diabetestalk.net

Can Ssri Cause Hypoglycemia?

Serotonin Syndrome

Serotonin Syndrome

What is serotonin syndrome? Serotonin syndrome is a potentially serious negative drug reaction. It’s believed to occur when too much serotonin builds up in your body. Nerve cells normally produce serotonin. Serotonin is a neurotransmitter, which is a chemical. It helps regulate: digestion blood flow body temperature breathing It also plays an important role in the proper functioning of nerve and brain cells and is believed to impact mood. If you take different prescribed medications together, you may end up with too much serotonin in your body. The types of medication that could lead to serotonin syndrome include those used to treat depression and migraine headaches, and manage pain. Too much serotonin can cause a variety of mild to severe symptoms. These symptoms can affect the brain, muscles, and other parts of the body. Serotonin syndrome can occur when you start a new medication that interferes with serotonin. It can also occur if you increase the dosage of a medication you’re already taking. The condition is most likely to occur when two or more drugs are taken together. Serotonin syndrome can be fatal if you don’t receive prompt treatment. You may have symptoms within minutes or hours of taking a new medication or increasing the dose of an existing medication. The symptoms may include: confusion disorientation irritability anxiety muscle spasms muscle rigidity tremors shivering diarrhea rapid heartbeat, or tachycardia high blood pressure nausea hallucinations overactive reflexes, or hyperreflexia dilated pupils In more severe cases, the symptoms may include: unresponsiveness coma seizures irregular heartbeat Typically, the condition occurs when you combine two or more medications, illicit drugs, or nutritional supplements that increase serotonin levels. For Continue reading >>

Acute Effect Of Different Antidepressants On Glycemia In Diabetic And Non-diabetic Rats

Acute Effect Of Different Antidepressants On Glycemia In Diabetic And Non-diabetic Rats

R. Gomez, J. Huber, G. Tombini and H.M.T. Barros Divisão de Farmacologia, Fundação Faculdade Federal de Ciências Médicas de Porto Alegre, Porto Alegre, RS, Brasil Diabetic patients have a 20% higher risk of depression than the general population. Treatment with antidepressant drugs can directly interfere with blood glucose levels or may interact with hypoglycemic agents. The treatment of depression in diabetic patients must take into account variations of glycemic levels at different times and a comparison of the available antidepressant agents is important. In the present study we evaluated the interference of antidepressants with blood glucose levels of diabetic and non-diabetic rats. In a first experiment, male adult Wistar rats were fasted for 12 h. Imipramine (5 mg/kg), moclobemide (30 mg/kg), clonazepam (0.25 mg/kg), fluoxetine (20 mg/kg) sertraline (30 mg/kg) or vehicle was administered. After 30 min, fasting glycemia was measured. An oral glucose overload of 1 ml of a 50% glucose solution was given to rats and blood glucose was determined after 30, 60 and 90 min. Imipramine and clonazepam did not change fasting or overload glycemia. Fluoxetine and moclobemide increased blood glucose at different times after the glucose overload. Sertraline neutralized the increase of glycemia induced by oral glucose overload. In the second experiment, non-diabetic and streptozotocin-induced diabetic rats were fasted, and the same procedures were followed for estimation of glucose tolerance 30 min after glucose overload. Again, sertraline neutralized the increase in glycemia after glucose overload both in diabetic and non-diabetic rats. These data raise the question of whether sertraline is the best choice for prolonged use for diabetic individuals, because of its antihyperg Continue reading >>

Antidepressants That Cause High Blood Sugar

Antidepressants That Cause High Blood Sugar

High blood sugar--abnormal, even dangerous levels of sugar in the blood--is known as hyperglycemia and is most often associated with the disease diabetes mellitus. However, different types of medications may also cause high blood sugar; this is sometimes known as medication-induced, or drug-induced, diabetes. Within the list of drugs are several medications that are used to treat depression. While only one medication is officially considered an "antidepressant," certain antipsychotics--which may also be used in the treatment of depression--may cause hyperglycemia as well. Video of the Day Fluoxetine is a commonly-used antidepressant; it belongs to a class called the “serotonin-specific reuptake inhibitors,” and may also be known by one of its brand names, Prozac. It is used to treat both depression that occurs as a result of major depressive disorder and, in combination with the antipsychotic medication olanzepine, to treat the depression that may occur in patients with bipolar disorder. In addition to its effects on blood sugar levels, fluoxetine may Medline Plus reports that fluoxetine can cause nausea, lack of appetite, weight loss, nervousness, and changes in sex drive. The medical reference UpToDate reports that in patients with diabetes, fluoxetine affects blood sugar regulation in an interesting way. Patients who take fluoxetine may have more episodes of hypoglycemia, or low blood sugar--but when they stop taking fluoxetine, instead of their blood sugar reaching normal levels, patients’ blood sugar level goes above normal. This is called hyperglycemia, and this observation suggests that fluoxetine is somehow impacting the blood sugar regulation mechanism of patients with diabetes. Because of this, a patient who is taking medication for his diabetes and is a Continue reading >>

The Selective Serotonin Reuptake Inhibitor Sertraline Enhances Counterregulatory Responses To Hypoglycemia

The Selective Serotonin Reuptake Inhibitor Sertraline Enhances Counterregulatory Responses To Hypoglycemia

Go to: Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed for patients with comorbid diabetes and depression. Clinical case studies in diabetic patients, however, suggest that SSRI therapy may exacerbate hypoglycemia. We hypothesized that SSRIs might increase the risk of hypoglycemia by impairing hormonal counterregulatory responses (CRR). We evaluated the effect of the SSRI sertraline on hormonal CRR to single or recurrent hypoglycemia in nondiabetic rats. Since there are time-dependent effects of SSRIs on serotonin neurotransmission that correspond with therapeutic action, we evaluated the effect of 6- or 20-day sertraline treatment on hypoglycemia CRR. We found that 6-day sertraline (SERT) treatment specifically enhanced the epinephrine response to a single bout of hypoglycemia vs. vehicle (VEH)-treated rats (t = 120: VEH, 2,573 ± 448 vs. SERT, 4,202 ± 545 pg/ml, P < 0.05). In response to recurrent hypoglycemia, VEH-treated rats exhibited the expected impairment in epinephrine secretion (t = 60: 678 ± 73 pg/ml) vs. VEH-treated rats experiencing first-time hypoglycemia (t = 60: 2,081 ± 436 pg/ml, P < 0.01). SERT treatment prevented the impaired epinephrine response in recurrent hypoglycemic rats (t = 60: 1,794 ± 276 pgl/ml). In 20-day SERT-treated rats, epinephrine, norepinephrine, and glucagon CRR were all significantly elevated above VEH-treated controls in response to hypoglycemia. Similarly to 6-day SERT treatment, 20-day SERT treatment rescued the impaired epinephrine response in recurrent hypoglycemic rats. Our data demonstrate that neither 6- nor 20-day sertraline treatment impaired hormonal CRR to hypoglycemia in nondiabetic rats. Instead, sertraline treatment resulted in an enhancement of hypoglycemia CRR and prevented the impaired adr Continue reading >>

Antidepressants Not Depression Associated With Obesity

Antidepressants Not Depression Associated With Obesity

There is a major contributor to the so-called "obesity epidemic" which never gets cited in the press--the antidepressant drugs which are the most frequently prescribed class of drugs in the pharmacopoeia. Now a study that analyzes data from the Canadian National Population Health Survey (NPHS), a longitudinal study of a representative cohort of household residents in Canada, finds a strong correlation between the use of SSRIs, Effexor, and the development obesity. Lest you think that this is because depression makes people fat, this same study found no correlation between a history of a major depressive episode and the development of obesity. It's the drugs, folks. Here's the study: Major Depression, Antidepressant Medication and the Risk of Obesity Scott B. Patten et al. Psychother Psychosom 2009;78:182-186 (DOI: 10.1159/000209349) Vol. 78, No. 3, 2009 How widespread use of these antidepressant drugs is, is very hard to pin down. Anecdotally, it sometimes seems like everyone who has good health insurance is on them. A report published in 2005 that analyzed Canadian data reported that "...one in five women (19%) in the province over the age of thirty received at least one prescription for SSRIs in the period between August 1, 2002 and July 30, 2003." Canada's public health system controls access to prescriptions in the way the US system does not. The data for the US is 7 years old and at that time the CDC reported that 1 in 10 American Women were taking antidepressants which were the single most highly prescribed class of drugs in the US. That 2002 report also reported that antidepressant use had tripled over the previous decade, which makes it likely that antidepressant use has risen significantly in the 7 years since those statistics were analyzed. The Canadian report Continue reading >>

Neonate Characteristics After Maternal Use Of Antidepressants In Late Pregnancy

Neonate Characteristics After Maternal Use Of Antidepressants In Late Pregnancy

Background Exposure to antidepressants during the third trimester of pregnancy has been associated with an increased risk for adverse birth outcomes, including preterm birth, respiratory distress, and hypoglycemia. Objective To investigate neonatal outcomes in 997 infants (987 mothers) after maternal use of antidepressants based on prospectively recorded information in antenatal care documents. Results An increased risk for preterm birth (odds ratio [OR], 1.96) and low birth weight (OR, 1.98) was verified, but the gestational week-specific birth weight was increased notably after exposure to tricyclic antidepressants. An increased risk for a low Apgar score (OR, 2.33), respiratory distress (OR, 2.21), neonatal convulsions (OR,1.90), and hypoglycemia (OR, 1.62) was found, the latter especially after exposure to tricyclic drugs, but no significant effect on the frequency of neonatal jaundice was seen (OR, 1.13). Most effects seemed not to be selective serotonin reuptake inhibitor drug specific, and outcomes after exposure to paroxetine hydrochloride were not worse than after exposure to other selective serotonin reuptake inhibitors. Conclusions Neonatal effects after maternal use of antidepressant drugs during late pregnancy were seen. Selective serotonin reuptake inhibitors may be the drugs of choice during pregnancy. Some studies1- 8 have been published on the occurrence of birth defects after maternal use of antidepressants without any certain teratogenic effect being demonstrable. Less is published on the neonatal outcome besides birth defects, and published studies are all small. Most studies4,7,9 have found evidence for increased rates of premature delivery; admission to special-care nurseries; poor neonatal adaptation, including respiratory difficulties; low Apgar Continue reading >>

Important Safety Information

Important Safety Information

ZYVOX® (linezolid) should not be used if you have any known allergies or hypersensitivity to linezolid or any of the other product components. ZYVOX should not be used in patients taking any medicines which inhibit monoamine oxidases A or B (e.g. phenelzine, isocarboxazid) or within 2 weeks of taking any such product. Before you use ZYVOX talk to your doctor if you have a history of anemia (low hemoglobin), thrombocytopenia (low platelets), neutropenia (low white blood cells), a history of bleeding problems, or any other blood related disorders. Tell your doctor if you experience changes in vision as nerve injury has been reported in patients taking ZYVOX longer than 28 days. You may want to undergo an eye examination to see if you are at risk and discuss the continued use of ZYVOX with your doctor. Before taking ZYVOX, tell your doctor if you take a serotonin re-uptake inhibitor (SSRI) for depression or other antidepressants. Taking ZYVOX with antidepressants can cause serious or even life-threatening side effects. Do not take ZYVOX within 14 days of stopping an antidepressant SSRI. Associated diarrhea has been reported with use of nearly all antibacterial agents, including ZYVOX, and may range in severity from mild diarrhea to fatal colitis. Tell your doctor right away if you experience severe diarrhea, even after you have stopped taking ZYVOX. You may need to be monitored for increases in blood pressure. Tell your doctor about all the medical conditions you have or had including uncontrolled high blood pressure or history of hypertension. Tell your doctor about all the prescription and over the counter medications you are taking or plan to take including cold remedies and decongestants such as pseudoephedrine HCl or phenylpropanolamine HCl. Tell your doctor or seek Continue reading >>

Hypoglycemia Associated Autonomic Failure In Type 1 Diabetes Mellitus (dm)

Hypoglycemia Associated Autonomic Failure In Type 1 Diabetes Mellitus (dm)

Exercise is a cornerstone of diabetes management. It helps reduce blood pressure, promote weight loss, lower insulin resistance and improve glucose and lipid (triglyceride and HDL-cholesterol) profiles. Unfortunately, the benefits of exercise are often not embraced by diabetic individuals because of the fear of low blood sugar (hypoglycemia). My laboratory has demonstrated that Autonomic nervous system (ANS) counterregulatory failure plays an important role in exercise associated hypoglycemia in Type 1 DM. ANS responses are significantly reduced in Type 1 DM and are further blunted by antecedent episodes of hypoglycemia. Furthermore, there is a large sexual dimorphism of reduced ANS responses during submaximal exercise in both Type 1 DM and healthy individuals that is unexplained. Accumulating data are demonstrating that serotonergic pathways can regulate ANS discharge. Generally, serotonergic pathways are inhibitory but both single and longer term administration of selective serotonin reuptake inhibitors (SSRI's) such as Prozac has been demonstrated to increase basal epinephrine levels and enhance baroreflex control of Sympathetic nervous system (SNS) activity. What is unknown is whether fluoxetine can also enhance SNS responses and also override the large ANS sexual dimorphism present during sub maximal exercise. Therefore, the purpose of this study is to determine if the SSRI fluoxetine (Prozac) can improve SNS responses during exercise. Study Type : Interventional (Clinical Trial) Estimated Enrollment : 64 participants Allocation: Randomized Intervention Model: Crossover Assignment Masking: Double (Participant, Investigator) Primary Purpose: Treatment Official Title: Hypoglycemia Associated Autonomic Failure in Type 1 DM, SSRI and Exercise Study Start Date : October Continue reading >>

Antidepressant Discontinuation Syndrome

Antidepressant Discontinuation Syndrome

Not to be confused with Serotonin syndrome. Antidepressant discontinuation syndrome is a condition that can occur following the interruption, dose reduction, or discontinuation of antidepressant drugs, including selective serotonin re-uptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs). The symptoms can include flu-like symptoms and disturbances in sleep, senses, movement, mood, and thinking. In most cases symptoms are mild, short-lived, and resolve without treatment. More severe cases may be successfully treated by reintroduction of the drug, provided reintroduction is done in a timely fashion. Symptoms, including tardive akathisia, and Post SSRI Sexual Dysfunction (PSSD) may persist for months to years, yet may spontaneously resolve after prolonged presence. Signs and symptoms[edit] People with discontinuation syndrome have been on an antidepressant for at least four weeks and have recently stopped taking the medication, whether abruptly, after a fast taper, or each time the medication is reduced on a slow taper.[1] Commonly reported symptoms include flu-like symptoms (nausea, vomiting, diarrhea, headaches, sweating) and sleep disturbances (insomnia, nightmares, constant sleepiness). Sensory and movement disturbances have also been reported, including imbalance, tremors, vertigo, dizziness, and electric-shock-like experiences in the brain, often described by sufferers as "brain zaps". Mood disturbances such as dysphoria, anxiety, or agitation are also reported, as are cognitive disturbances such as confusion and hyperarousal. In cases associated with sudden discontinuation of MAO inhibitors, acute psychosis has been observed.[1][2][3] Over fifty symptoms have been reported.[4] Most cases of discontinuation syndrome last between one and Continue reading >>

Antidepressants Cause 40,000 Deaths A Year - But They're Handed Out Like Candy

Antidepressants Cause 40,000 Deaths A Year - But They're Handed Out Like Candy

My recent article on the dangers of psychiatric drugs ignited a firestorm of controversy. Part of the outrage may have been caused by some general misunderstandings, which I hope to clear up here. This is particularly important at this time as it is abundantly clear that suicide rates rise as the economy worsens. The image of people jumping from windows after the stock market crash of 1929 graphically illustrates this risk. Many may not agree, but I have been studying the economy for over 30 years now and it seems crystal clear to me that the economy has yet to hit bottom, and this will only serve to increase the risk of depression. My Personal Experiences with Depression First of all, I would like to set the record straight as many were confused about my personal experiences with depression. They believed I had none, and therefore there is no way I could understand this disease. Well let me tell you, nothing could be further from the truth. Mental and emotional problems exact an extreme toll on family units and in some cases extended circles of friends. I've personally been a witness to the struggles of two people near and dear to me who suffered from deep chronic depression for a number of years that actually resulted in multiple suicide attempts. Suicide is a common complication of depression, and is one of the primary reasons why it must be taken seriously as it can become a terminal illness. Many also might be unaware that I was a full-time practicing physician for over 20 years before I determined that I could help more people by committing myself full time to this newsletter and web site, than treating patients one on one. Before making that choice however, I treated tens of thousands of people for all sorts of problems, and I've seen my fair share of depressed p Continue reading >>

Effects Of A Selective Serotonin Reuptake Inhibitor, Fluoxetine, On Counterregulatory Responses To Hypoglycemia In Healthy Individuals

Effects Of A Selective Serotonin Reuptake Inhibitor, Fluoxetine, On Counterregulatory Responses To Hypoglycemia In Healthy Individuals

OBJECTIVE—Hypoglycemia commonly occurs in intensively-treated diabetic patients. Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk for further hypoglycemic events. Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not been established. Therefore, the specific aim of this study was to test the hypothesis that 6 weeks’ administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine would amplify autonomic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia. RESEARCH DESIGN AND METHODS—A total of 20 healthy (10 male and 10 female) subjects participated in an initial single-step hyperinsulinemic (9 pmol · kg−1 · min−1)-hypoglycemic (means ± SE 2.9 ± 0.1 mmol/l) clamp study and were then randomized to receive 6 weeks’ administration of fluoxetine (n = 14) or identical placebo (n = 6) in a double-blind fashion. After 6 weeks, subjects returned for a second hypoglycemic clamp. Glucose kinetics were determined by three-tritiated glucose, and muscle sympathetic nerve activity (MSNA) was measured by microneurography. RESULTS—Despite identical hypoglycemia (2.9 ± 0.1 mmol/l) and insulinemia during all clamp studies, key ANS (epinephrine, norepinephrine, and MSNA but not symptoms), neuroendocrine (cortisol), and metabolic (endogenous glucose production, glycogenolysis, and lipolysis) responses were increased (P < 0.01) following fluoxetine. CONCLUSIONS—This study demonstrated that 6 weeks’ administration of the SSRI fluoxetine can amplify a wide spectrum of ANS and metabolic counterregulatory responses during hypoglycemia in healthy individuals. These data further suggest that serotonergic transmission may be an important mechani Continue reading >>

Call Us: 303-973-3529

Call Us: 303-973-3529

Most of these supplements can be found on-line, at your local pharmacy or vitamin store, or through a number of supplement companies. We have included the link to a website for Xymogen, which is a supplement company that Dr. Jill Quigley and Eric Adrid, PA-C have reviewed and found to be a reliable source for supplements. Please check with your provider prior to starting supplements to make sure they will benefit you and will not interact with other medications or supplements you are taking. Your provider will inform you of the dose of each supplement that you should take. If you are interested in purchasing supplements online, please speak to your medical provider about how to create your online account. Alpha Lipoic Acid: Antioxidant, helps turn glucose into energy Can cause permanent hypothyroidism when dose greater than 1800mg/day is taken Beta-glucan: Fiber from cell walls; decreases hunger; also lowers LDL and A1c and increases HDL No known side effects Not available through Metagenics Chromium (Trivalent Chromium Picolinate): Improves the efficiency of insulin; improves fat loss with muscle sparing Can cause hypoglycemia so do not use if not overweight Green Tea Extract (Epigallocatechin Gallate (EGCG): Releases norepinephrine at the hypothalamus (like phentermine) Can cause abnormal liver function tests (AST and ALT) Requires a good supplement company to ensure extraction of ingredient Green Coffee Extract (Chlorogenic Acid): Increases production of norepinephrine at the hypothalamus (like phentermine) No serious side effects noted; side effects are those associated with caffeine Standardization and extraction is important, so make sure a good company makes it; should say chlorogenic acids, not green coffee extracts on ingredients 5-Hydroxytryptophan (5-HTP): Co Continue reading >>

Can Prozac Affect My Blood Sugar Levels?

Can Prozac Affect My Blood Sugar Levels?

Hi. It’s Jenny at AnxietyBoss.com. Our question today is from Donna in Columbus, Ohio. Can Prozac affect my blood sugar levels? Although Prozac serves as a superb drug for depression, little research has actually been done on its side effects on those who suffer from diabetes or those who are looking to reduce their blood sugar levels. Now because of this, many doctors who prescribe anti-depressants to their patients are not aware of the possibility that SSRIs or Selective Serotonin Reuptake Inhibitors can actually lower blood sugar levels. When this occurs, patients may find that it’s necessary to decrease the amount of diabetes medication that they’re taking. In accordance to Prozac’s drug label which is posted on the FDA website, in patients with diabetes, Prozac may alter glycemic control. Hypoglycemia has occurred during therapy with Prozac and Hyperglycemia has developed following discontinuation of the drug. As is true with many other types of medication when taken concurrently by patients with diabetes, insulin and oral hypoglycemic dosage may need to be adjusted when therapy with Prozac is instituted or discontinued. Continue reading >>

Celexa Induced Hypoglycemia

Celexa Induced Hypoglycemia

Abstract: 56-year-old African-American male from nursing home was admitted to the hospital with an acute drop in his hemoglobin concentration to 5.6 mg/dL (baseline Hgb of 10 mg/dL). His past medical history was notable for type 2 diabetes controlled with diet, end-stage renal disease on hemodialysis (HD), hepatitis B and C, HIV (last viral load undetectable), hypertension and depression. His nursing home medications included aspirin, hydralazine, lisinopril, lamivudine, zidovudine, raltegravir and sertraline. Patient received packed red cell transfusion and an upper endoscopy/colonoscopy showed clean shallow ulcer at ileocecal valve. During his hospital course, patient became increasingly somnolent and sertraline was switched to citalopram 20 mg oral daily. A week later, he started complaining of sweating, tremors, anxiety and agitation with random glucose values ranging from 37 to 56 mg/dL (both before and after meals) that were confirmed with venous blood samples. Hypoglycemia was relieved with meals. Common causes of hypoglycemia were ruled out by thyroid and liver related tests, anti-insulin antibodies, adrenal insufficiency, insulinoma and surreptious abuse of sulfonylureas or insulin. His 72-hour fast was aborted, as he had low glucose of 45 at the end of 36 hours. Patient was experiencing new onset hypoglycemia and the only change made was addition of citalopram. Hence, because of rare reports of citalopram induced hypoglycemia this medication was discontinued, and within 24 hours patient's daily hypoglycemia episodes ceased. Citalopram (Celexa) is a selective serotonin reuptake inhibitor (SSRI) commonly used in the treatment of depression in diabetics. Within the class of SSRI's hypoglycemia is rarely reported. We found 2 case reports of citalopram causing hypo Continue reading >>

The Serotonin Connection

The Serotonin Connection

By Jurriaan Plesman, BA(Psych), Post Grad Dip Clin Nutr I will attempt to describe briefly The Serotonin Connection as asequence of psychological and biochemical events in the development of emotional disorders. Most of the statements below can be verified by scientific studies, but some are still controversial, especially the relationship between insulin resistance and absorption of amino acids. Much research needs to be done in this area. The events appear to follow a predetermined sequence as follows; 1) An extended period of physical or psychological stress, will produce stress hormones such as cortisol and adrenaline, that can interfere with the synthesis of the brain neurotransmitter, Serotonin. 2) A neurotransmitter is any one of numerous chemicals that occupy the gap (synapse) between two or more nerve cells (neurons) and thereby allows the triggering of a tiny electrical currents in adjacent cells. Each neurotransmitter fits into a unique receptor – like a key fitting into a lock – thus allowing messages to be carried along nerve pathways. See Figure 1 3) Serotonin is a neurotransmitter that conveys the positive sensations of satiety, satisfaction and relaxation. It regulates appetite and when converted to melatonin helps us to sleep. 4) A deficiency of Serotonin in the brain can cause endogenous depression, upsets the appetite mechanism and may lead to obesity or other eating disorders such as anorexia and bulimia nervosa and may be responsible for insomnia. Doctors usually prescribe Selective Serotonin Reuptake Inhibitors (SSRIs) which have the effects of increasing the amount Serotonin and thereby medically treat the above conditions. Unfortunately, SSRIs may have side effects in some patients, and generally do not address the underlying biochemical caus Continue reading >>

More in diabetes