Tag Archives: Depression

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The Brain on Fire: Depression and Inflammation

According to the World Health Organization, depression is the leading cause of disability. Unfortunately, 30 to 60 percent of patients are not responsive to available antidepressant treatments (Krishnan & Nestler, 2008). In other words, 40 to 70 percent of patients are not helped by existing treatments. One area of research might shed some light on why a sizable portion of patients are not helped by current antidepressants.

There is growing evidence that inflammation can exacerbate or even give rise to depressive symptoms. The inflammatory response is a key component of our immune system. When our bodies are invaded by bacteria, viruses, toxins, or parasites, the immune system recruits cells, proteins, and tissues, including the brain, to attack these invaders. The main strategy is to mark the injured body parts, so we can pay more attention to them. Local inflammation makes the injured parts red, swollen, and hot. When the injury is not localized, then the system becomes inflamed. These pro-inflammatory factors give rise to “sickness behaviors.” These include physical, cognitive and behavioral changes. Typically, the sick person experiences sleepiness, fatigue, slow reaction time, cognitive impairments, and loss of appetite. This constellation of changes that take place when we are sick is adaptive. It compels us to get more sleep to heal and remain isolated so as not to spread infections.

However, a prolonged inflammatory response can wreak havoc in our bodies and can put us at risk of depression and other illnesses. There is plenty of evidence solidifying the link between inflammation and depression. For example, markers of inflammation are elevated in people who suffer from depression compared to non-depressed ones (Happakoski et al., 2015). Also, indicators of inflammation can predict the severity of depressive symptoms. A study that examined twins who share 100 percent of the same genes found that the twin who had a higher CRP concentration (a measure of inflammation) was more likely to develop depression five years later.  

Doctors noticed that their cancer and Hepatitis C patients treated with IFN-alpha therapy (increases inflammatory response) also suffered from depression. This treatment increased the release of pro-inflammatory cytokines, which gave rise to a loss of appetite, sleep disturbance, anhedonia (loss of pleasure), cognitive impairment, and suicidal ideation (Lotrich et al., 2007). The prevalence of depression in these patients was high. These results add credence to the inflammation story of depression.

Subsequent careful studies showed that the increase in the prevalence of depression in patients treated with IFN-alpha was not only because they were sick. Using a simple method of injecting healthy subjects with immune system invaders, researchers found higher rates of depressive symptoms in the ones who were exposed compared to the placebo group. The subjects who were induced to have an inflammatory response complained of symptoms such as negative mood, anhedonia, sleep disturbances, social withdrawal, and cognitive impairments.

The link between inflammation and depression is even more solid for patients who don’t respond to current antidepressants. Studies have shown that treatment-resistant patients tend to have elevated inflammatory factors circulating at baseline than the responsive ones. This is clinically important; a clinician can utilize a measure like CRP levels, which are part of a routine physical, to predict the therapeutic response to antidepressants. In one study, they found that increased levels of an inflammation molecule prior to treatment predicted poor response to antidepressants (O’Brien et al., 2007).

There are environmental factors that cause inflammation and therefore elevate risk for depression: stress, low socioeconomic status, or a troubled childhood. Also, an elevated inflammatory response leads to increased sensitivity to stress. The effect has been reported in multiple studies in mice. For example, mice that have gone under chronic unpredictable stress have higher levels of inflammation markers (Tianzhu et al., 2014). Interestingly, there are individual differences that make some mice more resistant to stress, therefore initiating a calmer immune response (Hodes et al., 2014).

Depression is a heterogeneous disorder. Each patient’s struggle is unique given their childhood, genetics, the sensitivity of their immune system, other existing bodily illnesses, and their current status in society. Being on the disadvantageous end of these dimensions irritates our immune system and causes chronic inflammation. The brain is very responsive to these circulating inflammatory markers and initiates “sickness behavior.” When the inflammation is prolonged by stressors or other vulnerabilities, the sickness behavior becomes depression.

If you are a professional working with patients suffering from depression, I urge you to consider the health of your patients’ immune systems. If you are a patient suffering from an exaggerated immune disorder (e.g., arthritis), do not ignore the depressive symptoms that you might be experiencing. If you are suffering from depression, avoid anything that might exacerbate your immune response. This is another example of the beautiful dance between mind and body!

References

Haapakoski,R.,Mathieu,J.,Ebmeier,K.P.,Alenius,H.,Kivimäki,M., 2015. Cumulative meta-analysisofinterleukins6 and 1β,tumournecrosisfactorα and C-reactive protein in patients with major depressive disorder. Brain Behav.Immun. 49,206.

Hodes GE, Pfau ML, Leboeuf M, Golden SA, Christoffel DJ, Bregman D et al (2014). Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress. Proc Natl Acad Sci USA 111: 16136–16141.

Krishnan V, Nestler EJ (2008). The molecular neurobiology of depression. Nature 455: 894–902.

Lotrich,F.E.,Rabinovitz,M.,Gironda,P.,Pollock,B.G., 2007. Depression following pe-gylated interferon-alpha:characteristics and vulnerability.J.Psychosom.Res.63, 131–135.https://doi.org/10.1016/j.jpsychores.2007.05.013.

O’Brien, S.M., Scully, P., Fitzgerald, P., Scott, L.V., Dinan, T.G., 2007a. Plasma cytokine profiles in depressed patients who fail to respond to selective serotonin reuptake inhibitor therapy. J. Psychiatr. Res. 41, 326e331.

Tianzhu, Z., Shihai, Y., Juan, D., 2014. Antidepressant-like effects of cordycepin in a mice model of chronic unpredictable mild stress. Evid. Based Complement. Altern. Med. 2014, 438506.

The Serotonin Transporter Gene and Depression

A new large-scale study casts doubt on a widely reported association.

Why some people develop major depressive disorder and others do not is a complex and not well-understood process. Several factors have been discussed to contribute to depression, among them:

Genetic variation: Individuals carrying one or two copies of a specific risk allele on one or more “depression gene/s” have a higher risk of developing depression.

Environmental influences: Negative life events such as trauma, negligence, or abuse increase the risk of developing depression.

Gene-by-environment interactions: Negative life events only lead to depression in individuals with a specific genetic set-up that makes them risk-prone to develop depression.

The gene most commonly associated with depression is the serotonin transporter gene SLC6A4 (Bleys et al., 2018). Serotonin is a neurotransmitter affecting multiple physiological processes and cognitivebrain functions, among them mood and emotions, which is why it has been linked to mood disorders such as depression. Indeed, low serotonin levels have been associated with depressed mood (Jenkins et al., 2016), and selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. SSRIs block the reuptake of serotonin during cellular communication in the brain, making more serotonin available, and thus in theory helping to reduce depression.

Along these lines, the idea that the serotonin transporter gene could affect depression risk or severity intuitively made sense. Specifically, many scientists focused on the so-called 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene to research the effects of this gene on depression. Genetic polymorphism means that at a specific location in the genome, different people might have slight variations in their DNA which could affect how well the protein that the gene produces could do its job. In the case of the 5-HTTLPR polymorphism, there is a short allele (s) and a long allele (l). Already back in the 1990s, researchers showed that people with two or one short alleles have a higher chance of developing depression than those with two long alleles, as the short allele leads to reduced expression of the serotonin transporter (Collier et al., 1996).

This initial study sparked interest in the 5-HTTLPR polymorphism, but not all empirical works could find a clear association. In 2003, a surprising finding seemingly resolved this controversy. In a widely cited study, Caspi and colleagues were able to show that the effects of 5-HTTLPR polymorphism genotype on depression were moderated by a so-called gene-by-environment interaction (Caspi et al., 2003). This means that the genotype would only have an effect if individuals were also subjected to specific environmental conditions. Specifically, the scientists found that individuals reacted differently to highly stressful life events, depending on the 5-HTTLPR genotype. People with at least one short allele on the 5-HTTLPR polymorphism developed more depressive symptoms if they experienced a highly stressful life event than people with two long alleles. However, without a stressful life event, the genotype did not have an effect on the probability to develop depression.

This study further increased the interest in the 5-HTTLPR polymorphism and its relation to depression, leading to more studies on this topic. However, a problem of many of these studies was that their sample sizes were comparably small for genetic studies, potentially leading to erroneous results and overblown effects.

Almost a decade ago, Risch and co-workers (Risch et al., 2009) conducted a so-called meta-analysis, a statistical integration of empirical studies. They analyzed 14 studies on the 5-HTTLPR polymorphism and its relation to depression and on whether this relation was influenced by stressful life events as had been suggested by Caspi et al. (2003). Their result was clear: While more stressful life events led to a higher risk of depression, there was no effect of the 5-HTTLPR genotype on depression and no gene-by-environment interaction effect between genotype and stressful life events.

Despite this finding, hundreds of studies on the 5-HTTLPR polymorphism and depression have been published since 2009 (the scientific search engine PubMed lists more than 800 hits for the search term “5-HTTLPR depression” as of early May 2019). A new study recently published by Richard Border and colleagues in The American Journal of Psychiatry(Border et al., 2019) aimed to resolve the controversy about whether or not the 5-HTTLPR genotype affects depression and whether there is a gene-by-environment interaction between this genotype and stressful life events once and for all. To avoid the statistical problems of previous studies, they obtained data from several large genetic datasets available to researchers, leading to a sample size of several hundred thousand individuals. The results of the analysis were clear as well: There was no statistical evidence for a relation between the 5-HTTLPR polymorphism and depression, and there was also no evidence that traumatic life events or adverse socioeconomic conditions might show a gene-by-environment interaction with this genotype.

This, of course, does not mean that there is no relationship between serotonin and depression (there clearly is, as shown by the treatment success of SSRIs), but it lends further support to an emerging insight in psychiatry genetics: Mental illness is a highly complex process that is likely influenced by a large number of genetic and non-genetic effects. As such, it is unlikely that single genetic variations such as the 5-HTTLPR polymorphism have a huge impact on whether or not an individual develops depression or any other form of mental illness. Future psychiatry genetic studies will need to take this complexity into account by analyzing genetic variation across the whole genome and epigenome and relating it to mental illness (Meier & Deckert, 2019).



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703-844-0184 | Ketamine for depression | Alexandria, Va 22306 | Ketamine Treatment Center | Call for an appointment – Dr. Sendi

Is ketamine safe? What are some reasons I would not be eligible (contraindications)?

Ketamine is a unique among anesthetic medications in that it is extremely safe, having been used in various settings for more than fifty years, even in poorly monitored settings such as battlefield anesthesia and developing countries, “ketamine has a good safety profile and is easy to use, especially in under-resourced health systems and emergency settings where clinical conditions and medical equipment are generally not available” (World Health Organization).  Ketamine has an even higher margin of safety when used to treat depression because such doses are much lower than those used in surgery. Patients typically remain conscious the entire time, though may feel somewhat altered and experience perceptual changes.  When used in higher surgical and anesthetic doses, ketamine requires the presence of an anesthesiologist for full airway and cardiac monitoring, while the lower doses used in depression do not.  There are specific reasons you would not be eligible for ketamine, including recent myocardial infarction (heart attack), recent psychosis (hallucinations, delusions), or recent bladder inflammation (cystitis). Administration of ketamine and medical monitoring throughout the session is performed by Dr. Sendi, and not by nurses or personnel with less medical training.

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WHO Recommends against International Control of Ketamine

20160309_FactFile_Ketamine

What is the best route of administration for treatment of depression?

As noted above, ketamine can be administered in several different ways: by an intravenous infusion, an intramuscular injection, intranasally, sublingually, and orally. Intravenous ketamine infusions have been most studied because of their historical use and original FDA approval decades ago, though more and more studies are finding comparable efficacy with the other routes of administration.  It is not clear that intravenous ketamine infusions are more effective than other routes of administration, and further results in great patient discomfort, greater resource utilization, and ultimately result in a higher cost.  For this reason I typically offer ketamine via the intramuscular route, which appears to be non-inferior in terms of efficacy for depression.Here is a link to an article on Ketamine and depression:   the International Journal of Transpersonal Studies: Ketamine and depression: a review.

Am I a good candidate?  How are ketamine treatments structured?

Prior to initiating ketamine treatments, some  potential patients are scheduled for an initial psychiatric evaluation.  On this first meeting, we will determine a diagnosis, develop a treatment plan, and assess for any medical or psychiatric issues that may interfere with ketamine treatment. If we mutually agree that ketamine could be beneficial, then we can schedule a subsequent visit for the actual administration; with some planning, it is possible for both the intake and administration to be done on the same day.  The greatest benefit of ketamine is attained with multiple administrations over the first few weeks of treatment, which is then followed by periodic booster treatments to maintain freedom from depression.  I ask patients to commit to a series of 6 administrations over 3 weeks, and then return for periodic bimonthly to monthly booster treatments thereafter to prevent depression from returning. Please note, it is always your option to stop treatment at any time. Patients must have a friend or family member pick them up after the appointment, as ketamine temporarily impairs one’s ability to drive. Ketamine sessions are scheduled for 90 minutes in duration, and involve a brief medication management visit, the actual ketamine administration, followed by psychotherapy, all of which is integrated into one visit.

For individuals interested in ketamine treatments, please print out the informed consent  and bring it with you to our appointment.  I will have you sign it after an in depth discussion about the risks, benefits, and alternatives available to you.

Are there any precautions?

Individuals receiving ketamine should abstain from any food or drink for the 6 hours prior to receiving the medication, and furthermore, should not drive for the remainder of the day. This is a necessary precaution because the subtle after effects of ketamine can linger for hours after the treatment and impair the ability to drive.  Effects typically resolve by the following day, at which time driving is allowed. Typically patients arrange a ride home with a friend or family member, and once tolerability is established can later use a taxi or ride sharing service to return home.

What is the cost of ketamine treatments? Do insurance companies cover it?

I do not directly contract with insurance companies, but instead collect the full fee at time of the visit and provide patients with a superbill that can be submitted to their insurance provider for reimbursement.  Current fees can be found on the new patient intake form, available here.

Visits may be partially covered depending on your insurance plan.  The ketamine administration itself is generally not covered by insurance, however the typical 90 minute long ketamine treatment session involves several other components which may be reimbursed for: the brief medication management (99213, 99214, or 99215) and psychotherapy visit (90833 or 90834) are typically covered by insurance, though this cannot be guaranteed.  In addition, the initial psychiatric evaluation visit (99205) is also typically covered.  I suggest potential patients check with their insurance provider to see what their out-of-network coverage benefits are for the above procedures/CPT codes.  PPO type insurances usually allow for out-of-network benefits, while HMO plans do not.

What can you tell me about the use of ketamine for treatment of addiction or substance use disorders?

Ketamine has been studied for treatment of addiction, specifically to the opiate and street drug, heroin.  Findings suggest that ketamine, as part of a structured therapy program, is effective for the treatment of addiction, perhaps due to biochemical properties as an NMDA receptor antagonist. While studies examining this particular application of ketamine are more limited than those examining treatment of depression, work with compounds that create similar states of consciousness–such as the “classical hallucinogens”: LSD, psilocybin, mescaline, DMT, and ayahuasca–suggest a role for altered states independent of the biochemical effects of ketamine.  Such compounds seem to work to treat addiction via their ability to produce spiritual or mystical experiences. While such “classical hallucinogens” are not currently available for clinical use, there exists a growing literature detailing successful and robust treatment of tobacco and alcohol addiction. Use of the aforementioned compounds outside of a research setting is however illegal, except for ketamine which has been FDA approved for other indications and is consequently available for off-label use to treat such diagnoses as depression, post-traumatic stress disorder, and addiction / substance use disorders.

What other psychiatric conditions has ketamine been used for?

Treatment resistant depression is, by far, the most extensively studied psychiatric application of ketamine, and has a wealth of data to support its use.  Other indications (or reasons to use ketamine) include drug or alcohol use disorders (specifically for opioid or cocaine use disorders),  Post-Traumatic Stress Disorder (PTSD), and eating disorders such as anorexia or bulimia.  On the other hand, data suggests ketamine is less effective for treatment of Obsessive-Compulsive Disorder (OCD), but may be worth pursuing on a case by case basis.

Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder a randomized clinical trial.

Where can I learn more?

You are invited to read a review article on ketamine for depression.  The full text is available free of charge from the California Institute of Integral Studies [ full text ].  Ketamine and Depression_ A Review An updated version of this review is available as a book chapter in a larger publication on ketamine.  The book, entitled The Ketamine Papers–Science, Therapy and Transformation, is published by the non-profit Multidisciplinary Association for Psychedelic Studies (MAPS) and available for purchase through their website and amazon [ order the book via MAPS, or via amazon ].  Also available is a video recording of a presentation on ketamine that I gave for the Aware Project [ YouTube video ].

 

 

 

The Ketamine Papers

 

 2007 Mar;39(1):13-9.

Single versus repeated sessions of ketamine-assisted psychotherapy for people with heroin dependence.

Abstract

A prior study found that one ketamine-assisted psychotherapy session was significantly more effective than active placebo in promoting abstinence (Krupitsky et al. 2002). In this study of the efficacy of single versus repeated sessions of ketamine-assisted psychotherapy in promoting abstinence in people with heroin dependence, 59 detoxified inpatients with heroin dependence received a ketamine-assisted psychotherapy (KPT) session prior to their discharge from an addiction treatment hospital, and were then randomized into two treatment groups. Participants in the first group received two addiction counseling sessions followed by two KPT sessions, with sessions scheduled on a monthly interval (multiple KPT group). Participants in the second group received two addiction counseling sessions on a monthly interval, but no additional ketamine therapy sessions (single KPT group). At one-year follow-up, survival analysis demonstrated a significantly higher rate of abstinence in the multiple KPT group. Thirteen out of 26 subjects (50%) in the multiple KPT group remained abstinent, compared to 6 out of 27 subjects (22.2%) in the single KPT group (p < 0.05). No differences between groups were found in depression, anxiety, craving for heroin, or their understanding of the meaning of their lives. It was concluded that three sessions of ketamine-assisted psychotherapy are more effective than a single session for the treatment of heroin addiction.

How to use psychedelics

How to Take Ketamine to Treat Depression, Anxiety and PTSD

Ketamine is a legal prescription medication used for a variety of purposes– as a pain killer, sedative, anesthetic, and anti-depressant. It’s one of the safest anesthetics in the world and is available in every hospital. Ketamine’s use as an anti-depressant and PTSD treament is growing very quickly and research studies are expanding. Here’s a directory of US doctors offering ketamine treatment for depression, bipolar, PTSD, and other mood disorders.

As the BBC wrote in a 2014 article about ketamine, “Some patients who have faced incurable depression for decades have had symptoms disappear within hours of taking low doses of the drug.”

What makes Ketamine so remarkable for treating depression is that its positive effects begin almost immediately, within 1 – 12 hours, compared to SSRIs that may take weeks to start working, if they work at all. Ketamine also seems to have much fewer side effects than SSRIs (though it hasn’t been studied much for long term use) and is incredibly effective as a treatment for people who don’t respond well to SSRIs and other anti-depressants. If you’ve had limited success with other treatment methods you may respond very well to ketamine.

Before you begin, be sure to read our safety section and ensure that you aren’t taking any medication or supplements that interact with Ketamine.

Dosage

Dosage for ketamine varies depending on whether it’s taken intranasally, intravenously (IV), orally, or sublingually. We recommend taking ketamine orally or sublingually because it’s safe and easy. Many doctors and treatment centers will give ketamine in an IV. Treatment with a doctor / center can be quite expensive but you may be able to find a doctor or center in your area if you google around.

The anti-depressant effect of ketamine typically wears off after a while (a few days to a month), though the relief that is felt while it is active can often lead to lasting improvements. There are various protocols for using ketamine to treat depression– some people take small amounts daily, others weekly, and others monthly. We recommend starting with a moderate dose once a week and adjusting based on how it feels.

How to Take Ketamine Sublingually (Under the Tongue)

Sublingual ketamine seems much more potent than oral ketamine. We suggest starting with a very small “microdose” and trying a little more each session until you find the minimum amount that works for you. You should almost certainly see results using .3mg of ketamine per pound of body weight (or .75mg per kg of body weight). This works out to about 50mg for someone who weighs 160lbs (72kg). But start far below that.

  • STEP ONE
    Prepare your ketamine solution. You’ll want to use one of those little bottles that has an eyedropper in the lid. Maybe you have one around the house with some sort of herbal tincture. Boil some water, then let it cool. Using the eyedropper, wash out the dropper and the bottle with the water, just to get rid of any residue. Put a known amount of ketamine into the bottle. Then add water to the bottle using the eyedropper, carefully counting the drops. You want to use as few drops as possible to dissolve all the ketamine. In a lab you should be able to dissolve 5mg ketamine per drop. If you add this much water and you still see some undissolved ketamine in there, add just enough water to dissolve it all. Carefully swirl it around to speed things up. Now you can give yourself microdoses of ketamine. Just divide the amount of ketamine by the number of drops. If you had 1000mg of ketamine, and added 200 drops of water, you’d know there was 5mg ketamine per drop.
  • TWO
    Find a place where you can sit or lie down comfortably for an hour. Unlike traditional psychedelics like mushrooms, LSD, and even MDMA, the benefits of ketamine do not seem to derive from an exploratory experience while taking the medicine. In addition, the experience at an effective dose is much more gentle. You can read a book, watch TV, etc.
  • THREE
    Looking at yourself in a mirror, put one or two drops under your tongue. This is probably at most 5-10mg. Don’t swallow it, just leave it under your tongue. After 5 minutes or so, you can swallow.
  • FOUR
    The effects will be very subtle but you might feel a slight mellow or sleepy feeling in about 5-15 minutes.
  • FIVE
    The anti-depressant effects of the ketamine generally start to appear about two hours after taking the first dose. In some people the anti-depressant effect is strong right away and in some people it gradually grows over 1-4 days– so you might feel the most relief 4 days after taking the dose.
  • SIX
    See how you feel the next day. If you are less depressed, great! If not, the next time try the previous dose plus one more drop. Don’t take ketamine two days in a row. Once you find a dose that seems to work, see how many days you can wait between doses. Ideally, you would take a dose once a week or once a month. Worst-case, you’d take it every other day. If you get up to 50mg sublingually and it still doesn’t work, it might just not work for you in general.

How to Take Ketamine Orally

We suggest using .6mg of ketamine per pound of body weight (or 1.5mg per kg of body weight). This works out to about 100mg for someone who weighs 160lbs (72kg).

Remember these are oral doses– usually mixed with warm water and swallowed. If you are taking ketamine in an IV the doses should be much, much lower.

  • STEP ONE
    Find a place where you can sit or lie down comfortably for an hour. Unlike traditional psychedelics like mushrooms, LSD, and even MDMA, the benefits of ketamine do not seem to derive from an exploratory experience while taking the medicine. In addition, the experience at an effective dose is much more gentle. You can read a book, watch TV, etc.
  • TWO
    Make sure you have the right dose measured and ready. If you don’t have a mg scale, you can order them cheaply anywhere, including Amazon. They are about $20-$30.
  • THREE
    If it’s your first time, mix about 1/5th of the dose with about an inch of warm water in a mug. If you are taking about 100mg, that would be roughly 20mg. Once you mix it, drink it.
  • FOUR
    A 1/5th dose will be very subtle but you should be able to feel a nice mellow or sleepy feeling in about 5-15 minutes. After 15 minutes, if you feel comfortable with that test dose (and it’s fine if you don’t feel anything at all), then you can mix the rest of the dose with warm water and drink it.
  • FIVE
    As you feel the effects of the dose, again after 5-15 minutes, you will likely feel sleepy or mellow. You can rest, read, watch tv, etc. After about 45 minutes to an hour, the effects will be mostly gone, though you may still feel very relaxed or sleepy for a couple more hours.
  • SIX
    The anti-depressant effects of the ketamine generally start to appear about two hours after taking the first dose. In some people the anti-depressant effect is strong right away and in some people it gradually grows over 1-4 days– so you might feel the most relief 4 days after taking the dose.

Afterwards

The anti-depressant effects of ketamine last for days and sometimes weeks or even a month. We suggest starting with weekly re-dosing, using the same dose, and seeing how it goes. If you find that you don’t need to redose after a week, then wait longer and see how things go. It’s always good to err on the side of taking too little rather than too much. Some people need to redose more often, every few days. You’ll probably get a sense pretty quickly of what works for you.

Special Safety Considerations

Always research any supplements or other medicines that you may be taking to avoid interactions. Here’s a Medscape list of potential interactions. (Note that the dosing levels listed on that site are for inducing anesthesia, which is way way more than what is use for anti-depressant effects.)

Articles and Research on Ketamine for Anxiety and Depression

Research on ketamine is growing quickly and some drug companies are trying to create new versions of ketamine that they can patent.

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Reasons to treat depression rapidly – Depression causes rapid aging> Consider using a rapid – acting antidepressant!

Depression ‘makes us biologically older’  BBC Article

Major depressive disorder and accelerated cellular aging

Patients with major depressive disorder (MDD) have an increased onset risk of aging-related somatic diseases such as heart disease,
diabetes, obesity and cancer. This suggests mechanisms of accelerated biological aging among the depressed, which can be
indicated by a shorter length of telomeres. We examine whether MDD is associated with accelerated biological aging, and whether
depression characteristics such as severity, duration, and psychoactive medication do further impact on biological aging. Data are
from the Netherlands Study of Depression and Anxiety, including 1095 current MDD patients, 802 remitted MDD patients and 510
control subjects. Telomere length (TL) was assessed as the telomere sequence copy number (T) compared to a single-copy gene
copy number (S) using quantitative polymerase chain reaction. This resulted in a T/S ratio and was converted to base pairs (bp).
MDD diagnosis and MDD characteristics were determined by self-report questionnaires and structured psychiatric interviews.
Compared with control subjects (mean bp = 5541), sociodemographic-adjusted TL was shorter among remitted MDD patients
(mean bp = 5459; P = 0.014) and current MDD patients (mean bp = 5461; P = 0.012). Adjustment for health and lifestyle variables did
not reduce the associations. Within the current MDD patients, separate analyses showed that both higher depression severity
(P<0.01) and longer symptom duration in the past 4 years (P = 0.01) were associated with shorter TL. Our results demonstrate that
depressed patients show accelerated cellular aging according to a ‘dose–response’ gradient: those with the most severe and
chronic MDD showed the shortest TL. We also confirmed the imprint of past exposure to depression, as those with remitted MDD
had shorter TL than controls

In this large cohort study we demonstrated that currently
depressed persons had shorter TL than never-depressed controls.
Based on an estimated mean telomere shortening rate of 14–20
bp per year as found in this and other studies,20,23,26 the
differences observed indicate 4–6 years of accelerated aging for
the current MDD sample as compared to controls. We also showed
evidence for the imprint of past exposure to depression since
those with remitted MDD also had shorter TL than control
subjects. These observed associations remained significant after
controlling for lifestyle and somatic health variables, suggesting that the shortened telomeres were not simply due to unhealthylifestyle or poorer somatic health among depressed persons.
Finally, the association between MDD and TL showed a ‘dose–
response’ gradient, since the most severely and chronically
depressed patients had the shortest telomeres.

MDD is thus associated with shortened TL, which resembles
accelerated biological aging. The disorder has previously also been
associated with dysregulations of the hypothalamus–pituitary–
adrenal (HPA) axis,43,45 the immune system,46,47 the autonomic
nervous system (ANS)48,49 and increased oxidative stress.50
Shortened telomeres, in turn, are suggested to be a consequence
or a concomitant of these dysregulated biological stress systems.
In line with this, several in vitro and in vivo studies found increased
cortisol,51 oxidative stress52 and pro-inflammatory cytokines53
to be associated with shorter TL. Dysregulations of these stress systems could contribute to telomere shortening in MDD patients.9,12
However, the exact biological mechanisms that mediate the relation
between depression and telomere shortening, as well as the
direction of the link, remain to be further explored.

Oxidative stress shortens telomeres

Elevated DNA Oxidation and DNA Repair Enzyme Expression in Brain White Matter in Major Depressive Disorder.

The Role of Oxidative Stress in Depressive Disorders

Abstract:

Studies of the World Health Organization suggest that in the year 2020, depressive disorder will be the illness with the highest
burden of disease. Especially unipolar depression is the psychiatric disorder with the highest prevalence and incidence, it is cost-intensive and has a relatively high morbidity. Lately, the biological process involved in the aetiology of depression has been the focus of research.
Since its emergence, the monoamine hypothesis has been adjusted and extended considerably. An increasing body of evidence points to
alterations not only in brain function, but also in neuronal plasticity. The clinical presentations demonstrate these dysfunctions by accompanying cognitive symptoms such as problems with memory and concentration. Modern imaging techniques show volume reduction of the hippocampus and the frontal cortex. These findings are in line with post-mortem studies of patients with depressive disorder and they point to a significant decrease of neuronal and glial cells in cortico-limbic regions which can be seen as a consequence of alterations in
neuronal plasticity in this disorder. This could be triggered by an increase of free radicals which in turn eventually leads to cell death and consequently atrophy of vulnerable neuronal and glial cell population in these regions. Therefore, research on increased oxidative stress in unipolar depressive disorder, mediated by elevated concentrations of free radicals, has been undertaken. This review gives a comprehensive overview over the current literature discussing the involvement of oxidative stress and free radicals in depression.

Membrane damage in blood of patients with depression has
been shown by elevated of omega 3- fatty-acids [45] and by increased
lipid peroxidation products in patients with DD [42, 45,
[46, 47]. Furthermore, DNA-strand brakes have been reported in
the blood of these patients [48]. DD has been linked to increased
serum levels of malondialdehyde (MDA), a breakdown product of
oxidized apolipoprotein B-containing lipoproteins, and thus a
marker of the rate of peroxide breakdown [49, 50].

In patients with DD (Depressive Disorders), elevated levels of MDA adversely affect
the efficiency of visual-spatial and auditory-verbal working memory,
short-term declarative memory and delayed recall declarative
memory [51]. Higher concentration of plasma MDA in patients
with recurrent depression is associated with the severity of depressive
symptoms, both at the beginning of antidepressant pharmacotherapy,
and after 8 weeks of treatment. Statistically significant
differences were found in the intensity of depressive symptoms,
measured on therapy onset versus the examination results after
8 weeks of treatment [51]. Although this is used as a marker of lipid peroxidation, it is considered to be less stable than 8-iso-PGF2a, and more susceptible to confounding factors such as antioxidants from diet [52]. Therefore, the best way to investigate oxidative disruptions to lipids in humans is via assessing levels of F2-
isoprostanes [52-54]. These are stable compounds produced in the
process of lipid peroxidation [52, 54]. 8-iso-PGF2a are specific F2-
isoprostane molecules produced during the peroxidation of arachnidonic acid. However, the mean serum level of 8-iso-PGF2a was shown to be significantly higher in a group of patients with DD,
controlling for lifestyle variables such as body mass index, alcohol
consumption, and physical activity [55, 56]. Cerebral membrane
abnormalities and altered membrane phospholipids have been suggested by an increased choline-containing compound seen in the
putamen of patients with DD [57] which has been interpreted as a
result of increased oxidative stress in patients with DD.

A Meta-Analysis of Oxidative Stress Markers in Depression

Results
115 articles met the inclusion criteria. Lower TAC was noted in acute episodes (AEs) of depressed patients (p<0.05). Antioxidants, including serum paraoxonase, uric acid, albumin,
high-density lipoprotein cholesterol and zinc levels were lower than controls (p<0.05); the serum uric acid, albumin and vitamin C levels were increased after antidepressant therapy
(p<0.05). Oxidative damage products, including red blood cell (RBC) malondialdehyde (MDA), serum MDA and 8-F2-isoprostanes levels were higher than controls (p<0.05). After
antidepressant medication, RBC and serum MDA levels were decreased (p<0.05). Moreover, serum peroxide in free radicals levels were higher than controls (p<0.05). There were
no difference

Conclusion
This meta-analysis supports the facts that the serum TAC, paraoxonase and antioxidant levels are lower, and the serum free radical and oxidative damage product levels are higher
than controls in depressed patients. Meanwhile, the antioxidant levels are increased and the oxidative damage product levels are decreased after antidepressant medication. The
pathophysiological relationships between oxidative stress and depression, and the potential benefits of antioxidant supplementation deserve further research.

Some studies have demonstrated that depressed patients’ oxidative product levels in their peripheral blood [3, 4], red blood cells (RBC) [4], mononuclear cells [5], urine [6], cerebrospinal
fluid [7] and postmortem brains [8] were abnormal. Antioxidant system disturbance in peripheral blood has also been reported [9]. Autoimmune responses against neoepitopes
induced by oxidative damage of fatty acid and protein membranes have been reported [10, 11].
Lower glutathione (GSH) levels [12] and a negative relationship between anhedonia severity
and occipital GSH levels [13] were found through magnetic resonance spectroscopy (MRS).

Oxidative stress is defined as a persistent imbalance between oxidation and anti-oxidation, which leads to the damage of cellular macromolecules [14, 15]. The free radicals consist of reactive
oxygen species (ROS) and reactive nitrogen species (RNS). The main ROS includes superoxide anion, hydroxy radical and hydrogen peroxide, and the RNS consists of nitric oxide
(NO), nitrogen dioxide and peroxynitrite. Nitrite is often used as a marker of NO activity. Interestingly, the brain appears to be more susceptible to the ROS/RNS because of the high
content of unsaturated fatty acids, high oxygen consumption per unit weight, high content of key ingredients of lipid peroxidation (LP) and scarcity of antioxidant defence systems [16].
The oxidative products include products of oxidative damage of LP, protein and DNA in depression. As a product of LP, abnormal malondialdehyde (MDA) levels in depression have
been reported [17]. 8-F2-isoprostane (8-iso-PGF2α) is another product of LP [18] that is considered
to be a marker of LP because of its chemical stability [19]. The protein carbonyl (PC), 8-hydroxy-2-deoxyguanosine (8-OHdG) and 8-oxo-7, 8-dihydroguanosine (8-oxoGuo) are
the markers of protein, DNA and RNA oxidative damage, respectively [3, 20, 21]. The oxidative damage to cellular macromolecules changes the structure of original epitopes, which leads to the generation of new epitopes modified (neoepitopes). The antibodies against oxidative neoepitopes
in depression have been found [10, 11, 22–24]. On the other hand, the antioxidant defence systems can be divided into enzymatic and non-enzymatic antioxidants. The nonenzymatic
antioxidants include vitamins C and E, albumin, uric acid, high-density lipoprotein cholesterol (HDL-C), GSH, coenzyme Q10 (CoQ10), ceruloplasmin, zinc, selenium, and so on.
The enzymatic antioxidants include superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), glutathione reductase (GR), paraoxonase 1 (PON1), and so on.

Discussion
The present findings support oxidative stress may be disordered in depressed patients, which is demonstrated by abnormal oxidative stress marker levels. In this meta-analysis, at first we
found in depressed patients: 1) the serum TAC, PON, uric acid, albumin, HDL-C and zinc levels were lower than controls; 2) the serum peroxide, MDA, 8-iso-PGF2α and RBC MDA levels
were higher than controls. To explore the effect of the antidepressant therapy to oxidative stress
markers, we reviewed the studies which had changes. And it came to the conclusions: 1) the serum uric acid, albumin, and vitamin C levels were increased; 2) the serum nitrite, RBC and
serum MDA levels were decreased.

The serum antioxidant levels are significantly lower in depression in our study and previous
reports, including PON, albumin, zinc, uric acid HDL-C, CoQ10 [146] and GSH [4, 38].
Meanwhile, the oxidative damage product levels are significantly higher. The body couldn’t
scavenge the excess free radicals (peroxide), leading to damages of main parts of cellular macromolecules
such as fatty acids, protein, DNA, RNA and mitochondria. The longitudinal antidepressant
therapy can reverse these abnormal oxidative stress parameters. It has proved
these phenomena occur in depression, such as increased levels of MDA, 8-iso-PGF2α, 8-oxoGuo
and 8-OHdG [3, 21]. Oxidative stress plays a crucial role in the pathophysiology of
depression. Some genes may be a potential factor. Lawlor et al (2007) reported the R allele of
PON1Q192R was associated with depression [147]. In addition, poor appetite, psychological
stressors, obesity, metabolic syndrome, sleep disorders, cigarette smoking and unhealthy lifestyle
may also contribute to it [148]. Furthermore, oxidative stress activates the immuneinflammatory
pathways [148]. But some studies supported decrease in albumin, zinc and
HDL-C levels was probably related to increased levels of pro-inflammatory cytokines (such as
interleukin-1 (IL-1) and IL-6) [59, 70–72, 117] during an acute phase response, which illustrated the activated immune-inflammatory pathways also activates the oxidative stress. These two mechanisms influence each other. On the other hand, the oxidative damage to cellular macromolecules changes the structure of original epitopes, which leads to generation of newepitopes modified (neoepitopes). Oxidative neoepitopes reported up to now include the conjugated oleic and azelaic acid, MDA, phosphatidyl inositol (Pi), NO-modified adducts and oxidized low density lipoprotein (oxLDL) [11, 22–24]. Maes et al reported the levels of serum IgG antibody against the oxLDL and IgM antibodies against the conjugated oleic and azelaic acid, MDA, Pi and NO-modified adducts were increased in depression [11, 22–24]. Depleted antioxidant defence in depression suggests that antioxidant supplements may be useful in clinical management. Preliminary evidence has indicated that patients treated with CoQ10 showed improvement in depressive symptoms and decrease in hippocampal oxidative DNA damage [149]. In our analyses, vitamin C and E levels did not differ between depressed patients and controls, but many studies have reported that vitamin C and E supplements could improve depressive moods [150, 151].

Malondialdehyde plasma concentration correlates with declarative and working memory in patients with recurrent depressive disorder

Abstract

Oxidative stress has been implicated in the cognitive decline, especially in memory impairment. The purpose of this study was to determine the concentration of malondialdehyde (MDA) in patients with recurrent depressive disorders (rDD) and to define relationship between plasma levels of MDA and the cognitive performance. The study comprised 46 patients meeting criteria for rDD. Cognitive function assessment was based on: The Trail Making Test , The Stroop Test, Verbal Fluency Test and Auditory-Verbal Learning Test. The severity of depression symptoms was assessed using the Hamilton Depression Rating Scale (HDRS). Statistically significant differences were found in the intensity of depression symptoms, measured by the HDRS on therapy onset versus the examination results after 8 weeks of treatment (P < 0.001). Considering the 8-week pharmacotherapy period, rDD patients presented better outcomes in cognitive function tests. There was no statistically significant correlation between plasma MDA levels, and the age, disease duration, number of previous depressive episodes and the results in HDRS applied on admission and on discharge. Elevated levels of MDA adversely affected the efficiency of visual-spatial and auditory-verbal working memory, short-term declarative memory and the delayed recall declarative memory. 1. Higher concentration of plasma MDA in rDD patients is associated with the severity of depressive symptoms, both at the beginning of antidepressants pharmacotherapy, and after 8 weeks of its duration. 2. Elevated levels of plasma MDA are related to the impairment of visual-spatial and auditory-verbal working memory and short-term and delayed declarative memory.

Antioxidant /Antidepressant-like Effect of Ascorbic acid (Vitamine
C) and Fluoxetine
Another study investigated the influence of ascorbic acid
(which is an antioxidant with antidepressant-like effects in animals)
on both depressive-like behaviour induced by a chronic unpredictable
stress (CUS) paradigm and on serum markers of oxidative
stress and in cerebral cortex and hippocampus of mice [120]. The
CUS-model is an animal model for induced depression-like behaviour
in animals. Depressive-like behaviour induced by CUS was
accompanied by significantly increased lipid peroxidation (cerebral
cortex and hippocampus), decreased catalase (CAT) (cerebral cortex
and hippocampus) and glutathione reductase (GR) (hippocampus)
activities and reduced levels of glutathione (cerebral cortex).
Repeated ascorbic acid as well as fluoxetine administration significantly
reversed CUS-induced depressive-like behaviour as well as
oxidative damage. No alterations were observed in locomotor activity
and glutathione peroxidase (GPx) activity in the same sample.
These findings pointed to a rapid and robust effect of ascorbic acid
in reversing behavioural and biochemical alterations induced in an
animal model [120].  Ascorbic acid treatment, similarly to fluoxetine, reverses depressive-like behavior and brain oxidative damage induced by chronic unpredictable stress.

 

Ketamine | Fairfax | Alexandria | 703-844-0184| Ketamine therapy | Ketamine as an anti-depressant – Is it right for you? | Dr. Sendi | Ketamine physician | Mt. Vernon | Harrisonburg | Virginia

I am posting a Ketamine article I published in “Your Health Magazine” below. There is excellent studies demonstrating the efficacy of Ketmine in multiple disorders, especially depression, PTSD, post-partum depression, suicidality, Obsessive-compulsive disorder, and severl other mental health problems. Likewise, Ketamine is effective in numerous painful conditions, including CRPS, neuropathy, fibromyalgia, post-herpetic neuralgia, phantom-limb pain, and others. I will discuss articles on each in the ensuing months.

I have used Ketamine over the past 20 years with excellent results in multiple settings. I have always been impressed by it’s safety, especially when it comes to respiratory and cardiac situations.

More and more information is coming about Ketamine’s versatility. Even Time magazine had a recent posting regarding it’s use in depression:

New hope in Depression

Ketamine treatment | Dr. Sendi | Fairfax | Alexandria | Virginia | 703-844-0184

Also, a mention in November JAMA 2017 with Dr. Zarate:

Abbasi J. Ketamine Minus the Trip: New Hope for Treatment-Resistant DepressionJAMA.2017;318(20):1964–1966. doi:10.1001/jama.2017.12975

Ketamine minus the trip

Ketamine minus the trip – a new hope in treating depression  < Article

Here is the audio file link regarding Ketamine in JAMA : https://jamanetwork.com/learning/audio-player/14890187

 

 

 

Ketamine has been safely used for over 45 years, serving as an effective anesthetic agent that has also been shown to have benefits in the treatment of a wide variety of painful conditions as well as mood-related disorders. Treatment-resistant depression is an example of a life-threatening disorder that can be improved through the use of specific protocols that involve the infusion of Ketamine. Depression causes tremendous suffering in both quality of life as well as medical problems that result from the stress it produces. Many individuals have tried numerous therapies that have had little to no impact on their depression, leaving them feeling hopeless over their condition. It turns out that for properly selected individuals, Ketamine can provide acute relief within hours to days. Unlike typical antidepressants, Ketamine interacts with certain brain-derived factors that encourage nerve cells to make meaningful connections that can diminish depression within a much shorter time than a standard depression medication. It is a ‘brain reset’ of sorts, allowing underlying medications to be adjusted while your mood is rapidly elevated through genuine changes of brain circuitry.

Ketamine also provides potentially effective treatment in cases of painful conditions, such as RSD/CRPS, trigeminal neuralgia, post-herpetic neuralgia, and several other nerve conditions. Ketamine can be used in an office-based intravenous protocol and then continued in a topical treatment for those who respond well.

Although Ketamine is FDA approved for anesthetic use, it has not been sent to the FDA for approval of any other medical states. However, the evidence for Ketamine’s ability to provide relief in conditions such as PTSD, anxiety disorders, depression, suicidality, post-herpetic neuralgia, CRPS, trigeminal neuralgia, and multiple other conditions has accumulated over 45 years of use in multiple studies. Ketamine is also being evaluated for drug addictions as well as alcohol use disorder. More recently, Ketamine was featured in Time magazine (August 2017) and in JAMA (November 2017) due to the  positive effects it has had in difficult-to-treat depression.

More and more clinics are offering this treatment, which creates new possibilities for improving conditions that formerly had so few options. With proper patient selection and appropriate monitoring, Ketamine can be safely and comfortably used in an office setting. With a standard slow infusion, most people do not even notice any significant side effects. If you have suffered from any of these conditions then ask your specialist if Ketamine may be a solution for you.

Pictagram from Your health magazine

Fed up with dieting? Dr. Christopher Sendi MD explains dietary success. Link in bio. • #weightloss #nutrition #exercise #washingtondc #virginia #maryland #novaaddictionspecialists #yourhealth #transformation#washingtondc #weightloss#virginia #nutrition #maryland #novaaddictionspecialists #yourhealth #exercise #transformation

“Addiction is a devastating disease that affects an individual physically and psychologically. Counseling may help the psychological component but medications can be much more effective for the physical changes that result from alcohol and opioid abuse.” – Christopher Sendi MD • Link in bio #alcoholaddiction #addiction #opioidaddiction #counseling #medication #recovery#addiction #medication #recovery#counseling #opioidaddiction #alcoholaddiction

 

 

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I copied an pasted an article from people’s pharmacy below that has several excellent links:

Time magazine has a cover story (August 7, 2017) titled:

“THE ANTI
ANTIDEPRESSANT

Depression afflicts 16 million Americans.
One third don’t respond to treatment
A surprising new drug may change that”

The drug in question is ketamine. Will ketamine stop suicidal thoughts better than traditional antidepressants?

When someone is suicidal seconds count!

Q. Is ketamine infusion safe for the elderly? My son’s mother-in-law (age 69) has been diagnosed with major depression. She has made two suicide attempts.

I am not sure what she is taking now, but she seems apathetic, worries about everything and interacts inappropriately with family. She is almost completely unresponsive to her grandchildren. This is a total change from her personality five years ago, when she was devoted to her family and engaged with the world.

A. Major depression takes a terrible toll on the individual, family and friends. Suicide attempts are a clear signal that your son’s mother-in-law is desperate and requires expert medical intervention.

Ketamine (Ketalar) is a fascinating drug that has been used since 1962 as a general anesthetic. Over the last several years researchers have discovered that this medication has profound antidepressant activity that kicks in within hours instead of the usual weeks of standard drugs. When someone is suicidal it is dangerous to wait weeks for an antidepressant drug to work.

Will Ketamine Stop Suicidal Thoughts?

A recent meta-analysis found that ketamine is effective in reducing suicidal ideation within four hours (Neuroscience and Biobehavioral Reviews, June 2017).  Unfortunately, research has not yet shown how long this effect may last.

This isn’t the first assessment of ketamine in the treatment of suicidal thoughts.

Here are some other reports in the medical literature:

“Sublingual (under the tongue) Ketamine for Rapid Relief of Suicidal Ideation”:

“These cases demonstrate that low doses of sublingual ketamine repeated over a span of hours can induce rapid remission of suicidality in unipolar or bipolar depression.

“Chronic use of oral or sublingual ketamine has been helpful in the past 4 years for many of my patients with mild depressive symptoms.

“Sublingual ketamine may be a practical option for managing suicidality in outpatients as an adjunct to traditional antidepressants and mood stabilizers and could shorten the hospital stay of psychiatric inpatients. Sublingual ketamine is worthy of systematic study as a treatment to provide rapid relief of suicidal ideation.”

Reduction in Suicidal Ideation Following Repeated Doses of Intravenous Ketamine?

…”the evidence to date supporting the clinical use of ketamine as antisuicidal treatment is extremely preliminary, and on the basis of the article by Ionescu et al, conclusions concerning the effects of ketamine on suicidal ideation should be drawn with caution.”

Ketamine Rapidly Relieves Acute Suicidal Ideation in Cancer Patients: A Randomized Controlled Clinical Trial

“Cancer patients experience increased risk and incidence of suicide and other psychiatric disorders.

“In the past 10 years, evidence has emerged showing that sub-anesthetic doses of ketamine (0.5 mg/kg) induce fast-acting antidepressant effects on depressed patients. Antidepressant effects of ketamine were observed as soon as 40 min after infusion and typically lasted at most for 7 days, with some patients experiencing more prolonged mood improvement.

” Collectively, this study provides novel information about the rapid antidepressant effect of ketamine on acute depression and suicidal ideation in newly-diagnosed cancer patients.”

“Ketamine for Treatment of Suicidal Ideation and Reduction of Risk for Suicidal Behavior”

(in Current Psychiatry Reports, June, 2016).

“Our review concludes that ketamine treatment can be seen as a double-edged sword, clinically to help provide treatment for acutely suicidal patients and experimentally to explore the neurobiological nature of suicidal ideation and suicidal behavior.”

Ketamine and Your Mother-In-Law:

There is inadequate research on ketamine infusion in older patients (Expert Opinion on Pharmacotherapy, April 2017).  Since this medication may alter blood pressure and heart rate, the latest recommendations from the American Psychiatric Association call for monitoring so that immediate care may be provided if necessary (JAMA Psychiatry, April 1, 2017).

More articles from The People’s Pharmacy about whether Ketamine can stop suicidal thoughts are available at these links:

Can Ketamine Jump Start Antidepressant Action?

Radio Show # 983 (FREE): Intriguing Approaches to Overcoming Depression

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Dr. Sendi graduated from Georgetown University Medical School and trained at Pitt County Memorial Hospital, East Carolina University, Greenville, N.C. for his Board Certification in Internal Medicine. He is also ABPSUS Board Certified in Emergency Medicine and Board Certified in Obesity Medicine with the American Board of Obesity Medicine.

Practice Philosophy

NOVA Health Recovery was founded to provide the optimal care to patients suffering from life-altering, preventable illnesses such as Obesity, Addiction, and Pain. We provide progressive therapies for challenging cases of depression, PTSD, neuropathy, CRPS/RSD, and other painful conditions using Ketamine infusions in a comfortable and safely monitored setting. We also use state-of-the-art interventions for addictions of multiple types, providing the tools and support to allow one to move forward in a healthy, successful manner. There is no need to suffer from treatable conditions in which progressive medication assisted therapies, behavioral support, wellness plans, and general health screening can allow you to improve your quality of life. We also use telemedicine to make it easy for you to see your physician from the comfort of your own home.

Professional Memberships:

American College of Physicians, American Society of Addiction Medicine, American Society for Nutrition, The Obesity Society.

Special Interests:

Dr. Sendi has 21 years experience in the medical field. Included experiences are Addiction and Pain Management, Obesity and weight management, lipidology, and wellness. Dr. Sendi is Board Certified in Internal Medicine, Emergency Medicine, and Obesity Medicine. His additional interests include wellness, aging, and health-risk mitigation.

Have you Tried all options for depression and pain?

At NOVA Health Recovery, we understand how painful conditions, such as CRPS, post-herpetic neuralgia, and neuropathies rob your life of comfort and quality. We also recognize the suffering that mental health problems, such as anxiety, depression, and PTSD inflict on people and destroy the ability to enjoy even their best years. Many have exhausted multiple therapies and feel hopeless about any treatment at all. NOVA Health Recovery offers Ketamine treatments to appropriate patients who suffer such conditions. In conjunction with other regimens, Ketamine infusion, offered in a monitored, comfortable setting, may provide improvement. This option may just be what you need to pick up your mood and decrease you pain while your regular medications take effect.

Want to learn more? Schedule a consultation today by calling 703-844-0184.