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How Does Use Of Insulin Lead To Hypokalemia?

Insulin And Potassium

Insulin And Potassium

Insulin has a number of actions on the body besides lowering your blood glucose levels. Insulin suppresses the breakdown and buildup of glycogen, which is the storage form of glucose, it blocks fat metabolism and the release of fatty acids, and it puts potassium into the cells by activating the sodium-potassium cellular channels. Insulin stimulates the uptake of glucose and potassium in all cells of the body but primarily fuels the muscle cells as well as some of the fat cells. In type 2 diabetes or metabolic syndrome (a form of metabolic disease), insulin is not functioning up to its normal level. The cells of the body become resistant to insulin and the blood sugar levels are elevated. The serum potassium (K+) level is a reflection of the total body stores of potassium, although it can be inaccurate in some conditions that affect the distribution of potassium in the body’s cells. The plasma potassium level determines the resting potential of the cells of the body. A person can have low potassium (hypokalemia) or high potassium (hyperkalemia), both of which are asymptomatic conditions that can be serious as they both cause heart arrhythmias. The Relationship between Insulin and Potassium Shortly after insulin was discovered, scientists revealed that insulin had something to do with the potassium levels in both the cells and in the blood. The insulin is the hormone in the body that keeps the potassium level in the blood within the normal range. When insulin is decreased, the potassium level rises and can rise even further if you eat something high in potassium, such as salt substitutes and bananas. When the potassium level is high, it causes the pancreas to release insulin in order to counteract the effects of high potassium levels. When you eat something that is high Continue reading >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Physiology of Potassium Handling Potassium (K+) is the most abundant cation in the body. About 90% of total body potassium is intracellular and 10% is in extracellular fluid, of which less than 1% is composed of plasma. The ratio of intracellular to extracellular potassium determines neuromuscular and cardiovascular excitability, which is why serum potassium is normally regulated within a narrow range of 3.5 to 5.0 mmol/L. Dietary K+ intake is highly variable, ranging from as low as 40 mmol/day to more than 100 mmol/day.1, 2 Homeostasis is maintained by two systems. One regulates K+ excretion, or external balance through the kidneys and intestines, and the second regulates K+ shifts, or internal balance between intracellular and extracellular fluid compartments. Internal balance is mainly mediated by insulin and catecholamines. Cellular Shifts Ingested K+ is absorbed rapidly and enters the portal circulation, where it stimulates insulin secretion. Insulin increases Na+,K+-ATPase activity and facilitates potassium entry into cells, thereby averting hyperkalemia. β2-Adrenergic stimulation also promotes entry of K+ into cells through increased cyclic adenosine monophosphate (cAMP) activation of Na+,K+-ATPase. Renal Handling An increase in extracellular potassium concentration also stimulates aldosterone secretion (via angiotensin II), and aldosterone increases K+ excretion. In the steady state, K+ excretion matches intake, and approximately 90% is excreted by the kidneys and 10% in the stool. Renal K+ excretion is mediated by aldosterone and sodium (Na+) delivery (glomerular filtration rate [GFR]) in principal cells of the collecting ducts.3 K+ is freely filtered by the glomerulus, and almost all the filtered K+ is reabsorbed in the proximal tubule and loop of Henle (Fig. Continue reading >>

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5 Continue reading >>

Physiologic Effects Of Insulin

Physiologic Effects Of Insulin

Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>

Hypokalemia: Video, Anatomy, Definition & Function | Osmosis

Hypokalemia: Video, Anatomy, Definition & Function | Osmosis

Rishi Desai, MD, MPH , Tanner Marshall, MS , Tanner Marshall, MS , Jake Ryan , Tanner Marshall, MS With hypokalemia, hypo- means under and -kal- refers to potassium, and -emia refers to the blood, so hypokalemia means lower than normal potassium levels in the blood, generally under 3.5 mEq/L. Now, total body potassium can essentially be split into two componentsintracellular and extracellular potassium, or potassium inside and outside cells, respectively. The extracellular component includes both the intravascular space, which is the space within the blood and lymphatic vessels and the interstitial spacethe space between cells where you typically find fibrous proteins and long chains of carbohydrates which are called glycosaminoglycans. Now, the vast majority, around 98%, of all of the bodys potassium is intracellular, or inside of the cells. In fact, the concentration of potassium inside the cells is about 150 mEq/L whereas outside the cells its only about 4.5 mEq/L. Keep in mind that these potassium ions carry a charge, so the difference in concentration also leads to a difference in charge, which establishes an overall electrochemical gradient across the cell membrane . And this is called the internal potassium balance. This balance is maintained by the sodium-potassium pump, which pumps 2 potassium ions in for every 3 sodium ions out, as well as potassium leak channels and inward rectifier channels that are scattered throughout the membrane. This concentration gradient is extremely important for setting the resting membrane potential of excitable cell membranes, which is needed for normal contraction of smooth, cardiac, and skeletal muscle . Also, though, in addition to this internal potassium balance, theres also an external potassium balance, which refers to the Continue reading >>

Hypokalemia & Diabetes

Hypokalemia & Diabetes

According to a 2011 national diabetes fact sheet from the Centers for Disease Control and Prevention, over 25 million people, or 8.3 percent of the United States population, have diabetes. Diabetes is the condition that results from the lack of insulin production or from insulin resistance; in diabetes, there is abnormal metabolism of glucose, which results in elevated blood glucose levels. Diabetes is associated with dysregulation of potassium, but several studies suggest that hypokalemia may mediate the development of diabetes. Video of the Day According to "Davidson's Principles & Practice of Medicine," hypokalemia, or low blood potassium, is defined as blood potassium levels below 3.5 millimoles per liter, or mmol/L, of blood. Potassium facilitates the function of insulin in the delivery of glucose to cells; when insulin binds to its receptors on the cell membrane, it causes potassium to flow into the cells. As levels of insulin increase in the blood, more potassium is driven into cells; therefore, hyperinsulinemia, or high blood insulin, is commonly associated with hypokalemia. Hypokalemia and Diabetes Studies Since a clear relationship exists between insulin and potassium, researchers have speculated the possibility of potassium's involvement in the development of diabetes. According to a 2008 article in the journal "Hypertension," several studies have collectively demonstrated a strong inverse relationship between blood glucose levels and potassium levels during the use of thiazides diuretics; therefore, as potassium levels decrease, blood glucose levels should increase. This inverse relationship between glucose and potassium, concurs with the notion that total body potassium has a role in determining person's sensitivity to insulin. In diabetics, excessive use o Continue reading >>

Hypokalemia (low Potassium)

Hypokalemia (low Potassium)

What Is Hypokalemia? Hypokalemia is an electrolyte imbalance and is indicated by a low level of potassium in the blood. The normal adult value for potassium is 3.5-5.3 mEq/L. Potassium is one of many electrolytes in your body. It is found inside of cells. Normal levels of potassium are important for the maintenance of heart, and nervous system function. What Causes Hypokalemia? One way your body regulates blood potassium levels is by shifting potassium into and out of cells. When there is a breakdown or destruction of cells, the electrolyte potassium moves from inside of the cell to outside of the cell wall. This shift of potassium into the cells causes hypokalemia. Trauma or insulin excess, especially if diabetic, can cause a shift of potassium into cells (hypokalemia). Potassium is excreted (or "flushed out" of your system) by your kidneys. Certain drugs or conditions may cause your kidneys to excrete excess potassium. This is the most common cause of hypokalemia. Other causes of hypokalemia include: Increased excretion (or loss) of potassium from your body. Some medications may cause potassium loss which can lead to hypokalemia. Common medications include loop diuretics (such as Furosemide). Other drugs include steroids, licorice, sometimes aspirin, and certain antibiotics. Renal (kidney) dysfunction - your kidneys may not work well due to a condition called Renal Tubular Acidosis (RTA). Your kidneys will excrete too much potassium. Medications that cause RTA include Cisplatin and Amphotericin B. You may have hypokalemia from a loss of body fluids due to excessive vomiting, diarrhea, or sweating. Endocrine or hormonal problems (such as increased aldosterone levels) - aldosterone is a hormone that regulates potassium levels. Certain diseases of the endocrine system, s Continue reading >>

Potassium As A Link Between Insulin And The Renin-angiotensin-aldosterone System.

Potassium As A Link Between Insulin And The Renin-angiotensin-aldosterone System.

Abstract PURPOSE: To focus on the interactions between insulin secretion, glucose tolerance and insulin sensitivity on the one hand and the renin-angiotensin-aldosterone system on the other. EFFECTS ON INSULIN: Insulin is a potent stimulus for hypokalaemia, sparing body potassium from urinary excretion by transporting it into cells. Potassium also appears to play a key role in the antinatriuretic effect of insulin. Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release. EFFECTS OF ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITION: Interference with the renin-angiotensin-aldosterone system by ACE inhibition blunts the hypokalaemic response to insulin, thereby improving glucose-induced insulin release and oral glucose tolerance. ACE inhibition, however, does not cause major changes in insulin sensitivity. POTASSIUM AND BLOOD PRESSURE: Plasma potassium levels are inversely related to blood pressure, both in population surveys and in intervention studies. In addition, in patients with essential hypertension, the level of plasma potassium appears to predict the blood pressure response to ACE inhibition. SUMMARY: Potassium metabolism is an important link between carbohydrate metabolism and the renin-angiotensin-aldosterone system by way of a double-feedback mechanism. Through the potential effects on blood pressure control, plasma levels of potassium represent a link between insulin and blood pressure in humans. Continue reading >>

Potassium Disorders: Hypokalemia And Hyperkalemia

Potassium Disorders: Hypokalemia And Hyperkalemia

Hypokalemia and hyperkalemia are common electrolyte disorders caused by changes in potassium intake, altered excretion, or transcellular shifts. Diuretic use and gastrointestinal losses are common causes of hypokalemia, whereas kidney disease, hyperglycemia, and medication use are common causes of hyperkalemia. When severe, potassium disorders can lead to life-threatening cardiac conduction disturbances and neuromuscular dysfunction. Therefore, a first priority is determining the need for urgent treatment through a combination of history, physical examination, laboratory, and electrocardiography findings. Indications for urgent treatment include severe or symptomatic hypokalemia or hyperkalemia; abrupt changes in potassium levels; electrocardiography changes; or the presence of certain comorbid conditions. Hypokalemia is treated with oral or intravenous potassium. To prevent cardiac conduction disturbances, intravenous calcium is administered to patients with hyperkalemic electrocardiography changes. Insulin, usually with concomitant glucose, and albuterol are preferred to lower serum potassium levels in the acute setting; sodium polystyrene sulfonate is reserved for subacute treatment. For both disorders, it is important to consider potential causes of transcellular shifts because patients are at increased risk of rebound potassium disturbances. Potassium disorders are common. Hypokalemia (serum potassium level less than 3.6 mEq per L [3.6 mmol per L]) occurs in up to 21% of hospitalized patients and 2% to 3% of outpatients.1–3 Hyperkalemia (serum potassium level more than 5 mEq per L [5 mmol per L] in adults, more than 5.5 mEq per L [5.5 mmol per L] in children, and more than 6 mEq per L [6 mmol per L] in neonates) occurs in up to 10% of hospitalized patients and ap Continue reading >>

Diabetes Mellitus And Electrolyte Disorders

Diabetes Mellitus And Electrolyte Disorders

Go to: Abstract Diabetic patients frequently develop a constellation of electrolyte disorders. These disturbances are particularly common in decompensated diabetics, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. These patients are markedly potassium-, magnesium- and phosphate-depleted. Diabetes mellitus (DM) is linked to both hypo- and hyper-natremia reflecting the coexistence of hyperglycemia-related mechanisms, which tend to change serum sodium to opposite directions. The most important causal factor of chronic hyperkalemia in diabetic individuals is the syndrome of hyporeninemic hypoaldosteronism. Impaired renal function, potassium-sparing drugs, hypertonicity and insulin deficiency are also involved in the development of hyperkalemia. This article provides an overview of the electrolyte disturbances occurring in DM and describes the underlying mechanisms. This insight should pave the way for pathophysiology-directed therapy, thus contributing to the avoidance of the several deleterious effects associated with electrolyte disorders and their treatment. Keywords: Glucose, Osmotic diuresis, Hyponatremia, Hyperkalemia, Hypomagnesemia Core tip: Diabetic patients frequently develop a constellation of electrolyte disorders. These patients are often potassium-, magnesium- and phosphate-depleted, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. Diabetes is linked to both hypo- and hyper-natremia, as well as to chronic hyperkalemia which may be due to hyporeninemic hypoaldosteronism. This article provides an overview of the electrolyte disturbances occurring in diabetes and describes the underlying mechanisms. This insight should pave the way for pathophysiology-direct Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patients With Diabetes Mellitus? - Quora

Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patients With Diabetes Mellitus? - Quora

Why doesn't regular insulin therapy cause hypokalemia in patients with diabetes mellitus? aMdy OofybgFyGIBs ANQDwVwumjkcmIZkAsDWDuacvXokTydYhGNQYxwovlz Did you know that unlike searching on DuckDuckGo, when you search on Google, they keep your search history forever? That means ... Originally Answered: Why doesn't regular insulin therapy cause hypokalemia in patient with diabetes mellitus? Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely... Read More Loading Originally Answered: Why doesn't regular insulin therapy cause hypokalemia in patient with diabetes mellitus? Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium atpas Continue reading >>

Hypokalemia Induced Insulin Resistance In Bartter's Syndrome. 522

Hypokalemia Induced Insulin Resistance In Bartter's Syndrome. 522

HYPOKALEMIA INDUCED INSULIN RESISTANCE IN BARTTER'S SYNDROME. 522 Bartter's Syndrome (BS) is characterized by renal tubular dysfunction with resultant severe hypokalemia. These patients exhibit poor linear growth, but clinicians have been reluctant to treat with growth hormone secondary to insulin resistance (IR) which could be worsened by growth hormone (hGH). The goal of this study was to determine insulin sensitivity in BS, utilizing the hyperinsulinemic euglycemic clamp model, and to determine the relationship between IR and hypokalemia. We studied a male BS (12 yrs, 33 kg, Tanner II, Z score-2). Serum potassium(K+) averaged 3.9meq/L over the previous 4 months. All medications were held for 18 hours prior to the study. The patient underwent two hyperinsulinemic euglycemic clamps (40 mU/m2/min): clamp #1 K+=2.5meq/L & clamp #2 K+=4.1meq/L. K+ was maintained at the initial level during each clamp. Total body potassium, 40K, was measured prior to the second clamp in BS. Growth hormone levels were measured at the initiation of each clamp. Results were compared to an age, weight, Z score and Tanner stage matched volunteer (C). Insulin sensitivity is reported as one-half maximal glucose disposal rate (GDR,mg/kg/min) measured at steady state after 2.5 hrs. GDR for the normal volunteer was 8.8 mg/kg/min. GDR for the BS patient was: clamp #1, hypokalemia, 4.0 mg/kg/min; clamp #2, normokalemia, 8.5 mg/kg/min. The peripheral insulin levels achieved during all clamp studies were similar(70mU/ml4). 40K was normal prior to clamp #2 in BS. hGH levels were undetectable in the BS patient and did not change with normalization of K+ (BS#1=<1.0,BS#2=<1.0,C=1.8 ng/ml). In conclusion: 1) insulin resistance is present in Bartter's Syndrome, but occurs secondarily to hypokalemia; 2) Insul Continue reading >>

What Is The Connection Between Diabetes And Potassium?

What Is The Connection Between Diabetes And Potassium?

Usually, your body processes the food you eat and turns it into a sugar called glucose. Your body uses glucose for energy. Insulin is a hormone your pancreas produces. Your body uses the insulin to help move glucose into cells throughout your body. If you have diabetes, your body is unable to produce or use insulin efficiently. Type 1 diabetes isn’t preventable, but you can prevent type 2 diabetes. Type 2 diabetes, or adult-onset diabetes, usually occurs in people ages 35 and older. Potassium is an electrolyte and mineral that helps keep your bodily fluids at the proper level. Your body can do the following if your fluids are in check: contract your muscles without pain keep your heart beating correctly keep your brain functioning at its highest capability If you don’t maintain the right level of potassium, you can experience a variety of symptom that include simple muscle cramps to more serious conditions, such as seizures. According to recent research, there may be a link between type 2 diabetes and low potassium levels. Although people recognize that potassium affects diabetes, research is ongoing to determine why this may happen. Researchers in one study at Johns Hopkins University School of Medicine linked low levels of potassium with high levels of insulin and glucose in people who were otherwise healthy. Low levels of potassium with high levels of insulin and glucose are both traits doctors associate with diabetes. One 2011 study found that people taking thiazides to treat high blood pressure experienced a loss of electrolytes, such as potassium. Researchers noted that this loss might increase a person’s risk of developing diabetes. And along with that, researchers have also linked potassium levels to high blood pressure. Even though low potassium may incre Continue reading >>

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