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How to cite generic viagra sildenafil this article:Singh OP. The National Commission for Allied and Healthcare Professions Act, 2020 and its implication for mental health. Indian J Psychiatry 2021;63:119-20The National Commission for Allied and Healthcare Professions Act, 2020 has been notified on March 28, 2021, by the Gazette of India published by generic viagra sildenafil the Ministry of Law and Justice. This bill aims to “provide for regulation and maintenance of standards of education and services by allied and healthcare professionals, assessment of institutions, maintenance of a Central Register and State Register and creation of a system to improve access, research and development and adoption of latest scientific advancement and for matters connected therewith or incidental thereto.”[1]This act has created a category of Health Care Professionals which is defined as.

€œhealthcare professional” includes a scientist, therapist, or other professional who studies, advises, researches, supervises or provides preventive, curative, rehabilitative, therapeutic or promotional health services and who has obtained any qualification of degree under this Act, the duration of which shall not be <3600 h spread over a period of 3 years to 6 years divided into specific semesters.[1]According to the act, “Allied health professional” includes an associate, technician, or technologist who is trained to perform any technical and practical task to support diagnosis and treatment of illness, disease, injury or impairment, and to support implementation of any healthcare treatment and referral plan recommended by a medical, nursing, or any other healthcare professional, and who has obtained any qualification of diploma or degree under this Act, the duration of which shall not be less than 2000 h spread over a period of 2 years to 4 years divided into specific semesters.”[1]It is noticeable that while the term “Health Care Professionals” does not include doctors who are registered under National Medical Council, Mental Health Care Act (MHCA), 2017 includes psychiatrists under the ambit of Mental Health Care Professionals.[2] This discrepancy needs to be corrected - psychiasts, being another group of medical specialists, should be kept out of the broad umbrella of “Mental Healthcare Professionals.”The category of Behavioural Health Sciences generic viagra sildenafil Professional has been included and defined as “a person who undertakes scientific study of the emotions, behaviours and biology relating to a person's mental well-being, their ability to function in everyday life and their concept of self. €œBehavioural health” is the preferred term to “mental health” and includes professionals such as counselors, analysts, psychologists, educators and support workers, who provide counseling, therapy, and mediation services to individuals, families, groups, and communities in response to social and personal difficulties.”[1]This is a welcome step to the extent that it creates a diverse category of trained workforce in the field of Mental Health (Behavioural Health Science Professionals) and tries to regulate their training although it mainly aims to promote mental wellbeing. However there generic viagra sildenafil is a huge lacuna in the term of “Mental Illness” as defined by MHCA, 2017. Only severe disorders are included as per definition and there is no clarity regarding inclusion of other psychiatric disorders, namely “common mental disorders” such as anxiety and depression.

This leaves a strong possibility of concept of “psychiatric illnesses” being limited to only “severe psychiatric disorders” (major psychoses) generic viagra sildenafil thus perpetuating the stigma and alienation associated with psychiatric patients for centuries. Psychiatrists being restricted to treating severe mental disorders as per MHCA, 2017, there is a strong possibility that the care of common mental disorders may gradually pass on under the care of “behavioural health professionals” as per the new act!. There is need to look into this aspect by the leadership in psychiatry, both organizational and academic psychiatry, and reduce the contradictions between the MHCA, generic viagra sildenafil 2017 and this nascent act. All disorders classified in ICD 10 and DSM 5 should be classified as “Psychiatric Disorders” or “Mental Illness.” This will not only help in fighting the stigma associated with psychiatric illnesses but also promote the integration of psychiatry with other specialties.

References 1.The National Commission for Allied and generic viagra sildenafil Healthcare Professions Act, 2021. The Gazette of India. Published by generic viagra sildenafil Ministry of Law and Justice. 28 March, 2021.

2.The Mental Healthcare Act, generic viagra sildenafil 2017. The Gazette of India. Published by Ministry generic viagra sildenafil of Law and Justice. April 7, 2017.

Correspondence generic viagra sildenafil Address:Om Prakash SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/indianjpsychiatry.indianjpsychiatry_268_21Abstract Thiamine is essential for the activity of several enzymes associated generic viagra sildenafil with energy metabolism in humans.

Chronic alcohol use is associated with deficiency of thiamine along with other vitamins through several mechanisms. Several neuropsychiatric syndromes have been associated with thiamine deficiency in the context of alcohol use generic viagra sildenafil disorder including Wernicke–Korsakoff syndrome, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, and possibly, Marchiafava–Bignami syndrome. High-dose thiamine replacement is suggested for these neuropsychiatric syndromes.Keywords. Alcohol use disorder, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, Marchiafava–Bignami syndrome, thiamine, Wernicke–Korsakoff syndromeHow to generic viagra sildenafil cite this article:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS.

High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry 2021;63:121-6How to cite this URL:Praharaj SK, Munoli RN, Shenoy S, Udupa generic viagra sildenafil ST, Thomas LS. High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry [serial online] 2021 [cited 2021 May generic viagra sildenafil 6];63:121-6.

Available from. Https://www.indianjpsychiatry.org/text.asp?. 2021/63/2/121/313716 Introduction Thiamine is a water-soluble vitamin (B1) that plays a key role in the activity of several enzymes associated with energy metabolism. Thiamine pyrophosphate (or diphosphate) is the active form that acts as a cofactor for enzymes.

The daily dietary requirement of thiamine in adults is 1–2 mg and is dependent on carbohydrate intake.[1],[2] The requirement increases if basal metabolic rate is higher, for example, during alcohol withdrawal state. Dietary sources include pork (being the major source), meat, legume, vegetables, and enriched foods. The body can store between 30 and 50 mg of thiamine and is likely to get depleted within 4–6 weeks if the diet is deficient.[2] In those with alcohol-related liver damage, the ability to store thiamine is gradually reduced.[1],[2]Lower thiamine levels are found in 30%–80% of chronic alcohol users.[3] Thiamine deficiency occurs due to poor intake of vitamin-rich foods, impaired intestinal absorption, decreased storage capacity of liver, damage to the renal epithelial cells due to alcohol, leading to increased loss from the kidneys, and excessive loss associated with medical conditions.[2],[3] Furthermore, alcohol decreases the absorption of colonic bacterial thiamine, reduces the enzymatic activity of thiamine pyrophosphokinase, and thereby, reducing the amount of available thiamine pyrophosphate.[4] Since facilitated diffusion of thiamine into cells is dependent on a concentration gradient, reduced thiamine pyrophosphokinase activity further reduces thiamine uptake into cells.[4] Impaired utilization of thiamine is seen in certain conditions (e.g., hypomagnesemia) which are common in alcohol use disorder.[2],[3],[4] This narrative review discusses the neuropsychiatric syndromes associated with thiamine deficiency in the context of alcohol use disorder, and the treatment regimens advocated for these conditions. A PubMed search supplemented with manual search was used to identify neuropsychiatric syndromes related to thiamine deficiency in alcohol use disorder patients.

Neuropsychiatric Syndromes Associated With Thiamine Deficiency Wernicke–Korsakoff syndromeWernicke encephalopathy is associated with chronic alcohol use, and if not identified and treated early, could lead to permanent brain damage characterized by an amnestic syndrome known as Korsakoff syndrome. Inappropriate treatment of Wernicke encephalopathy with lower doses of thiamine can lead to high mortality rates (~20%) and Korsakoff syndrome in ~ 80% of patients (ranges from 56% to 84%).[5],[6] The classic triad of Wernicke includes oculomotor abnormalities, cerebellar dysfunction, and confusion. Wernicke lesions are found in 12.5% of brain samples of patients with alcohol dependence.[7] However, only 20%–30% of them had a clinical diagnosis of Wernicke encephalopathy antemortem. It has been found that many patients develop Wernicke–Korsakoff syndrome (WKS) following repeated subclinical episodes of thiamine deficiency.[7] In an autopsy report of 97 chronic alcohol users, only16% had all the three “classical signs,” 29% had two signs, 37% presented with one sign, and 19% had none.[8] Mental status changes are the most prevalent sign (seen in 82% of the cases), followed by eye signs (in 29%) and ataxia (23%).[8] WKS should be suspected in persons with a history of alcohol use and presenting with signs of ophthalmoplegia, ataxia, acute confusion, memory disturbance, unexplained hypotension, hypothermia, coma, or unconsciousness.[9] Operational criteria for the diagnosis of Wernicke encephalopathy have been proposed by Caine et al.[10] that requires two out of four features, i.e., (a) dietary deficiency (signs such as cheilitis, glossitis, and bleeding gums), (b) oculomotor abnormalities (nystagmus, opthalmoplegia, and diplopia), (c) cerebellar dysfunction (gait ataxia, nystagmus), and (d) either altered mental state (confusion) or mild memory impairment.As it is very difficult to clinically distinguish Wernicke encephalopathy from other associated conditions such as delirium tremens, hepatic encephalopathy, or head injury, it is prudent to have a lower threshold to diagnose this if any of the clinical signs is seen.

Magnetic resonance imaging (MRI) brain scan during Wernicke encephalopathy shows mammillary body atrophy and enlarged third ventricle, lesions in the medial portions of thalami and mid brain and can be used to aid diagnosis.[11],[12] However, most clinical situations warrant treatment without waiting for neuroimaging report. The treatment suggestions in the guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with alcohol use disorder.[13] There are very few studies that have evaluated the dose and duration of thiamine for WKS, but higher doses may result in a greater response.[6],[14] With thiamine administration rapid improvement is seen in eye movement abnormalities (improve within days or weeks) and ataxia (may take months to recover), but the effects on memory, in particular, are unclear.[4],[14] Severe memory impairment is the core feature of Korsakoff syndrome. Initial stages of the disease can present with confabulation, executive dysfunction, flattened affect, apathy, and poor insight.[15] Both the episodic and semantic memory are affected, whereas, procedural memory remains intact.[15]Thomson et al.[6] suggested the following should be treated with thiamine as they are at high risk for developing WKS.

(1) all patients with any evidence of chronic alcohol misuse and any of the following. Acute confusion, decreased conscious level, ataxia, ophthalmoplegia, memory disturbance, and hypothermia with hypotension. (2) patients with delirium tremens may often also have Wernicke encephalopathy, therefore, all of these patients should be presumed to have Wernicke encephalopathy and treated, preferably as inpatients. And (3) all hypoglycemic patients (who are treated with intravenous glucose) with evidence of chronic alcohol ingestion must be given intravenous thiamine immediately because of the risk of acutely precipitating Wernicke encephalopathy.Alcoholic cerebellar syndromeChronic alcohol use is associated with the degeneration of anterior superior vermis, leading to a clinical syndrome characterized by the subacute or chronic onset of gait ataxia and incoordination in legs, with relative sparing of upper limbs, speech, and oculomotor movements.[16] In severe cases, truncal ataxia, mild dysarthria, and incoordination of the upper limb is also found along with gait ataxia.

Thiamine deficiency is considered to be the etiological factor,[17],[18] although direct toxic effects of alcohol may also contribute to this syndrome. One-third of patients with chronic use of alcohol have evidence of alcoholic cerebellar degeneration. However, population-based studies estimate prevalence to be 14.6%.[19] The effect of alcohol on the cerebellum is graded with the most severe deficits occurring in alcohol users with the longest duration and highest severity of use. The diagnosis of cerebellar degeneration is largely clinical.

MRI can be used to evaluate for vermian atrophy but is unnecessary.[20] Anterior portions of vermis are affected early, with involvement of posterior vermis and adjacent lateral hemispheres occurring late in the course could be used to differentiate alcoholic cerebellar degeneration from other conditions that cause more diffuse involvement.[21] The severity of cerebellar syndrome is more in the presence of WKS, thus could be related to thiamine deficiency.[22],[23] Therefore, this has been considered as a cerebellar presentation of WKS and should be treated in a similar way.[16] There are anecdotal evidence to suggest improvement in cerebellar syndrome with high-dose thiamine.[24]Alcoholic peripheral neuropathyPeripheral neuropathy is common in alcohol use disorder and is seen in 44% of the users.[25] It has been associated predominantly with thiamine deficiency. However, deficiency of other B vitamins (pyridoxine and cobalamin) and direct toxic effect of alcohol is also implicated.[26] Clinically, onset of symptoms is gradual with the involvement of both sensory and motor fibers and occasionally autonomic fibers. Neuropathy can affect both small and large peripheral nerve fibers, leading to different clinical manifestations. Thiamine deficiency-related neuropathy affects larger fiber types, which results in motor deficits and sensory ataxia.

On examination, large fiber involvement is manifested by distal limb muscle weakness and loss of proprioception and vibratory sensation. Together, these can contribute to the gait unsteadiness seen in chronic alcohol users by creating a superimposed steppage gait and reduced proprioceptive input back to the movement control loops in the central nervous system. The most common presentations include painful sensations in both lower limbs, sometimes with burning sensation or numbness, which are early symptoms. Typically, there is a loss of vibration sensation in distal lower limbs.

Later symptoms include loss of proprioception, gait disturbance, and loss of reflexes. Most advanced findings include weakness and muscle atrophy.[20] Progression is very gradual over months and involvement of upper limbs may occur late in the course. Diagnosis begins with laboratory evaluation to exclude other causes of distal, sensorimotor neuropathy including hemoglobin A1c, liver function tests, and complete blood count to evaluate for red blood cell macrocytosis. Cerebrospinal fluid studies may show increased protein levels but should otherwise be normal in cases of alcohol neuropathy and are not recommended in routine evaluation.

Electromyography and nerve conduction studies can be used to distinguish whether the neuropathy is axonal or demyelinating and whether it is motor, sensory, or mixed type. Alcoholic neuropathy shows reduced distal, sensory amplitudes, and to a lesser extent, reduced motor amplitudes on nerve conduction studies.[20] Abstinence and vitamin supplementation including thiamine are the treatments advocated for this condition.[25] In mild-to-moderate cases, near-complete improvement can be achieved.[20] Randomized controlled trials have showed a significant improvement in alcoholic polyneuropathy with thiamine treatment.[27],[28]Marchiafava–Bignami syndromeThis is a rare but fatal condition seen in chronic alcohol users that is characterized by progressive demyelination and necrosis of the corpus callosum. The association of this syndrome with thiamine deficiency is not very clear, and direct toxic effects of alcohol are also suggested.[29] The clinical syndrome is variable and presentation can be acute, subacute, or chronic. In acute forms, it is predominantly characterized by the altered mental state such as delirium, stupor, or coma.[30] Other clinical features in neuroimaging confirmed Marchiafava–Bignami syndrome (MBS) cases include impaired gait, dysarthria, mutism, signs of split-brain syndrome, pyramidal tract signs, primitive reflexes, rigidity, incontinence, gaze palsy, diplopia, and sensory symptoms.[30] Neuropsychiatric manifestations are common and include psychotic symptoms, depression, apathy, aggressive behavior, and sometimes dementia.[29] MRI scan shows lesions of the corpus callosum, particularly splenium.

Treatment for this condition is mostly supportive and use of nutritional supplements and steroids. However, there are several reports of improvement of this syndrome with thiamine at variable doses including reports of beneficial effects with high-dose strategy.[29],[30],[31] Early initiation of thiamine, preferably within 2 weeks of the onset of symptoms is associated with a better outcome. Therefore, high-dose thiamine should be administered to all suspected cases of MBS. Laboratory Diagnosis of Thiamine Deficiency Estimation of thiamine and thiamine pyrophosphate levels may confirm the diagnosis of deficiency.

Levels of thiamine in the blood are not reliable indicators of thiamine status. Low erythrocyte transketolase activity is also helpful.[32],[33] Transketolase concentrations of <120 nmol/L have also been used to indicate deficiency, while concentrations of 120–150 nmol/L suggest marginal thiamine status.[1] However, these tests are not routinely performed as it is time consuming, expensive, and may not be readily available.[34] The ETKA assay is a functional test rather than a direct measurement of thiamin status and therefore may be influenced by factors other than thiamine deficiency such as diabetes mellitus and polyneuritis.[1] Hence, treatment should be initiated in the absence of laboratory confirmation of thiamine deficiency. Furthermore, treatment should not be delayed if tests are ordered, but the results are awaited. Electroencephalographic abnormalities in thiamine deficiency states range from diffuse mild-to-moderate slow waves and are not a good diagnostic option, as the prevalence of abnormalities among patients is inconsistent.[35]Surrogate markers, which reflect chronic alcohol use and nutritional deficiency other than thiamine, may be helpful in identifying at-risk patients.

This includes gamma glutamate transferase, aspartate aminotransferase. Alanine transaminase ratio >2:1, and increased mean corpuscular volume.[36] They are useful when a reliable history of alcohol use is not readily available, specifically in emergency departments when treatment needs to be started immediately to avoid long-term consequences. Thiamine Replacement Therapy Oral versus parenteral thiamineIntestinal absorption of thiamine depends on active transport through thiamine transporter 1 and 2, which follow saturation kinetics.[1] Therefore, the rate and amount of absorption of thiamine in healthy individuals is limited. In healthy volunteers, a 10 mg dose results in maximal absorption of thiamine, and any doses higher than this do not increase thiamine levels.

Therefore, the maximum amount of thiamine absorbed from 10 mg or higher dose is between 4.3 and 5.6 mg.[37] However, it has been suggested that, although thiamine transport occurs through the energy-requiring, sodium-dependent active process at physiologic concentrations, at higher supraphysiologic concentrations thiamine uptake is mostly a passive process.[38] Smithline et al. Have demonstrated that it is possible to achieve higher serum thiamine levels with oral doses up to 1500 mg.[39]In chronic alcohol users, intestinal absorption is impaired. Hence, absorption rates are expected to be much lower. It is approximately 30% of that seen in healthy individuals, i.e., 1.5 mg of thiamine is absorbed from 10 mg oral thiamine.[3] In those consuming alcohol and have poor nutrition, not more than 0.8 mg of thiamine is absorbed.[2],[3],[6] The daily thiamine requirement is 1–1.6 mg/day, which may be more in alcohol-dependent patients at risk for Wernicke encephalopathy.[1] It is highly likely that oral supplementation with thiamine will be inadequate in alcohol-dependent individuals who continue to drink.

Therefore, parenteral thiamine is preferred for supplementation in deficiency states associated with chronic alcohol use. Therapy involving parenteral thiamine is considered safe except for occasional circumstances of allergic reactions involving pruritus and local irritation.There is a small, but definite risk of anaphylaxis with parenteral thiamine, specifically with intravenous administration (1/250,000 intravenous injections).[40] Diluting thiamine in 50–100 mg normal saline for infusion may reduce the risk. However, parenteral thiamine should always be administered under observation with the necessary facilities for resuscitation.A further important issue involves the timing of administration of thiamine relative to the course of alcohol abuse or dependence. Administration of thiamine treatment to patients experiencing alcohol withdrawal may also be influenced by other factors such as magnesium depletion, N-methyl-D-aspartate (NMDA) receptor upregulation, or liver impairment, all of which may alter thiamine metabolism and utilization.[6],[14]Thiamine or other preparations (e.g., benfotiamine)The thiamine transporters limit the rate of absorption of orally administered thiamine.

Allithiamines (e.g., benfotiamine) are the lipid-soluble thiamine derivatives that are absorbed better, result in higher thiamine levels, and are retained longer in the body.[41] The thiamine levels with orally administered benfotiamine are much higher than oral thiamine and almost equals to intravenous thiamine given at the same dosage.[42]Benfotiamine has other beneficial effects including inhibition of production of advanced glycation end products, thus protecting against diabetic vascular complications.[41] It also modulates nuclear transcription factor κB (NK-κB), vascular endothelial growth factor receptor 2, glycogen synthase kinase 3 β, etc., that play a role in cell repair and survival.[41] Benfotiamine has been found to be effective for the treatment of alcoholic peripheral neuropathy.[27]Dosing of thiamineAs the prevalence of thiamine deficiency is very common in chronic alcohol users, the requirement of thiamine increases in active drinkers and it is difficult to rapidly determine thiamine levels using laboratory tests, it is prudent that all patients irrespective of nutritional status should be administered parenteral thiamine. The dose should be 100 mg thiamine daily for 3–5 days during inpatient treatment. Commonly, multivitamin injections are added to intravenous infusions. Patients at risk for thiamine deficiency should receive 250 mg of thiamine daily intramuscularly for 3–5 days, followed by oral thiamine 100 mg daily.[6]Thiamine plasma levels reduce to 20% of peak value after approximately 2 h of parenteral administration, thus reducing the effective “window period” for passive diffusion to the central nervous system.[6] Therefore, in thiamine deficient individuals with features of Wernicke encephalopathy should receive thiamine thrice daily.High-dose parenteral thiamine administered thrice daily has been advocated in patients at risk for Wernicke encephalopathy.[43] The Royal College of Physicians guideline recommends that patients with suspected Wernicke encephalopathy should receive 500 mg thiamine diluted in 50–100 ml of normal saline infusion over 30 min three times daily for 2–3 days and sometimes for longer periods.[13] If there are persistent symptoms such as confusion, cerebellar symptoms, or memory impairment, this regimen can be continued until the symptoms improve.

If symptoms improve, oral thiamine 100 mg thrice daily can be continued for prolonged periods.[6],[40] A similar treatment regimen is advocated for alcoholic cerebellar degeneration as well. Doses more than 500 mg intramuscular or intravenous three times a day for 3–5 days, followed by 250 mg once daily for a further 3–5 days is also recommended by some guidelines (e.g., British Association for Psychopharmacology).[44]Other effects of thiamineThere are some data to suggest that thiamine deficiency can modulate alcohol consumption and may result in pathological drinking. Benfotiamine 600 mg/day as compared to placebo for 6 months was well tolerated and found to decrease psychiatric distress in males and reduce alcohol consumption in females with severe alcohol dependence.[45],[46] Other Factors During Thiamine Therapy Correction of hypomagnesemiaMagnesium is a cofactor for many thiamine-dependent enzymes in carbohydrate metabolism. Patients may fail to respond to thiamine supplementation in the presence of hypomagnesemia.[47] Magnesium deficiency is common in chronic alcohol users and is seen in 30% of individuals.[48],[49] It can occur because of increased renal excretion of magnesium, poor intake, decreased absorption because of Vitamin D deficiency, the formation of undissociated magnesium soaps with free fatty acids.[48],[49]The usual adult dose is 35–50 mmol of magnesium sulfate added to 1 L isotonic (saline) given over 12–24 h.[6] The dose has to be titrated against plasma magnesium levels.

It is recommended to reduce the dose in renal failure. Contraindications include patients with documented hypersensitivity and those with heart block, Addison's disease, myocardial damage, severe hepatitis, or hypophosphatemia. Do not administer intravenous magnesium unless hypomagnesemia is confirmed.[6]Other B-complex vitaminsMost patients with deficiency of thiamine will also have reduced levels of other B vitamins including niacin, pyridoxine, and cobalamin that require replenishment. For patients admitted to the intensive care unit with symptoms that may mimic or mask Wernicke encephalopathy, based on the published literature, routine supplementation during the 1st day of admission includes 200–500 mg intravenous thiamine every 8 h, 64 mg/kg magnesium sulfate (≈4–5 g for most adult patients), and 400–1000 μg intravenous folate.[50] If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal saline.[50] Precautions to be Taken When Administering Parenteral Thiamine It is recommended to monitor for anaphylaxis and has appropriate facilities for resuscitation and for treating anaphylaxis readily available including adrenaline and corticosteroids.

Anaphylaxis has been reported at the rate of approximately 4/1 million pairs of ampoules of Pabrinex (a pair of high potency vitamins available in the UK containing 500 mg of thiamine (1:250,000 I/V administrations).[40] Intramuscular thiamine is reported to have a lower incidence of anaphylactic reactions than intravenous administration.[40] The reaction has been attributed to nonspecific histamine release.[51] Administer intravenous thiamine slowly, preferably by slow infusion in 100 ml normal saline over 15–30 min. Conclusions Risk factors for thiamine deficiency should be assessed in chronic alcohol users. A high index of suspicion and a lower threshold to diagnose thiamine deficiency states including Wernicke encephalopathy is needed. Several other presentations such as cerebellar syndrome, MBS, polyneuropathy, and delirium tremens could be related to thiamine deficiency and should be treated with protocols similar to Wernicke encephalopathy.

High-dose thiamine is recommended for the treatment of suspected Wernicke encephalopathy and related conditions [Figure 1]. However, evidence in terms of randomized controlled trials is lacking, and the recommendations are based on small studies and anecdotal reports. Nevertheless, as all these conditions respond to thiamine supplementation, it is possible that these have overlapping pathophysiology and are better considered as Wernicke encephalopathy spectrum disorders.Figure 1. Thiamine recommendations for patients with alcohol use disorder.

AHistory of alcohol use, but no clinical features of WE. BNo clinical features of WE, but with risk factors such as complicated withdrawal (delirium, seizures). CClinical features of WE (ataxia, opthalmoplegia, global confusion)Click here to viewFinancial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Frank LL.

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Neuropsychol Rev 2012;22:170-80. 13.Pruckner N, Baumgartner J, Hinterbuchinger B, Glahn A, Vyssoki S, Vyssoki B. Thiamine substitution in alcohol use disorder. A narrative review of medical guidelines.

Eur Addict Res 2019;25:103-10. 14.Day E, Bentham PW, Callaghan R, Kuruvilla T, George S. Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033.

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A critical review. Neuropsychiatr Dis Treat 2017;13:2875-90. 16.Laureno R. Nutritional cerebellar degeneration, with comments on its relationship to Wernicke disease and alcoholism.

Handb Clin Neurol 2012;103:175-87. 17.Maschke M, Weber J, Bonnet U, Dimitrova A, Bohrenkämper J, Sturm S, et al. Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI. J Neurol 2005;252:704-11.

18.Mulholland PJ, Self RL, Stepanyan TD, Little HJ, Littleton JM, Prendergast MA. Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro. Neuroscience 2005;135:1129-39. 19.Del Brutto OH, Mera RM, Sullivan LJ, Zambrano M, King NR.

Population-based study of alcoholic cerebellar degeneration. The Atahualpa Project. J Neurol Sci 2016;367:356-60. 20.Hammoud N, Jimenez-Shahed J.

Chronic neurologic effects of alcohol. Clin Liver Dis 2019;23:141-55. 21.Lee JH, Heo SH, Chang DI. Early-stage alcoholic cerebellar degeneration.

Diagnostic imaging clues. J Korean Med Sci 2015;30:1539. 22.Phillips SC, Harper CG, Kril JJ. The contribution of Wernicke's encephalopathy to alcohol-related cerebellar damage.

Drug Alcohol Rev 1990;9:53-60. 23.Baker KG, Harding AJ, Halliday GM, Kril JJ, Harper CG. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke's encephalopathy. Neuroscience 1999;91:429-38.

24.Graham JR, Woodhouse D, Read FH. Massive thiamine dosage in an alcoholic with cerebellar cortical degeneration. Lancet 1971;2:107. 25.Julian T, Glascow N, Syeed R, Zis P.

Alcohol-related peripheral neuropathy. A systematic review and meta-analysis. J Neurol 2018;22:1-3. 26.Chopra K, Tiwari V.

Alcoholic neuropathy. Possible mechanisms and future treatment possibilities. Br J Clin Pharmacol 2012;73:348-62. 27.Woelk H, Lehrl S, Bitsch R, Köpcke W.

Benfotiamine in treatment of alcoholic polyneuropathy. An 8-week randomized controlled study (BAP I Study). Alcohol Alcohol 1998;33:631-8. 28.Peters TJ, Kotowicz J, Nyka W, Kozubski W, Kuznetsov V, Vanderbist F, et al.

Treatment of alcoholic polyneuropathy with vitamin B complex. A randomised controlled trial. Alcohol Alcohol 2006;41:636-42. 29.Fernandes LM, Bezerra FR, Monteiro MC, Silva ML, de Oliveira FR, Lima RR, et al.

Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity. How poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. Eur J Clin Nutr 2017;71:580-6. 30.Hillbom M, Saloheimo P, Fujioka S, Wszolek ZK, Juvela S, Leone MA.

Diagnosis and management of Marchiafava-Bignami disease. A review of CT/MRI confirmed cases. J Neurol Neurosurg Psychiatry 2014;85:168-73. 31.Nemlekar SS, Mehta RY, Dave KR, Shah ND.

Marchiafava. Bignami disease treated with parenteral thiamine. Indian J Psychol Med 2016;38:147-9. [Full text] 32.Brin M.

Erythrocyte transketolase in early thiamine deficiency. Ann N Y Acad Sci 1962;98:528-41. 33.Dreyfus PM. Clinical application of blood transketolase determinations.

N Engl J Med 1962;267:596-8. 34.Edwards KA, Tu-Maung N, Cheng K, Wang B, Baeumner AJ, Kraft CE. Thiamine assays – Advances, challenges, and caveats. ChemistryOpen 2017;6:178-91.

35.Chandrakumar A, Bhardwaj A, 't Jong GW. Review of thiamine deficiency disorders. Wernicke encephalopathy and Korsakoff psychosis. J Basic Clin Physiol Pharmacol 2018;30:153-62.

36.Torruellas C, French SW, Medici V. Diagnosis of alcoholic liver disease. World J Gastroenterol 2014;20:11684-99. 37.Thomson AD, Leevy CM.

Observations on the mechanism of thiamine hydrochloride absorption in man. Clin Sci 1972;43:153-63. 38.Hoyumpa AM Jr., Strickland R, Sheehan JJ, Yarborough G, Nichols S. Dual system of intestinal thiamine transport in humans.

J Lab Clin Med 1982;99:701-8. 39.Smithline HA, Donnino M, Greenblatt DJ. Pharmacokinetics of high-dose oral thiamine hydrochloride in healthy subjects. BMC Clin Pharmacol 2012;12:4.

40.Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44:911-5. 41.Raj V, Ojha S, Howarth FC, Belur PD, Subramanya SB.

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Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital. Drug Alcohol Rev 2015;34:323-8. 48.Flink EB. Magnesium deficiency in alcoholism.

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Correspondence Address:Samir Kumar PraharajDepartment of Psychiatry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_440_20 Figures [Figure 1].

How to cite viagra online canada this article:Singh http://iciutah.com/buy-zithromax-with-prescription/ OP. The National Commission for Allied and Healthcare Professions Act, 2020 and its implication for mental health. Indian J Psychiatry 2021;63:119-20The National Commission for Allied and Healthcare Professions Act, 2020 has been viagra online canada notified on March 28, 2021, by the Gazette of India published by the Ministry of Law and Justice. This bill aims to “provide for regulation and maintenance of standards of education and services by allied and healthcare professionals, assessment of institutions, maintenance of a Central Register and State Register and creation of a system to improve access, research and development and adoption of latest scientific advancement and for matters connected therewith or incidental thereto.”[1]This act has created a category of Health Care Professionals which is defined as.

€œhealthcare professional” includes viagra online canada a scientist, therapist, or other professional who studies, advises, researches, supervises or provides preventive, curative, rehabilitative, therapeutic or promotional health services and who has obtained any qualification of degree under this Act, the duration of which shall not be <3600 h spread over a period of 3 years to 6 years divided into specific semesters.[1]According to the act, “Allied health professional” includes an associate, technician, or technologist who is trained to perform any technical and practical task to support diagnosis and treatment of illness, disease, injury or impairment, and to support implementation of any healthcare treatment and referral plan recommended by a medical, nursing, or any other healthcare professional, and who has obtained any qualification of diploma or degree under this Act, the duration of which shall not be less than 2000 h spread over a period of 2 years to 4 years divided into specific semesters.”[1]It is noticeable that while the term “Health Care Professionals” does not include doctors who are registered under National Medical Council, Mental Health Care Act (MHCA), 2017 includes psychiatrists under the ambit of Mental Health Care Professionals.[2] This discrepancy needs to be corrected - psychiasts, being another group of medical specialists, should be kept out of the broad umbrella of “Mental Healthcare Professionals.”The category of Behavioural Health Sciences Professional has been included and defined as “a person who undertakes scientific study of the emotions, behaviours and biology relating to a person's mental well-being, their ability to function in everyday life and their concept of self. €œBehavioural health” is the preferred term to “mental health” and includes professionals such as counselors, analysts, psychologists, educators and support workers, who provide counseling, therapy, and mediation services to individuals, families, groups, and communities in response to social and personal difficulties.”[1]This is a welcome step to the extent that it creates a diverse category of trained workforce in the field of Mental Health (Behavioural Health Science Professionals) and tries to regulate their training although it mainly aims to promote mental wellbeing. However there is a huge lacuna viagra online canada in the term of “Mental Illness” as defined by MHCA, 2017. Only severe disorders are included as per definition and there is no clarity regarding inclusion of other psychiatric disorders, namely “common mental disorders” such as anxiety and depression.

This leaves a strong possibility of concept of “psychiatric illnesses” viagra online canada being limited to only “severe psychiatric disorders” (major psychoses) thus perpetuating the stigma and alienation associated with psychiatric patients for centuries. Psychiatrists being restricted to treating severe mental disorders as per MHCA, 2017, there is a strong possibility that the care of common mental disorders may gradually pass on under the care of “behavioural health professionals” as per the new act!. There is need to look into this aspect by the leadership in psychiatry, both organizational and academic psychiatry, and viagra online canada reduce the contradictions between the MHCA, 2017 and this nascent act. All disorders classified in ICD 10 and DSM 5 should be classified as “Psychiatric Disorders” or “Mental Illness.” This will not only help in fighting the stigma associated with psychiatric illnesses but also promote the integration of psychiatry with other specialties.

References 1.The National Commission for Allied and viagra online canada Healthcare Professions Act, 2021. The Gazette of India. Published by Ministry of Law viagra online canada and Justice. 28 March, 2021.

2.The Mental viagra online canada Healthcare Act, 2017. The Gazette of India. Published by Ministry of Law and Justice viagra online canada. April 7, 2017.

Correspondence Address:Om Prakash SinghAA 304, Ashabari viagra online canada Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/indianjpsychiatry.indianjpsychiatry_268_21Abstract Thiamine is essential for the activity of several enzymes associated with viagra online canada energy metabolism in humans.

Chronic alcohol use is associated with deficiency of thiamine along with other vitamins through several mechanisms. Several neuropsychiatric syndromes have been associated with thiamine deficiency viagra online canada in the context of alcohol use disorder including Wernicke–Korsakoff syndrome, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, and possibly, Marchiafava–Bignami syndrome. High-dose thiamine replacement is suggested for these neuropsychiatric syndromes.Keywords. Alcohol use disorder, alcoholic cerebellar syndrome, alcoholic peripheral neuropathy, Marchiafava–Bignami syndrome, thiamine, Wernicke–Korsakoff syndromeHow viagra online canada to cite this article:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS.

High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry 2021;63:121-6How to viagra online canada cite this URL:Praharaj SK, Munoli RN, Shenoy S, Udupa ST, Thomas LS. High-dose thiamine strategy in Wernicke–Korsakoff syndrome and related thiamine deficiency conditions associated with alcohol use disorder. Indian J Psychiatry viagra online canada [serial online] 2021 [cited 2021 May 6];63:121-6.

Available from. Https://www.indianjpsychiatry.org/text.asp?. 2021/63/2/121/313716 Introduction Thiamine is a water-soluble vitamin (B1) that plays a key role in the activity of several enzymes associated with energy metabolism. Thiamine pyrophosphate (or diphosphate) is the active form that acts as a cofactor for enzymes.

The daily dietary requirement of thiamine in adults is 1–2 mg and is dependent on carbohydrate intake.[1],[2] The requirement increases if basal metabolic rate is higher, for example, during alcohol withdrawal state. Dietary sources include pork (being the major source), meat, legume, vegetables, and enriched foods. The body can store between 30 and 50 mg of thiamine and is likely to get depleted within 4–6 weeks if the diet is deficient.[2] In those with alcohol-related liver damage, the ability to store thiamine is gradually reduced.[1],[2]Lower thiamine levels are found in 30%–80% of chronic alcohol users.[3] Thiamine deficiency occurs due to poor intake of vitamin-rich foods, impaired intestinal absorption, decreased storage capacity of liver, damage to the renal epithelial cells due to alcohol, leading to increased loss from the kidneys, and excessive loss associated with medical conditions.[2],[3] Furthermore, alcohol decreases the absorption of colonic bacterial thiamine, reduces the enzymatic activity of thiamine pyrophosphokinase, and thereby, reducing the amount of available thiamine pyrophosphate.[4] Since facilitated diffusion of thiamine into cells is dependent on a concentration gradient, reduced thiamine pyrophosphokinase activity further reduces thiamine uptake into cells.[4] Impaired utilization of thiamine is seen in certain conditions (e.g., hypomagnesemia) which are common in alcohol use disorder.[2],[3],[4] This narrative review discusses the neuropsychiatric syndromes associated with thiamine deficiency in the context of alcohol use disorder, and the treatment regimens advocated for these conditions. A PubMed search supplemented with manual search was used to identify neuropsychiatric syndromes related to thiamine deficiency in alcohol use disorder patients.

Neuropsychiatric Syndromes Associated With Thiamine Deficiency Wernicke–Korsakoff syndromeWernicke encephalopathy is associated with chronic alcohol use, and if not identified and treated early, could lead to permanent brain damage characterized by an amnestic syndrome known as Korsakoff syndrome. Inappropriate treatment of Wernicke encephalopathy with lower doses of thiamine can lead to high mortality rates (~20%) and Korsakoff syndrome in ~ 80% of patients (ranges from 56% to 84%).[5],[6] The classic triad of Wernicke includes oculomotor abnormalities, cerebellar dysfunction, and confusion. Wernicke lesions are found in 12.5% of brain samples of patients with alcohol dependence.[7] However, only 20%–30% of them had a clinical diagnosis of Wernicke encephalopathy antemortem. It has been found that many patients develop Wernicke–Korsakoff syndrome (WKS) following repeated subclinical episodes of thiamine deficiency.[7] In an autopsy report of 97 chronic alcohol users, only16% had all the three “classical signs,” 29% had two signs, 37% presented with one sign, and 19% had none.[8] Mental status changes are the most prevalent sign (seen in 82% of the cases), followed by eye signs (in 29%) and ataxia (23%).[8] WKS should be suspected in persons with a history of alcohol use and presenting with signs of ophthalmoplegia, ataxia, acute confusion, memory disturbance, unexplained hypotension, hypothermia, coma, or unconsciousness.[9] Operational criteria for the diagnosis of Wernicke encephalopathy have been proposed by Caine et al.[10] that requires two out of four features, i.e., (a) dietary deficiency (signs such as cheilitis, glossitis, and bleeding gums), (b) oculomotor abnormalities (nystagmus, opthalmoplegia, and diplopia), (c) cerebellar dysfunction (gait ataxia, nystagmus), and (d) either altered mental state (confusion) or mild memory impairment.As it is very difficult to clinically distinguish Wernicke encephalopathy from other associated conditions such as delirium tremens, hepatic encephalopathy, or head injury, it is prudent to have a lower threshold to diagnose this if any of the clinical signs is seen.

Magnetic resonance imaging (MRI) brain scan during Wernicke encephalopathy shows mammillary body atrophy and enlarged third ventricle, lesions in the medial portions of thalami and mid brain and can be used to aid diagnosis.[11],[12] However, most clinical situations warrant treatment without waiting for neuroimaging report. The treatment suggestions in the guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with alcohol use disorder.[13] There are very few studies that have evaluated the dose and duration of thiamine for WKS, but higher doses may result in a greater response.[6],[14] With thiamine administration rapid improvement is seen in eye movement abnormalities (improve within days or weeks) and ataxia (may take months to recover), but the effects on memory, in particular, are unclear.[4],[14] Severe memory impairment is the core feature of Korsakoff syndrome. Initial stages of the disease can present with confabulation, executive dysfunction, flattened affect, apathy, and poor insight.[15] Both the episodic and semantic memory are affected, whereas, procedural memory remains intact.[15]Thomson et al.[6] suggested the following should be treated with thiamine as they are at high risk for developing WKS.

(1) all patients with any evidence of chronic alcohol misuse and any of the following. Acute confusion, decreased conscious level, ataxia, ophthalmoplegia, memory disturbance, and hypothermia with hypotension. (2) patients with delirium tremens may often also have Wernicke encephalopathy, therefore, all of these patients should be presumed to have Wernicke encephalopathy and treated, preferably as inpatients. And (3) all hypoglycemic patients (who are treated with intravenous glucose) with evidence of chronic alcohol ingestion must be given intravenous thiamine immediately because of the risk of acutely precipitating Wernicke encephalopathy.Alcoholic cerebellar syndromeChronic alcohol use is associated with the degeneration of anterior superior vermis, leading to a clinical syndrome characterized by the subacute or chronic onset of gait ataxia and incoordination in legs, with relative sparing of upper limbs, speech, and oculomotor movements.[16] In severe cases, truncal ataxia, mild dysarthria, and incoordination of the upper limb is also found along with gait ataxia.

Thiamine deficiency is considered to be the etiological factor,[17],[18] although direct toxic effects of alcohol may also contribute to this syndrome. One-third of patients with chronic use of alcohol have evidence of alcoholic cerebellar degeneration. However, population-based studies estimate prevalence to be 14.6%.[19] The effect of alcohol on the cerebellum is graded with the most severe deficits occurring in alcohol users with the longest duration and highest severity of use. The diagnosis of cerebellar degeneration is largely clinical.

MRI can be used to evaluate for vermian atrophy but is unnecessary.[20] Anterior portions of vermis are affected early, with involvement of posterior vermis and adjacent lateral hemispheres occurring late in the course could be used to differentiate alcoholic cerebellar degeneration from other conditions that cause more diffuse involvement.[21] The severity of cerebellar syndrome is more in the presence of WKS, thus could be related to thiamine deficiency.[22],[23] Therefore, this has been considered as a cerebellar presentation of WKS and should be treated in a similar way.[16] There are anecdotal evidence to suggest improvement in cerebellar syndrome with high-dose thiamine.[24]Alcoholic peripheral neuropathyPeripheral neuropathy is common in alcohol use disorder and is seen in 44% of the users.[25] It has been associated predominantly with thiamine deficiency. However, deficiency of other B vitamins (pyridoxine and cobalamin) and direct toxic effect of alcohol is also implicated.[26] Clinically, onset of symptoms is gradual with the involvement of both sensory and motor fibers and occasionally autonomic fibers. Neuropathy can affect both small and large peripheral nerve fibers, leading to different clinical manifestations. Thiamine deficiency-related neuropathy affects larger fiber types, which results in motor deficits and sensory ataxia.

On examination, large fiber involvement is manifested by distal limb muscle weakness and loss of proprioception and vibratory sensation. Together, these can contribute to the gait unsteadiness seen in chronic alcohol users by creating a superimposed steppage gait and reduced proprioceptive input back to the movement control loops in the central nervous system. The most common presentations include painful sensations in both lower limbs, sometimes with burning sensation or numbness, which are early symptoms. Typically, there is a loss of vibration sensation in distal lower limbs.

Later symptoms include loss of proprioception, gait disturbance, and loss of reflexes. Most advanced findings include weakness and muscle atrophy.[20] Progression is very gradual over months and involvement of upper limbs may occur late in the course. Diagnosis begins with laboratory evaluation to exclude other causes of distal, sensorimotor neuropathy including hemoglobin A1c, liver function tests, and complete blood count to evaluate for red blood cell macrocytosis. Cerebrospinal fluid studies may show increased protein levels but should otherwise be normal in cases of alcohol neuropathy and are not recommended in routine evaluation.

Electromyography and nerve conduction studies can be used to distinguish whether the neuropathy is axonal or demyelinating and whether it is motor, sensory, or mixed type. Alcoholic neuropathy shows reduced distal, sensory amplitudes, and to a lesser extent, reduced motor amplitudes on nerve conduction studies.[20] Abstinence and vitamin supplementation including thiamine are the treatments advocated for this condition.[25] In mild-to-moderate cases, near-complete improvement can be achieved.[20] Randomized controlled trials have showed a significant improvement in alcoholic polyneuropathy with thiamine treatment.[27],[28]Marchiafava–Bignami syndromeThis is a rare but fatal condition seen in chronic alcohol users that is characterized by progressive demyelination and necrosis of the corpus callosum. The association of this syndrome with thiamine deficiency is not very clear, and direct toxic effects of alcohol are also suggested.[29] The clinical syndrome is variable and presentation can be acute, subacute, or chronic. In acute forms, it is predominantly characterized by the altered mental state such as delirium, stupor, or coma.[30] Other clinical features in neuroimaging confirmed Marchiafava–Bignami syndrome (MBS) cases include impaired gait, dysarthria, mutism, signs of split-brain syndrome, pyramidal tract signs, primitive reflexes, rigidity, incontinence, gaze palsy, diplopia, and sensory symptoms.[30] Neuropsychiatric manifestations are common and include psychotic symptoms, depression, apathy, aggressive behavior, and sometimes dementia.[29] MRI scan shows lesions of the corpus callosum, particularly splenium.

Treatment for this condition is mostly supportive and use of nutritional supplements and steroids. However, there are several reports of improvement of this syndrome with thiamine at variable doses including reports of beneficial effects with high-dose strategy.[29],[30],[31] Early initiation of thiamine, preferably within 2 weeks of the onset of symptoms is associated with a better outcome. Therefore, high-dose thiamine should be administered to all suspected cases of MBS. Laboratory Diagnosis of Thiamine Deficiency Estimation of thiamine and thiamine pyrophosphate levels may confirm the diagnosis of deficiency.

Levels of thiamine in the blood are not reliable indicators of thiamine status. Low erythrocyte transketolase activity is also helpful.[32],[33] Transketolase concentrations of <120 nmol/L have also been used to indicate deficiency, while concentrations of 120–150 nmol/L suggest marginal thiamine status.[1] However, these tests are not routinely performed as it is time consuming, expensive, and may not be readily available.[34] The ETKA assay is a functional test rather than a direct measurement of thiamin status and therefore may be influenced by factors other than thiamine deficiency such as diabetes mellitus and polyneuritis.[1] Hence, treatment should be initiated in the absence of laboratory confirmation of thiamine deficiency. Furthermore, treatment should not be delayed if tests are ordered, but the results are awaited. Electroencephalographic abnormalities in thiamine deficiency states range from diffuse mild-to-moderate slow waves and are not a good diagnostic option, as the prevalence of abnormalities among patients is inconsistent.[35]Surrogate markers, which reflect chronic alcohol use and nutritional deficiency other than thiamine, may be helpful in identifying at-risk patients.

This includes gamma glutamate transferase, aspartate aminotransferase. Alanine transaminase ratio >2:1, and increased mean corpuscular volume.[36] They are useful when a reliable history of alcohol use is not readily available, specifically in emergency departments when treatment needs to be started immediately to avoid long-term consequences. Thiamine Replacement Therapy Oral versus parenteral thiamineIntestinal absorption of thiamine depends on active transport through thiamine transporter 1 and 2, which follow saturation kinetics.[1] Therefore, the rate and amount of absorption of thiamine in healthy individuals is limited. In healthy volunteers, a 10 mg dose results in maximal absorption of thiamine, and any doses higher than this do not increase thiamine levels.

Therefore, the maximum amount of thiamine absorbed from 10 mg or higher dose is between 4.3 and 5.6 mg.[37] However, it has been suggested that, although thiamine transport occurs through the energy-requiring, sodium-dependent active process at physiologic concentrations, at higher supraphysiologic concentrations thiamine uptake is mostly a passive process.[38] Smithline et al. Have demonstrated that it is possible to achieve higher serum thiamine levels with oral doses up to 1500 mg.[39]In chronic alcohol users, intestinal absorption is impaired. Hence, absorption rates are expected to be much lower. It is approximately 30% of that seen in healthy individuals, i.e., 1.5 mg of thiamine is absorbed from 10 mg oral thiamine.[3] In those consuming alcohol and have poor nutrition, not more than 0.8 mg of thiamine is absorbed.[2],[3],[6] The daily thiamine requirement is 1–1.6 mg/day, which may be more in alcohol-dependent patients at risk for Wernicke encephalopathy.[1] It is highly likely that oral supplementation with thiamine will be inadequate in alcohol-dependent individuals who continue to drink.

Therefore, parenteral thiamine is preferred for supplementation in deficiency states associated with chronic alcohol use. Therapy involving parenteral thiamine is considered safe except for occasional circumstances of allergic reactions involving pruritus and local irritation.There is a small, but definite risk of anaphylaxis with parenteral thiamine, specifically with intravenous administration (1/250,000 intravenous injections).[40] Diluting thiamine in 50–100 mg normal saline for infusion may reduce the risk. However, parenteral thiamine should always be administered under observation with the necessary facilities for resuscitation.A further important issue involves the timing of administration of thiamine relative to the course of alcohol abuse or dependence. Administration of thiamine treatment to patients experiencing alcohol withdrawal may also be influenced by other factors such as magnesium depletion, N-methyl-D-aspartate (NMDA) receptor upregulation, or liver impairment, all of which may alter thiamine metabolism and utilization.[6],[14]Thiamine or other preparations (e.g., benfotiamine)The thiamine transporters limit the rate of absorption of orally administered thiamine.

Allithiamines (e.g., benfotiamine) are the lipid-soluble thiamine derivatives that are absorbed better, result in higher thiamine levels, and are retained longer in the body.[41] The thiamine levels with orally administered benfotiamine are much higher than oral thiamine and almost equals to intravenous thiamine given at the same dosage.[42]Benfotiamine has other beneficial effects including inhibition of production of advanced glycation end products, thus protecting against diabetic vascular complications.[41] It also modulates nuclear transcription factor κB (NK-κB), vascular endothelial growth factor receptor 2, glycogen synthase kinase 3 β, etc., that play a role in cell repair and survival.[41] Benfotiamine has been found to be effective for the treatment of alcoholic peripheral neuropathy.[27]Dosing of thiamineAs the prevalence of thiamine deficiency is very common in chronic alcohol users, the requirement of thiamine increases in active drinkers and it is difficult to rapidly determine thiamine levels using laboratory tests, it is prudent that all patients irrespective of nutritional status should be administered parenteral thiamine. The dose should be 100 mg thiamine daily for 3–5 days during inpatient treatment. Commonly, multivitamin injections are added to intravenous infusions. Patients at risk for thiamine deficiency should receive 250 mg of thiamine daily intramuscularly for 3–5 days, followed by oral thiamine 100 mg daily.[6]Thiamine plasma levels reduce to 20% of peak value after approximately 2 h of parenteral administration, thus reducing the effective “window period” for passive diffusion to the central nervous system.[6] Therefore, in thiamine deficient individuals with features of Wernicke encephalopathy should receive thiamine thrice daily.High-dose parenteral thiamine administered thrice daily has been advocated in patients at risk for Wernicke encephalopathy.[43] The Royal College of Physicians guideline recommends that patients with suspected Wernicke encephalopathy should receive 500 mg thiamine diluted in 50–100 ml of normal saline infusion over 30 min three times daily for 2–3 days and sometimes for longer periods.[13] If there are persistent symptoms such as confusion, cerebellar symptoms, or memory impairment, this regimen can be continued until the symptoms improve.

If symptoms improve, oral thiamine 100 mg thrice daily can be continued for prolonged periods.[6],[40] A similar treatment regimen is advocated for alcoholic cerebellar degeneration as well. Doses more than 500 mg intramuscular or intravenous three times a day for 3–5 days, followed by 250 mg once daily for a further 3–5 days is also recommended by some guidelines (e.g., British Association for Psychopharmacology).[44]Other effects of thiamineThere are some data to suggest that thiamine deficiency can modulate alcohol consumption and may result in pathological drinking. Benfotiamine 600 mg/day as compared to placebo for 6 months was well tolerated and found to decrease psychiatric distress in males and reduce alcohol consumption in females with severe alcohol dependence.[45],[46] Other Factors During Thiamine Therapy Correction of hypomagnesemiaMagnesium is a cofactor for many thiamine-dependent enzymes in carbohydrate metabolism. Patients may fail to respond to thiamine supplementation in the presence of hypomagnesemia.[47] Magnesium deficiency is common in chronic alcohol users and is seen in 30% of individuals.[48],[49] It can occur because of increased renal excretion of magnesium, poor intake, decreased absorption because of Vitamin D deficiency, the formation of undissociated magnesium soaps with free fatty acids.[48],[49]The usual adult dose is 35–50 mmol of magnesium sulfate added to 1 L isotonic (saline) given over 12–24 h.[6] The dose has to be titrated against plasma magnesium levels.

It is recommended to reduce the dose in renal failure. Contraindications include patients with documented hypersensitivity and those with heart block, Addison's disease, myocardial damage, severe hepatitis, or hypophosphatemia. Do not administer intravenous magnesium unless hypomagnesemia is confirmed.[6]Other B-complex vitaminsMost patients with deficiency of thiamine will also have reduced levels of other B vitamins including niacin, pyridoxine, and cobalamin that require replenishment. For patients admitted to the intensive care unit with symptoms that may mimic or mask Wernicke encephalopathy, based on the published literature, routine supplementation during the 1st day of admission includes 200–500 mg intravenous thiamine every 8 h, 64 mg/kg magnesium sulfate (≈4–5 g for most adult patients), and 400–1000 μg intravenous folate.[50] If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal saline.[50] Precautions to be Taken When Administering Parenteral Thiamine It is recommended to monitor for anaphylaxis and has appropriate facilities for resuscitation and for treating anaphylaxis readily available including adrenaline and corticosteroids.

Anaphylaxis has been reported at the rate of approximately 4/1 million pairs of ampoules of Pabrinex (a pair of high potency vitamins available in the UK containing 500 mg of thiamine (1:250,000 I/V administrations).[40] Intramuscular thiamine is reported to have a lower incidence of anaphylactic reactions than intravenous administration.[40] The reaction has been attributed to nonspecific histamine release.[51] Administer intravenous thiamine slowly, preferably by slow infusion in 100 ml normal saline over 15–30 min. Conclusions Risk factors for thiamine deficiency should be assessed in chronic alcohol users. A high index of suspicion and a lower threshold to diagnose thiamine deficiency states including Wernicke encephalopathy is needed. Several other presentations such as cerebellar syndrome, MBS, polyneuropathy, and delirium tremens could be related to thiamine deficiency and should be treated with protocols similar to Wernicke encephalopathy.

High-dose thiamine is recommended for the treatment of suspected Wernicke encephalopathy and related conditions [Figure 1]. However, evidence in terms of randomized controlled trials is lacking, and the recommendations are based on small studies and anecdotal reports. Nevertheless, as all these conditions respond to thiamine supplementation, it is possible that these have overlapping pathophysiology and are better considered as Wernicke encephalopathy spectrum disorders.Figure 1. Thiamine recommendations for patients with alcohol use disorder.

AHistory of alcohol use, but no clinical features of WE. BNo clinical features of WE, but with risk factors such as complicated withdrawal (delirium, seizures). CClinical features of WE (ataxia, opthalmoplegia, global confusion)Click here to viewFinancial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Frank LL.

Thiamin in clinical practice. JPEN J Parenter Enteral Nutr 2015;39:503-20. 2.Thomson AD, Marshall EJ. The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis.

Alcohol Alcohol 2006;41:151-8. 3.Thomson AD, Guerrini I, Marshall EJ. Wernicke's encephalopathy. Role of thiamine.

Pract Gastroenterol 2009;33:21-30. 4.Isenberg-Grzeda E, Kutner HE, Nicolson SE. Wernicke-Korsakoff-syndrome. Under-recognized and under-treated.

Psychosomatics 2012;53:507-16. 5.Wood B, Currie J, Breen K. Wernicke's encephalopathy in a metropolitan hospital. A prospective study of incidence, characteristics and outcome.

Med J Aust 1986;144:12-6. 6.Thomson AD, Cook CC, Touquet R, Henry JA, Royal College of Physicians, London. The Royal College of Physicians report on alcohol. Guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department.

Alcohol Alcohol 2002;37:513-21. 7.Harper C. Thiamine (vitamin B1) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe!. Eur J Neurol 2006;13:1078-82.

8.Harper CG, Giles M, Finlay-Jones R. Clinical signs in the Wernicke-Korsakoff complex. A retrospective analysis of 131 cases diagnosed at necropsy. J Neurol Neurosurg Psychiatry 1986;49:341-5.

9.Cook CC. Prevention and treatment of Wernicke-Korsakoff syndrome. Alcohol Alcohol 2000;35:19-20. 10.Caine D, Halliday GM, Kril JJ, Harper CG.

Operational criteria for the classification of chronic alcoholics. Identification of Wernicke's encephalopathy. J Neurol Neurosurg Psychiatry 1997;62:51-60. 11.Sullivan EV, Pfefferbaum A.

Neuroimaging of the Wernicke-Korsakoff syndrome. Alcohol Alcohol 2009;44:155-65. 12.Jung YC, Chanraud S, Sullivan EV. Neuroimaging of Wernicke's encephalopathy and Korsakoff's syndrome.

Neuropsychol Rev 2012;22:170-80. 13.Pruckner N, Baumgartner J, Hinterbuchinger B, Glahn A, Vyssoki S, Vyssoki B. Thiamine substitution in alcohol use disorder. A narrative review of medical guidelines.

Eur Addict Res 2019;25:103-10. 14.Day E, Bentham PW, Callaghan R, Kuruvilla T, George S. Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033.

Doi. 10.1002/14651858.CD004033.pub3. 15.Arts NJ, Walvoort SJ, Kessels RP. Korsakoff's syndrome.

A critical review. Neuropsychiatr Dis Treat 2017;13:2875-90. 16.Laureno R. Nutritional cerebellar degeneration, with comments on its relationship to Wernicke disease and alcoholism.

Handb Clin Neurol 2012;103:175-87. 17.Maschke M, Weber J, Bonnet U, Dimitrova A, Bohrenkämper J, Sturm S, et al. Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI. J Neurol 2005;252:704-11.

18.Mulholland PJ, Self RL, Stepanyan TD, Little HJ, Littleton JM, Prendergast MA. Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro. Neuroscience 2005;135:1129-39. 19.Del Brutto OH, Mera RM, Sullivan LJ, Zambrano M, King NR.

Population-based study of alcoholic cerebellar degeneration. The Atahualpa Project. J Neurol Sci 2016;367:356-60. 20.Hammoud N, Jimenez-Shahed J.

Chronic neurologic effects of alcohol. Clin Liver Dis 2019;23:141-55. 21.Lee JH, Heo SH, Chang DI. Early-stage alcoholic cerebellar degeneration.

Diagnostic imaging clues. J Korean Med Sci 2015;30:1539. 22.Phillips SC, Harper CG, Kril JJ. The contribution of Wernicke's encephalopathy to alcohol-related cerebellar damage.

Drug Alcohol Rev 1990;9:53-60. 23.Baker KG, Harding AJ, Halliday GM, Kril JJ, Harper CG. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke's encephalopathy. Neuroscience 1999;91:429-38.

24.Graham JR, Woodhouse D, Read FH. Massive thiamine dosage in an alcoholic with cerebellar cortical degeneration. Lancet 1971;2:107. 25.Julian T, Glascow N, Syeed R, Zis P.

Alcohol-related peripheral neuropathy. A systematic review and meta-analysis. J Neurol 2018;22:1-3. 26.Chopra K, Tiwari V.

Alcoholic neuropathy. Possible mechanisms and future treatment possibilities. Br J Clin Pharmacol 2012;73:348-62. 27.Woelk H, Lehrl S, Bitsch R, Köpcke W.

Benfotiamine in treatment of alcoholic polyneuropathy. An 8-week randomized controlled study (BAP I Study). Alcohol Alcohol 1998;33:631-8. 28.Peters TJ, Kotowicz J, Nyka W, Kozubski W, Kuznetsov V, Vanderbist F, et al.

Treatment of alcoholic polyneuropathy with vitamin B complex. A randomised controlled trial. Alcohol Alcohol 2006;41:636-42. 29.Fernandes LM, Bezerra FR, Monteiro MC, Silva ML, de Oliveira FR, Lima RR, et al.

Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity. How poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. Eur J Clin Nutr 2017;71:580-6. 30.Hillbom M, Saloheimo P, Fujioka S, Wszolek ZK, Juvela S, Leone MA.

Diagnosis and management of Marchiafava-Bignami disease. A review of CT/MRI confirmed cases. J Neurol Neurosurg Psychiatry 2014;85:168-73. 31.Nemlekar SS, Mehta RY, Dave KR, Shah ND.

Marchiafava. Bignami disease treated with parenteral thiamine. Indian J Psychol Med 2016;38:147-9. [Full text] 32.Brin M.

Erythrocyte transketolase in early thiamine deficiency. Ann N Y Acad Sci 1962;98:528-41. 33.Dreyfus PM. Clinical application of blood transketolase determinations.

N Engl J Med 1962;267:596-8. 34.Edwards KA, Tu-Maung N, Cheng K, Wang B, Baeumner AJ, Kraft CE. Thiamine assays – Advances, challenges, and caveats. ChemistryOpen 2017;6:178-91.

35.Chandrakumar A, Bhardwaj A, 't Jong GW. Review of thiamine deficiency disorders. Wernicke encephalopathy and Korsakoff psychosis. J Basic Clin Physiol Pharmacol 2018;30:153-62.

36.Torruellas C, French SW, Medici V. Diagnosis of alcoholic liver disease. World J Gastroenterol 2014;20:11684-99. 37.Thomson AD, Leevy CM.

Observations on the mechanism of thiamine hydrochloride absorption in man. Clin Sci 1972;43:153-63. 38.Hoyumpa AM Jr., Strickland R, Sheehan JJ, Yarborough G, Nichols S. Dual system of intestinal thiamine transport in humans.

J Lab Clin Med 1982;99:701-8. 39.Smithline HA, Donnino M, Greenblatt DJ. Pharmacokinetics of high-dose oral thiamine hydrochloride in healthy subjects. BMC Clin Pharmacol 2012;12:4.

40.Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44:911-5. 41.Raj V, Ojha S, Howarth FC, Belur PD, Subramanya SB.

Therapeutic potential of benfotiamine and its molecular targets. Eur Rev Med Pharmacol Sci 2018;22:3261-73. 42.Xie F, Cheng Z, Li S, Liu X, Guo X, Yu P, et al. Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride.

J Clin Pharmacol 2014;54:688-95. 43.Cook CC, Hallwood PM, Thomson AD. B Vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol 1998;33:317-36.

44.Lingford-Hughes AR, Welch S, Peters L, Nutt DJ, British Association for Psychopharmacology, Expert Reviewers Group. BAP updated guidelines. Evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity. Recommendations from BAP.

J Psychopharmacol 2012;26:899-952. 45.Manzardo AM, He J, Poje A, Penick EC, Campbell J, Butler MG. Double-blind, randomized placebo-controlled clinical trial of benfotiamine for severe alcohol dependence. Drug Alcohol Depend 2013;133:562-70.

46.Manzardo AM, Pendleton T, Poje A, Penick EC, Butler MG. Change in psychiatric symptomatology after benfotiamine treatment in males is related to lifetime alcoholism severity. Drug Alcohol Depend 2015;152:257-63. 47.Dingwall KM, Delima JF, Gent D, Batey RG.

Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital. Drug Alcohol Rev 2015;34:323-8. 48.Flink EB. Magnesium deficiency in alcoholism.

Alcohol Clin Exp Res 1986;10:590-4. 49.Grochowski C, Blicharska E, Baj J, Mierzwińska A, Brzozowska K, Forma A, et al. Serum iron, magnesium, copper, and manganese levels in alcoholism. A systematic review.

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Correspondence Address:Samir Kumar PraharajDepartment of Psychiatry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_440_20 Figures [Figure 1].

What is Viagra?

Generic Viagra is used to treat male Impotence also known as Erectile Dysfunction. Also, it has been approved by US FDA for treating pulmonary arterial hypertension.

Viagra interactions

€‹â€‹NSW has reported two new cases of locally transmitted erectile dysfunction treatment viagra interactions in the 24 hours to 8pm last night.Three cases in overseas travellers in hotel quarantine were also diagnosed, bringing the total number visit this website of cases in NSW to 4,158. Confirmed cases (including interstate residents in NSW health care facilities) 4,158 Deaths (in NSW from confirmed cases)​ 55 Total tests carried out 2,917,454 There were 7,401 tests reported to 8pm last night, compared with 6,952 in the viagra interactions previous 24 hours.Anyone with symptoms of a cold should assume it’s erectile dysfunction treatment until proven otherwise by a test. Get tested on the day you get those symptoms – don’t wait to see if they go away. Of the new cases to 8pm last viagra interactions night. Three were acquired overseas and are now in hotel quarantine Two were locally acquired, both linked to known cases and clusters One locally acquired case is a household contact of a previously confirmed case linked to the Liverpool private clinic cluster, which now has a total of 12 cases.

The other locally acquired case is a close contact of a confirmed case linked to someone who attended the childcare centre viagra interactions at Oran Park.NSW Health is treating 64 erectile dysfunction treatment cases, with one patient in intensive care. This patient does not require ventilation. Ninety-four per cent of cases being treated by NSW viagra interactions Health are in non-acute, out-of-hospital care.NSW is at a critical point, and the only way to find undiagnosed cases and prevent further transmission is to increase testing.NSW Health particularly thanks the Oran Park community for its brilliant response to our calls for increased testing. From 1 August to 10 October 2020, the average number of erectile dysfunction treatment tests conducted each week among residents of Oran Park was 227, but during the week ending 17 October 2020, the number of tests increased almost four-fold to 895.However, increases in surrounding suburbs were far more modest and NSW Health continues to appeal to the community in South Western Sydney to come forward for testing right away if anyone has even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment. This is also particularly important in Western Sydney and South Eastern Sydney, where there have also been locally transmitted cases recently.There are more than 300 viagra interactions erectile dysfunction treatment testing locations across NSW.

To find your nearest clinic visit erectile dysfunction treatment testing clinics or contact your GP.erectile dysfunction treatment is still likely circulating in the community and we must all be vigilant. To help stop the spread of viagra interactions erectile dysfunction treatment. If you are unwell, get tested and isolate right away – don’t delay.Wash your hands regularly. Take hand sanitiser with you when viagra interactions you go out.Keep your distance. Leave 1.5 metres between yourself and others.

Wear a mask when using public transport, rideshares and taxis, and in shops, places of worship and other viagra interactions places where you can’t physically distance. When taking taxis or rideshares, commuters should also sit in the back. Confirmed viagra interactions cases to date Overseas​ 2,218 Interstate acquired 91 Loca​lly acquired – contact of a confirmed case and/or in a known cluster 1,455 Locally acquired – contact not identified 394 Under investigation 0 Counts reported for a particular day may vary over time with ongoing enhanced surveillance activities.Returned travellers in hotel quarantine to date Symptomati​c travellers tested 5,970 Found positive 138 Asymptomatic travellers sc​reened at day 2 36,406 Found positive 181 Asymptomatic travellers screened at day 10 48,768 Found positive 129 ​​​NSW has reported no new cases of locally transmitted erectile dysfunction treatment in the 24 hours to 8pm last night. The last time there were no new locally transmitted cases in NSW was the 24 hours to 6 October.Four cases http://omalandro.com/?page_id=33 in overseas travellers in hotel quarantine were diagnosed, bringing the total number of cases in NSW to 4,153. Confirmed viagra interactions cases (including interstate residents in NSW health care facilities) 4,153 Deaths (in NSW from confirmed cases)​ 55 Total tests carried out 2,910,053 There were 6,952 tests reported to 8pm last night, compared with 12,985 in the previous 24 hours.Testing numbers have dropped recently, which is a concern.

NSW is at a critical point, and the only way to find new cases and prevent further transmission is to increase testing.NSW Health is appealing to the community to come forward for testing right away if anyone has even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment. This is particularly important in South Western Sydney, Western Sydney and South Eastern Sydney where there have been recent locally transmitted cases.Everyone plays an important viagra interactions role in helping to contain the viagra by getting tested quickly and following social distancing rules. Get tested on the day you get symptoms – don’t wait to see if they go away. Assume it’s erectile dysfunction treatment until proven otherwise by a test, and remember there is no limit on how many tests you can have.Testing is quick, free, viagra interactions and easy and most people receive their test result within 24 hours. If you have even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment, please come forward for testing right away.

There are more than 300 erectile dysfunction treatment testing viagra interactions locations across NSW. To find your nearest clinic visit erectile dysfunction treatment testing clinics or contact your GP.NSW Health is treating 69 erectile dysfunction treatment cases, with one patient in intensive care. This patient does not require viagra interactions ventilation. Ninety-six per cent of cases being treated by NSW Health are in non-acute, out-of-hospital care.erectile dysfunction treatment is still likely circulating in the community and we must all be vigilant. To help stop viagra interactions the spread of erectile dysfunction treatment.

If you are unwell, get tested and isolate right away – don’t delay. Wash your viagra interactions hands regularly. Take hand sanitiser with you when you go out. Keep your viagra interactions distance. Leave 1.5 metres between yourself and others.

Wear a mask when using public transport, rideshares and taxis, and in shops, places of worship and other places where you can’t physically distance. When taking taxis or rideshares, commuters should also sit in the back.Locations linked to known cases, advice on testing and isolation, and areas identified for increased testing can be at NSW Government - Latest news and updates.Confirmed cases to date Overseas​ 2,215 Interstate acquired 91 Loca​lly acquired – contact of a confirmed case and/or in a known cluster 1,452 Locally acquired – contact not identified 395 Under investigation 0 Counts reported for a particular day may vary over time with ongoing enhanced surveillance activities.Returned travellers in hotel quarantine to date Symptomati​c travellers tested 5,954 Found positive 138 Asymptomatic travellers sc​reened at day 2 36,037 Found positive 179 Asymptomatic travellers screened at day 10 48,458 Found positive 129.

€‹â€‹NSW has reported two new cases of locally transmitted viagra online canada erectile dysfunction treatment in the 24 hours to 8pm last night.Three cases in overseas travellers in hotel quarantine were also diagnosed, bringing the total number of cases in NSW to 4,158. Confirmed cases (including interstate residents in NSW health care facilities) 4,158 Deaths (in NSW from confirmed cases)​ 55 Total tests carried out 2,917,454 There were 7,401 tests reported to 8pm last night, compared with 6,952 in the viagra online canada previous 24 hours.Anyone with symptoms of a cold should assume it’s erectile dysfunction treatment until proven otherwise by a test. Get tested on the day you get those symptoms – don’t wait to see if they go away. Of the new cases to 8pm viagra online canada last night. Three were acquired overseas and are now in hotel quarantine Two were locally acquired, both linked to known cases and clusters One locally acquired case is a household contact of a previously confirmed case linked to the Liverpool private clinic cluster, which now has a total of 12 cases.

The other locally acquired case is a close contact of a confirmed case linked to someone who attended the viagra online canada childcare centre at Oran Park.NSW Health is treating 64 erectile dysfunction treatment cases, with one patient in intensive care. This patient does not require ventilation. Ninety-four per cent of cases being treated by NSW Health are in non-acute, out-of-hospital care.NSW is at a critical point, and the only way viagra online canada to find undiagnosed cases and prevent further transmission is to increase testing.NSW Health particularly thanks the Oran Park community for its brilliant response to our calls for increased testing. From 1 August to 10 October 2020, the average number of erectile dysfunction treatment tests conducted each week among residents of Oran Park was 227, but during the week ending 17 October 2020, the number of tests increased almost four-fold to 895.However, increases in surrounding suburbs were far more modest and NSW Health continues to appeal to the community in South Western Sydney to come forward for testing right away if anyone has even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment. This is also particularly important in viagra online canada Western Sydney and South Eastern Sydney, where there have also been locally transmitted cases recently.There are more than 300 erectile dysfunction treatment testing locations across NSW.

To find your nearest clinic visit erectile dysfunction treatment testing clinics or contact your GP.erectile dysfunction treatment is still likely circulating in the community and we must all be vigilant. To help stop the spread of viagra online canada erectile dysfunction treatment. If you are unwell, get tested and isolate right away – don’t delay.Wash your hands regularly. Take hand sanitiser with you viagra online canada when you go out.Keep your distance. Leave 1.5 metres between yourself and others.

Wear a mask when using public transport, rideshares and taxis, and in shops, places of worship and other places viagra online canada where you can’t physically distance. When taking taxis or rideshares, commuters should also sit in the back. Confirmed cases to date Overseas​ 2,218 Interstate acquired 91 Loca​lly acquired – contact of a confirmed case and/or in a known cluster 1,455 Locally acquired – contact not identified 394 Under investigation 0 Counts reported for a viagra online canada particular day may vary over time with ongoing enhanced surveillance activities.Returned travellers in hotel quarantine to date Symptomati​c travellers tested 5,970 Found positive 138 Asymptomatic travellers sc​reened at day 2 36,406 Found positive 181 Asymptomatic travellers screened at day 10 48,768 Found positive 129 ​​​NSW has reported no new cases of locally transmitted erectile dysfunction treatment in the 24 hours to 8pm last night. The last time there were no new locally transmitted cases in NSW was the 24 hours to 6 October.Four cases in overseas travellers in hotel quarantine were diagnosed, bringing the total number of cases in NSW to 4,153. Confirmed cases (including interstate viagra online canada residents in NSW health care facilities) 4,153 Deaths (in NSW from confirmed cases)​ 55 Total tests carried out 2,910,053 There were 6,952 tests reported to 8pm last night, compared with 12,985 in the previous 24 hours.Testing numbers have dropped recently, which is a concern.

NSW is at a critical point, and the only way to find new cases and prevent further transmission is to increase testing.NSW Health is appealing to the community to come forward for testing right away if anyone has even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment. This is particularly important in South Western Sydney, Western viagra online canada Sydney and South Eastern Sydney where there have been recent locally transmitted cases.Everyone plays an important role in helping to contain the viagra by getting tested quickly and following social distancing rules. Get tested on the day you get symptoms – don’t wait to see if they go away. Assume it’s erectile dysfunction treatment until proven otherwise by viagra online canada a test, and remember there is no limit on how many tests you can have.Testing is quick, free, and easy and most people receive their test result within 24 hours. If you have even the mildest of symptoms like a runny nose or scratchy throat, cough, fever or other symptoms that could be erectile dysfunction treatment, please come forward for testing right away.

There are more than 300 erectile dysfunction treatment testing viagra online canada locations across NSW. To find your nearest clinic visit erectile dysfunction treatment testing clinics or contact your GP.NSW Health is treating 69 erectile dysfunction treatment cases, with one patient in intensive care. This patient viagra online canada does not require ventilation. Ninety-six per cent of cases being treated by NSW Health are in non-acute, out-of-hospital care.erectile dysfunction treatment is still likely circulating in the community and we must all be vigilant. To help viagra online canada stop the spread of erectile dysfunction treatment.

If you are unwell, get tested and isolate right away – don’t delay. Wash your hands regularly viagra online canada. Take hand sanitiser with you when you go out. Keep your viagra online canada distance. Leave 1.5 metres between yourself and others.

Wear a mask when using public transport, rideshares and taxis, and in shops, places of worship and other places where you can’t physically viagra online canada distance. When taking taxis or rideshares, commuters should also sit in the back.Locations linked to known cases, advice on testing and isolation, and areas identified for increased testing can be at NSW Government - Latest news and updates.Confirmed cases to date Overseas​ 2,215 Interstate acquired 91 Loca​lly acquired – contact of a confirmed case and/or in a known cluster 1,452 Locally acquired – contact not identified 395 Under investigation 0 Counts reported for a particular day may vary over time with ongoing enhanced surveillance activities.Returned travellers in hotel quarantine to date Symptomati​c travellers tested 5,954 Found positive 138 Asymptomatic travellers sc​reened at day 2 36,037 Found positive 179 Asymptomatic travellers screened at day 10 48,458 Found positive 129.

Blue viagra

The term “mRNA” only blue viagra entered the average household in the past few months, as Moderna and Pfizer-BioNTech released their erectile dysfunction treatment Buy zithromax treatments. But a handful of scientists have spent decades studying this novel approach to immunization. By the start of the viagra the technology was already so advanced that, when Chinese researchers published the genetic sequence for the erectile dysfunction in mid-January, blue viagra Moderna was able to concoct a treatment within 48 hours.

Clinical trials began a matter of weeks after that. In nine months, the world was well on its way blue viagra to viral security.It was a stunning debut for mRNA — shorthand for messenger ribonucleic acid, DNA’s sidekick — which had long ranked as a promising but unproven treatment. After this encouraging success, its proponents predict an equally impressive future.

They have always believed in mRNA’s ability to protect against not only the likes of erectile dysfunction, but also a host of deadly diseases that resist traditional treatments, from malaria to HIV to cancer. In 2018, long before the past year’s confidence-boosting display, a group of researchers announced “a new era in vaccinology.”It remains to blue viagra be seen whether mRNA will live up to the hype. With concrete results attesting to its potential, though, interest is growing among investors and researchers alike.

It helps that regulatory agencies and the public are familiar blue viagra with it now, too, says Yale immunologist Rick Bucala. €œThat has really changed the landscape.”Andrew Geall, co-founder of one company testing RNA treatments and chief scientific officer of another, notes that mRNA has only just entered its infancy after a long gestation. Such is the nature of scientific progress.

€œWe’ve had the technology bubbling for 20 years, and the major blue viagra breakthrough is this clinical proof of two treatments,” he says. €œNow we’re set for 10 years of excitement.”Next Steps for mRNAThe goal of any treatment is to train the immune system to recognize and defend against a viagra. Traditional treatments do so by exposing the body to the viagra itself, weakened or blue viagra dead, or to a part of the viagra, called an antigen.

The new shots, as their name suggests, introduce only mRNA — the genetic material that, as you may remember from high school biology, carries instructions for making proteins. Once the mRNA enters the cells, particles called ribosomes read its instructions and use them to build the encoded proteins. In the blue viagra case of the erectile dysfunction treatments, those proteins are the crown-shaped “spike” antigens from which the erectile dysfunction derives its name (“corona” means crown in Latin).

By themselves they are harmless, but the immune system attacks them as foreign invaders, and in doing so learns how to ward off the real viagra. If it ever rears its spiky head thereafter, the body will remember and swiftly destroy it.But besides liberating the world from the worst viagra in generations, mRNA could help to vanquish many an blue viagra intractable illness. If all the dreams of its advocates are realized, the erectile dysfunction treatments may, in hindsight, be only a proof of concept.

In February, for example, Bucala and his colleagues patented a treatment against malaria, which has likely killed more humans than any other single cause and has mostly withstood immunization.Justin Richner, an immunologist with the University of Illinois, Chicago, is developing an mRNA treatment for dengue, another highly resistant viagra. Because mRNA blue viagra is simply a genetic sequence, scientists can easily tweak it as necessary to find the most effective combination. €œOne of the advantages of the mRNA platform is how it can be so easily modified and manipulated to test novel hypotheses,” Richner says.Read more.

Dengue Fever Is on the Rise — a Ticking Time Bomb in Many Places Around the WorldGeall says the obvious candidates for mRNA treatments include what he calls the “Big 6,” all of which remain crafty foes blue viagra. Malaria, cancer, tuberculosis HIV, cytomegaloviagra, and respiratory syncytial viagra. His own company, Replicate Bioscience, is working on the cancer front, as are several others, including BioNTech.

Through genetic analysis of individual blue viagra tumors, patients could one day receive personalized treatments, designed to target the specific mutations afflicting them.Currently, it’s difficult to tell whether an mRNA treatment will work on any particular pathogen. Many have shown promise in animal trials, only to falter in our species. As Geall put it, “mice are not humans.” Some appear to be better bets than others — cytomegaloviagra and RSV respiratory syncytial viagra in particular — but for now, it’s too early to say where mRNA will blue viagra next bear fruit.

€œDespite all we know about immunology, a lot of it is really empiric,” Bucala says. €œYou just have to try things and see if they work.” The viagra TamerBased on its recent achievements, mRNA’s next act may well involve the next viagra. Perhaps its biggest blue viagra strength is that it can be manufactured at speeds unheard of in the realm of traditional treatments, making it well-suited to addressing sudden surges of viagraes.

€œOne of the great things about the mRNA field is how quickly you can go from a concept into a therapy that is ready for clinical trials,” Richner says. €œWe can make multiple different treatments and test them in blue viagra a really rapid process.”Read more. erectile dysfunction treatment.

A Basic Guide to Different treatment Types and How They WorkSince 2018, Pfizer and BioNTech have been working on an mRNA treatment for seasonal flu. Under the status quo, experts must predict which variation of the viagra will pose the greatest threat each blue viagra year and produce treatments to match it. But because mRNA is so easy to edit, it can be modified more efficiently to keep pace with the ever-mutating strains.

€œI do think the influenza treatment field blue viagra will be transformed in the not too distant future,” Richner says. A similar kind of gene-based treatment, made with self-amplifying RNA (saRNA), is even more nimble. Whereas basic mRNA treatments — like Moderna’s and Pfizer-BioNTech’s — inject all the genetic material at once, the self-amplifying version replicates itself inside the cell.

Just a small dose of this potent product can trigger the same immune response as a syringe-full of blue viagra the current shots. Bucala’s malaria treatment and Geall’s cancer treatments both use this technology. €œThe big problem is blue viagra that treatments don’t prevent s,” Bucala says.

€œVaccinations prevent s.” With saRNA, manufacturers can ensure a lot more of them. After mRNA’s brilliant battle against erectile dysfunction treatment, it’s tempting to think of it as a panacea. But, Bucala says, “Is there blue viagra something intrinsically revolutionary about mRNA?.

We don’t know yet.”It does come with some logistical challenges. For example, mRNA breaks down easily, so it must be refrigerated throughout the blue viagra distribution process. Hurdles aside, though, the possibilities are vast, and investment may rise to meet the industry’s ambitions.

treatment development isn’t typically a lucrative business, but erectile dysfunction treatment has made more than a few billionaires, “and others are watching,” Bucala says. €œI think it should become blue viagra economically viable in our [current] model to get into treatment work again.”Geall agrees. Even if some mRNA endeavors fizzle out, at least a few are bound to make the world proud.

€œThere’s a lot of money out there that is blue viagra going to be invested into these new approaches,” he says. €œWe’re going to see failures, but we’re going to see successes for sure.”When the U.S. Cracked down on drugs in the 1970s, the effort dried up most funding and research into psychedelic substances — which only in the past few years have regained momentum in the field of psychotherapy.

In the ’70s, rather than shut down all his work, one psychedelic researcher at Johns Hopkins University, Stan Grof, turned his attention to another blue viagra potential avenue for attaining non-ordinary states of consciousness. Breathing.Grof, alongside his wife at the time, Christina Grof, developed the term Holotropic Breathwork for this technique, which loosely translates as “moving toward wholeness.” The practice in experiential psychotherapy emerged in the 1980s as a tool for self-exploration and inner healing, and has certified teaches who now facilitate it around the world. The framework integrates music with modern consciousness research, psychology and Eastern spiritual blue viagra practices, according to the Grof Transpersonal Training program.Many people today teach this intense breathing practice, and other similar techniques that preceded it, such as kundalini yoga or pranayama.

But questions remain about the science behind what exactly is happening in the mind and body while practitioners lie on the floor and breathe persistently in rapid patterns. And some clinicians have raised concerns about the safety, and risks, in a field with limited peer-reviewed studies.Meditation on a Freight TrainStacia Butterfield has been a certified Holotropic Breathwork teacher with Grof Transpersonal Training for roughly 15 years. She committed to the work after having her own life-changing experience at a workshop, and has since worked closely with Grof himself and guided thousands of people blue viagra in the practice.

€œIt’s deceptively simple. It seems like just turning on music, laying down and taking some breaths, and away blue viagra you go,” Butterfield says. €œWhat we’re actually relying on is the spontaneous mobilization of the psyche.”First and foremost, a guided Holotropic Breathwork session requires creating a safe container, Butterfield says, where people can let go of inhibitions or mental blocks.

Facilitators are trained to guide people through that process in a group setting.One session lasts between two and three hours — often as part of a weekend or week-long retreat. People pair off and alternate in the blue viagra roles of “sitter” (assisting the other) and “breather” (the person doing the heavy breathing). To begin, rhythmic drumming sets the mood.

The breather lays down and starts breathing rapidly, in a continuous way with no real break between inhales and blue viagra exhales.The music typically has an emotional arc, almost like a movie soundtrack. It might start off evocative and stimulating, then turn “increasingly dramatic and dynamic, and finally it reaches a breakthrough quality,” according to a guide written by Stan and Christina Grof. This guide notes that when the breathing leads to non-ordinary states of consciousness in a practitioner, “there is a potential for unusually intense projections, including regressed longings for nurturing, sexual contact, or spiritual connection.” Facilitators are advised to assist clients with these feelings as they arise, while following their agreement to conduct the practice in an ethical manner.Butterfield says one core principle, like somatic therapy, is for participants to become aware of the messages and wisdom in their own body.

€œSo many people are so busy, just cruising around [and] keeping blue viagra the lid on everything else that is going on internally,” she says. €œ[In a session] they can just close their eyes and go inward, and see what’s there.” She says visions, strong bodily sensations and emotions often arise. And she has watched people who had tried years of talk therapy make substantial progress in processing blue viagra grief and loss, past trauma, life changes or even mental illnesses.One practitioner aptly described this practice as “meditation on a freight train,” Butterfield adds.

The reported dramatic experiences spark questions about what might actually be happening within the body and brain.Mysticism or Hyperventilation?. Pulmonologist Michael Stephen, author of the book Breath Taking, says the practice of Holotropic Breathwork raises red flags for him because of its use of over-breathing, or hyperventilation. Biologically, when someone breathes heavily blue viagra for an extended period, they can lose too much carbon dioxide, which makes the blood overly alkaline.

The phenomenon often triggers an immediately physiological response. €œWe start to get tingly in our fingers and dizzy when we hyperventilate, as our pH is rising too much,” says Stephen.Prolonged, excessive blue viagra pH levels in the blood can also cause seizures, he adds. €œJust before seizures happen, you can get lightheaded, a sort of high.” He attributes this to the non-ordinary states of consciousness that people might feel during Holotropic Breathwork.

But he says few proper studies have been done on the practice because of the dangers and ethics involved.Casualties of Heavy BreathingAnother breath specialist and integrative psychiatrist, Patricia Gerbarg, says that Holotropic Breathwork, and other forceful respiratory practices such as breath of fire, do have the potential to alter the mind. They can also bring about a lasting impact blue viagra on people, but it’s not always beneficial or predictable.“It’s a stress on the system. You’re going through rapid changes in oxygen levels and the balance of various substances in the body and the brain,” she says.

And similar to drugs, “people can use them to attain different mental states,” she adds.Read More blue viagra. Can Breathing Like Wim Hof Make Us Super Human?. Healthy people tend to have a broader tolerance to endure these shifts and unpredictable outcomes.

But the same behavior can be harmful to someone who is less healthy, or dealing with a psychological disorder, says Gerbarg, who teaches psychiatry at New York Medical College.“Those kinds of intense, rapid shifts in your brain chemistry can cause adverse effects,” blue viagra she says, adding that she is familiar with cases where people feel they “never recovered” from what these states did to them. Some literature uses the term kundalini psychosis, or physio kundalini syndrome, to describe people who cognitively lose touch with reality in pursuit of "spiritual awakening."One of Gerbarg’s concerns about the rise in popularity of these advanced, Eastern breathing practices is how they are inserted into the Western world and modern mindset. (Two other intense and forceful breathing practices include Tummo breathing, with a Tibetan buddhist lineage, and the Wim Hof Method.) The blue viagra breathwork is often tied closely to a lifestyle and belief system, and many traditional practitioners dedicate hours a day for many years to master the techniques in a healthy way.

Alternatively, people in modern Western cultures often struggle to commit to a new practice for 20 minute a day. €œ[Intense breathwork] is becoming increasingly popular and people are doing it online,” Gerbarg says. €œThey aren’t often aware that there are risks,” blue viagra or they might not know the pre-existing conditions their students have.

The big responsibility ultimately falls on the teachers and facilitators to ensure everyone is safe. A Gentler TouchGerbarg and her husband Richard Brown, a professor of psychiatry at Columbia College of Physicians and blue viagra Surgeons, have published several books on the healing potential of breath. And they offer evidence-based workshops and teaching resources through their Breath-Body-Mind Foundation.One of their most popular techniques, called coherent breathing, teaches gentle, slower and relaxed respiration.

Once practitioners learn it, they can use it any point throughout the day when stress or anxiety is likely to rise up — even in mundane circumstances like being stuck in a long line — and trigger a string of reactions in the body.The goal is to inhale and exhale slowly through the nose at a rate of about five breaths per minute, or one breath cycle every 12 seconds. Gerbarg says blue viagra this process can promptly activate the rest-and-restore parasympathetic nervous system throughout the body, with millions of reactions and signals firing every second.Read More. How Slow, Deep Breathing Taps Into a Natural Rhythm in Our Bodies“It tells the brain, ‘the conditions are safe,’ ” she says.

€œThe less effort, blue viagra the more you get out of this one.”The results of this technique may not feel like the freight-train experience of altered consciousness. But it carries less risk and broader appeal to anyone interested in channeling their own breath for health and wellness.In a year marked by a viagra, economic downturn, racial unrest, and an election that culminated with a mob storming the U.S. Capitol, we’ve come face to face with stressors we could never have imagined prior to 2020.

The causes and health impacts of stress have been widely discussed as blue viagra have a host of tools for tackling the mounting anxiety we feel in our daily lives. But cortisol, among the body’s most important steroid hormones, at the helm of our stress response, remains largely a mystery. Is our blue viagra fight-or-flight response really tied to our prehistoric ancestors?.

Has our modern world evolved beyond the antiquated workings of our endocrine system?. Here’s what we know. A Caveman blue viagra Instinct?.

Cortisol, along with epinephrine and norepinephrine, activate the body’s sympathetic nervous system, triggering a lineup of physiological responses that speed up respiration, constrict blood vessels, dilate pupils, and slow down the digestive system. It’s called a fight-or-flight response, and it allows muscles to react more powerfully and move faster, priming us to, well, fight or blue viagra flee. Alan Goodman, a biological anthropologist at Hampshire College in Amherst, MA, studies stress in prehistoric humans.

He agrees that cortisol and the entire acute stress response system is an evolutionary design. “It’s an ancient mammalian system adapted to protect hunter blue viagra gathers,” says Goodman. Still, getting a window into the daily stress levels of prehistoric humans is difficult because we can’t look at their blood, he says, and cortisol doesn’t preserve well.

Research published in the International Journal of Paleopathology, looked at cortisol accumulation in the hair of 2,000-year-old blue viagra Peruvian mummies and found “repeated exposure to stress.” Another small pilot study of the same population found that hair samples suggest social, physiological, and environmental circumstances “strongly impacted stress levels.” But the research, says Goodman, has its shortcomings. The study authors can’t rule out chemical changes to the samples over time and we’re not sure how accumulation in the hair corresponds to that of the blood. Goodman prefers to look at skeletal indicators of prehistoric stress because cortisol production can also impact bone and teeth metabolism.

He studies ancient populations in the Illinois River Valley from around 1200 AD, during the transition from hunting and blue viagra gathering to farming. “Enamel on the teeth grows like an onion and you can tell from teeth’s layers the years when the body was stressed,” says Goodman. His research shows a stress response likely brought on by the move from blue viagra hunting and gathering to the building of civilizations and establishment of society.

€œLife becomes more complicated because societal structures have a hierarchy,” he says. With the haves and have-nots, the winners and losers, stress becomes more convoluted, no longer confined to immediate threats. Goodman notices this in the teeth as humans blue viagra build societies under chieftains.

Although the enamel stops growing once permanent teeth develop, a growth stunt, known as enamel dysplasia, is frozen in time. Like the rings of a blue viagra tree, you can see the years when life was stressful. This too, says Goodman, is an imperfect model because and malnutrition can also impact enamel production.

But after spending his career studying these populations, Goodman suspects it’s likely a combination of all three. He says that it’s clear stress has been around blue viagra since the dawn of time but today our response has become more prolonged and in some cases, maladaptive. Chronic Disease and Cortisol Production In ancient populations high cortisol levels meant good health, basically indicating that a human could still compete for survival, but in modern populations it can spell disaster.

Sudha Seshadri, a professor of neurology and founder of the Glenn Biggs Institute for blue viagra Alzheimer's &. Neurodegenerative Diseases at the University of Texas Health Science Center in San Antonio, studies the link between neurodegenerative diseases and high cortisol levels. Cortisol levels, she says, should vary throughout the day, highest in the morning when we’re the most active and lowest late at night when we should be sleeping.

If levels don’t vary or are overly elevated in the morning, cortisol production can start to impact blue viagra other parts of the body. €œChronic activation of fight or flight can cause problems in certain regions of the brain,” says Seshadri. Her research blue viagra published in the journal Neurology, has shown that those with higher morning cortisol levels are more likely to have problems with parts of the brain responsible for memory retention like the hypothalamus, which can be an early indicator of dementia and Alzheimer’s disease.

Chronic high cortisol levels are also linked to high blood pressure, heart disease, anxiety, and depression. Reducing Cortisol Levels People respond to stress with different degrees of cortisol activation, says Seshadri, partially based on genetics and partially based on life experiences. €œHyper-activation” of fight blue viagra or flight especially during early childhood, is linked to exaggerated responses to stress later in life.

€œIt’s a vicious cycle, the more you’re exposed to stress, the more likely you are to have an exaggerated response to it,” says Seshadri. For parents, monitoring responses to stress can have blue viagra lifelong implications for children. Studies also suggest that meditation seems to reduce cortisol levels, as does biofeedback, a technique that monitors heart rate, respiration, brain waves, muscle contractions, and perspiration and allows patients to respond to indicators in the moment, building awareness around and slowing their stress response.

Additionally, exercise generates its own positive chemicals for counteracting cortisol like dopamine, norepinephrine, and serotonin. Both Goodman and Seshadri agree that fight or flight is found in both modern blue viagra and prehistoric populations. But it’s meant to help humans rapidly react to a physical threat and then laugh off their brush with death later, not stew all night over a perceived danger that never happens.

“The problem with humans is that we’re symbolic beings, blue viagra constantly finding meaning in situations where there wasn’t any,” Goodman says. Experts contend that cortisol still plays an important role in keeping us safe in our modern world. But the key is dampening your response once the threat has lifted, instead of constantly fearing the imagined sabertooth tiger lunging from around the corner..

The term “mRNA” only entered the average household in the past few months, as Moderna and viagra online canada Pfizer-BioNTech released their erectile dysfunction treatments. But a handful of scientists have spent decades studying this novel approach to immunization. By the start of the viagra the technology was already so advanced that, when Chinese researchers published viagra online canada the genetic sequence for the erectile dysfunction in mid-January, Moderna was able to concoct a treatment within 48 hours.

Clinical trials began a matter of weeks after that. In nine months, the world was well on its way to viral security.It was a stunning debut for mRNA — shorthand for messenger ribonucleic acid, DNA’s viagra online canada sidekick — which had long ranked as a promising but unproven treatment. After this encouraging success, its proponents predict an equally impressive future.

They have always believed in mRNA’s ability to protect against not only the likes of erectile dysfunction, but also a host of deadly diseases that resist traditional treatments, from malaria to HIV to cancer. In 2018, long before the past year’s confidence-boosting display, a viagra online canada group of researchers announced “a new era in vaccinology.”It remains to be seen whether mRNA will live up to the hype. With concrete results attesting to its potential, though, interest is growing among investors and researchers alike.

It helps that regulatory agencies and the public are familiar with it now, viagra online canada too, says Yale immunologist Rick Bucala. €œThat has really changed the landscape.”Andrew Geall, co-founder of one company testing RNA treatments and chief scientific officer of another, notes that mRNA has only just entered its infancy after a long gestation. Such is the nature of scientific progress.

€œWe’ve had the technology bubbling for 20 years, and viagra online canada the major breakthrough is this clinical proof of two treatments,” he says. €œNow we’re set for 10 years of excitement.”Next Steps for mRNAThe goal of any treatment is to train the immune system to recognize and defend against a viagra. Traditional treatments do so by exposing the body viagra online canada to the viagra itself, weakened or dead, or to a part of the viagra, called an antigen.

The new shots, as their name suggests, introduce only mRNA — the genetic material that, as you may remember from high school biology, carries instructions for making proteins. Once the mRNA enters the cells, particles called ribosomes read its instructions and use them to build the encoded proteins. In the case of viagra online canada the erectile dysfunction treatments, those proteins are the crown-shaped “spike” antigens from which the erectile dysfunction derives its name (“corona” means crown in Latin).

By themselves they are harmless, but the immune system attacks them as foreign invaders, and in doing so learns how to ward off the real viagra. If it ever rears its spiky head thereafter, the body will remember and swiftly destroy it.But besides liberating the world from the worst viagra in generations, mRNA viagra online canada could help to vanquish many an intractable illness. If all the dreams of its advocates are realized, the erectile dysfunction treatments may, in hindsight, be only a proof of concept.

In February, for example, Bucala and his colleagues patented a treatment against malaria, which has likely killed more humans than any other single cause and has mostly withstood immunization.Justin Richner, an immunologist with the University of Illinois, Chicago, is developing an mRNA treatment for dengue, another highly resistant viagra. Because mRNA is simply a genetic sequence, scientists can easily tweak it as viagra online canada necessary to find the most effective combination. €œOne of the advantages of the mRNA platform is how it can be so easily modified and manipulated to test novel hypotheses,” Richner says.Read more.

Dengue Fever Is on the Rise — a Ticking Time Bomb in Many Places Around the WorldGeall says the obvious candidates for mRNA treatments include what he calls viagra online canada the “Big 6,” all of which remain crafty foes. Malaria, cancer, tuberculosis HIV, cytomegaloviagra, and respiratory syncytial viagra. His own company, Replicate Bioscience, is working on the cancer front, as are several others, including BioNTech.

Through genetic analysis of individual viagra online canada tumors, patients could one day receive personalized treatments, designed to target the specific mutations afflicting them.Currently, it’s difficult to tell whether an mRNA treatment will work on any particular pathogen. Many have shown promise in animal trials, only to falter in our species. As Geall put it, “mice are not humans.” Some appear to be better bets than others — cytomegaloviagra and RSV respiratory syncytial viagra in particular — but for now, it’s too early to say where mRNA viagra online canada will next bear fruit.

€œDespite all we know about immunology, a lot of it is really empiric,” Bucala says. €œYou just have to try things and see if they work.” The viagra TamerBased on its recent achievements, mRNA’s next act may well involve the next viagra. Perhaps its biggest viagra online canada strength is that it can be manufactured at speeds unheard of in the realm of traditional treatments, making it well-suited to addressing sudden surges of viagraes.

€œOne of the great things about the mRNA field is how quickly you can go from a concept into a therapy that is ready for clinical trials,” Richner says. €œWe can make multiple different treatments and test them in a really rapid process.”Read viagra online canada more. erectile dysfunction treatment.

A Basic Guide to Different treatment Types and How They WorkSince 2018, Pfizer and BioNTech have been working on an mRNA treatment for seasonal flu. Under the status quo, experts must predict which variation of the viagra will pose the greatest threat each viagra online canada year and produce treatments to match it. But because mRNA is so easy to edit, it can be modified more efficiently to keep pace with the ever-mutating strains.

€œI do think the viagra online canada influenza treatment field will be transformed in the not too distant future,” Richner says. A similar kind of gene-based treatment, made with self-amplifying RNA (saRNA), is even more nimble. Whereas basic mRNA treatments — like Moderna’s and Pfizer-BioNTech’s — inject all the genetic material at once, the self-amplifying version replicates itself inside the cell.

Just a small dose of this potent product can trigger the same immune response as a syringe-full of the viagra online canada current shots. Bucala’s malaria treatment and Geall’s cancer treatments both use this technology. €œThe big viagra online canada problem is that treatments don’t prevent s,” Bucala says.

€œVaccinations prevent s.” With saRNA, manufacturers can ensure a lot more of them. After mRNA’s brilliant battle against erectile dysfunction treatment, it’s tempting to think of it as a panacea. But, Bucala says, “Is viagra online canada there something intrinsically revolutionary about mRNA?.

We don’t know yet.”It does come with some logistical challenges. For example, mRNA breaks down easily, so it must be refrigerated viagra online canada throughout the distribution process. Hurdles aside, though, the possibilities are vast, and investment may rise to meet the industry’s ambitions.

treatment development isn’t typically a lucrative business, but erectile dysfunction treatment has made more than a few billionaires, “and others are watching,” Bucala says. €œI think it should become economically viable in our [current] model to get viagra online canada into treatment work again.”Geall agrees. Even if some mRNA endeavors fizzle out, at least a few are bound to make the world proud.

€œThere’s a lot of money out there that is going to be invested into these new approaches,” viagra online canada he says. €œWe’re going to see failures, but we’re going to see successes for sure.”When the U.S. Cracked down on drugs in the 1970s, the effort dried up most funding and research into psychedelic substances — which only in the past few years have regained momentum in the field of psychotherapy.

In the ’70s, rather than shut down all his work, one psychedelic researcher at viagra online canada Johns Hopkins University, Stan Grof, turned his attention to another potential avenue for attaining non-ordinary states of consciousness. Breathing.Grof, alongside his wife at the time, Christina Grof, developed the term Holotropic Breathwork for this technique, which loosely translates as “moving toward wholeness.” The practice in experiential psychotherapy emerged in the 1980s as a tool for self-exploration and inner healing, and has certified teaches who now facilitate it around the world. The framework viagra online canada integrates music with modern consciousness research, psychology and Eastern spiritual practices, according to the Grof Transpersonal Training program.Many people today teach this intense breathing practice, and other similar techniques that preceded it, such as kundalini yoga or pranayama.

But questions remain about the science behind what exactly is happening in the mind and body while practitioners lie on the floor and breathe persistently in rapid patterns. And some clinicians have raised concerns about the safety, and risks, in a field with limited peer-reviewed studies.Meditation on a Freight TrainStacia Butterfield has been a certified Holotropic Breathwork teacher with Grof Transpersonal Training for roughly 15 years. She committed to the work after having her viagra online canada own life-changing experience at a workshop, and has since worked closely with Grof himself and guided thousands of people in the practice.

€œIt’s deceptively simple. It seems viagra online canada like just turning on music, laying down and taking some breaths, and away you go,” Butterfield says. €œWhat we’re actually relying on is the spontaneous mobilization of the psyche.”First and foremost, a guided Holotropic Breathwork session requires creating a safe container, Butterfield says, where people can let go of inhibitions or mental blocks.

Facilitators are trained to guide people through that process in a group setting.One session lasts between two and three hours — often as part of a weekend or week-long retreat. People pair off and alternate in the roles of “sitter” (assisting the other) and “breather” (the viagra online canada person doing the heavy breathing). To begin, rhythmic drumming sets the mood.

The breather lays down and starts breathing rapidly, in a continuous way with no real break between inhales viagra online canada and exhales.The music typically has an emotional arc, almost like a movie soundtrack. It might start off evocative and stimulating, then turn “increasingly dramatic and dynamic, and finally it reaches a breakthrough quality,” according to a guide written by Stan and Christina Grof. This guide notes that when the breathing leads to non-ordinary states of consciousness in a practitioner, “there is a potential for unusually intense projections, including regressed longings for nurturing, sexual contact, or spiritual connection.” Facilitators are advised to assist clients with these feelings as they arise, while following their agreement to conduct the practice in an ethical manner.Butterfield says one core principle, like somatic therapy, is for participants to become aware of the messages and wisdom in their own body.

€œSo many people are so busy, just cruising around [and] keeping the lid on everything else that is going viagra online canada on internally,” she says. €œ[In a session] they can just close their eyes and go inward, and see what’s there.” She says visions, strong bodily sensations and emotions often arise. And she has watched people who had tried years of talk therapy make substantial progress in processing grief and loss, past trauma, life changes or even mental illnesses.One practitioner aptly described this practice as “meditation on viagra online canada a freight train,” Butterfield adds.

The reported dramatic experiences spark questions about what might actually be happening within the body and brain.Mysticism or Hyperventilation?. Pulmonologist Michael Stephen, author of the book Breath Taking, says the practice of Holotropic Breathwork raises red flags for him because of its use of over-breathing, or hyperventilation. Biologically, when someone breathes heavily for an extended period, they can viagra online canada lose too much carbon dioxide, which makes the blood overly alkaline.

The phenomenon often triggers an immediately physiological response. €œWe start to get tingly viagra online canada in our fingers and dizzy when we hyperventilate, as our pH is rising too much,” says Stephen.Prolonged, excessive pH levels in the blood can also cause seizures, he adds. €œJust before seizures happen, you can get lightheaded, a sort of high.” He attributes this to the non-ordinary states of consciousness that people might feel during Holotropic Breathwork.

But he says few proper studies have been done on the practice because of the dangers and ethics involved.Casualties of Heavy BreathingAnother breath specialist and integrative psychiatrist, Patricia Gerbarg, says that Holotropic Breathwork, and other forceful respiratory practices such as breath of fire, do have the potential to alter the mind. They can also bring about a lasting impact on people, but it’s not always beneficial or predictable.“It’s a viagra online canada stress on the system. You’re going through rapid changes in oxygen levels and the balance of various substances in the body and the brain,” she says.

And similar to drugs, “people can use them to viagra online canada attain different mental states,” she adds.Read More. Can Breathing Like Wim Hof Make Us Super Human?. Healthy people tend to have a broader tolerance to endure these shifts and unpredictable outcomes.

But the same behavior can viagra online canada be harmful to someone who is less healthy, or dealing with a psychological disorder, says Gerbarg, who teaches psychiatry at New York Medical College.“Those kinds of intense, rapid shifts in your brain chemistry can cause adverse effects,” she says, adding that she is familiar with cases where people feel they “never recovered” from what these states did to them. Some literature uses the term kundalini psychosis, or physio kundalini syndrome, to describe people who cognitively lose touch with reality in pursuit of "spiritual awakening."One of Gerbarg’s concerns about the rise in popularity of these advanced, Eastern breathing practices is how they are inserted into the Western world and modern mindset. (Two other intense and forceful breathing practices include Tummo breathing, with a Tibetan buddhist lineage, and the Wim Hof Method.) The breathwork is often tied closely to a lifestyle and belief viagra online canada system, and many traditional practitioners dedicate hours a day for many years to master the techniques in a healthy way.

Alternatively, people in modern Western cultures often struggle to commit to a new practice for 20 minute a day. €œ[Intense breathwork] is becoming increasingly popular and people are doing it online,” Gerbarg says. €œThey aren’t often aware viagra online canada that there are risks,” or they might not know the pre-existing conditions their students have.

The big responsibility ultimately falls on the teachers and facilitators to ensure everyone is safe. A Gentler TouchGerbarg and her husband Richard Brown, a professor of psychiatry at Columbia College of Physicians and Surgeons, have published several books viagra online canada on the healing potential of breath. And they offer evidence-based workshops and teaching resources through their Breath-Body-Mind Foundation.One of their most popular techniques, called coherent breathing, teaches gentle, slower and relaxed respiration.

Once practitioners learn it, they can use it any point throughout the day when stress or anxiety is likely to rise up — even in mundane circumstances like being stuck in a long line — and trigger a string of reactions in the body.The goal is to inhale and exhale slowly through the nose at a rate of about five breaths per minute, or one breath cycle every 12 seconds. Gerbarg says this process can promptly activate the rest-and-restore parasympathetic nervous system throughout the body, with millions of reactions and viagra online canada signals firing every second.Read More. How Slow, Deep Breathing Taps Into a Natural Rhythm in Our Bodies“It tells the brain, ‘the conditions are safe,’ ” she says.

€œThe less effort, the more you get out of this one.”The viagra online canada results of this technique may not feel like the freight-train experience of altered consciousness. But it carries less risk and broader appeal to anyone interested in channeling their own breath for health and wellness.In a year marked by a viagra, economic downturn, racial unrest, and an election that culminated with a mob storming the U.S. Capitol, we’ve come face to face with stressors we could never have imagined prior to 2020.

The causes and health impacts of stress have been widely discussed as have a host of tools for tackling the mounting anxiety we feel in our daily viagra online canada lives. But cortisol, among the body’s most important steroid hormones, at the helm of our stress response, remains largely a mystery. Is our fight-or-flight response really tied to viagra online canada our prehistoric ancestors?.

Has our modern world evolved beyond the antiquated workings of our endocrine system?. Here’s what we know. A Caveman Instinct? viagra online canada.

Cortisol, along with epinephrine and norepinephrine, activate the body’s sympathetic nervous system, triggering a lineup of physiological responses that speed up respiration, constrict blood vessels, dilate pupils, and slow down the digestive system. It’s called viagra online canada a fight-or-flight response, and it allows muscles to react more powerfully and move faster, priming us to, well, fight or flee. Alan Goodman, a biological anthropologist at Hampshire College in Amherst, MA, studies stress in prehistoric humans.

He agrees that cortisol and the entire acute stress response system is an evolutionary design. “It’s an ancient mammalian system adapted to protect hunter gathers,” viagra online canada says Goodman. Still, getting a window into the daily stress levels of prehistoric humans is difficult because we can’t look at their blood, he says, and cortisol doesn’t preserve well.

Research published in the International Journal of Paleopathology, looked at cortisol accumulation in the viagra online canada hair of 2,000-year-old Peruvian mummies and found “repeated exposure to stress.” Another small pilot study of the same population found that hair samples suggest social, physiological, and environmental circumstances “strongly impacted stress levels.” But the research, says Goodman, has its shortcomings. The study authors can’t rule out chemical changes to the samples over time and we’re not sure how accumulation in the hair corresponds to that of the blood. Goodman prefers to look at skeletal indicators of prehistoric stress because cortisol production can also impact bone and teeth metabolism.

He studies ancient populations in the Illinois River Valley from around viagra online canada 1200 AD, during the transition from hunting and gathering to farming. “Enamel on the teeth grows like an onion and you can tell from teeth’s layers the years when the body was stressed,” says Goodman. His research shows a stress viagra online canada response likely brought on by the move from hunting and gathering to the building of civilizations and establishment of society.

€œLife becomes more complicated because societal structures have a hierarchy,” he says. With the haves and have-nots, the winners and losers, stress becomes more convoluted, no longer confined to immediate threats. Goodman notices this in the teeth as humans build societies under chieftains viagra online canada.

Although the enamel stops growing once permanent teeth develop, a growth stunt, known as enamel dysplasia, is frozen in time. Like the rings of viagra online canada a tree, you can see the years when life was stressful. This too, says Goodman, is an imperfect model because and malnutrition can also impact enamel production.

But after spending his career studying these populations, Goodman suspects it’s likely a combination of all three. He says that it’s clear stress has been around since the dawn of time but today our response has become more prolonged and viagra online canada in some cases, maladaptive. Chronic Disease and Cortisol Production In ancient populations high cortisol levels meant good health, basically indicating that a human could still compete for survival, but in modern populations it can spell disaster.

Sudha Seshadri, a professor of neurology and founder of the Glenn viagra online canada Biggs Institute for Alzheimer's &. Neurodegenerative Diseases at the University of Texas Health Science Center in San Antonio, studies the link between neurodegenerative diseases and high cortisol levels. Cortisol levels, she says, should vary throughout the day, highest in the morning when we’re the most active and lowest late at night when we should be sleeping.

If levels viagra online canada don’t vary or are overly elevated in the morning, cortisol production can start to impact other parts of the body. €œChronic activation of fight or flight can cause problems in certain regions of the brain,” says Seshadri. Her research published in the journal Neurology, has shown that those viagra online canada with higher morning cortisol levels are more likely to have problems with parts of the brain responsible for memory retention like the hypothalamus, which can be an early indicator of dementia and Alzheimer’s disease.

Chronic high cortisol levels are also linked to high blood pressure, heart disease, anxiety, and depression. Reducing Cortisol Levels People respond to stress with different degrees of cortisol activation, says Seshadri, partially based on genetics and partially based on life experiences. €œHyper-activation” of fight or flight especially during early childhood, is linked to exaggerated viagra online canada responses to stress later in life.

€œIt’s a vicious cycle, the more you’re exposed to stress, the more likely you are to have an exaggerated response to it,” says Seshadri. For parents, monitoring responses viagra online canada to stress can have lifelong implications for children. Studies also suggest that meditation seems to reduce cortisol levels, as does biofeedback, a technique that monitors heart rate, respiration, brain waves, muscle contractions, and perspiration and allows patients to respond to indicators in the moment, building awareness around and slowing their stress response.

Additionally, exercise generates its own positive chemicals for counteracting cortisol like dopamine, norepinephrine, and serotonin. Both Goodman and Seshadri agree viagra online canada that fight or flight is found in both modern and prehistoric populations. But it’s meant to help humans rapidly react to a physical threat and then laugh off their brush with death later, not stew all night over a perceived danger that never happens.

“The problem with humans is that we’re viagra online canada symbolic beings, constantly finding meaning in situations where there wasn’t any,” Goodman says. Experts contend that cortisol still plays an important role in keeping us safe in our modern world. But the key is dampening your response once the threat has lifted, instead of constantly fearing the imagined sabertooth tiger lunging from around the corner..

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Noch 2 Tage gültig
WAZ
Noch 2 Tage gültig
WAZ
Noch 2 Tage gültig
WAZ
Noch 2 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 3 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 4 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 5 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ
Noch 6 Tage gültig
WAZ