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How Does Ketamine Work? How Does Ketamine Prevent Deaths of Despair? Serotonin 1B Receptors and Ketamine | Northern Virginia Ketamine Infusion Center | Ketamine Assisted Psychotherapy

For more information about ketamine treatment or to schedule for a ketamine consultation or infusion in Northern Virginia, call 703-844-0184 or email us below. No referral is needed.

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How Does Ketamine Work? How Does Ketamine Prevent Deaths of Despair? 

There are numerous pathways through which ketamine appears to work to resolve depression. Ketamine demonstrates efficacy the rapid relief of suicidalityPTSDBipolar depression, and pain. Glutamate is the neurotransmitter that appears to be a primary molecule involved in learning and is an excitatory neurotransmitter in the cerebrum. Disorders in glutamate result in depression and mood disorders. A recent study demonstrated the importance of Serotonin 1B receptors in depression and how ketamine improves that. 

A randomized placebo-controlled PET study of ketamine´s effect on serotonin1B receptor binding in patients with SSRI-resistant depression 

Low Serotonin 1B receptors have been found in limbic areas of the brain in major depression disorder (MDD). Ketamine upregulates AMPA receptor activity and results in increased 5-HT1B receptor binding in the ventral striatum (involved in depression). 

In the study, PET scans were used to image serotonin receptor binding after ketamine infusions in 30 patients. Low levels of serotonin correlate with severe depression. During the study, a certain portion of the patients underwent ketamine infusions twice a week for two weeks, and 70% of those patients had improvement in their depression scores. Based in the PET scans, ketamine reduces the output of serotonin and increased dopamine (the reward molecule). Ketamine increased the number of Serotonin 1B receptors and the higher number of Serotonin 1B receptors correlates with less depression. 

Key points: 

Subanesthetic dosing of ketamine has been effective in the rapid reduction of depression over hours as opposed to weeks with traditional treatments: 

Antidepressant effects of ketamine in depressed patients 

Glutamate is the key neurotransmitter involved in mood disorders based on recent theories: 

The role of glutamate in mood disorders: results from the ketamine in major depression study and the presumed cellular mechanism underlying its antidepressant effects 

The NMDA receptor (N-methyl-D-aspartate ) antagonism by ketamine plays a key role in the effectiveness of ketamine’s antidepressant effect: 

 
The acute effects of NMDA antagonism: from the rodent to the human brain 

Ketamine interacts with several receptors in the brain and impacts neurotransmitters through affinity for opioid, muscarinic, nicotinic, and serotonin (5-HT)2 receptors: 

 
Classics in Chemical Neuroscience: Ketamine 

Ketamine, much like other antidepressants, seems to increase serotonin in areas of the brain such as the prefrontal cortex and depletion of serotonin results in decreased antidepressant effects with ketamine: 

Role of Serotonin and Noradrenaline in the Rapid Antidepressant Action of Ketamine 

In the positron emission tomography (PET) studies of in vivo 5-HT1B receptor binding in MDD, low binding in the hippocampus and in the anterior cingulate cortex (ACC) has been reported both in patients with recurrent MDD: 

Low serotonin1B receptor binding potential in the anterior cingulate cortex in drug-free patients with recurrent major depressive disorder 

PTSD also presents with reduced serotonin 1B receptors as well: 

The Effect of Early Trauma Exposure on Serotonin Type 1B Receptor Expression Revealed by Reduced Selective Radioligand Binding 

In patients with a family history of depression, it is noted that 5-HT1B receptor binding was low in the ventral striatum (VST) and ventral pallidum: 

Reduced ventral striatal/ventral pallidal serotonin1B receptor binding potential in major depressive disorder 

The VST is a key structure in the reward system, implicated in anhedonia – the presence of no mood that can accompany MDD and 5-HT1B receptor binding is high in the VST: 

Circuit-based frameworks of depressive behaviors: The role of reward circuitry and beyond 

Per this studyketamine increased 5-HT1B receptor binding in regions with reported low 5-HT1B receptor levels, such as the hippocampus, ACC (Anterior Cingulate Cortex), and VST and this resulted in diminished depression. 

What does this mean for you? 

The bottom line is that ketamine still improved depression in 70% of treatment failures through still-debated mechanisms. The improvement of the Serotonin 1B receptor is just another piece of the puzzle.  

Ketamine Infusions for Anhedonia and Bipolar Depression | How Ketamine Therapy can Help Improve Loss of Interest and Improve Motivation | Northern Virginia Ketamine Infusion Center

Contact NOVA Health Recovery Ketamine Infusion Center in Fairfax, Virginia for more information about ketamine infusion therapy. Don’t forget to include your phone number:

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What is Anhedonia?  It is defined as the diminished pleasure from, or interest in previously rewarding activity and this is considered to be part of a depressive episode However, depression may be relieved with medical treatments, yet the anhedonia can remain with associated reward blunting.  

Depression is a major cause of disability in the world and its symptoms include loss of interest, depressed mood, and loss of pleasure in daily activities with frequent associated loss of sleep, appetite changes, intrusive thoughts, suicidal thoughts, and issues with focus and concentration (brain fog). 

Anhedonia is a component of depression and other mental health disorders that is not tracked as closely. The loss of excitement in anticipating activities that were once pleasurable defines anhedonia. The treatment of depression with traditional medications may relieve depression without restoring the circuits involved with the enjoyment of anticipation – the “wanting’ of something. This leaves an anhedonic person without hope or passions for the future. They may enjoy consuming things placed before them, but effectively they are unable to achieve the motivation to reach out for their old hobbies and passions. They aren’t interested in learning about new rewarding experiences.  

The fulfilment of life experiences hinges on the anticipation and excitement of future adventures. Anhedonia robs people of this treat and can be as life-threatening as the depression itself through an increase suicidality or overall medical illnesses such as heart disease due to the stress and anxiety that remains. 

Either way, anhedonia may indicate a poorer prognosis in depressed people as they are unable to achieve the motivation and cognition to return to work, accrue more medical problems, have an increased risk of substance abuse, and an increased risk of suicidality. The loss of emotions, sexual interests, and physical blunting (decreased activity) frequently accompanies depressed patients who are treated with traditional antidepressants.  

Ketamine has been shown to be one of the only effective therapies for anhedonia. 

Anhedonia as a Clinical Correlate of Suicidal Thoughts in Clinical Ketamine Trials 

Can Anhedonia Be Considered a Suicide Risk Factor? A Review of the Literature 

Relationships between anhedonia, suicidal ideation and suicide attempts in a large sample of physicians 

The Neurobiology of Anhedonia and Other Reward-Related Deficits 

Anhedonia is commonly present in bipolar disorder, anxiety, Major Depressive Disorder (MDD), and other psychiatric illnesses. Some studies have demonstrated that ketamine can reduce anhedonia symptoms as measured by the Snaith-Hamilton Pleasure Scale (SHAPS). Anhedonia responds to treatment differently than does depression . In fact, regular antidepressant treatment may lead to sexual anhedonia and anorgasmia, and emotionablunting. Anti-anhedonic effects of ketamine were found to be related to increased glucose metabolism in the dorsal anterior cingulate cortex and putamen.   

Standard treatments for depression do little to alleviate anhedonia. These standard treatments also cause other issues: 

Anhedonia can be seen as having a consummatory component, such as the enjoyment of a good meal, and a motivational component, such as the anticipation and drive towards rewarding stimuli, such as looking towards a good movie. These have a biological basis. Most patients with MDD and Bipolar depression have normal consummatory behaviors but low motivation to obtain the consumable items they might enjoy. 

Although someone who is depressed may find sugar to be enjoyable or cartoons to be funny as do non-depressed people, they will not have the actual motivation to seek out such enjoyments. Thus again, the consumption of rewards is still present in MDD patients, but the positive anticipatory stimulus and motivation to obtain these rewards is diminished. Anhedonia in depression is primarily associated with a deficit in non-consummatory reward behaviors

Anticipation, motivation, and learning is a result of dopaminergic signaling as related to pleasurable stimuli; However, dopamine signaling is not related to the consumption of pleasurable items. When there is an unexpected result, the Ventral tegmental area (VTA) fires off signals as there is ‘new learning’ to be had regarding the event. A violation of an expected reward involves dopamine signaling and reward learning. The VTA connects to the Nucleus accumbens where reward motivation is processed. 

Other areas involved with reward processing and receive or send out dopaminergic neurons include: 

These areas are recruited during reward processing. 

We are aware of motivational disorders in MDD yet there is not much direct evidence of dopamine signaling errors in MDD. However, medications that involve dopaminergic stimulation, such as Pramipexole, a D2 agonist, has been found to help MDD and Bipolar Depression (BD). 

Ketamine acts on the glutamate system, which is impacted in depression. Blocking glutamate uptake into astrocytes in animal models resulted in anhedonia, and ketamine, an NMDA-receptor antagonist, reversed anhedonia-type behaviors in lab animals placed under stressful conditions.  

Ketamine improved dopaminergic and glutamate signaling pathways  to the prefrontal cortex and decreased anhedonia symptoms. Ketamine reverses anticipatory anhedonia through these pathways. 

18FDG-PET measures glucose metabolism.  Glial uptake of glucose in response to glutamate release from neurons principally reflects glutamatergic neurotransmitter release and cycling which determines much of glucose metabolism in the brain. Glucose in the brain is transformed into glutamate and this is the basis for using PET scanning to determine regional brain metabolism and glutamate metabolism. 

One study used a randomized, placebo-controlled, double-blind crossover design to examine whether a single ketamine infusion could reduce anhedonia levels in 36 patients with treatment-resistant bipolar depression and also evaluated PET scans of the brain to determine the neurobiological basis of anhedonia. The study demonstrated that the reduction of anhedonia was independent from the reduction of depression, and the reduction of anhedonia was related to increased glucose metabolism in the dorsal anterior cingulate cortex and putamen.   

The study evaluating the efficacy of ketamine for anhedonia involved 36 patients with BD who were given one dose of ketamine and a follow-up PET scan to determine glucose metabolism in the brain.  

  • Ketamine rapidly reduced anhedonia with results lasting 14 days in many. 
  • Anhedonia reduction was independent of depressive symptom reduction. 
  • PET scanning revealed that the dorsal anterior cingulate nucleus (DACC) had a resulting increase in metabolism. 
  • There are no other treatments available for anhedonia despite its presence in many mental health disorders. 
  • Improvement in depression was associated with increased ventral striatum glucose metabolism following ketamine infusions yet this area is not involved in anhedonia relief. 
  • Areas of the nucleus accumbens (NAC) that have opioid receptors are involved with the ‘liking’ of hedonistic activities or consummatory pleasures. 
  • Motivational behavior centers in the brain achieve their innervation from multiple receptors in the NAC. 
  •  Patients showing the greatest antidepressant response to ketamine, as measured by the MADRS ( a depression scoring system) , may be experiencing high levels of pleasure. The anhedonia scale (SHAPS) might not be sensitive enough to distinguish the pleasure of being less depressed from low motivation that anhedonia produces. 
  • This study found that increased glucose metabolism in the putamen and DACC resulted in much improvement in anhedonia separate from the relief in depression. 
  • Both the dACC and putamen are highly involved in reward processinglearning and decision-making
  • The dACC has also been strongly linked with the anticipation of rewarding events in humans. 
  • Deficits in the ability to imagine future events, particularly positive ones, have been reliably identified in MDD patients experiencing an MDE. The ability to anticipate pleasure is associated with the diminishing of depression. 
  • Other studies, as did this one, demonstrated that anticipating a reward such as a sugary snack elicited heightened activity in the right putamen compared with anticipating a punishment (salt water). Levels of anhedonia, as measured by the Fawcett–Clark Pleasure Scale, were positively correlated with activity in the right putamen during an emotional face-processing task that required MDD patients to compare sad and neutral faces. Other measures of anhedonia include a SAAS self-assessment scale for anhedonia
  • Studies of the medial prefrontal cortex (mPFC) (an area of decision-making and anti-depressant area) demonstrate that the synaptogenic and antidepressant-like effects of a single dose of ketamine in rodents are dependent upon activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) signaling pathway together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its inhibitory in influence on mTOR. The use of lithium allows this inhibition of GSK-3 and may be useful for improvement of the anti-anhedonia effects of ketamine as found in one study
  • Lithium may enhance the anti-anhedonic effects of ketamine in individuals with BD through enhanced plasticity and antidepressant-like effects. 
  • Glutamate has a central role in anhedonia and depression
  • Ketamine is also a partial agonist of the dopamine D2 receptor and it has been found to increase dopamine levels in the striatum, including the caudate and the putamen. Of note, in MDD patients with motor retardation, there are lower extracellular levels of dopamine. Ketamine may, in part, modulate dopamine levels in anhedonia and depression through its initial effects of glutamate, which then affect the dopamine systems of reward. 
  • recent study in primates demonstrated that an “area 25” of the brain was overactive in anhedonia models of depression and ketamine could decrease that overactivity. 
  • Anhedonia is present in many psychiatric and neurological illnesses, such as schizophrenia, Parkinson’s disease, drug addiction and both mood and anxiety disorders. Anhedonia influences outcomes of treatment and needs to be monitored. 
  • Ketamine ameliorates anhedonia independent of its already considerable antidepressant effects. 
  • Ketamine is the only medication available to treat and improve anhedonia. 

recent study from the Canadian Rapid Treatment Center for Depression demonstrated that ketamine infusions can rapidly treat consummatory anhedonia symptoms in depression and relieve suicidality, depression, and anxiety. Again, there are no effective treatments outside of ketamine therapy for the anhedonia that accompanies depression, so if you have improved your depression but still have no energy, motivation, or sense of enjoyment, ketamine therapy may offer an additional line of treatment to make you feel more excited about the basic things in life. It is time to find the next great adventure. 

NOVA Health Recovery Ketamine Infusion Center utilizes ketamine therapies for the treatment of depression and anhedonia. Why suffer with low motivation, loss of pleasure and interest, anxiety, and brain fog? Traditional medications may improve some measures of depression, but ketamine can provide rapid relief in many for both their depression and anhedonia. No other medication has demonstrated the ability to restore hope and anticipation of pleasures as can ketamine therapy in the setting of anhedonia. Ketamine targets key areas of the brain to restore the appropriate reward circuitry to lead a more fulfilling life. The ability to have the energy and motivation for your next adventure is crucial for your happiness. This is where ketamine therapy may be able to bridge the gaps your other treatments could not. 

NOVA Health Recovery is a Ketamine Treatment Center in Fairfax, Virginia (Northern Virginia Ketamine) that specializes in the treatment of depression, anxiety, bipolar disorder, OCD, and chronic pain such as CRPS, cluster headaches, and fibromyalgia using Ketamine therapies. We offer ketamine infusions and home-based ketamine nasal spray and oral tablets. For CRPS, we offer multi-day, high-dose infusions and prescriptions for maintenance ketamine therapies for home. We utilize integrative psychiatric therapies for mood disorders as well and offer IV Vitamin support as well as IV NAD+ for mental health, pain, opioid detox, and mood disorders. We also offer addiction treatment services with Suboxone, Vivitrol, and Sublocade therapies for opiate addiction as well as alcohol treatment regimens. Contact us at 703-844-0184 for more information or to schedule. No referral is needed. 

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Ketamine Provider | Ketamine near me | Psychedelic assisted therapy | Mushrooms | Ketamine assisted psychotherapy | Ketamine psychedelic therapy | KAP | K hole | New depression Treatments | Areas we serve: 

Maryland (MD): 

Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902 

Washington DC: 

Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016 

Northern Virginia: 

McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304  Fairfax – 20191 – Reston – 22009 – Springfield – 22152  22015  Lorton 22199 

Fairfax, Va 

2303 –  22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312 

22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 –  20124 

22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043 

22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101 

22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153 

22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 –  22182 

Woodbridge – 22191 – 22192 -22193 -22194 – 22195  

Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161  

Front Royal 22630 

Warren County 22610 22630 22642 22649 

Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412  

Please call Sendi Hair Loss Center now at 703-574-0974 for quality Hair Restoration services in Alexandria, VA. 

20105 Aldie Loudoun County 20106 Amissville Culpeper County 20107 Arcola Loudoun County 

20108 Manassas Manassas City 20109 Sudley Springs Prince William County 

20109 Manassas Prince William County 20110 Manassas Manassas City 

20111 Manassas Prince William County 20111 Manassas Park Prince William County 

20112 Manassas Prince William County 20113 Manassas Park Manassas Park City 

20115 Marshall Fauquier County 20116 Marshall Fauquier County 

20117 Middleburg Loudoun County 20118 Middleburg Loudoun County 

20119 Catlett Fauquier County – 20120 Sully Station Fairfax County 

20120 Centreville Fairfax County – 20121 Centreville Fairfax County 

20122 Centreville Fairfax County – 20124 Clifton Fairfax County 

20128 Orlean Fauquier County -20129 Paeonian Springs Loudoun County 

20130 Paris Clarke County 

20131 Philomont Loudoun County 20132 Purcellville Loudoun County 

20134 Hillsboro Loudoun County 20134 Purcellville Loudoun County 

20135 Bluemont Clarke County 20136 Bristow Prince William County 

20137 Broad Run Fauquier County 20138 Calverton Fauquier County 

20139 Casanova Fauquier County 20140 Rectortown Fauquier County 

20141 Round Hill Loudoun County 20142 Round Hill Loudoun County 

20143 Catharpin Prince William County 

20144 Delaplane Fauquier County20146 Ashburn Loudoun County 

20147 Ashburn Loudoun County 20148 Brambleton Loudoun County 

20148 Ashburn Loudoun County 20151 Chantilly Fairfax County 

20151 Fairfax Fairfax County 20152 South Riding Loudoun County 

20152 Chantilly Loudoun County 20152 Fairfax Loudoun County 

20153 Chantilly Fairfax County 20153 Fairfax Fairfax County 

20155 Gainesville Prince William County 20156 Gainesville Prince William County 

20158 Hamilton Loudoun County 20159 Hamilton Loudoun County 

20160 Lincoln Loudoun County 20160 Purcellville Loudoun County 

20163 Sterling Loudoun County 20164 Sterling Loudoun County 

20165 Potomac Falls Loudoun County 20165 Sterling Loudoun County 

20166 Dulles Loudoun County 20166 Sterling Loudoun County 

20167 Sterling Loudoun County 20168 Haymarket Prince William County 

20169 Haymarket Prince William County 20170 Herndon Fairfax County 

20171 Oak Hill Fairfax County 20171 Herndon Fairfax County 

20172 Herndon Fairfax County 20175 Leesburg Loudoun County 

20176 Lansdowne Loudoun County 20176 Leesburg Loudoun County 

20177 Leesburg Loudoun County 20178 Leesburg Loudoun County 

20180 Lovettsville Loudoun County 20181 Nokesville Prince William County 

20182 Nokesville Prince William County 20184 Upperville Fauquier County 

20185 Upperville Fauquier County 20186 Warrenton Fauquier County 

20187 New Baltimore Fauquier County 20187 Vint Hill Farms Fauquier County 20187 Warrenton Fauquier County 

20188 Vint Hill Farms Fauquier County 20188 Warrenton Fauquier County 

20190 Reston Fairfax County 20190 Herndon Fairfax County 

20191 Reston Fairfax County 20191 Herndon Fairfax County 

20194 Reston Fairfax County 20194 Herndon Fairfax County 

20195 Reston Fairfax County 20195 Herndon Fairfax County 

20197 Waterford Loudoun County 20198 The Plains Fauquier County 

Loudon County: 

Loudoun County, VA – Standard ZIP Codes 

20105 | 20117 | 20120 | 20129 | 20130 | 20132 | 20135 | 20141 | 20147 | 20148 | 20152 | 20158 | 20164 | 20165 | 20166 | 20175 | 20176 | 20180 | 20184 | 20189 | 20197 | 22066 

Ketamine Infusions for Depression and Psychedelic Assisted Psychotherapy – Ketamine and psilocybin therapy | Northern Virginia Ketamine Infusion Center

NOVA Health Recovery Ketamine Infusion Center offers Ketamine infusions for Depression, Anxiety, PTSD, Chronic pain. We use intravenous and oral ketamine along with ketamine assisted psychotherapy (KAP) to treat multiple mood disorders. Northern Virginia Ketamine | Contact us below by email and leave your phone number as well, or call 703-844-0184 for an immediate appointment. 

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Recently, the United Kingdom has opened the first centers for psychedelic therapy for depression. Awakn Life is the name of the psychedelic-assisted psychotherapy center and is providing psychedelics to treat mood disorders and addictions. A recent article in the Guardian addressed the state of psychedelics in the U.K. where more permissive laws have enabled more productive research into psychedelic use in depression and addictions. The traditional psychiatric approach of FDA approved medications results in poor outcomes with addiction still remaining a significant cause of morbidity and over 1/3 of patients with depression failing multiple courses of medications. Talk therapy is effective in 50% of patients. In fact, if you see a psychiatrist at the age of twenty, you will still be his patient at the age of sixty in all likelihood.  

Psilocybins can be grown with home kits ordered online. Although illegal in many areas of the United States, many people have tried to use ‘magic mushrooms’ to heal their depressed or inflamed brain. Studies demonstrate the efficacy of 10-25 mg of psylocibins with talk therapy as being effective for depression for up to 6 months. Currently, psilocybin therapy is being studied in the United States and has been given a break-through status with the FDA. A study of 24 patients at Johns Hopkins demonstrated a significant improvement in treatment resistant depression in 70% of patients that lasted 4 weeks. 

Ketamine is currently available and FDA approved as a nasal spray Esketamine. Ketamine, in the form of infusions, is being used in centers throughout the United States and has demonstrated significant efficacy for TRD in studies dating back to 2000 and 2006. Continued studies have shown its effect in Bipolar depression and suicidality. Intravenous forms of ketamine are more reliable and rapid, yet other formulations can be effective, including nasal sprays and oral formulations. Chronic suicidality has been successfully treated with low-dose oral ketamine in one study in which weekly doses of oral ketamine at doses of 0.5 mg/kg up to 3 mg/kg were administered. Other studies of oral therapies for depression have demonstrated efficacy as well.  The effects of ketamine infusions have been found to be potentially more effective as a series of six infusions and then can be maintained effectively with home-based oral and nasal spray therapies, intermittent infusions, and medications such as D-cycloserine

Ketamine and psychedelic therapy represent a potentially more effective and rapid treatment of depression and mood disorders. Contact NOVA Health Recovery Ketamine Infusion Center in Alexandria, Virginia for more information on ketamine treatments that include infusions, oral ketamine, and home-based ketamine support for depression, anxiety, PTSD, Bipolar disorder, and pain.  

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NOVA Health Recovery is a Ketamine Treatment Center in Fairfax, Virginia (Northern Virginia Ketamine) that specializes in the treatment of depression, anxiety, bipolar disorder, OCD, and chronic pain such as CRPS, cluster headaches, and fibromyalgia using Ketamine therapies, both infusion and home-based ketamine nasal spray and oral tablets. We also offer addiction treatment services with Suboxone, Vivitrol, and Sublocade therapies for opiate addiction as well as alcohol treatment regimens. Contact us at 703-844-0184 or at this link: NOVA Health Recovery Ketamine Infusion Center Near me Ketamine Infusion 

Ketamine Provider | Ketamine near me | Psychedelic assisted therapy | Mushrooms | Ketamine assisted psychotherapy | Ketamine psychedelic therapy | KAP | K hole | New depression Treatments | Areas we serve: 

Maryland (MD): 

Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902 

Washington DC: 

Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016 

Northern Virginia: 

McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304  Fairfax – 20191 – Reston – 22009 – Springfield – 22152  22015  Lorton 22199 

Fairfax, Va 

2303 –  22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312 

22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 –  20124 

22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043 

22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101 

22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153 

22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 –  22182 

Woodbridge – 22191 – 22192 -22193 -22194 – 22195  

Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161  

Front Royal 22630 

Warren County 22610 22630 22642 22649 

Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412  

Please call Sendi Hair Loss Center now at 703-574-0974 for quality Hair Restoration services in Alexandria, VA. 

20105 Aldie Loudoun County 20106 Amissville Culpeper County 20107 Arcola Loudoun County 

20108 Manassas Manassas City 20109 Sudley Springs Prince William County 

20109 Manassas Prince William County 20110 Manassas Manassas City 

20111 Manassas Prince William County 20111 Manassas Park Prince William County 

20112 Manassas Prince William County 20113 Manassas Park Manassas Park City 

20115 Marshall Fauquier County 20116 Marshall Fauquier County 

20117 Middleburg Loudoun County 20118 Middleburg Loudoun County 

20119 Catlett Fauquier County – 20120 Sully Station Fairfax County 

20120 Centreville Fairfax County – 20121 Centreville Fairfax County 

20122 Centreville Fairfax County – 20124 Clifton Fairfax County 

20128 Orlean Fauquier County -20129 Paeonian Springs Loudoun County 

20130 Paris Clarke County 

20131 Philomont Loudoun County 20132 Purcellville Loudoun County 

20134 Hillsboro Loudoun County 20134 Purcellville Loudoun County 

20135 Bluemont Clarke County 20136 Bristow Prince William County 

20137 Broad Run Fauquier County 20138 Calverton Fauquier County 

20139 Casanova Fauquier County 20140 Rectortown Fauquier County 

20141 Round Hill Loudoun County 20142 Round Hill Loudoun County 

20143 Catharpin Prince William County 

20144 Delaplane Fauquier County20146 Ashburn Loudoun County 

20147 Ashburn Loudoun County 20148 Brambleton Loudoun County 

20148 Ashburn Loudoun County 20151 Chantilly Fairfax County 

20151 Fairfax Fairfax County 20152 South Riding Loudoun County 

20152 Chantilly Loudoun County 20152 Fairfax Loudoun County 

20153 Chantilly Fairfax County 20153 Fairfax Fairfax County 

20155 Gainesville Prince William County 20156 Gainesville Prince William County 

20158 Hamilton Loudoun County 20159 Hamilton Loudoun County 

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Ketamine infusions for depression | Depression scoring | Inflammation and brain shrinkage from depression – why you should worry | NOVA Health Recovery Ketamine Infusion Center Fairfax, Virginia 22304

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Depression may be, in part, a chemical imbalance in the brain, such as aberrant serotonin (‘the happy neurotransmitter) or dopamine (the molecule of reward) levels. However, depression can be initiated at several levels, including the gut, due to alterations in the gut microbiome and general inflammation. It has been found that elevated markers of inflammation, such as C-reactive protein (CRP) and Interleukin-6 (IL-6) can be markers of and lead to increased depression. These markers rise in stress, obesity, general medical illness, and from gut dysbiosis (poor microbial health in the gut) to name a few. This can lead to brain fog, poor motivation, difficulty with concentration, memory loss, difficulty making decisions (executive functioning), poor processing speed, and even weight gain.  

Over 7 % of the nation suffers from depression – that is about 16.1 million people, per the National Institutes of Mental Health. Women are twice as likely to be depressed as are men. Some of this may be due to hormonal imbalances. The chance of women becoming depressed in their lifetime is 21-45 % while it is 10-30% for men. 

There are multiple causes for depression, which include stress, poor nutrition, genetics, medications, general medical illness, obesity, lack of exercise, poor sleep, drugs and alcohol, leaky gut, hormonal imbalances, inflammation, and several other factors.  

We frequently assess depression by using the basic PHQ-9 – the physicians health questionnaire that is 9 questions based on a scale of 0-3. The questions are based on the last two weeks of feelings: Link to a PHQ calculator 

1.Little interest or pleasure in doing things 

2.Feeling down, depressed or hopeless 

3.Trouble falling asleep, staying asleep, or sleeping too much 

4.Feeling tired or having little energy 

5.Poor appetite or overeating 

6.Feeling bad about yourself – or that you’re a failure or have let yourself or your family down 

7.Trouble concentrating on things, such as reading the newspaper or watching television 

8.Moving or speaking so slowly that other people could have noticed. Or the opposite – being so fidgety or restless that you have been moving around a lot more than usual 

9.Thoughts that you would be better off dead or of hurting yourself in some way 

These are scored on a scale of 0-3: 

0 – for not at all 

1- For several days in the past two weeks 

2- For more than half the days 

3–  For nearly every day. 

The score results are graded as the following: 

Score Depression Severity Treatment 
0 – 4 None-minimal None 
5 – 9 Mild Watchful waiting; repeat PHQ-9 at follow-up 
10 – 14 Moderate Treatment plan, considering counseling, follow-up and/or pharmacotherapy 
15 – 19 Moderately Severe Active treatment with pharmacotherapy and/or psychotherapy 
20 – 27 Severe Immediate initiation of pharmacotherapy and, if severe impairment or poor response to therapy, expedited referral to a mental health specialist for psychotherapy and/or collaborative management 

The importance of treating depression is several fold. One is to get you feeling better. Many patients will eat excessively and gain weight to comfort themselves. Excess adipose tissue results in inflammation in the brain that leads to further depression and cognitive deficits. Others may resort to self-medication with alcohol or opioids that leads to addiction. In other cases, the person may continue a downward spiral in both their personal life, with family discord and personal unfulfillment, as well as work-related loss, such as absenteeism and presenteeism (showing up but not doing their job). The ability to concentrate and focus is much worse when depression sets in. In fact, depression has been found to physically decrease the size of the hippocampus on MRI(the memory center of the brain) as well as the prefrontal cortex (involved with decision-making and executive functioning).  See the following general mainstream article: Chronic Depression Shrinks the Brain’s Memories and Emotions  (ENIGMA research) .  

An individual who is depressed and sitting in a room will continue to have their hippocampus and prefrontal cortex shrink due to depression and the inflammation that results. Such individuals will have difficult with memory, emotional regulation, processing speed, and decision-making. Aggressive treatment for depression should be sought as it is possible to regenerate these vital areas of the brain with treatment, such as Ketamine therapy and lifestyle interventions like exercise and nutrition. Concerning nutritionhigh adherence to dietary recommendations, anti-inflammatory diet, fish consumption, exclusion of processed foods, and adequate intake of folic acid, magnesium different fatty acids, were associated with a reduced risk of mental illness. Suggestions for nutritional changes can be found at nutritionfactshealthyplacenutritionkits, and everydayhealth as a few options for ideas. 

Ketamine therapy, as a series of infusions, demonstrates rapid reversal of depression and suicidality. It is an anti-inflammatory agent that increases Brain Derived Neurotrophic Factor (BDNF) to increase neuroplasticity and allows the formation of new connections in the brain. This decreases depression and can be seen on MRI’s to increase the volume and functioning of the hippocampus (memory center). We will discuss more information regarding ketamine therapies in upcoming articles. Refer to NOVA Health Recovery for more information as well. 

Structural changes in the hippocampus in major depressive disorder: contributions of disease and treatment  

J Psychiatry Neurosci. 2010 Sep; 35(5): 337–343.doi: 10.1503/jpn.100002 

Redlich, R., Opel, N., Bürger, C. et al. The Limbic System in Youth Depression: Brain Structural and Functional Alterations in Adolescent In-patients with Severe Depression. Neuropsychopharmacol. 43, 546–554 (2018). https://doi.org/10.1038/npp.2017.246 

Hippocampal Volume and Depression: A Meta-Analysis of MRI Studies  

Jacka, F.N., Cherbuin, N., Anstey, K.J. et al. Western diet is associated with a smaller hippocampus: a longitudinal investigation. BMC Med 13, 215 (2015). https://doi.org/10.1186/s12916-015-0461-x 

Gujral S, Aizenstein H, Reynolds CF 3rd, Butters MA, Erickson KI. Exercise effects on depression: Possible neural mechanisms. Gen Hosp Psychiatry. 2017 Nov;49:2-10. doi: 10.1016/j.genhosppsych.2017.04.012. PMID: 29122145; PMCID: PMC6437683

Evidence of the Importance of Dietary Habits Regarding Depressive Symptoms and Depression Ljungberg T, Bondza E, Lethin C. Evidence of the Importance of Dietary Habits Regarding Depressive Symptoms and Depression. Int J Environ Res Public Health. 2020;17(5):1616. Published 2020 Mar 2. doi:10.3390/ijerph17051616 

Huang Q, Liu H, Suzuki K, Ma S, Liu C. Linking What We Eat to Our Mood: A Review of Diet, Dietary Antioxidants, and Depression. Antioxidants (Basel). 2019;8(9):376. Published 2019 Sep 5. doi:10.3390/antiox8090376 

Koebnick C, Black MH, Wu J, et al. A diet high in sugar-sweetened beverage and low in fruits and vegetables is associated with adiposity and a pro-inflammatory adipokine profile. Br J Nutr. 2018;120(11):1230-1239. doi:10.1017/S0007114518002726 

Vermeulen E, Stronks K, Snijder MB, Schene AH, Lok A, de Vries JH, Visser M, Brouwer IA, Nicolaou M. A combined high-sugar and high-saturated-fat dietary pattern is associated with more depressive symptoms in a multi-ethnic population: the HELIUS (Healthy Life in an Urban Setting) study. Public Health Nutr. 2017 Sep;20(13):2374-2382. doi: 10.1017/S1368980017001550. Epub 2017 Jul 20. PMID: 28724468. 

Opie RS, Itsiopoulos C, Parletta N, Sanchez-Villegas A, Akbaraly TN, Ruusunen A, Jacka FN. Dietary recommendations for the prevention of depression. Nutr Neurosci. 2017 Apr;20(3):161-171. doi: 10.1179/1476830515Y.0000000043. Epub 2016 Mar 2. PMID: 26317148. 

Depression Nutrition Fact Sheet  

Healthy Eating and depression 

Eating your way to recovery in depression 

Food For the Brain 

Ketamine and its effects on the brain and mental health 

Zhou, Y., Wu, F., Liu, W. et al. Volumetric changes in subcortical structures following repeated ketamine treatment in patients with major depressive disorder: a longitudinal analysis. Transl Psychiatry 10, 264 (2020). https://doi.org/10.1038/s41398-020-00945-9  

Ionescu DF, Felicione JM, Gosai A, et al. Ketamine-Associated Brain Changes: A Review of the Neuroimaging Literature. Harv Rev Psychiatry. 2018;26(6):320-339. doi:10.1097/HRP.0000000000000179 

https://www.researchgate.net/publication/264794534_Hippocampal_Volume_And_The_Rapid_Antidepressant_Effect_Of_Ketamine

Prefrontal Cortex Connectivity and BDNF Fluctuations May Play a Role in Ketamine Mechanism of Action 

Corriger A, Pickering G. Ketamine and depression: a narrative review. Drug Des Devel Ther. 2019;13:3051-3067. Published 2019 Aug 27. doi:10.2147/DDDT.S221437 

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Recent research has shown that ketamine has considerable promise for treating a wide range of treatment-refractory neuropsychiatric disorders, including obsessive compulsive disorder (OCD), post-traumatic stress disorder (PTSD), bipolar disorder, suicide ideation, addiction and, most notably, treatment-resistant major depressive disorder (MDD). Although this research has taken place almost exclusively within the past two decades, evidence of ketamine’s neuropsychiatric effects appeared long before this. For example, ketamine was used throughout the 1970s in Mexico as part of psychedelic therapy sessions that combined traditional healing practices with psychoanalytic techniques.

In 2000, researchers found that ketamine had strong, fast-acting, and long-term effects in depression. In a randomized, placebo-controlled, crossover design study, patients with depression received 0.5 mg/kg of ketamine or saline on the first day of testing. Treatments were switched 1 week later. Researchers found that the antidepressant effects of ketamine began within 4 hours, peaked at 72 hours, and lasted for 1 to 2 weeks thereafter.1 In a 2006 study, this finding was replicated in an independent group of 18 patients with major depressive disorder who were resistant to other treatments. Compared with participants who received placebo, those who received ketamine showed significant improvement in symptoms within 110 minutes, with 35% maintaining significant response for at least 1 week.

Many of today’s depression treatments are monoaminergic-based, including monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin-norepinephrine reuptake inhibitors. These treatments have been proven effective for a large number of patients. However, a significant subset of patients with major depressive disorder do not respond to these agents. Despite its undisputed value to the field, the monoamine hypothesis of depression cannot fully explain the heterogeneity of MDD. In the 1990s, animal models began to implicate glutamate – one of the major excitatory neurotransmitters in the mammalian central nervous system (CNS) – as well as its ionotropic NMDA receptor in the etiology and treatment of mood disorders .

Existing antidepressant treatments [MAOIs, TCAs, SSRIs, and serotonin-norepinephrine reuptake inhibitors (SNRIs)] are monoaminergic-based treatments. Although they have been in use for decades and have helped many patients, a significant subset of MDD patients showed little to no therapeutic benefit in response to these agents. For instance, the NIMH-funded, communitybased Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study of >4000 MDD patients found that, even after four unique medication trials, augmentation, or switch, 33% of the patients did not respond to standard monoaminergic-based treatments .

In 2000, Berman and colleagues discovered that ketamine exerted rapid, robust, and relatively sustained antidepressant effects in depressed patients . Using a randomized, placebo-controlled, crossover design, each patient received an i.v. infusion of 0.5 mg/kg of either ketamine or saline on the first test day. On the following test day, which took place at least 1 week later, treatments were switched. The authors found that ketamine exerted antidepressant effects that began within 4 h of the infusion, peaked at 72 h, and persisted for 1–2 weeks post-infusion. .Ketamine has also been shown to have distinct and independent antisuicidal and anti-anhedonic effects in patients with mood disorders .

Another limitation of currently available antidepressants is that their clinical effects take more time to reach their full therapeutic potential (for instance, the mean onset for paroxetine is 13 days). This is a substantial disadvantage during an acute depressive crisis. Furthermore, even when these agents do alleviate depressive symptoms, evidence regarding their ability to successfully reduce suicide ideation and behavior remains inconclusive . In contrast, a single dose (0.5 mg/kg) of i.v. ketamine exerts rapid and profound antidepressant effects within hours to days of administration . Ketamine also rapidly reduces suicidel ideation, an effect that appears to occur independently of its antidepressant properties . Ketamine has dose-dependent neuropsychological effects even at subanesthetic doses, with antidepressant properties peaking at 0.5–1.0 mg/kg.

Ketamine’s pan-therapeutic effects also include alleviating fatigue and anhedonia as well as improving sleep measures such as circadian rhythm and slow-wave activity in MDD patients .

The positive effects of Ketamine has led to research into other rapidly acting antisdepressants, including nasal ketamine. Lapidus and colleagues demonstrated that intranasal ketamine had antidepressant effects and led to sufficiently high ketamine plasma concentrations. We use a compounded intranasal ketamine miuxture in our office at NOVA Health Recovery. There is also an FDA approved version more recently, which has only the S-Ketamine in it . There are heavy restrictions and high costs to the FDA approved version, yet efficacy may not be any better.

Noitrois Oxide also has antidepressant effects. Like ketamine, it exhibits NMDA receptor antagonism, has partial agonism for mu, kappa, and delta opioid receptors, inhibits AMPA, kainite, and gamma-aminobutyric acid receptors A and C (GABAA, GABAC), affects serotonin-3 receptors (5-HT3), and releases dopamine . In a double-blind, placebo-controlled, crossover trial, depressive symptoms improved for participants receiving nitrous oxide within 2 h compared with those receiving placebo, an effect that remained significant at 1 day post-treatment. Phase I and II trials are ongoing to determine optimal dose, safety, and efficacy.

Sarcosine also has antidepressant effects. t, sarcosine (also known as N-methylglycine), is an amino acid that functions as a glycine transporter-1 inhibitor and a 6- week, double-blind, randomized, citalopram-controlled trial in 20 MDD patients found that sarcosine possessed superior antidepressant properties compared with citalopram after 2 weeks . Notably, and in contrast to ketamine, sarcosine did not result in rapid-acting effects on the timescale of several days. Sarcosine has co-agonistic properties at the NMDA receptor and is an agonist at the inhibitory glycine receptor. It also exhibits NMDA-enhancing properties, suggesting that AMPA-receptor-mediated or other downstream mechanisms might elicit antidepressant effects. NMDA receptor downregulation might also play a part .

Suboxone (Buprenorphine) also has antidepressant effects as well. Intrigued by the potential of nonaminergic antidepressant mechanisms, researchers have begun to re-evaluate the role of endogenous opioids in depression. For instance, buprenorphine (BUP), a drug currently used to treat opioid addiction and pain disorders, is being explored as a treatment for MDD. The compound has a wide variety of actions throughout the brain, including partial agonism at the mu opioid receptor and antagonism at the kappa and delta opioid receptors ; these are connected to intracellular signaling cascades that potentially mediate antidepressant effects Several open-label studies of BUP in MDD have shown promising preliminary results, and a double-blind, randomized, placebo-controlled trial examining the effect of low-dose BUP on suicidal ideation similarly yielded positive results .

NOVA Health Recovery has used buprenorphine succesfully in the treatment of depression.

Ketamine and Future Depression Treatments

1. Kraus C, Wasserman D, Henter ID, Acevedo-Diaz E, Kadriu B, Zarate CA Jr. The influence of ketamine on drug discovery in depression [published online August 2, 2019]. Drug Discov Today. doi: 10.1016/j.drudis.2019.07.007

2. Zarate CA Jr, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depressionArch Gen Psychiatry. 2006;63(8):856-64.

3. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trialBiol Psychiatry. 2015;78(1):10-18.

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Treating Alcohol Use with Ketamine? New Research Finds It May Help

  • Results from new studies suggest that ketamine may be effective in treating alcohol use disorder.
  • Researchers found that when participants were treated with ketamine instead of midazolam, a sedative that helps with alcohol withdrawal, they had higher rates of stopping drinking following treatment.
  • They were also less likely to relapse, had fewer days of drinking, and had fewer days of heavy drinking.

Once derided as a “club drug,” the anesthetic ketamine is facing a surge of interest from doctors and researchers who say it could treat certain psychiatric disorders. The most prominent among them: depression.

However, a pair of new studies show promise for a new area of ketamine therapy: alcohol use disorder.

Both studies are early indicators that ketamine could, along with other alcohol interventions like therapy, some day help people decrease or stop drinking. But there’s a lot more research to be done.

The first study, published earlier this month in The American Journal of Psychiatry, was a pilot study, the first of its kind, to test the effects of ketamine and mindfulness practice against a control for alcohol use disorder.

The study included 40 participants who, on average, consumed about 5 drinks per day. Most of the participants were white, and most were employed.

Participants were randomly assigned to either receive a single infusion of ketamine along with a 5-week regimen of motivational enhancement therapy, or midazolam, a sedative that helps with alcohol withdrawal, and the same therapy.

Researchers found that participants who received ketamine rather than midazolam had higher rates of abstinence (stopping drinking) following treatment, were less likely to relapse, had fewer days of drinking, and had fewer days of heavy drinking.

The beneficial results of the ketamine also persisted for several weeks after the single dose infusion.

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If you would like a consultation for Ketamine for alcoholism treatment in Virginia, call 703-844-0184 or email Northern Virginia Ketamine Infusion Center

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Ketamine may treat harmful drinking behavior by ‘rewriting drinking memories,’ researchers say

(CNN)A single dose of ketamine may be able to curb harmful drinking behavior by “rewriting drinking memories,” according to a study published Tuesday in the journal Nature Communications.The researchers say that, when coupled with an exercise involving beer that pulls memories of alcohol to the foreground, there’s evidence that the drug can disrupt how the brain associates these cues — like the smell or taste of beer — to its perceived “reward,” making relapse less likely.”It’s those kinds of associations that we’re trying to break down,” explained study author Ravi Das, an associate professor at University College London who specializes in psychopharmacology. “We’re not talking about people’s explicit recollection of the fact that they drank in the past.” FDA approves ketamine-like nasal spray for depressionKetamine is a powerful medication used in hospitals primarily as an anesthetic, though it has also been used illegally as a club drug, often referred to as Special K. It generates an intense high and dissociative effects.  “It’s an intriguing approach that builds on existing literature in a couple of areas,” said Dr. Henry Kranzler, a professor of psychiatry at the University of Pennsylvania Perelman School of Medicine, who was not involved in the study.Earlier studies have explored ketamine for alcohol, cocaine and opioid addiction — but many had small sample sizes, limited follow-up and lack of placebo, according to experts. Das said it’s also difficult to blind participants to whether they’ve received ketamine or a placebo because of its “strong effects.”Other research has shown the drug’s potential to counter depression and suicidal ideation. In March, a close relative of ketamine — called esketamine and sold under the name Spravato in the form of a nasal spray — was approved by the US Food and Drug Administration for treatment-resistant depression.The new study recruited 90 “beer-preferring” people with potentially harmful drinking patterns from internet ads and separated them into groups: those who underwent an exercise involving alcohol-related cues and received intravenous ketamine in a controlled environment; those who completed the exercise but received a placebo; and those who received ketamine alone. While the authors said participants “showed a clearly harmful and problematic pattern of drinking,” they were not seeking treatment for an alcohol use disorder and had not been formally diagnosed with such.  But there was some heterogeneity between the groups. While the first group reduced their drinking to the largest degree, they also happened to drink more to begin with — “and therefore their consumption was more likely to decline, a phenomenon known as regression to the mean,” explained Matt Field, a professor of psychology at the University of Sheffield in the UK, in an emailed statement.After the treatment, there wasn’t a significant difference between the three groups in terms of how much alcohol they drank. Nine months later, average weekly consumption was roughly the same across the board. The authors say this may have been influenced by losing participants to follow-up.Field said the findings are “promising,” but the claim that the full treatment protocol “leads to ‘unprecedented’ long-lasting reductions in alcohol consumption are not justified on the basis of this data.”Das pointed out other layers to the data, however: Those who completed the exercise and received ketamine had less desire to drink, and they drank less frequently. In addition, there was a correlation among that group between concentrations of ketamine and its breakdown products in the blood, and the reduction in how much participants drank.”People all vary in how quickly they metabolize” and excrete ketamine and its byproducts, Das said. “That level of individual variability with ketamine actually predicts drinking outcomes subsequently.” 

The group that received ketamine alone saw improvements, too, but not to the same degree as those presented with alcohol-related cues, according to the authors.Kranzler said the study is an intriguiguing proof-of-principle that he suspects will spur subsequent studies needed to replicated these findings.But an important question, he added, “is to what degree could combined psychosocial intervention — cognitive behavioral intervention, for example — synergize with or at least augment the pharmacological effect” of ketamine.”That’s the kind of treatment study that I think would make a lot of sense,” he added. “So this wouldn’t be used in isolation.”

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A dose of ketamine could lessen the lure of alcohol

The hallucinogenic drug may help treat addiction by weakening past memories of drinking

Ketamine can reduce harmful drinking by pharmacologically rewriting drinking memories

A single dose of ketamine may cut down problematic drinking. Taken in the right context, the hallucinogenic drug may be able to weaken the pull of the cues that trigger people to drink beer, researchers report November 26 in Nature Communications.

Ketamine’s influence on people’s drinking was modest. Still, the results might be a time when “small effects tell a big story,” says addiction researcher David Epstein of the National Institute on Drug Abuse in Baltimore. “If a seemingly small one-time experience in a lab produces any effects that are detectable later in real life, the data are probably pointing toward something important.”

The study hinges on the idea that addiction, in a way, is a memory disorder. People learn to associate a drug or alcohol with the good feelings it brings. Cues in the world, such as the smell or picture of a beer, can trigger those memories — and cravings. “We’re trying to break down those memories to stop that process from happening, and to stop people from relapsing,” says study coauthor Ravi Das, a psychopharmacologist at University College London.

Ketamine is an anesthetic, that at lower doses, has also shown promise as a treatment for severe depression (SN: 3/21/19). The drug can also affect memories. One of ketamine’s effects in the body is to interfere with a molecule called NMDA, which is involved in reforming memories after they are called up.

Das and his colleagues recruited 90 people who said they drank too much beer, though none was formally diagnosed with alcohol addiction. First, participants were exposed to pictures of beer and even got to drink one in the lab. During the experience, they rated their beer cravings, enjoyment of drinking, and after the beer was gone, the desire to have another one.

A few days later, the participants returned to the lab and were split into three groups. People in one group were again shown pictures of beer to jog their memories. To make the memory recall extra strong, the researchers served up actual beer, but then, in a twist, took it away before participants could drink it. The bait-and-switch maneuver was key, Das says. “You have to generate the element of surprise,” he says.

As a comparison, a second group was shown images of orange juice instead of beer. Then people in both of these groups got an intravenous dose of ketamine. A third group had beer memories called up, but received no ketamine.

A week after the procedure, the people who had their beer memories jogged before receiving ketamine reported less desire to drink, and less enjoyment of beer — a reduction that wasn’t as strong for the other two groups of participants. The people who had their beer-drinking memories jogged and received ketamine also reported drinking less.

The results were surprising, Das says, because attempts to curb people’s drinking in their daily lives are rarely successful (SN: 8/9/17). “You get jaded. Not a lot seems to work,” he says.

Nine months after the procedure, all of the participants, including those who hadn’t received ketamine, had roughly halved their beer drinking — an across-the-board drop that could be explained by the self-awareness that comes simply from enrolling in a study, says Epstein. “Behavior can change for all sorts of reasons that aren’t specific to the experimental treatment,” he says. The interesting thing here, he says, is the initial decline in drinking among people who had ketamine while they were reminded of beer.

More research is needed to confirm ketamine’s short-term effect on drinking, and see how long it might last. Das and his colleagues plan on testing ketamine on more people with problematic drinking habits in clinical trials. The researchers are also trying to weaken other sorts of problematic memories, such as those involved in post-traumatic stress disorder.

As a drug that can be abused, ketamine comes with baggage that may make people reluctant to see it as a way to treat addictions. But if a single dose of ketamine can slow excessive drinking, “then that’s quite an easy trade-off from a health perspective,” Das says. “If it works, it works.”

A Single Dose Of Ketamine Might Help Heavy Drinkers, Study Finds

What if a single dose of ketamine could make a heavy drinker dramatically cut back on booze?

A team at University College London thinks that ketamine may be able to “rewrite” memories that shape a person’s relationship with alcohol. Scientists say that participants who were given ketamine as part of an experimental study dramatically reduced their average alcohol intake for months after the initial dose. Their research was published Tuesday in Nature Communications.

Ketamine — sometimes known as a club drug called Special K that can produce hallucinations — has been shown to be a powerful and fast-acting treatment for depression. Researchers also are looking into whether ketamine can help patients with post-traumatic stress disorder.

The U.K. findings may signal yet another use for the drug for hard-to-treat conditions.

In general, the treatment options for alcoholism “aren’t particularly effective for the majority of people, particularly over the long term,” says Ravi Das, a UCL psychopharmacologist and the study’s lead researcher.

Das thinks part of the problem is that current remedies don’t necessarily help patients deal with positive memories of drinking that could make them want to drink again.

“When people become addicted, they’re learning that kind of behavior in response to things in their environment,” he says. “Those memories, those associative trigger memories, can be really long lasting and really kind of ingrained. And current treatments don’t target those.”

The researchers thought ketamine might be able to target a heavy drinker’s memories, particularly if people had their memories of drinking triggered just before they received a dose of the drug.

To test this, they recruited 90 people who drank much more than average — an average of about four to five pints of beer a day, or about five times the U.K.’s recommended maximum — but had not previously been diagnosed with alcoholism and were not receiving treatment.

On the first day of the experiment, participants were shown pictures of alcoholic drinks and were asked to rate how strong their urge to drink was. All of them were then allowed to drink a beer.

The next day, they were divided into three groups, and none of them received beer. One group did the exercise in which they saw pictures of drinks — to stimulate their memories — and then received a dose of ketamine. The second group saw the drinks and then got a placebo drug. The final group was shown no pictures and received ketamine.

The results were dramatic. Ten days later, those people who did the memory exercise and got ketamine reported a significant drop in their alcohol intake. A follow-up nine months into the experiment showed that their alcohol consumption was half of what it had been.

Meanwhile, the group that got ketamine and didn’t have their memories triggered saw a smaller but still significant reduction in drinking, both at the 10-day mark and nine months later. The placebo group also reported a decrease, albeit a more modest one.

From Chaos To Calm: A Life Changed By Ketamine

From Chaos To Calm: A Life Changed By Ketamine

So why would stimulating memories of drinking prior to a ketamine dose seem to be so effective in reducing alcohol consumption? Das says ketamine is thought to block certain receptors in the brain that help to “restabilize” a memory — such as pleasure from drinking. “You’re kind of stopping the restabilization, and the memory is weakened,” he notes.

John Krystal, head of the psychiatry department at Yale School of Medicine, was among the first researchers to study how ketamine could be helpful to patients who have depression. He says ketamine doesn’t erase memories but can help rewrite them.

“You can help them have a better and more balanced approach to it,” Krystal says. “Like instead of the idea that alcohol is always good no matter how much you drink … someone could instead say, ‘You know, I don’t really need to drink this much.’ “

That lines up with what the participants in the U.K. experiment reported. Das says they “kind of felt the urge to drink less” and “that might be because of this reduction in the way that environmental triggers can spark off the urge to drink.”

Krystal, who was not involved in the research, says this suggests that ketamine could be useful for other conditions that are exacerbated by certain kinds of memories. The drug, he says, could “help them to get control of what they really think and believe about things like alcohol or other drugs, abuse or their traumatic experiences, which otherwise kind of take over their lives in ways that are very maladaptive.”

“I would say this is a very cool study,” Krystal says. “And I think if the findings can be replicated, then it opens up a new window about a strategy to treat alcohol-use disorders.”

Still, he cautions that this is a fairly new idea and that “there are a lot of complexities here that need to be worked out.” Complexities such as whether people with high tolerance to alcohol respond differently to ketamine or whether there’s something inherent about ketamine that makes people want to drink less even without memory recall. “That’s just the nature of research — no single study can really answer all of the questions,” Krystal says.

Das says he hopes that one day, following more study and testing, ketamine could be used in clinical settings to help patients with alcoholism.

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Weekly Ketamine Infusions Show Initial, Repeated Depression Benefits

A new study shows that weekly ketamine infusions are associated with continued and maintained reductions in depressive symptoms among patients with treatment-resistant depression.

The findings, which are considered novel among studies assessing ketamine administration for patients with treatment-resistant depression, evidence the promising role the controversial drug could play in psychiatric care.

A team of investigators, led by Jennifer L. Phillips, PhD, an associate scientist in the Mood Disorders Research Unit at The Royal’s Institute of Mental Health Research, conducted a randomized, double-blind crossover comparison of single ketamine infusion versus active placebo control midazolam. The assessment, held with 41 participants with treatment-resistant depression at single treatment center, observed patients receive 6 open-label ketamine infusions 3 times per week over 2 once patients had a relapse of depressive symptoms.

Patients who reported a decrease of at least 50% in the Montgomery-Åsberg Depression Rating Scale (MADRS) received another 4 additional infusions once weekly in a maintenance phase.

Those administered a single ketamine infusion reported significantly reduced depressive symptoms at the primary efficacy endpoint of 24 hours post-care versus those treated with midazolam. The therapy showed cumulative antidepressant effects over repeated infusions, as well a doubling of antidepressant response rate in patients, according to linear mixed models.

Investigators found that 59% of patients met the response criteria following repeated infusions, with 3 infusions serving as the median dosage required to reach achieved response. In patients receiving weekly maintenance infusions, no further improvement in MADRS scores were reported.

The first-of-its-kind findings come just 1 month following the US Food and Drug Administration (FDA) approval of esketamine nasal spray (Spravato) for the treatment of patients with treatment-resistant depression. At the time, the therapy made history as the first novel treatment indicated for depression in 30 years—and headlines as one of the first hallucinogenic drugs to reach indication for a common condition.

Dennis Charney, MD, Dean of Icahn School of Medicine at Mount Sinai and a member of the Yale University team that led pioneering antidepressant ketamine trials in the 1990s, told MD Magazine® that microdosing or implementing controversial therapies for psychiatric care require what any other trial requires: control, safety, and a carefully-assessed standard for efficacy.

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‘Nothing less than transformational:’ Ketamine brings relief to people with severe depression

Ketamine gave Rachel Morgan her life back.

The 33 year old has struggled to beat back severe depression and post-traumatic stress disorder for much of her life. She’s tried more than 30 psychiatric medications, none of which helped. Her inner pain reached a level so unbearable that she retreated from the world. She stayed in bed. She stopped doing the dishes and taking out the trash, which piled up in her San Francisco apartment. She stopped socializing.

She lost the will to live.

“I had gotten to a point where I disappeared, mentally and physically,” Morgan said. “My psychiatrist kind of put his hands up in the air and said, ‘There’s nothing else I can do for you.'”

But he did suggest something different she could try, albeit not through him: ketamine. The only legally available psychedelic in the U.S., the drug is widely used as an anesthetic in hospitals and medical settings. But it has been found to give people with severe mood disorders, including treatment-resistant depression and suicidal ideation, almost unbelievably fast-acting relief from their symptoms — some with a single dose, though more commonly it takes several treatments.

Morgan received her first ketamine infusion in a Palo Alto psychiatry clinic in June. By her second treatment, she took out the trash for the first time in months. After several infusions, friends told her she was talking more than she had in a year.

For the first time in her life, “I felt like there is a future for me,” Morgan said. “It’s left me a different person than I was a year ago.”

Ketamine is starting to shed its reputation as a psychedelic club drug and experimental mental health treatment as more patients like Morgan see results and more research is conducted on the drug’s impact on the brain. A watershed moment came in March when the U.S. Food and Drug Administration (FDA) approved Spravato, or esketamine, a ketamine nasal spray for adults with treatment-resistant major depression. One short-term clinical trial showed the spray had a statistically significant effect on depression compared to a placebo, and patients saw some effect within two days, according to the FDA.

A handful of local private psychiatry clinics, including in Palo Alto, Menlo Park and Woodside, have in recent years started offering ketamine. They are working at the forefront of a promising new treatment in psychiatry, a field that has seen little medication innovation for decades.

Many of the psychiatrists who run these clinics said they were initially skeptical of the drug’s potential, with little still known about how exactly ketamine works as an antidepressant and its long-term effects, but became believers when they saw life-changing improvements in patients for whom nothing else had worked.

“I think we’re on the brink of an amazing revolution in psychiatry,” said Alex Dimitriu, who offers ketamine treatments at his Menlo Park private psychiatry clinic. “We’re on the brink of understanding that a lot of drugs that previously we thought were drugs of abuse are actually turning out to be some very powerful agents.”

Exploring ketamine’s potential

Ketamine was developed in 1962 as a fast-acting anesthetic and continues to be widely used as such today, particularly for surgery and pain relief, including with children and in veterinary medicine. The drug is a schedule III controlled substance, meaning its medical use is accepted and it has moderate to low potential for abuse. The World Health Organization has included ketamine on its list of essential medicines since 1985 and calls it “possibly the most widely used anesthetic in the world.” As an anesthetic, it is incredibly safe (it does not depress breathing or blood pressure) and is easy to administer, according to the World Health Organization.

In higher doses, ketamine produces a “dissociative” state that can include hallucinations and out-of-body experiences. The drug’s conscious-altering potential led to its recreational use in the psychedelic era of the 1960s and 1970s.

Reports of ketamine use to treat psychological or psychiatric disorders first emerged in the 1970s, including in Argentina, Mexico and Russia, according to a study co-authored by Jennifer Dore, who offers ketamine at her private Helios Psychiatry practice in Woodside.

In 2000, a group of Yale University researchers published a seminal but small-scale study that found seven patients with major depression who received ketamine showed significant improvement in their symptoms within 72 hours, suggesting the drug could be used as an antidepressant.

Six years later, a National Institute of Mental Health study showed that ketamine reduced depression symptoms more quickly than a placebo.

Dore, who trained as a resident at the Stanford University Department of Psychiatry, became curious about ketamine several years ago while treating patients with severe PTSD and treatment-resistant depression. They simply weren’t getting better.

Dore dug into the available research on the drug’s antidepressant effects, which suggested that ketamine inhibits the action of the brain’s NMDA receptors and triggers glutamate production, which causes the brain to form new neural connections. She reached out to Phil Wolfson, director of the Center for Transformational Psychotherapy in San Anselmo, who pioneered ketamine-assisted psychotherapy, in which ketamine is administered while simultaneously patients receive therapy. She was compelled by taking this approach rather than the more medical model of providing the drug in isolation.

The results with her early patients in 2016 were like nothing she had ever seen.

“They had immediate relief,” she said.

Dore said her clinic was the first on the Peninsula to offer ketamine-assisted psychotherapy. She now offers trainings for other providers and sits on the board of the Ketamine Research Foundation.

In March, Dore published a five-year study with two other psychiatry practices that found patients who received ketamine saw clinically significant improvements in depression and anxiety, particularly so for people who came in with more severe symptoms like suicidality and a history of psychiatric hospitalization. At their clinics, they saw the drug help people suffering from obsessive compulsive disorder, bipolar disorder, personality disorders, substance abuse, psychological reactions to physical illness and even relationship issues and social anxiety.

“Ketamine promotes a time-out from (the) ordinary, usual mind, relief from negativity, and an openness to the expansiveness of mind with access to self in the larger sense,” Dore’s study states. “These effects enhance a patient’s ability to engage in meaningful psychotherapy during and after administration.”

Dore is a staunch champion of combining ketamine with psychotherapy, which she believes is necessary to harness the full potential of the drug. She doesn’t see ketamine as a magic bullet, but rather one tool she can use in concert with others — talk therapy, medication, nutrition — to treat people in serious psychological pain.

Before patients start ketamine, Dore carefully evaluates them to determine if it’s an appropriate next step in their treatment, as recommended by the American Psychiatric Association, including through therapy sessions, psychological tests and a review of their medical history. If they choose to proceed, Dore requires patients to sign a lengthy consent form that explains how ketamine works and its potential benefits and risks.

During a patient’s initial treatment, Dore monitors their physical and emotional responses, including blood pressure and heart rate, to decide on an appropriate dose going forward. The highest doses can produce the dissociative state, or the dream-like sensation of disconnecting from reality, Dore said. (Some people believe they have died and are in a new reality, she said. One patient described it as being in a lucid dream.) At lower doses, it can feel more like having a glass of wine, she said. The peak effects last about 15 to 30 minutes, according to Dore.

Patients can take the ketamine via a small lozenge that dissolves under their tongues, intravenously or an intra-muscular injection.

They receive the ketamine in a large second-floor space at Dore’s practice. It resembles a homey living room more than a psychiatric setting — a reflection of the importance of creating “set and setting” for a psychedelic experience, including a comforting physical environment. A large, soft corner couch is strewn with pillows, including one that says “anger” and another, “love.” During treatments, Dore pulls down the blinds on the windows, adjusts the temperature and offers patients weighted blankets, eyeshades and quiet music. The sessions last two to three hours.

Gaining a new perspective

Andy Mathis was at the end of his mental rope when he found Dore. A father, husband and successful tech industry executive, he had quietly suffered from self-doubt and insomnia since he was a young child. By the time he reached his mid-40s, it had escalated to depression. He felt his well-being and very brain chemistry was at risk.

A friend of a friend referred him to Dore, who prescribed him antidepressant and anti-anxiety medications that finally helped him sleep. But she suspected there was more to understand about the root causes of his symptoms, he said, and suggested ketamine as a means for exploring that.

A former professional tennis player, Mathis said he had never taken any drugs before. He did his own research on ketamine and thought it sounded “groundbreaking.” He was more curious than fearful about embarking on a psychedelic experience.

He received his first infusion two and a half years ago and continues to get ketamine every four to eight weeks today.

“It was indeed transformational,” Mathis said. “Nothing less than transformational.”

Mathis described the experience as taking him out of his own ego, a “tilt(ing) of the prism on how I see things.”

“It allowed me to have a detached, philosophical view on all things — me, my place in the world, my relationships,” he said.

This helps him make sense of his emotions “in a way that can be extremely difficult and sometimes even impossible to do when I am inside of myself,” referring to his default, day-to-day mental state.

Over the course of the infusions, Mathis started feeling more comfortable in his own skin, which he said improved his relationships and even his work performance. He realized he has a love for music and at age 47, started to learn how to play the saxophone. He came to a better understanding of his relationship to food and how he had used it as a coping mechanism.

Combining the ketamine-induced realizations with therapy was crucial, Mathis said.

“It was the post-experience discussions that we would have that would also unravel and unwind some of the unhealthy habits,” he said. “I’m 47 now, almost 48. I am healthier now than I was probably, maybe, ever.”

Dore likened ketamine’s power as a catalyst for psychological change to “a year of psychotherapy in three hours.”

Unlike antidepressants, patients don’t have to take ketamine every day and do not experience significant side effects; they can become nauseous or slur their words during the treatment, psychiatrists said. They require patients to have someone to drive them home after the treatment.

Mathis, for his part, did not experience any negative side effects. A patient at another local psychiatry clinic, Lisa Ward, however, said her mind feels “foggy” if she has two infusions in a single week. According to the FDA, the most common side effects experienced by patients treated with Spravato, the esketamine nasal spray, in clinical trials including disassociation, dizziness, nausea, lethargy and increased blood pressure.

“It would be inhumane,” Dore said, to not offer ketamine to people in intractable mental anguish. “We need things that are transformative, that aren’t putting a Band-Aid on a problem.”

Psychiatrist calls it ‘life-changing’

When Rameen Ghorieshi first looked into ketamine as an option for a patient with treatment-resistant depression about five years ago, it was still “very much fringe,” he said. His colleagues at Stanford, where he completed his psychiatric training, knew about the drug but had no idea how to actually use it as a treatment.

He decided to offer ketamine at his small private practice in downtown Palo Alto, Palo Alto Mind Body. He trained with an anesthesiologist and started with two patients. One suicidal young woman who had dealt with a chronic illness since childhood and didn’t intend to live past 30 years old, he said, got to the point where she was working four days a week, socializing and planning to go back to school.

“That just blew my mind,” Ghorieshi said. “I knew it would help just reading the studies but seeing it firsthand was pretty incredible.”

He has done more than 1,000 ketamine infusions at his downtown Palo Alto practice. Eighty-seven percent of patients rated their improvements as significant and 35% of those described it as “life-changing.” It particularly helped suicidal patients, he said. About 13% of patients said the improvement in their symptoms was not worth the time and effort of the infusions.

“This is a bit of a departure for me. I’m a very conservative prescriber,” Ghorieshi said. “My patients tend to be on one, two, maybe three medications. … But it was so remarkable that it seemed hard not to offer it to people.”

Ghorieshi said his was the first clinic in the Bay Area to treat someone with the tightly controlled, FDA-approved nasal spray. A handful of his patients have since received it, with good results, he said.

Esketamine is attached to a federal Risk Evaluation and Mitigation Strategy, which the FDA “can require for certain medications with serious safety concerns to help ensure the benefits of the medication outweigh its risks.” Providers and patients must register and the drug must be administered in a certified medical office under the supervision of a health care professional.

At Palo Alto Mind Body, patients receive eight ketamine infusions over several weeks. They are strongly encouraged to also pursue therapy but it’s not part of the treatment itself, Ghorieshi said.

He or a nurse supervises patients over the course of the 90-minute appointments. Morgan likes to sit upright on the couch in Ghorieshi’s office, covered by a blanket that keeps her warm and gives her a sense of emotional security. She listens to relaxing elevator music. After, she goes home and naps off the residual effects.

Years ago, she was given much higher doses of ketamine as a pain treatment for chronic physical illnesses and had horrible hallucinations, which she described as “having my head slammed against a wall repeatedly by a slime monster from a deep black bog.”

At the dose Ghorieshi gives her, she feels like the floor and ceiling switch. Her inhibitions dissolve. Afterwards, she feels more open to trying new experiences, from coping mechanisms for her depression to new foods. She feels her perfectionism, which for a long time had prevented her from being vulnerable with others, soften.

“To me, that’s the magic of ketamine,” Menlo Park psychiatrist Dimitriu said of the drug’s tendency to destabilize entrenched behaviors. “I think that speaks to the magic of future psychedelic research, which is down the pipeline, in that it increases our openness to new experience. The general belief here is if you’re depressed severely, you get stuck in maladaptive patterns.”

Lisa Ward didn’t see immediate relief from her life-long depression after her first ketamine infusion with Ghorieshi in March.

Then, a week later as the drug continued to work in her system, “the whole cloud just lifted,” she said. (It takes most patients several treatments to see results, according to Ghorieshi.)

She had more energy. She felt more productive. The benefits extended to her loved ones, as she’s engaged more with her two young children, husband, her parents and her sister.

“It’s enough for me to have more fun with my kids. It’s enough for me to spend more time with my husband instead of going to bed because I just can’t deal with the day anymore,” she said. “Being in depression you don’t realize it but it takes a big toll on other people.”

For Ward, a photographer, the effects of ketamine last about five weeks before she feels the cloud returning. There was one period where the ketamine seemed to stop working all together. Because she lives in Hollister — a three-hour round trip drive from Palo Alto, not including the time of the session itself — and pays out of pocket for the expensive treatment, gaps between her appointments stretch longer than she’d like.

She actually doesn’t enjoy the experience of being on ketamine, which she described as mind-bending and often intense. But she said the disruption of her depression allows her to focus on shifting the underpinning behavior and thought patterns.

Ketamine “doesn’t magically lift all … your problems away,” Ward said. “You’re more apt to make changes when you’re thinking clearly and you’re not so focused on the depression.”

While esketamine, the nasal spray, is covered by insurance because of the FDA approval, most other ketamine administrations are not. Morgan pays almost $1,000 out of pocket for each infusion, though Ghorieshi said some of his patients have been reimbursed for their treatments. Dore charges patients for her time as a provider, about $1,000 for a several-hour session, rather than for the drug itself.

Morgan felt strongly about using her full name in this article to dispel stigma around ketamine in the hopes it will be more widely accepted — and thus available to more people in need.

“Just because you hear something in one context, like ketamine being used as an illicit drug, doesn’t mean it doesn’t exist in another,” she said. “I think that’s what scares insurance companies away from covering it for patients. And that’s what makes me angry because I wish this treatment was out there for everybody to see. I’m lucky enough to be able to handle the financial portion, but the average person might not be.”

The as-yet-unknown risks

Despite the success stories, ketamine has not yet been fully accepted by the broader psychiatric community. The unanswered questions and possible risks that surround ketamine — how it works as an antidepressant, the long-term effects, the potential for abuse — are cause for caution, said Alan Schatzberg, a Stanford School of Medicine psychiatry professor and former president of the American Psychiatric Association.

“Rarely has there been so much anticipation for a new antidepressant as has been seen for intranasal esketamine,” he wrote in the American Journal of Psychiatry in May about the newly FDA-approved ketamine nasal spray.

“Do we have clear evidence of efficacy? Maybe. How strong is the efficacy? Apparently mild. Do we have a real sense of how long and how often to prescribe it? It’s not entirely clear.

“Taken together,” he wrote, “there are more questions than answers with intranasal esketamine, and care should be exercised in its application in clinical practice.”

In an interview, Schatzberg said he’s concerned about repetitive, extended use of any form of ketamine and the drug’s potential for dependence. The American Psychiatric Association has said that the literature on ketamine’s longer-term effectiveness and safety is so limited that the organization cannot “make a meaningful statement” on such use.

“The scarcity of this information is one of the major drawbacks to be considered before initiating ketamine therapy for patients with mood disorders and should be discussed with the patient before beginning treatment,” an American Psychiatric Association task force wrote in a consensus statement on ketamine in 2017.

Schatzberg co-authored a 2018 study that suggests ketamine’s antidepressant effects are tied to the brain’s opioid system and said the implications of this for dependency should be studied further.

“This is the same as any potential drug of abuse, any kind of opioid type drug. Serial use is less the issue. It’s when you get into repetitive use that one needs to be careful,” Schatzberg said. “That’s the clarion call that we’ve been sounding.”

One of his study co-authors, Carolyn Rodriguez, a Stanford associate professor of psychiatry and behavioral sciences, has been blown away by the rapid benefits of ketamine in studies she’s conducted with patients with obsessive compulsive order, or OCD. In the first-ever randomized clinical trial of ketamine compared to placebo in OCD, she found that a single low dose of ketamine prompted a decrease in OCD symptoms within hours for all participants.

Yet she remains cautious and said more research is needed to fully understand the powerful drug. She’s currently studying the mechanisms of how ketamine works so quickly on OCD patients, with funding from the National Institute of Mental Health.

“I believe that the state of the field of ketamine and how it works on OCD is not at the point yet where I would recommend it clinically because I always like to see science, (including) my own science, replicated,” Rodriguez said.

With pause about the long-term effects, she and other researchers have suggested a national registry be created to monitor side effects.

Ghorieshi said he is frank with his patients about the unknowns and potential downsides of ketamine, which must be weighed against other risks.

“We do know the immediate mortality and morbidity of things like suicide and depression.

I think that’s, as with anything, the risk-benefit. What are the risks of suicide, but also depression and anxiety in general?” he said. “You have to balance that versus these unknown risks of ketamine.”

Mathis, for his part, said he’s not concerned about the long-term effects of taking ketamine.

“What I worry about,” Mathis said, “is what my health would have done without it.”