadwinner of the family now.”

In India, several research groups are on the trail of a cause. But each team has used its own methods and tools, often in isolation, making it hard to compare findings. Taduri and Singh, for example, have both worked in Andhra Pradesh for years, and both have pursued the hypothesis that the high levels of silica in drinking water could be responsible. Silica dust is known to damage lungs and kidneys when inhaled, but no one knows what it does when ingested.

Yet the two researchers had never met until recently. “I wasn’t even aware that this work was going on,” Singh says about Taduri’s work. Whereas Singh thinks the silica comes from pesticides, Taduri believes it leaches into the groundwater from bedrock. Singh admits the researchers could have benefitted from a collaboration. “We need to develop a coordinated approach.”

That is true beyond India. As scientists and public health experts realize that CKDu is a global disease or set of diseases, they are casting a wider net for possible causes. “We need to look at this from a global perspective,” Weaver says.

Some 30 Indian and international scientists, physicians, and public health experts sit at a round table in a nondescript conference room at The Energy and Resources Institute in New Delhi. The group is here for a CKD workshop spearheaded by the La Isla Foundation, a nonprofit group that works with affected communities in Central America. The goal of the January meeting: to create a global network of scientists studying the disease.

The first task for the network is to determine prevalence, says Ben Caplin, a nephrologist at University College London who works in Nicaragua. “We need to know where are the hot spots of CKDnT,” he says. “Are there common environmental, occupational, and social factors shared between CKDnT hot spots?”

But participants differ about how to define the disease. Caplin proposes a working definition: “no alternative cause of CKD diagnosed by medical professional, absence of diabetes, absence of hypertension.” But Singh says that the condition may well be a collection of diseases caused by different factors in different places. By insisting on a single definition, we are “already starting to have a bias on what the causes may be.”

Neil Pearce of the London School of Hygiene & Tropical Medicine, the only epidemiologist in the room, says screening for impaired kidney function can be done without making assumptions about causes. “We’re trying to find populations with high prevalence and low prevalence. This says nothing about the individual.”

Getting a handle on prevalence will require a standard screening test, however. Caplin, Pearce, and their colleagues are developing a protocol that can be adapted for different populations: a blood test for kidney function, a urine test, and a basic questionnaire recording the participant’s age, sex, occupation, and income. The team is trying to keep it simple and inexpensive, Caplin says. “We don’t want to make it too complicated and put people off.”

The team hopes to publish the protocol in a peer-reviewed journal, so that scientists in any country can use it to screen local or regional populations with their own funds. “I think that using a simple protocol that will be affordable in different settings would really shed light on the extent and global distribution of the disease,” says Catharina Wesseling, an occupational and environmental health expert at the Karolinska Institute in Stockholm.

Wesseling studies CKDnT in Central America, where it takes an even heavier toll than in India. “Just look at the mortality numbers,” says Jason Glaser of La Isla. In Chichigalpa, Nicaragua, for example, “46% of all male deaths are due to CKD,” he says. “Seventy-five percent of deaths of men between 35 and 55 years are due to CKD.” By some estimates, the disease has already killed at least 20,000 people in the region.

If the disease hitting India is identical, research in Central America could narrow the search for a cause. Recent studies there have bolstered the hypothesis that CKDu results from long hours of work in the heat with too little drinking water, leading to chronic dehydration. Last year, for example, a study by Wesseling and her colleagues showed that the disease has existed in Costa Rica at least since the 1970s, but that the death rate in Guanacaste province has shot up from 4.4 per 100,000 men between 1970 and 1972 to 38.5 in 2008 to 2012 with the expansion of industrial-scale sugarcane farms. In another study, the same group showed that the kidney function of cane cutters in one Nicaraguan community declined through a single harvest period. “These people have a very scary deterioration of kidney function over the harvest time,” Wesseling says.

The mysterious new form of chronic kidney disease strikes mainly poor, agricultural areas in the tropics. It takes its heaviest toll in Central America, but it has now been reported in other regions.

A pilot study she and her colleagues did last year hinted at how chronic dehydration does its damage. They found high levels of uric acid crystals in cane cutters’ urine, especially at the ends of their shifts. Those crystals could be injuring the kidneys, the researchers proposed. “This is an important mechanism we hadn’t thought about,” says Richard Johnson, a nephrologist at the University of Colorado, Denver, and an author on the study.

But the case is far from closed. “I absolutely don’t think that heat stress and dehydration are the only part of the story,” Glaser says. “You see different severity [of the disease] in different places.” Like him, most scientists are not yet ruling out other factors.

Even before scientists know for sure what causes the disease, Taduri says communities can take steps to reduce the risks. Providing clean surface water sources for drinking, urging people to drink more water at work, and advising them to stay away from pain- killers will improve their health anyway, he contends. In El Salvador, Glaser and his colleagues are working to expand a pilot study called the Worker Health and Efficiency program, which prescribes frequent rest and hydration for workers.

Meanwhile, in CKDu-affected communities in southern India, fear and frustration are on the rise. Now, says Taduri, villagers in Andhra Pradesh refuse to come for screening, fearing stigma. When a man is diagnosed with the kidney condition, “his entire family will feel him as a burden,” explains Dolai, the village chief in Balliputtuga.

On a nearby farm, a group of men stand in a circle peeling coconuts. Most are sweating in the midmorning sun. Each stands over a blade longer than his forearm, its wooden handle planted firmly in the soil. They pluck coconuts from a pile and swiftly pull each one over the blade, peeling the thick husk away from the hard, brown inner shell.

The men talk as they work, and the conversation turns to their creatinine levels. “Mine is 1.4,” says a young man in his 30s. “Mine is 1.3,” another says. “One point nine.” “Two.” For half the men, the levels are either borderline or high. All work long hours under the sun, with too little water to drink. Their legs and backs often hurt when they return home in the evenings, and they turn to painkillers or alcohol, even though they know both are bad for their kidneys.

The men understand they are at risk of chronic kidney disease, but believe they can do little to stop it from progressing. Rest is not an option, one says. “We have the dsease, but we still have to work to earn a living.”
credit
sciencemag.org

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