You are likely in Cymbalta Duloxetine withdrawal at the moment. This page gives you quick solutions to the existing Cymbalta Duloxetine withdrawal side effects and gives guidance on how to proceed with a safe and effective Cymbalta Duloxetine withdrawal.
The most debilitating Cymbalta Duloxetine withdrawal side effect is something called brain zaps. An electrical jolt that usually starts at the base of the skull and feels like it runs into the brain. Cymbalta Duloxetine brain zaps is the leading cause of people stopping the Effexor Venlafaxine withdrawal process and they go back on a higher dosage of the Effexor Venlafaxine in the hope of relief.
What to do: Go to any store that sells supplements and look for omega 3 fish oil. Select a bottle that is highest in EPA. Look at the back label and you will see the amount of DHA and EPA per serving. Choose the one that is highest in EPA. Ideally, around 400mg per softgel in EPA works the best.
Take 4 softgels as soon as you can, and you should begin to feel relief from the Cymbalta Duloxetine withdrawal brain zaps. We will provide long-term solutions for you later on this page.
Nausea from Cymbalta Duloxetine withdrawal – While at the store getting the omega 3, get a box of ginger tea. Drink at least 2 cups of ginger tea a day and the nausea should ease.
Doing the two suggestions above will help you begin to feel better quickly but there are a few other things you will need to do for a successful Cymbalta Duloxetine withdrawal.
Next – Go back up to the last Cymbalta Duloxetine dosage you felt stable at. Hopefully, it was the last dosage you reduced from. If you were not stable when you reduced the last dosage of Cymbalta Duloxetine, you need to consider going back up further on the Effexor Venlafaxine. Let your prescribing physician know what you are going to do. The sooner you go back up to the last dosage you felt stable on the Cymbalta Duloxetine the better off you will be.
You may feel hesitant about going back up on the Cymbalta Duloxetine dosage because you do not want to lose the ground you have gained but there really is not another option for you. The further you proceed doing what you have been doing the harder it will be to dig out of the Cymbalta Duloxetine withdrawal side effects.
Again, go back up on the Effexor Venlafaxine and get stable.
Cymbalta Duloxetine Withdrawal Timeline
Cymbalta Duloxetine needs to be reduced by no more than 10% of the original dosage every 2 weeks. However, you should not reduce Cymbalta after 2 weeks if you are having Cymbalta withdrawal side effects. You need to remain on that dosage until you feel very stable.
How to reduce Cymbalta
Reducing Cymbalta
With Cymbalta being a time-release medication, you have one choice.
Open 1 capsule of the Cymbalta and count the balls inside of the capsule. As an example, let’s say there are 60 balls in the capsule. To reduce the Cymbalta by 10 percent, you will remove 6 of the balls. The next reduction you will remove 12 of the Cymbalta balls and the next reduction you will remove 18 of the Cymbalta balls. Just remove an additional 6 Cymbalta balls with each reduction.
When you are opening the Cymbalta and removing the balls you should wear sterile gloves. Do not reuse the gloves. You want to avoid the chance you will get body oil on the Cymbalta balls.
Here is an example you might follow for removing the Cymbalta from the capsule.
Put on your clean gloves.
Get a clean saucer or bowl.
Pour the Cymbalta into the saucer or into the bowl.
Remove 6 of the Cymbalta and discard them.
Now you have the remaining 54 balls of Cymbalta. If you can put them back into the original Cymbalta capsule do that. Make sure the capsule is sealed tightly again.
If you can’t use the original capsule again, you will need to put the Cymbalta balls into applesauce. Mott’s applesauce is the recommended brand to use.
Get a tablespoon and fill with the applesauce and then pour the Cymbalta onto the top of the applesauce.
When you take the Cymbalta balls and applesauce, DO NOT CHEW THE BALLS. THIS IS VERY IMPORTANT. You want the Cymbalta balls to slowly release as they would normally.
The Mott’s applesauce gives you the same pH level as you would with taking the Cymbalta in a capsule. Keeping the pH level the same in your gut is what makes the Cymbalta breakdown slowly just as they are intended to do.
I would go to Walmart or a pharmacy and pick up a pill container that gives you 14 days’ worth of slots. Using the 60 Cymbalta balls as an example and removing 6 of the Cymbalta balls, open the first container slot and put 54 Cymbalta balls into it and snap the lid shut. Then do the other 13 days’ worth of Cymbalta balls. This way you only need to go through this process once every 14 days, instead of every day.
Since you are changing how the Cymbalta is being taken, your first 14 days of the Cymbalta taper should be taking the entire 60 Cymbalta balls for 14 days. Again, this allows you to know if there is any reaction, it is from taking the Cymbalta balls with applesauce and not a reduction reaction.
Using either of the two options above gives you a 50% chance of completing the Cymbalta withdrawal. Are you shocked by such a low percentage? Probably so. So were we in the early 2000’s when we first developed this withdrawal program.
We were assisting hundreds of thousands off Cymbalta and 50% of the people simply went back up on the Cymbalta and stayed on the Cymbalta due to withdrawal.
The other 50% made it off the Cymbalta but still struggled with Cymbalta withdrawal side effects. Most eventually went back on the Cymbalta to get relief.
In 2004, Jim Harper started a DNA testing laboratory with the hope of finding some answer for Cymbalta withdrawal based upon an individual’s DNA and how fast or slow they metabolized Cymbalta. The test results showed why some went into withdrawal quicker than other but no real answers for a more successful Cymbalta withdrawal.
In 2005, Jim began researching other areas that might help with Cymbalta withdrawal, and he looked at specific nutritional supplements. The first sign of success was found early on with this approach. Over the past 26 years Jim has continued to research and formulate new supplements as new evidence came to light. Basically, Cymbalta and other medications make certain genes and proteins become too active and this is part of what makes the Cymbalta withdrawal begin.
Bringing those genes and proteins back to a normal balance, while not changing how the Cymbalta metabolizes turned out to be the answer for an effecting Cymbalta withdrawal.
As of December 2024, our estimated Cymbalta withdrawal success rate is now around 90%.
Next on this page is how we recommend you do a Cymbalta withdrawal.
You start with what we call a Pre-Taper. These are the things you do before reducing the Effexor. If you have already started reducing the Cymbalta, your step is to be at a dosage of the Cymbalta you feel stable on.
You will need to start taking supplements that have been formulated to help reduce Cymbalta withdrawal side effects.
Click here for the link to the supplements you will need.
You need to take the supplements below and how they are described to take each one before reducing the Cymbalta.
How to take the supplements
You will need to take these supplements:
Neuro Day
JNK Formula
Maca Supreme
Omega 3 Supreme
Neuro Night
Maca Supreme – You need to slowly increase the Maca Supreme. Start by taking 1 capsule in the morning.
After 3 days, take 1 capsule in the morning and 1 capsule at noon.
After 3 days, take 2 capsules in the morning and take 1 capsule at noon.
After 3 days, take 2 capsules in the morning and 2 capsules at noon.
After 3 days you can now start the rest of the supplements.
Morning – Take 2 Maca Supreme capsules, 1 Neuro Day capsule and 1 Omega 3 Supreme.
Mid-Morning – Take 1 JNK Formula capsule.
Noon – Take 1 Neuro Day, 1 Omega 3 Supreme and 2 Maca Supreme.
Mid-Afternoon – Take 1 JNK Formula capsule.
Night (15-minutes before bed) – Take 2 Neuro Night capsules.
This is the ideal way to take each supplement.
Try your best to keep a constant schedule with the supplements.
Omega 3 Supreme – Cymbalta is known for a withdrawal side effect called, brain zaps. A brain zap is an electrical jolt that tends to start at the base of the skull and run up and into the head. Omega 3 Supreme is the only supplement that will give you relief.
You can increase the Omega 3 Supreme to as much as 2 softgels in the morning and 2 softgels at noon if needed to get relief from the Cymbalta brain zaps.
You can also adjust the time you take the Omega 3 Supreme if needed. An example of this could be – let’s say brain zaps start around 4pm every day. Instead of taking the Omega 3 Supreme at noon, take the Omega 3 Supreme at 2pm.
If Cymbalta brain zaps tend to start around 11am, wait until around 9am before you take the morning Omega 3 Supreme.
You should take all the supplements for at least 1 full week before starting to taper the Cymbalta.
Use the graphs to track your symptoms before you start this method and during the Cymbalta taper process.
Get all symptoms below a 5 on a 1-10 scale before you start reducing the Cymbalta. If this takes a few extra days or a few weeks, it is more than worth it in the long term.
Goal of Cymbalta Pre-taper
If anxiety is present, have it eliminated
If fatigue is present, have it eliminated
If flu like symptoms are present, have them eliminated
If depression is present, have it eliminated
Eliminate all other antidepressant side effects
Set up the body correctly to eliminate potential withdrawal symptoms. The goal of the pre-taper may seem unobtainable to you at this moment, but after you experience a day to two of taking the supplements used with this program, you should begin to experience the changes we suggest will happen. It is not out of character for people to feel as though they are no longer even on an antidepressant as all side effects vanish quickly.
Action:
Rate your daytime anxiety, panic attacks, insomnia and other side effects. Use the Daily Journal and rate anxiety, sleep and any additional symptoms you may be experiencing from 1 to 10. Rate with number 10 being the worst and number 1 being no side effect or symptom remaining.
Rate the previous night’s sleep first thing the next morning. Rate the daytime anxiety just before bedtime of that day.
If you take the Cymbalta first thing in the morning, take the Cymbalta as normal and 1 hour later take the morning supplements.
Finishing the Pre-Taper
Do the Cymbalta pre-taper at least 7-full days. Do not cut the pre-taper short no matter how well you may feel after a few days. Give your body a chance to balance, give yourself the chance to fully experience relief before you tackle the reduction of the Cymbalta. If you wish to stay on the pre-taper for an extended time, that is fine to do, many have.
You may have experienced extreme trauma the last time you tried to get off the Cymbalta and the apprehension you may feel now is normal, not a mental disorder. This is your time; do not let yourself get rushed by your physician or by the information in this book. The drug manufacturer, the F.D.A., and even the American Medical Association state a gradual reduction of the Cymbalta is required. We cannot stress enough, take your time. This is when the tortoise beats the hare to the finish line.
Let’s say you have a reaction of some type when you change how you take the Cymbalta.
This is where the pre-taper comes in handy as well as taking good notes during that time.
Keep good notes on these new symptoms, what they are and the time of the day they start.
Let’s say you normally take the Cymbalta at 10am and the negative feelings started at 1pm. The negative is anxiety. The odds are you had anxiety before adjusting the Cymbalta. If the anxiety was lowered during the pre-taper and you can tell the Neuro Day is what lowered the anxiety, adjust the time of day you take the Neuro Day. Instead of taking the Neuro Day as the first supplement in the morning, take the JNK Formula first and then take your first Neuro Day at noon. Just before the negative symptom tends to begin.
If you get a head symptom the Omega 3 Supreme will always be the answer. Take another capsule of Omega 3 Supreme at noon.
I hope you see where we are going with this. Using your notes from the pre-taper you will know which supplement helped with which symptom. Adjust the supplements around so you are taking the one that helped with that negative symptom an hour before it tends to start.
The good news. Any symptom that might start at this point is likely one you had before the pre-taper and you know which supplement it was that helped.
Slow and steady will win this race!
There is Hope and There is a Solution
1. Serotonin and Norepinephrine Reuptake Inhibitors
This chapter covers antidepressants that fall into the class of serotonin (5-HT) and norepinephrine (NE) reuptake inhibitors. That is, they bind to the 5-HT and NE transporters with varying levels of potency and binding affinity ratios. Unlike the selective serotonin (5-HT) reuptake inhibitors (SSRIs), most of these antidepressants have an ascending rather than a flat dose-response curve. The chapter provides a brief review of the chemistry, pharmacology, metabolism, safety and adverse effects, clinical use, and therapeutic indications of each antidepressant. Venlafaxine, a phenylethylamine, is a relatively weak 5-HT and weaker NE uptake inhibitor with a 30-fold difference in binding of the two transporters. Therefore, the drug has a clear dose progression, with low doses predominantly binding to the 5-HT transporter and more binding of the NE transporter as the dose ascends. Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism. The half-life of venlafaxine is short at about 5 h, with the ODV metabolite being 12 h. Both parent compound and metabolite have low protein binding and neither inhibit CYP enzymes. Therefore, both venlafaxine and desvenlafaxine are potential options if drug-drug interactions are a concern, although venlafaxine may be subject to drug-drug interactions with CYP2D6 inhibitors. At low doses, the adverse effect profile is similar to an SSRI with nausea, diarrhea, fatigue or somnolence, and sexual side effects, while venlafaxine at higher doses can produce mild increases in blood pressure, diaphoresis, tachycardia, tremors, and anxiety. A disadvantage of venlafaxine relative to the SSRIs is the potential for dose-dependent blood pressure elevation, most likely due to the NE reuptake inhibition caused by higher doses; however, this adverse effect is infrequently observed at doses below 225 mg per day. Venlafaxine also has a number of potential advantages over the SSRIs, including an ascending dose-antidepressant response curve, with possibly greater overall efficacy at higher doses. Venlafaxine is approved for MDD as well as generalized anxiety disorder, social anxiety disorder, and panic disorder. Desvenlafaxine is the primary metabolite of venlafaxine, and it is also a relatively low-potency 5-HT and NE uptake inhibitor. Like venlafaxine it has a favorable drug-drug interaction profile. It is subject to CYP3A4 metabolism, and it is therefore vulnerable to enzyme inhibition or induction. However, the primary metabolic pathway is direct conjugation. It is approved in the narrow dose range of 50-100 mg per day. Duloxetine is a more potent 5-HT and NE reuptake inhibitor with a more balanced profile of binding at about 10:1 for 5HT and NE transporter binding. It is also a moderate inhibitor of CYP2D6, so that modest dose reductions and careful monitoring will be needed when prescribing duloxetine in combination with drugs that are preferentially metabolized by CYP2D6. The most common side effects identified in clinical trials are nausea, dry mouth, dizziness, constipation, insomnia, asthenia, and hypertension, consistent with its mechanisms of action.
2. Burning mouth syndrome: a review and update
Burning mouth syndrome (BMS) is mainly found in middle aged or elderly women and is characterized by intense burning or itching sensation of the tongue or other regions of the oral mucosa. It can be accompanied by xerostomia and dysgeusia. The syndrome generally manifests spontaneously, and the discomfort is typically of a continuous nature but increases in intensity during the evening and at night. Although BMS classically has been attributed to a range of factors, in recent years evidence has been obtained relating it peripheral (sensory C and/or trigeminal nerve fibers) or central neuropathic disturbances (involving the nigrostriatal dopaminergic system). The differential diagnosis requires the exclusion of oral mucosal lesions or blood test alterations that can produce burning mouth sensation. Patient management is based on the avoidance of causes of oral irritation and the provision of psychological support. Drug treatment for burning sensation in primary BMS of peripheral origin can consist of topical clonazepam, while central type BMS appears to improve with the use of antidepressants such as duloxetine, antiseizure drugs such as gabapentin, or amisulpride.
3. Bioaccumulation of therapeutic drugs by human gut bacteria
Bacteria in the gut can modulate the availability and efficacy of therapeutic drugs. However, the systematic mapping of the interactions between drugs and bacteria has only started recently1 and the main underlying mechanism proposed is the chemical transformation of drugs by microorganisms (biotransformation). Here we investigated the depletion of 15 structurally diverse drugs by 25 representative strains of gut bacteria. This revealed 70 bacteria-drug interactions, 29 of which had not to our knowledge been reported before. Over half of the new interactions can be ascribed to bioaccumulation; that is, bacteria storing the drug intracellularly without chemically modifying it, and in most cases without the growth of the bacteria being affected. As a case in point, we studied the molecular basis of bioaccumulation of the widely used antidepressant duloxetine by using click chemistry, thermal proteome profiling and metabolomics. We find that duloxetine binds to several metabolic enzymes and changes the metabolite secretion of the respective bacteria. When tested in a defined microbial community of accumulators and non-accumulators, duloxetine markedly altered the composition of the community through metabolic cross-feeding. We further validated our findings in an animal model, showing that bioaccumulating bacteria attenuate the behavioural response of Caenorhabditis elegans to duloxetine. Together, our results show that bioaccumulation by gut bacteria may be a common mechanism that alters drug availability and bacterial metabolism, with implications for microbiota composition, pharmacokinetics, side effects and drug responses, probably in an individual manner.
4. Duloxetine for treating painful neuropathy, chronic pain or fibromyalgia
Background: Duloxetine is a balanced serotonin and noradrenaline reuptake inhibitor licensed for the treatment of major depressive disorders, urinary stress incontinence and the management of neuropathic pain associated with diabetic peripheral neuropathy. A number of trials have been conducted to investigate the use of duloxetine in neuropathic and nociceptive painful conditions. This is the first update of a review first published in 2010.
Objectives: To assess the benefits and harms of duloxetine for treating painful neuropathy and different types of chronic pain.
5. Withdrawal Symptoms after Serotonin-Noradrenaline Reuptake Inhibitor Discontinuation: Systematic Review
Background: Serotonin-noradrenaline reuptake inhibitors (SNRI) are widely used in medical practice. Their discontinuation has been associated with a wide range of symptoms. The aim of this paper is to identify the occurrence, frequency, and features of withdrawal symptoms after SNRI discontinuation.
Keywords: Adverse events; Antidepressant drugs; Desvenlafaxine; Discontinuation syndrome; Duloxetine; Levomilnacipran; Milnacipran; Serotonin-noradrenaline reuptake inhibitors; Venlafaxine; Withdrawal symptoms.
6. Optimal pharmacotherapy pathway in adults with diabetic peripheral neuropathic pain: the OPTION-DM RCT
Background: The mainstay of treatment for diabetic peripheral neuropathic pain is pharmacotherapy, but the current National Institute for Health and Care Excellence guideline is not based on robust evidence, as the treatments and their combinations have not been directly compared.
Objectives: To determine the most clinically beneficial, cost-effective and tolerated treatment pathway for diabetic peripheral neuropathic pain.
7. Is duloxetine an alternative in the treatment of osteoarthritis?
Introduction: Many osteoarthritis patients continue to present symptoms despite nonsurgical treatment. Duloxetine might be a viable alternative for such cases, but real clinical relevance remains unclear.
Methods: A literature review was conducted in Epistemonikos, the largest database for systematic reviews in health that compiles multiple sources, including MEDLINE, EMBASE, and Cochrane, among others. Relevant data were extracted, and information from the primary studies was reanalyzed. A subsequent meta-analysis was conducted, and summary of findings tables were constructed using the GRADE methodology.
Results and conclusions: Four systematic reviews including four randomized trials, were identified. In conclusion, while duloxetine slightly improves pain and functionality in osteoarthritis patients, its use is associated with frequent adverse side effects. Therefore, the benefit/risk balance appears unfavorable.
8. A randomized comparative study of methylcobalamin, methylcobalamin plus pregabalin and methylcobalamin plus duloxetine in patients of painful diabetic neuropathy
Context: Diabetic neuropathy affects 10.5%-32.2% of diabetic population posing clinical burden onto society.
Aims: We aimed to study the efficacy, safety, and tolerability of methylcobalamin, methylcobalamin plus pregabalin, and methylcobalamin plus duloxetine in patients of painful diabetic neuropathy.
9. Duloxetine Induced Hyponatremia
Hyponatremia can be asymptomatic or have a wide range of clinical presentations such as headaches, muscle cramps, nausea, seizures, coma, cerebral edema and may even result in death. Despite it has been suggested that duloxetine has a relatively less risk of hyponatraemia, the number of case reports are increasing. A 45- year old female patient with complaints of fear, anxiety, sleeplessness and headache was started on duloxetine (30 mg/day). In the first week of the treatment, she was admitted to the emergency service with dizziness, dry mouth, polyuria and polydipsia. She had to be transferred to the intensive care unit because of agitation, loss of consciousness and a generalized tonic-clonic seizure. Blood levels of Sodium (Na+), Potassium (K+) and Chlorine (Cl-) were, respectfully, 121 mmol/L, 2.7 mmol/L and 87 mmol/L. Brain imaging displayed cerebral edema. Electrolyte levels were regulated with saline infusions. Amitriptyline was initiated for the ongoing headache and anxiety. In outpatient visits, hyponatremia did not recur in the following 3 months. Low dose duloxetine was associated with severe hyponatremia signs and symptoms in an individual who was not previously considered as high risk for hyponatraemia. The patient’s history did not reveal any complaints related to hyponatremia when she was treated with sertraline two years ago. Based on these, we discussed the risk factors for hyponatremia and risky antidepressant classes.
10. Efficacy and safety of duloxetine in chronic musculoskeletal pain: a systematic review and meta-analysis
Background: Chronic musculoskeletal pain (CMP) is a complex condition that is mainly treated with analgesic drugs. However, antidepressant intervention is also an important factor in the treatment of CMP. Duloxetine is an effective treatment option for patients with CMP as its antidepressant effect. The purpose of this article is to evaluate the efficacy and safety of duloxetine in treating CMP.