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Depakote Withdrawal. Step by step Depakote withdrawal procedure. Depakote withdrawal. Withdrawal from Depakote no longer needs to be grueling and suffering from the Depakote withdrawal side effects can be a thing of the past.

Depakote Withdrawal

The web site you are on is The Road Back Program. The Road Back is a member of California Association of Alcoholism & Drug Abuse Counselors (CAADAC).  We have been assisting people off psychoactive medication since 1999, and have helped well over 50,000 people off their drugs.

Head symptoms? Anxiety? Insomnia? Of course you do.

You likely would prefer to cut to the chase and find out what you can do to get relief quickly.

You can use two natural supplements to help with the Depakote withdrawal and likely the underlying symptoms you were experiencing before starting Depakote.

The first supplement is CBD oil. You likely have heard or read about CBD oil already. We are taking about THC Free CBD oil only. The price of CBD oil may have limited you from using this amazing product. We have assisted the manufacturer of a CBD oil to help eliminate the cost problem and have helped formulate a high quality CBD oil in the process. How does $34.27 (30 servings) a bottle sound and with 26mg CBD oil in each serving, you will not find a lower price per mg of CBD oil anywhere. Plus, it's made in the United States in an F.F.A. registered facility. Click here for Harper Drops Supreme

Optimum Solace is the other supplement recommended. Undoing some of the unwanted harm Depakote can do is equally as important as getting off the medication. Click here

There was a time not so long ago the medical community felt Depakote was not addictive. In 2012, the Surgeon General for the U.S. Army acknowledged Depakote was not just addictive but he went further to remove Depakote from the psychoactive drug list approved to give our troops. Well intentioned physicians may still believe Depakote is not addictive but this does not make them a bad physician, it does mean they are still uninformed about Depakote.

The point I wish to make with the above text is; clinical studies may be accurate or they may even be completely false, we at The Road Back as well as physician’s need to listen to each of you. If the goal is to assist people off Depakote and have the person feel real well during the Depakote withdrawal process, we need to listen to you and not clinical studies only. This program was developed by taking Depakote clinical studies and putting that information to use. Some of the information has worked quite well, while other information turned out to be worthless.

An example of this regarding Depakote: If Depakote is used for a prolonged period of time the Depakote will deplete the B vitamin biotin from the body. A deficiency of biotin will cause numbness or tingling of the extremities, a reaction to loud noise or a reaction to bright light which could also include seizures. This is a biotin deficiency and not a medical problem. Put the right amount of biotin back in the body and these symptoms vanish. It is that simple.

This program is a culmination of 18-years of work, 18-years of failure and 18-years of success. None of us are exactly the same; the Depakote side effects you may be experiencing may not be the same Depakote side effects experienced by others, how you do while tapering the Depakote may not be the same for others, you may be able to taper Depakote a little faster than average or you may need to take this a little slower.

There are some basics that apply to all people though when it comes to being able to withdrawal from Depakote. We take those basics, the list of side effects from the Depakote drug approval process and from these, you have our program. Read through the Depakote side effect list found below on this page, you may have quite a few of them or only a small quantity. Either way, the program is designed to guide you through the Depakote withdrawal process.

You start out with what we call the Pre-Taper. The Pre-Taper are things you start doing before you ever reduce the Depakote.

Two of the side effects that tend to be common with each person taking Depakote are daytime anxiety and insomnia. Unless we can handle these two side effects, there really would not be a Depakote withdrawal program. These two side effects are that debilitating when left out of control. Once the daytime anxiety and insomnia are under control, other Depakote side effects you may be experiencing have a chance of simply going away on their own because they were anxiety and sleep related.

It would be hard to argue that constant anxiety on top of no sleep would not cause a person stress. We have gene in our cells called the JNK gene. This gene becomes too active when stress is chronic and this over activation of the JNK gene will lead to other body problems and some of those problems can be mentally related in time. So we also want to reduce the over activation of the JNK gene during the pre-taper and keep this gene in check throughout the taper process as well.

Natural supplements can be used to regulate the JNK gene, anxiety and insomnia. The Depakote creates a metabolic disorder bringing some enzymes too high and when the flow of the metabolic system becomes stuck or flowing too profusely the body can’t handle it and a cascading effect takes place. You may become anxious due to the calcium firing erratically or by the adrenals out of balance or a host of proteins being too abundant or even too few.

You will start the Pre-Taper by taking a supplement called JNK Capsules. This supplement contains botanicals that have been proven to regulate the JNK gene, reduce stress, and put back in the cells what the benzodiazepines have stripped out and more. As stated earlier, long term use of a benzodiazepine will create an inadequate amount of the B vitamin biotin. Biotin has been included in the JNK Capsule formula to address this issue.

A metabolic disorder will take place with Depakote usage in an area called nitric oxide and nitric oxide synthase. These are also known as NO/NOS. Too much NO will overwhelm NOS and then a substance called NMDA will go out of balance and this will lead to the misfiring of calcium. Here you have the rapid start of anxiety and the start of insomnia.

The Road Back does not sell these supplements. They are available at the U.S. manufacture Neuro Genetic Solutions.

Many of you are in the middle of Depakote withdrawal when you find our web site and the thought of reading hundreds of pages from the book How to Get Off Psychoactive Drugs safely is overwhelming. If you click How to Start which is located at the top of this page, all pages of the book are located there.

Divalproex Sodium 
Brand name (Epival and Depakote)


Divalproex sodium has anticonvulsant properties, and is chemically related to valproic acid. Although its mechanism of action has not yet been established, it has been suggested that its activity is related to increased brain levels of gamma-aminobutyric acid (GABA). The effect on the neuronal membrane is unknown. It dissociates into valproic acid in the gastrointestinal tract.

Peak serum levels of valproic acid occur in 3 to 4 hours.

The serum half-life of valproic acid is typically in the range of 6 to 16 hours. Half-lives in the lower part of the above range are usually found in patients taking other drugs capable of enzyme induction. Enzyme induction may result in enhanced clearance of valproic acid by glucuronidation and microsomal oxidation. Because of these changes in valproic acid clearance monitoring of valproate and concomitant drug concentrations should be intensified whenever enzyme inducing drugs are introduced or withdrawn.

A slight delay in absorption occurs when the drug is administered with meals but this does not affect the total absorption. Valproic acid is rapidly distributed throughout the body and the drug is strongly bound (90%) to human plasma proteins. Increases in dose may result in decreases in the extent of protein binding and variable changes in valproic acid clearance and elimination. In epilepsy, the therapeutic plasma concentration range is believed to be from 50 to 100 mcg/mL. Occasional patients may be controlled with serum levels lower or higher than this range. A good correlation has not been established between daily dose, serum level and therapeutic effect.

In placebo controlled clinical studies in acute mania, 79% of patients were dosed to a plasma concentration between 50 and 125 mcg/mL. Protein binding of valproate is saturable ranging from 90% at 50 mcg/mL to 82% at 125 mcg/mL.

Elimination of valproic acid and its metabolites occurs principally in the urine, with minor amounts in the feces and expired air. Very little unmetabolized parent drug is excreted in the urine. The principal metabolite formed in the liver is the glucuronide conjugate.

Other metabolites in the urine are products of C-3, C-4 and C-5 oxidation. The major oxidative metabolite in the urine is 2-propyl-3-keto-pentanoic acid; minor metabolites are 2-propyl-glutaric acid, 2-propyl-5-hydroxy-pentanoic acid, 2-propyl-3-hydroxy-pentanoic acid and 2-propyl-4-hydroxy-pentanoic acid.

See Warnings regarding statement on fatal hepatic dysfunction.


Divalproex is indicated for use as sole or adjunctive therapy in the treatment of simple or complex absence seizures, including petit mal and is useful in primary generalized seizures with tonic-clonic manifestations. Divalproex may also be used adjunctively in patients with multiple seizure types which include either absence or tonic-clonic seizures.

Acute Mania:
Divalproex is indicated in the treatment of the manic episodes associated with bipolar disorder (DSM-III-R).

The effectiveness of divalproex in long-term use, that is for more than 3 weeks, has not been systematically evaluated in controlled trials.

Dilvalproex is not indicated for use as a mood stabilizer in patients under 18 years of age.


Patients with hepatic disease or significant dysfunction. Hypersensitivity to the drug.


Hepatic failure resulting in fatalities has occurred in patients receiving valproic acid and its derivatives. These incidences usually occurred during the first 6 months of treatment with valproic acid. Experience has indicated that children under the age of 2 years are at a considerably increased risk of developing fatal hepatotoxicity, especially those on multiple anticonvulsants, those with congenital metabolic disorders, those with severe seizure disorders accompanied by mental retardation, and those with organic brain disease.

The risk in this age group decreased considerably in patients receiving valproate as monotherapy. Similarly, patients aged 3 to 10 years were at somewhat greater risk if they received multiple anticonvulsants than those who received only valproate. Risk generally declined with increasing age. No deaths have been reported in patients over 10 years of age who received valproate alone.

If divalproex is to be used for the control of seizures in children 2 years old or younger, it should be used with extreme caution and as a sole agent. The benefits of therapy should be weighed against the risks.

Serious or fatal hepatotoxicity may be preceded by nonspecific symptoms such as malaise, weakness, lethargy, facial edema, anorexia, vomiting, and in epileptic patients, loss of seizure control. Patients and parents should be instructed to report such symptoms. Because of the nonspecific nature of some of the early signs, hepatotoxicity should be suspected in patients who become unwell, other than through obvious cause, while taking divalproex.

Liver function tests should be performed prior to therapy and at frequent intervals thereafter especially during the first 6 months. However, physicians should not rely totally on serum biochemistry since these tests may not be abnormal in all instances, but should also consider the results of careful interim medical history and physical examination. Caution should be observed when administering Divalproex to patents with a prior history of hepatic disease. Patients with various unusual congenital disorders, those with severe seizure disorders accompanied by mental retardation, and those with organic brain disease may be at particular risk.

In high-risk patients, it might also be useful to monitor serum fibrinogen and albumin for decreases in concentrations and serum ammonia for increases in concentration. If changes occur, divalproex should be discontinued. Dosage should be titrated to and maintained at the lowest dose consistent with optimal seizure control.

The drug should be discontinued immediately in the presence of significant hepatic dysfunction, suspected or apparent. In some cases, hepatic dysfunction has progressed in spite of discontinuation of drug. The frequency of adverse effects (particularly elevated liver enzymes) may increase with increasing dose. The benefit of improved symptom control at higher doses should therefore be weighed against the possibility of a greater incidence of adverse effects.

According to recent reports in the medical literature, valproic acid may produce teratogenicity in the offspring of human females receiving the drug during pregnancy. The incidence of neural tube defects in the fetus may be increased in mothers receiving valproic acid during the first trimester of pregnancy. Based upon a single report, it was estimated that the risk of valproic acid exposed women having children with spina bifida is approximately 1 to 2%. This risk is similar to that which applies to nonepileptic women who have had children with neural tube defects (anencephaly and spina bifida).

Animal studies have demonstrated valproic acid-induced teratogenicity, and studies in human females have demonstrated placental transfer of the drug.

Multiple reports in the clinical literature indicate an association between the use of antiepileptic drugs and an elevated incidence of birth defects in children born to epileptic women taking such medication during pregnancy. The incidence of congenital malformations in the general population is regarded to be approximately 2%; in children of treated epileptic women, this incidence may be increased 2- to 3-fold. The increase is largely due to specific defects, e.g., congenital malformations of the heart, cleft lip and/or palate, craniofacial abnormalities and neural tube defects. Nevertheless, the great majority of mothers receiving antiepileptic medications deliver normal infants.

Data are more extensive with respect to phenytoin and phenobarbital, but these drugs are also the most commonly prescribed antiepileptics. Some reports indicate a possible similar association with the use of other antiepileptic drugs, including trimethadione, paramethadione, and valproic acid. However, the possibility also exists that other factors, e.g., genetic predisposition or the epileptic condition itself may contribute to or may be mainly responsible for the higher incidence of birth defects.

Patients taking valproic acid may develop clotting abnormalities. If valproic acid is used in pregnancy, the clotting parameters should be monitored carefully.

Antiepileptic drugs should not be discontinued in patients to whom the drug is administered to prevent major seizures, because of the strong possibility of precipitating status epilepticus with attendant hypoxia and risks to both the mother and the unborn child. With regard to drugs given for minor seizures, the risks of discontinuing medication prior to or during pregnancy should be weighed against the risk of congenital defects in the particular case and with the particular family history.

Epileptic women of childbearing age should be encouraged to seek the counsel of their physician and should report the onset of pregnancy promptly to him. Where the necessity for continued use of antiepileptic medication is in doubt, appropriate consultation is indicated.

Risk-benefit must be carefully considered when treating women of childbearing age for bipolar disorder.

Tests to detect neural tube and other defects using current accepted procedures should be considered a part of routine prenatal care in childbearing women receiving valproate.

Valproic acid is excreted in breast milk. Concentrations in breast milk have been reported to be 1 to 10% of serum concentrations. As a general rule, nursing should not be undertaken while a patient is receiving divaiproex. It is not known what effect this may have on a nursing infant.

The effect of valproate on testicular development and on sperm production and fertility in humans is unknown.

Long-term animal toxicity studies indicate that valproic acid is a weak carcinogen or promoter in rats and mice. The significance of these findings for man is unknown at present.


Hepatic dysfunction (see Contraindications and Warnings).

Because of reports of thrombocytopenia, inhibition of the second phase of platelet aggregation, platelet counts and coagulation tests are recommended before instituting therapy and at periodic intervals. It is recommended that patients receiving divalproex be monitored for platelet count and coagulation parameters prior to planned surgery.

Clinical evidence of hemorrhage, bruising or a disorder of hemostasis/coagulation is an indication for dosage reduction or withdrawal of therapy pending investigation.

Hyperammonemia with or without lethargy or coma has been reported and may be present in the absence of abnormal liver function tests; if elevation occurs the divalproex sodium should be discontinued.

Divalproex is partially eliminated in the urine as a ketone-containing metabolite which may lead to a false interpretation of the urine ketone test.

There have been reports of altered thyroid function tests associated with valproic acid: the clinical significance of these is unknown.

Renal Impairment:
Renal impairment is associated with an increase in the unbound fraction of valproate. In several studies, the unbound fraction of valproate in plasma from renally impaired patients was approximately double that for subjects with normal renal function.

Hemodialysis in renally impaired patients may remove up to 20% of the circulating valproate.

The safety and efficacy of divalproex in elderly patients with epilepsy and mania has not been systematically evaluated in clinical trials. Caution should thus be exercised in dose selection for an elderly patient, recognizing the more frequent hepatic and renal dysfunctions, and limited experience with Divalproex in this population.

Occupational Hazards:
Divalproex may produce CNS depression, especially when combined with another CNS depressant, such as alcohol. Therefore, patients should be advised not to engage in hazardous occupations, such as driving a car or operating dangerous machinery, until it is known that they do not become drowsy from the drug.

Drug Interactions:

Divalproex may potentiate the CNS depressant action of alcohol.

The concomitant administration of valproic acid with drugs that exhibit extensive protein binding (e.g., aspirin, carbamazepine and dicumarol) may result in alteration of serum drug levels.

Aspirin and Warfarin:
Caution is recommended when divalproex is administered with drugs affecting coagulation, (e.g., aspirin and warfarin) (see Adverse Effects).

There is evidence that valproic acid may cause an increase in serum phenobarbital levels, by impairment of nonrenal clearance. This phenomenon can result in severe CNS depression. The combination of valproic acid and phenobarbital has also been reported to produce CNS depression without significant elevations of barbiturate or valproic acid serum levels. Patients receiving concomitant barbiturate therapy should be closely monitored for neurological toxicity. Serum barbiturate drug levels should be obtained, if possible, and the barbiturate dosage decreased, if indicated.

Primidone is metabolized into a barbiturate and, therefore, may also be involved in a similar or identical interaction.

There is conflicting evidence regarding the interaction of valproic acid with phenytoin. It is not known if there is a change in unbound (free) phenytoin serum levels. The dosage of phenytoin should be adjusted as required by the clinical situation. There have been reports of breakthrough seizures occurring with the combination of valproic acid and phenytoin.

Because divalproex may interact with concurrently administered drugs which are capable of enzyme induction, periodic serum level determinations of these drugs are recommended during the early part of therapy.

The concomitant use of valproic acid and clonazepam may produce absence status in patients with a history of absence type seizures.

Oral contraceptives:
Evidence suggests that there is an association between the use of certain drugs capable of enzyme induction and failure of oral contraceptives. One explanation for this interaction is that enzyme-inducing antiepileptic drugs effectively lower plasma concentrations of the relevant steroid hormones, resulting in unimpaired ovulation. However, other mechanisms, not related to enzyme induction, may contribute to the failure of oral contraceptives. Valproic acid is not a significant enzyme inducer and would not be expected to decrease concentrations of steroid hormones. However, clinical data about the interaction of valproic acid with oral contraceptives are minimal.

In addition to enhancing CNS depression when used concurrently with valproic acid, tricyclic antidepressants, MAO inhibitors, and antipsychotics, may lower the seizure threshold. Dosage adjustments may be necessary to control seizures.

Concomitant use of carbamazepine with valproic acid may result in decreased serum concentrations and half-life of valproate due to increased metabolism induced by hepatic microsomal enzyme activity. Valproate causes an increase in the active 10, 11-epoxide metabolite of carbamazepine by inhibition of its breakdown. Monitoring of serum concentrations is recommended when either medication is added to or withdrawn from an existing regimen. Changes in the serum concentration of the 10, 11-epoxide metabolite of carbamazepine, however, will not be detected by routine serum carbamazepine assay.

Cimetidine may decrease the clearance and increase the half-life of valproic acid by altering its metabolism. In patients receiving valproic acid, serum valproic acid levels should be monitored when treatment with cimetidine is instituted, increased, decreased, or discontinued. The valproic acid dose should be adjusted accordingly.

A single study has shown that the concomitant use of chlorpromazine with valproic acid may result in a decrease in valproic acid clearance. Valproic acid serum concentrations and effects should be monitored when valproic acid is unadministered chlorpromazine due to possible inhibition of valproic acid metabolism.

Selective serotonin re-uptake inhibitors (SSRIs):
Some evidence suggests that SSRIs inhibit the metabolism of valproate, resulting in higher than expected levels of valproate.

Tricyclic antidepressants:
The metabolism of amitriptyline and nortriptyline after a single dose of amitriptyline (50 mg) was inhibited by multiple dosing with valproic acid (500 mg twice daily) in 16 healthy male and female volunteers. For the sum of amitriptyline and nortriptyline plasma concentrations, in the presence of valproic acid, the mean Cmax and AUC were increased by 19 and 42%, respectively.

In a double-blind placebo-controlled multiple dose crossover study in 16 healthy male volunteers, pharmacokinetic parameters of lithium were not altered by the presence or absence of divalproex. The presence of lithium, however, resulted in an 11 to 12% increase in the AUC and Cmax of valproate. Tmax was also reduced. Although these changes were statistically significant, they are not likely to have clinical importance.

Valproic acid may decrease oxidative liver metabolism of some benzodiazepines, resulting in increased serum concentrations. In two small studies in healthy volunteers, valproate produced a 17% decrease in the clearance of lorazepam, and 26% decrease in the clearance of unbound diazepam. Displacement of diazepam from plasma protein binding sites may also occur. During valproate administration the unbound fraction of diazepam in the senum increased approximately two-fold.

Adverse Effects

The most commonly reported adverse reactions are nausea, vomiting and indigestion. Since valproic acid has usually been used with other antiepileptics, it is not possible in most cases to determine whether the adverse reactions mentioned in this section are due to valproic acid alone or to the combination of drugs.

Nausea, vomiting and indigestion are the most commonly reported side effects at the initiation of therapy. These effects are usually transient and rarely require discontinuation of therapy. Diarrhea, abdominal cramps and constipation have also been reported. Anorexia with some weight loss and increased appetite with some weight gain have also been seen.

Sedative effects have been noted in patients receiving valproic acid alone but are found most often in patients on combination therapy. Sedation usually disappears upon reduction of other antiepileptic medication. Ataxia, headache, nystagmus, diplopia, asterixis, "spots before the eyes", tremor (may be dose-related), dysarthria, dizziness, and incoordination have rarely been noted. Rare cases of coma have been reported in patients receiving valproic acid alone or in conjunction with phenobarbital.

Transient increases in hair loss have been observed. Skin rash, photosensitivity, generalized pruritus, erythema multiforms, Stevens-Johnson syndrome and petechiae have rarely been noted.

There have been reports of irregular menses and secondary amenorrhea, breast enlargement, galactorrhea and parotid gland swelling in patients receiving valproic acid. Abnormal thyroid function tests have been reported (see Precautions).

Emotional upset, depression, psychosis, aggression, hyperactivity and behavioral deterioration have been reported.

Weakness has been reported.

Thrombocytopenia has been reported. Valproic acid inhibits the second phase of platelet aggregation (see Precautions). This may be reflected in altered bleeding time. Petechiae, bruising, hematoma formation and frank hemorrhage have been reported. Relative lymphocytosis macrocytosis and hypofibrinogenemia have been noted. Leukopenia and eosinophilia have also been reported. Anemia, including macrocytic with or without folate deficiency, bone marrow suppression and acute intermittent porphyria have been reported.

Minor elevations of transaminases (e.g., AST and ALT) and LDH are frequent and appear to be dose related. Occasionally, laboratory tests also show increases in serum bilirubin and abnormal changes in other liver function tests. These results may reflect potentially serious hepatotoxicity (see Warnings).

Hyperammonemia (see Precautions), hyponatremia and inappropriate ADH secretion. Hyperglycinemia has been reported and associated with a fall outcome in a patient with pre-existing nonketotic hyperglycinemia.


There have been reports of acute pancreatitis occurring in association with therapy with valproic acid.

Special Senses:
Hearing loss, either reversible or irreversible, has been reported however, a cause and effect relationship has not been established.

Edema of extremities has been reported.

Bipolar Disorder:
The incidence of adverse events has been ascertained based on data from 2 short-term (21 day) placebo-controlled clinical trials of divalproex in the treatment of acute mania, and from 2 long-term (up to 3 years) retrospective open trials.

Most Commonly Observed:
During the short-term placebo-controlled trials, the 6 most commonly reported adverse events in patients (N=89) exposed to divalproex were nausea (22%), headache (21%), somnolence (19%), pain (15%), vomiting (12%), and dizziness (12%).

In the long-term retrospective trials (634 patients exposed to divalproex), the 6 most commonly reported adverse events were somnolence (31%), tremor (29%), headache (24%), asthenia (23%), diarrhea (22%) and nausea (20%).

Associated With Discontinuation of Treatment:
In the placebo-controlled trials, adverse events which resulted in valproate discontinuation in at least 1% of patients were nausea (4%) abdominal pain (3%), somnolence (2%) and rash (2%).

In the long-term retrospective trials, adverse events which resulted in valproate discontinuation in at least 1% of patients were alopecia (2.4%), somnolence (1.9%), nausea (1.7%) and tremor (1.4%). The time to onset of these events was generally within the first 2 months of initial exposure to valproate. A notable exception was alopecia, which was first experienced after 3 to 6 months of exposure by 8 of the 15 patients who discontinued valproate in response to the event.

Controlled Trials:
Table I summarizes those treatment emergent adverse events reported for patients in the placebo-controlled trials when the incidence rate in the divalproex group was at least 5%. (Maximum treatment duration was 21 days; maximum dose in 83% of patients was between 1000 to 2500 mg/day).