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Lactic Acidosis An Update

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>

Role Of Lactate In Critically Ill Children Agrawal S, Sachdev A, Gupta D, Chugh K

Role Of Lactate In Critically Ill Children Agrawal S, Sachdev A, Gupta D, Chugh K

Lactic acidosis is a common finding in critically ill patients. It has been used as a prognostic marker of the outcome in Pediatric Intensive Care Unit patients. Lactic acid is produced as a product of anaerobic glycolysis and is reversibly converted to pyruvate in the presence of favorable metabolic environment. All the body tissues can produce and consume lactate with few having predominant function of production and others of consumption. Liver is a major organ for lactate consumption and it is the liver, which metabolizes the increased lactic acid produced in regional tissue beds.The lactate levels can be done on arterial, venous, or mixed venous blood and can be measured by various methods. Serial lactate concentrations and the difference in arterial and mixed venous lactate levels or between the arterial and regional blood lactate levels like jugular venous lactate levels have been shown to have better correlation with the outcome. High initial blood lactate levels and persistently high lactate levels have been correlated with poor outcome.There are various causes of lactic acid overproduction, which may produce either hyperlactatemia or lactic acidosis. High blood lactate levels are found in critically ill patients with shock of any etiology and sepsis due to various reasons, which include increased catecholamine induced glucose flux apart from the tissue hypoperfusion and hypoxia. Various other illnesses can cause an increase in blood lactate levels like acute lung/liver injury, severe asthma, poisoning, post cardiac surgery etc.Treating the underlying disease leading to lactic acidosis is the best measure to control lactic acidosis. Some therapeutic choices are available to neutralize the effect of lactic acid on cell function, but none has stood the test of t Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further clarifying the relationship between metformin, acute kidney injury and lactic acidosis Subscribe to Nature Reviews Nephrology for full access: Diabetes mellitus: complex interplay between metformin, AKI and lactic acidosis Bell, S., Soto-Pedre, E., Connelly, P., Livingstone, S. & Pearson, E. Clarifying the relationship between metformin, acute kidney injury and lactic acidosis . Nat. Rev. Nephrol. , (2017). Rhee, C. M., Kovesdy, C. P. & Kalantar-Zadeh, K. Risks of metformin in type 2 diabetes and chronic kidney disease: lessons learned from Taiwanese data Risk of acute kidney injury and survival in patients treated with metformin: an observational cohort study Acute kidney injury, plasma lactate concentrations and lactic acidosis in metformin users: a GoDarts study . Diabetes Obes. Metab. 19, 1579–1586 (2017). Inzucchi, S. E., Lipska, K. J., Mayo, H., Bailey, C. J. & McGuire, D. K. Metformin in patients with type 2 diabetes and kidney disease: a systematic review Restricting metformin in CKD: continued caution warranted . Am. J. Kidney Dis. 66, 1101–1102 (2015). Should restrictions be relaxed for metformin use in chronic kidney disease? Yes, they should be relaxed! What's the fuss? Should restrictions be relaxed for metformin use in chronic kidney disease? No, we should never again compromise safety! Metformin in chronic kidney disease: more harm than help? Lancet Diabetes Endocrinol. 3, 579–581 (2015). Metformin use in type 2 diabetes mellitus With CKD: is it time to liberalize dosing recommendations? Kalantar-Zadeh, K., Uppot, R. N. & Lewandrowski, K. B. Case records of the Massachusetts General Hospital. Case 23–2013. A 54-year-old woman with abdominal pain, vomiting, and confusion United States Renal Data System. USRDS 2017 Annual Data Report: Atlas Continue reading >>

Lactic Acidosis

Lactic Acidosis

WHAT YOU NEED TO KNOW: What is lactic acidosis and what causes it? Lactic acidosis is the buildup of lactic acid in your blood. Lactic acid is a substance that can build up in your body if you are not getting enough oxygen. It can also occur if you have a condition that causes an increased need for oxygen. The following may cause lactic acidosis: Shock from trauma or severe blood loss Sepsis (a serious condition that occurs when the body overreacts to an infection) Seizures Heart attack or heart failure Severe lung disease Liver or kidney disease Cancer or AIDS Diabetic ketoacidosis Certain medicines such as metformin (diabetes medicine) or some HIV medicines Intense exercise What are the signs and symptoms of lactic acidosis? Muscular weakness Breathing faster than normal Nausea and vomiting Coma How is lactic acidosis diagnosed and treated? Lactic acidosis is diagnosed with a blood test. The blood test measures the amount of lactate in your blood. Treatment depends on the cause of your lactic acidosis. The condition that caused lactic acidosis will need to be treated. When should I contact my healthcare provider? Your symptoms return. You have questions or concerns about your condition or care. Care Agreement You have the right to help plan your care. Learn about your health condition and how it may be treated. Discuss treatment options with your caregivers to decide what care you want to receive. You always have the right to refuse treatment. The above information is an educational aid only. It is not intended as medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you. © 2017 Truven Health Analytics Inc. Information is for End User's use only and Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H+) or a reduction in bicarbonate (HCO3-) concentrations. In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO2. Chronically, renal compensation occurs by means of reabsorption of HCO3. [ 1 , 2 ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. [ 2 , 3 , 4 ] It remains the most common cause of metabolic acidosis in hospitalized patients. Cohen R, Woods H. Clinical and Biochemical Aspects of Lactic Acidosis. London, United Kingdom: Blackwell Scientific Publications; 1976. Suetrong B, Walley KR. Lactic acidosis in sepsis: It's not all anaerobic. Implications for diagnosis and management. Chest. 2015 Sep 17. [Medline] . Forrest DM, Russell JA. Metabolic acidosis. Webb A, Shapiro M, Singer M, Suter P, eds. Oxford Textbook of Critical Care. Oxford, United Kingdom: Oxford University Press; 1999. 573-7. Seheult J, Fitzpatrick G, Boran G. Lactic acidosis: an update. Clin Chem Lab Med. 2017 Mar 1. 55 (3):322-33. [Medline] . [Full Text] . Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med. 1992 Jan. 20(1):80-93. [Medline] . Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA. Lactate clearance vs central venous oxygen saturation as goal Continue reading >>

Propofol Infusion Syndrome In Adults: A Clinical Update

Propofol Infusion Syndrome In Adults: A Clinical Update

Propofol Infusion Syndrome in Adults: A Clinical Update Department of Internal Medicine, Saint Joseph Hospital, 2900 N. Lake Shore, Chicago, IL 60657, USA Received 24 November 2014; Revised 21 March 2015; Accepted 28 March 2015 Copyright 2015 Aibek E. Mirrakhimov et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Propofol infusion syndrome is a rare but extremely dangerous complication of propofol administration. Certain risk factors for the development of propofol infusion syndrome are described, such as appropriate propofol doses and durations of administration, carbohydrate depletion, severe illness, and concomitant administration of catecholamines and glucocorticosteroids. The pathophysiology of this condition includes impairment of mitochondrial beta-oxidation of fatty acids, disruption of the electron transport chain, and blockage of beta-adrenoreceptors and cardiac calcium channels. The disease commonly presents as an otherwise unexplained high anion gap metabolic acidosis, rhabdomyolysis, hyperkalemia, acute kidney injury, elevated liver enzymes, and cardiac dysfunction. Management of overt propofol infusion syndrome requires immediate discontinuation of propofol infusion and supportive management, including hemodialysis, hemodynamic support, and extracorporeal membrane oxygenation in refractory cases. However, we must emphasize that given the high mortality of propofol infusion syndrome, the best management is prevention. Clinicians should consider alternative sedative regimes to prolonged propofol infusions and remain within recommended maximal dose limits. Propofol is a sedative-hypnotic m Continue reading >>

D-lactic Acidosis In Humans: Review Of Update

D-lactic Acidosis In Humans: Review Of Update

Your browser does not support the NLM PubReader view. Go to this page to see a list of supporting browsers. D-Lactic Acidosis in Humans: Review of Update Electrolyte Blood Press. 2006 Mar;4(1):53-56. Electrolyte Blood Press. 2006 Mar;4(1):53-56. English. Published online March 31, 2006. Copyright 2006 The Korean Society of Electrolyte and Blood Pressure Research D-Lactic Acidosis in Humans: Review of Update Kyung Pyo Kang, M.D.,Sik Lee, M.D. and Sung Kyew Kang, M.D. Department of Internal Medicine, and Research Institute of Clinical Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Correspondence author: Sung Kyew Kang, M.D., Department of Internal Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Tel: 063)250-1677, Fax: 063)254-1609, Email: [email protected] This article has been cited by 2 articles inPubMed Central. D-Lactic acidosis has been well documented in ruminants. In humans, D-lactic acidosis is very rare, but D-lactic acidosis may be more common than generally believed and should be looked for in a case of metabolic acidosis in which the cause of acidosis is not apparent. The clinical presentation of D-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The entity should be considered as a diagnosis in a patient who presents with metabolic acidosis accompanied by high anion gap, normal lactate level, negative Acetest, history of short bowel syndrome or malabsorption, and characteristic neurologic manifestations. Low carbohydrate diet, bicarbonate treatment, rehydration, and oral antibiotics would be helpful in controlling symptoms. Keywords: D-lactic acidosis; Metabolic acidosis; Humans D-Lactic acidosis has been well documented in ruminants. In humans, however, D-lactic acidosis is Continue reading >>

Lactic Acidosis: An Update

Lactic Acidosis: An Update

Clinical Chemistry and Laboratory Medicine (CCLM) Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R. Source Normalized Impact per Paper (SNIP) 2016: 1.112 [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * *Prices in US$ apply to orders placed in the Americas only. Prices in GBP apply to orders placed in Great Britain only. Prices in represent the retail prices valid in Germany (unless otherwise indicated). Prices are subject to change without notice. Prices do not include postage and handling if applicable. RRP: Recommended Retail Price. Department of Anaesthesia and Critical Care, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Department of Clinical Chemistry, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Published Online: 2016-08-15 | DOI: Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences Continue reading >>

Metformin-associated Lactic Acidosis Undergoing Renal Replacement Therapy In Intensive Care Units: A Five-million Population-based Study In The North-west Of Italy

Metformin-associated Lactic Acidosis Undergoing Renal Replacement Therapy In Intensive Care Units: A Five-million Population-based Study In The North-west Of Italy

Abstract Background: Metformin-associated lactic acidosis (MALA) is a severe complication of drug administration with significant morbidity and mortality. So far no study in large population areas have examined the incidence, clinical profile and outcome of acute kidney injury (AKI)-MALA patients admitted in intensive care units (ICUs) and treated by renal replacement therapy (MALA-RRT). Methods: Retrospective analysis over a 6-year period (2010-2015) in Piedmont and Aosta Valley regions (5,305,940 inhabitants, 141,174 diabetics treated with metformin) of all MALA-RRT cases. Results: One hundred and seventeen cases of AKI-MALA-RRT were observed (12.04/100,000 metformin treated diabetics, 1.45% of all RRT-ICU patients). Survival rate was 78.3%. The average duration of RRT was 4.0 days at mean dialysis effluent of 977 mL/kg/day. At admission most patients were dehydrated, and experienced shock and oliguria. Conclusion: Our data showed that MALA-RRT is a common complication, needing more prevention. Adopted policy of early, extended, continuous and high efficiency dialysis could contribute to an observed high survival rate. Video Journal Club “Cappuccino with Claudio Ronco” at © 2017 S. Karger AG, Basel Introduction Metformin, an old drug known for more than 45 years, is the first-line treatment for type 2 diabetes mellitus in the world [1]. Metformin reduces the risk of mortality and morbidity in diabetic population [2] and decreases insulin resistance [3]. Generally speaking, metformin is considered a safe drug, with some limitations. Due to increased risk of lactic acidosis, metformin is contraindicated in patients with organ dysfunction such as congestive heart failure, renal, or hepatic insufficiency, and in very elderly patients [4]. Since metformin prescription Continue reading >>

Acute Lactic Acidosis

Acute Lactic Acidosis

Author: Bret A Nicks, MD, MHA; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H+) or a reduction in bicarbonate (HCO3-) concentrations. In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO2. Chronically, renal compensation occurs by means of reabsorption of HCO3. [ 1 , 2 ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. [ 2 , 3 , 4 ] It remains the most common cause of metabolic acidosis in hospitalized patients. The normal blood lactate concentration in unstressed patients is0.5-1 mmol/L. Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L. Hyperlactatemia is defined as a mild to moderate persistent increase in blood lactate concentration (2-4 mmol/L) without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >4-5 mmol/L) in association with metabolic acidosis. [ 1 , 5 ] Elevated lactate levels, while typically thought of as a marker of inadequate tissue perfusion with concurrent shift toward increased anaerobic metabolism, can be present in patients in whom systemic hypoperfusion is not present and therefore should be considered wit Continue reading >>

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update for Critical Care Clinicians Franz Volhard Clinic and Max Delbrck Center for Molecular Medicine, Medical Faculty of the Charit Humboldt University of Berlin, Berlin, Germany. Correspondence to Dr. Friedrich C. Luft, Wiltberg Strasse 50, 13125 Berlin, Germany. Phone: 49-30-9417-2202; Fax: 49-30-9417-2206; E-mail: luft/{at}fvk-berlin.de Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO3 increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na2CO3 and NaHCO3 that buffers similarly to NaHCO3 but without net generation of CO2. The results from animal stud Continue reading >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>

European Medicines Agency - News And Events - Updated Advice On Body Fat Changes And Lactic Acidosis With Hiv Medicines

European Medicines Agency - News And Events - Updated Advice On Body Fat Changes And Lactic Acidosis With Hiv Medicines

Updated advice on body fat changes and lactic acidosis with HIV medicines Updated advice on body fat changes and lactic acidosis with HIV medicines EMA recommends removal of class warnings for several medicines The European Medicines Agency (EMA) has updated the advice on the risk of body fat changes and lactic acidosis with medicines for the treatment of human immunodeficiency virus (HIV) infection. As a result, HIV medicines will no longer require a warning concerning fat redistribution in their product information, and a number of medicines of the class nucleoside and nucleotide analogues will no longer require a warning about lactic acidosis. The warning about body fat changes (lipodystrophy) was introduced in the early 2000s in the light of clinical findings in patients taking combinations of medicines available at the time. The term lipodystrophy in this context refers to changes in the amount of body fat as well as the distribution of fat in the body. More recent analyses suggest that only some medicines cause fat changes (zidovudine, stavudine and, probably, didanosine), and that these fat changes concern the loss of subcutaneous fat (lipoatrophy). There is no clear evidence that HIV medicines cause fat accumulation. the general warning about lipodystrophy is therefore being removed for HIV medicines; a specific warning related to loss of subcutaneous fat will remain for medicines containing zidovudine, stavudine, and didanosine. Similarly, a warning about lactic acidosis, a harmful build-up of lactic acid in the body, was introduced in the early 2000s for nucleoside and nucleotide analogues. However, an analysis of studies, case reports and published literature now shows that the risk of lactic acidosis differs substantially between medicines in the class. In Continue reading >>

Lactic Acidosis | Neurology Update

Lactic Acidosis | Neurology Update

A neurology education blog from Dr Holland D-Lactate Encephalopathy and Periodic Ataxia Posted by Michael Twomey, Drexel MSIV, Class of 2014 Remember that pain in your side during a long hard workout? Thats the buildup of lactic acid or L-lactate which is a way for your body to burn energy when it there isnt much oxygen around (like when you think its a good idea to run 5 miles). This feeling, although uncomfortable, wont make you loopyits twin brother, however, has no such qualms. D-lactate is just like normal old lactic acid, only completely different. In fact, it is the mirror image of the molecule that causes us such grief. For those of us who have forgotten organic chemistry, or would rather walk on broken glass than take such a torturous class, think of it like a pair of gloves. L-lactate would be your left hand glove and D-lactate the right. They look like the same darn thing from a distance (made out of the same leather and thread, and stuffing), but no matter how you rotate them, you could never get them to match up. Our bodies happen to be finicky. Like the 7 year old fussy eater we all know and (hopefullystill) love, the human body can only make and break down L-lactate. Thus, under factorysettings, we all have an undetectable level of D-lactate in our blood. Bacteria, however, are wired a bit differently (shocking, I know). Some can take the same sugars that we eat, turnthem into D-lactate, and when those buggers are in your intestinal systemthis form of lacticacid can enter our blood stream. It just so happens that high levels of D-lactate effects the brain just as much as it does the rest of our bodies. We arent exactly sure the why or how this compound acts on our central nervous system, but it can cause anything from making you unbalanced to putting a p Continue reading >>

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