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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

NOVA Health Recovery Ketamine Infusion Center

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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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703-844-0184 | Arlington, Virginia Ketamine Infusion Provider | Sarcosine, Nitrous oxide, and buprenorphine for depression. Alexandria, Virginia Ketamine Infusion Center | Loudoun County Virginia Ketamine | IV Vitamin and Glutathione Center | IV NAD+ Virginia Center 22308

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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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