Seasonal affective Disorder and Ketamine Therapy –

If you are looking for ketamine therapy in Virginia, Maryland, or DC, feel free to contact NOVA Health Recovery at 571-999-2118 or 703-844-0184 or send us a web form. Please include your phone number so we can connect with you.


Seasonal Affective Disorder

If you Can Ketamine help treat seasonal depression? | New Depression Treatments | How Ketamine can help treat SAD? | Four causes of Seasonal Affective Disorder | Northern Virginia Ketamine Center or a loved one are suffering from depression, SAD, anxiety, OCD, PTSD, Bipolar Disorder, or chronic pain, consider ketamine therapy for rapid relief of your condition.  NO referral is needed. The treatment is not covered by insurance. The treatment is  effective in over 70% of treatment resistant patients. If you are located in the D.C., Northern Virginia, or Maryland area, contact us though the following web form below or through our website directly. We also offer oral and home ketamine therapy: 

About 70% of depressed patients feel worse in the wintertime. Seasonal Affective Disorder (SAD) is identified as a type of depression – Major Depressive Disorder with Seasonal Pattern in the Diagnostic Manual of Mental Disorders (DSM-5). Patients with this problem feel symptoms when there is less light in the fall and winter months. There is usually improvement in the spring months as the days grow longer. January and February can be the most difficult months and resolution may be seen in the summer, although some patients are seasonally depressed in the summertime. 

  • 5% of the population suffers from SAD 
  • Symptoms may last 40% of the year. 
  • These symptoms may be due to a shift in the biological clock. 
  • Women are affected more than men. 
  • The average age is between 18-30 years when it starts 

What symptoms are seen in this condition: 

  • Feeling sad or having a depressed mood 
  • Changes in appetite; usually eating more and craving carbohydrates 
  • Loss of energy or increased fatigue despite increased sleep hours 
  • Increase in purposeless physical activity (e.g., inability to sit still, pacing, handwringing) or slowed movements or speech.   
  • Feeling guilty or worthless 
  • Change in sleep with excess sleep being very common. 
  • Loss of interest or pleasure in activities once enjoyed and anhedonia. 
  • Difficulty thinking, concentrating, processing information, or making decisions 
  • Thoughts of self-harm, death, or suicide 

Circadian rhythm disruption either by change of daylight, social jetlag (from late night events and TV), shift work, change in seasons, travel, and exposure to artificial lights is a major cause of seasonal depression. These changes in circadian rhythms are associated with multiple mood disorders as mentioned in the links below: 

Circadian rhythm disruption and mental health 

In fact, circadian rhythm disruption plays a crucial role in the etiology of depression: 

Disruption of Circadian Rhythms: A Crucial Factor in the Etiology of Depression 

Chronotypes and affective disorders: A clock for mood? 

What are the risk factors for Seasonal Depression? 

  • Family history. People with SAD may be more likely to have relatives with SAD or another form of depression. 
  • Living far from the equator. SAD appears to be more common among people who live far north or south of the equator due to variations in light. 
  • Having major depression or bipolar disorder. Symptoms of depression may worsen seasonally when they suffer from another mood disorder. 

What else contributes to SAD? 

  • Melatonin – This hormone plays a role in sleep patterns and mood. It may be overproduced in SAD due to increased darkness: 

The circadian basis of winter depression 

The above study demonstrated the phase-shift hypothesis for SAD was a likely correlate of depression. 

  • Low Vitamin D 

Vitamin D is believed to play a role in serotonin activity, Vitamin D deficiency and insufficiency have been associated with clinically significant depressive symptoms: 

Associations between vitamin D levels and depressive symptoms in healthy young adult women 

  • Low Serotonin: People with seasonal affective disorder have difficulty regulating the neurotransmitter serotonin, a neurotransmitter believed to be responsible for balancing mood. In one study, people with SAD had 5% more SERT, a protein that assists with serotonin transport, in the winter months than in summer: 

Patients with seasonal affective disorder show seasonal fluctuations in their cerebral serotonin transporter binding 


Diagnostic Criteria for a Major Depressive Episode 

A. At least five of the following symptoms have been present during the same two-week period, nearly every day, and represent a change from previous functioning. At least one of the symptoms is either: 

  • Depressed mood (or alternatively can be irritable mood in children and adolescents). 
  •  Markedly diminished interest or pleasure in all, or almost all, activities 
  • Significant weight loss when not dieting or weight gain or decrease or increase in appetite. 
  • Insomnia or hypersomnia 
  • Psychomotor agitation or retardation. 
  • Fatigue or loss of energy. 
  • Feelings of worthlessness or excessive or inappropriate guilt. 
  • Diminished ability to think or concentrate, or indecisiveness. 
  • Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide. 

The symptoms are not better accounted for by a mood disorder due to a general medical condition, a substance-induced mood disorder, or bereavement (normal reaction to the death of a loved one). 

The symptoms are not better accounted for by a psychotic disorder like schizoaffective disorder. 

Criteria for Seasonal Pattern Specifier 

Regular temporal relationship between the onset of major depressive episodes and a particular time of the year (unrelated to obvious season-related psychosocial stressors) 

Full remissions (or a change from depression to mania or hypomania) also occur at a characteristic time of year 

Two major depressive episodes meeting criteria A and B in last two years and no nonseasonal episodes in the same period 

Seasonal major depressive episodes substantially outnumber the nonseasonal episodes over the individual’s lifetime 

American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D.C.: American Psychiatric Association, 1994:327. Copyright 1994. 

Treatments for SAD include

  1. Cognitive Behavioral Therapy (CBT) which is talk therapy. Problems helped by psychotherapy include difficulties in coping with daily life; the impact of trauma, medical illness or loss, like the death of a loved one; and specific mental disorders, like depression or anxiety. 
  1. Spending more time outside in the sun or by a window exposed to sunlight. 
  1. Structured exercise 
  1. Socialization with friends 
  1. Eating well. In particular, a Mediterranean Diet or anti-inflammatory diet. 
  1. Exposure to light therapy through a 10000 Lux light box for 30 minutes in the morning: 

Light therapy is used as a treatment for several conditions, including: 

  • SAD 
  • Dementia 
  • Jet lag 
  • Types of depression that don’t occur seasonally 
  • Sleep disorders 
  • Adjusting to a nighttime work schedule 

The light box should be used regularly and at the same time each day. The intensity of the light should be 10,000 Lux at a distance of 16-24 inches from you. This is used first thing in the morning. Tanning beds are not effective for this. 

Light regulates the circadian rhythm, and morning light therapy helps night owls with delayed sleep phase disorder fall asleep earlier. In primary insomnia, it improves daytime energy, boosts sleep quality, and helps patients fall asleep faster: 

The effects of light therapy on sleep problems: A systematic review and meta-analysis 

Light therapy has been used in older adults with Parkinson’s Disease, dementia, and cognitive impairment, and it improved mood and behavioral disturbances, but not the cognitive loss or quality of life: 

Application of light therapy in older adults with cognitive impairment: A systematic review 

The use of morning light at 10000 Lux and increasing evening darkness (or blue filtering lights or Phillips Hue Bulbs) may be an option to increase efficacy. Remember to not turn on lights at night if you wake up from sleep as it may disrupt your sleep rhythm. Consider specialty wall lights to avoid blue light at those times. 

For more information about improving your circadian clock and the timing of morning light for you, go to the CET website: Center for Environmental Therapeutics 

What is your chronotype? Here is an online test: AutoMEQ 

What is your seasonal pattern: AUTO-PIDS 

Also note that ADHD can worsen in the wintertime as well. Light therapy has been shown to improve this: 

An Open Trial of Light Therapy in Adult Attention-Deficit 

This trial demonstrated a shift towards earlier bedtimes and not so much of a mood benefit. 

Bright light therapy also helped reduce combat-related PTSD in a recent randomized trial as well: 

Bright Light Treatment of Combat-related PTSD: A Randomized Controlled Trial 

The light therapy was delivered across all seasons and decreased core PTSD symptoms. 

Medication options: 

Bupropion has been shown to be effective in the prevention of SAD by starting treatment prior to the winter season. 

Seasonal affective disorder and its prevention by anticipatory treatment with bupropion XL: 

Three prospective, randomized, placebo-controlled prevention trials were conducted on 1042 SAD patients, enrolled in autumn and treated while still well, across the northern US and Canada. Patients received either bupropion XL 150-300 mg or placebo daily by mouth from enrollment until spring and were then followed off medications for 8 additional weeks.   

Major depression recurrence rates during the three studies for bupropion XL and placebo groups were 19% versus 30% (p = 0.026), 13% versus 21% (p = 0.049), and 16% versus 31%; yielding a relative risk reduction across the three studies of 44% for patients taking bupropion XL.   

Of note, the use of Bupropion for SAD also helps the resolution of sleepiness and fatigue as depression resolves (relative to SSRI’s): 

Resolution of sleepiness and fatigue in major depressive disorder: A comparison of bupropion and the selective serotonin reuptake inhibitors 

Treatment of MDD with the NDRI, bupropion, resulted in a greater resolution of sleepiness and fatigue than SSRIs treatment. 

Ketamine Therapy for SAD 

Ketamine also offers a rapid ability to induce mood improvement from seasonal depression. Ketamine, through a series of infusions over two weeks can improve treatment resistant depression in 70% of patients. NOVA Health Recovery Ketamine Center in Fairfax, Virginia offers these infusions with follow-up oral and intranasal ketamine for use at home to maintain effects in combination with other therapies such as light box therapy. Ketamine works well in combination with other modalities and medications. 

Ketamine-Induced Glutamatergic Mechanisms of Sleep and Wakefulness: Insights for Developing Novel Treatments for Disturbed Sleep and Mood 

Effects of ketamine on circadian rhythm and synaptic homeostasis in patients with treatment-resistant depression: A protocol for mechanistic studies of its rapid and sustained antidepressant actions in humans 

Ketamine and Sleep: Bridging the Gap in the Treatment of Depressive Illness 

Motor-Activity Markers of Circadian Timekeeping Are Related to Ketamine’s Rapid Antidepressant Properties 

Contact Us Here:

National Suicide Prevention Lifeline – 800-273-TALK (8255). 

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Evidence that oral ketamine works for depression and chronic suicidal thoughts.

If you are interested in home oral ketamine therapy or nasal spray ketamine, contact NOVA Health Recovery Ketamine Center at 571-999-2118 or 703-844-0184 to start treatment. You can also fill out the web form below. Please include your phone number so we can contact you.


Oral ketamine can be an effective option in the treatment of depression and mood disorders. 

  • It has a significant antidepressant and anti-suicidal effect. 
  • Studies have not shown much abuse potential or adverse effects. 
  • It is cheap, convenient, and available
  • It is slower in onset than Intravenous formulations. It produces lower remission and response rates overall. 
  • It can be used to augment traditional antidepressant therapy

How is ketamine administered? 

  • Oral 
  •  Sublingual 
  • Transmucosal 
  • Intravenous 
  • Intramuscular 
  • Subcutaneous 
  • Intranasal 
  •  Rectally 

Intravenous ketamine is the most studied and demonstrates the best efficacy in mood disorders because it is 100% bioavailable. (4)(5) The dose of IV ketamine is 0.5 mg/kg over 40 minutes. The equivalent dose of oral ketamine would be 120-150 mg (2 mg/kg) in a standard adult.  

Oral ketamine is only 20% bioavailable to the blood stream. (1)(2)  

Oral ketamine is metabolized in the liver, which results in norketamine elevation (an active breakdown product). (2) 

A possible way to increase availability of oral ketamine is to increase the dose. 

Support for the use of oral ketamine comes from: 

  • Case reports 
  • Chart reviews 
  • Randomized controlled trials 
  • Case series 

Oral ketamine can augment traditional antidepressant therapies: 

In the study above, an RCT was performed in which 81 patients were followed with the combination of oral ketamine and sertraline or sertraline alone and monitored with the Hamilton Depression Rating Scale (HDRS) at baseline, 2,4 and 6 weeks later. 

The dosing of the oral ketamine was 25 mg twice a day with or without sertraline (150 mg/d)/ Antidepressant ratings were lower in the ketamine group starting at week 2 onward. Response rates were greater in the ketamine group, but remission rates did not differ from placebo (22% v 15% respectively) 

Conclusions of this study: 

Early improvement was significantly greater in the oral ketamine group with Sertraline (85.4%) compared to the placebo group (42.5%).  Oral ketamine may be considered as suitable adjuvant to sertraline in relieving depressive symptoms. 

A recent systematic review demonstrated that oral ketamine can improve depression symptoms, but remission rates and response rates were marginal compared to placebo. IV ketamine, however, has robust and rapid effects on depression. 

In this review, 890 studies were screened, with 10 studies included in the systematic review. Three randomized controlled trials with 160 total patients were included. They found: 

  • A significant antidepressant effect of oral ketamine. 
  • Remission rates and response rates were marginal relative to placebo at endpoints. 
  • Oral ketamine antidepressant effects seemed to take effect in the 2nd week (significant result). 
  • No significant differences in the overall side-effects between oral ketamine and the placebo group 

Other Randomized controlled trials have demonstrated efficacy with oral ketamine:(3) 

In the RCT with Domany et al. (2109) 41 patients were studied. Oral ketamine (1 mg/kg) or placebo was used. Doses were three times per week. 

Results: Ketamine was superior to placebo. At the treatment endpoint, the mean Montgomery-Asberg Depression Rating Scale scores dropped from 33.4 to 20.7 in the ketamine group and from 30.0 to 27.5 in the placebo group. 

Response (32% vs 6%) and remission (27% vs 0%) rates were also higher with ketamine than with placebo.   

What doses are used in oral ketamine for depression and suicidality? 

Doses of oral ketamine have ranged from 0.25 to 7 mg/kg and from 50 mg per occasion to 300 mg per occasion in multiple daily dosing, daily dosing, and intermittent dosing schedules. Periods of up to 3 years have been studied with oral ketamine. 

Oral ketamine was well tolerated in all studies. There was no misuse, dose escalation, craving, adverse effects, or dependence reported in these studies. 

Oral ketamine is cheaper, easily performed, and has few side-effects. However, it may take a few weeks to see the results of the antidepressant and anti-suicidal effects. 

Oral ketamine is poorly absorbed and tastes terrible. 

Titration of the oral dose to efficacy needs to be done and varies from person to person due to variable drug absorption. 

There has been no misuse of oral ketamine in any study groups for the RCT even though the medication was administered at home. 

  1. Yanagihara Y, Ohtani M, Kariya S, Uchino K, Hiraishi T, Ashizawa N, Aoyama T, Yamamura Y, Yamada Y, Iga T. Plasma concentration profiles of ketamine and norketamine after administration of various ketamine preparations to healthy Japanese volunteers. Biopharm Drug Dispos. 2003 Jan;24(1):37-43. doi: 10.1002/bdd.336. PMID: 12516077. 
  1. Clements JA, Nimmo WS, Grant IS. Bioavailability, pharmacokinetics, and analgesic activity of ketamine in humans. J Pharm Sci. 1982 May;71(5):539-42. doi: 10.1002/jps.2600710516. PMID: 7097501. 
  1. Domany Y, Bleich-Cohen M, Tarrasch R, Meidan R, Litvak-Lazar O, Stoppleman N, Schreiber S, Bloch M, Hendler T, Sharon H. Repeated oral ketamine for out-patient treatment of resistant depression: randomised, double-blind, placebo-controlled, proof-of-concept study. Br J Psychiatry. 2019 Jan;214(1):20-26. doi: 10.1192/bjp.2018.196. Epub 2018 Sep 24. PMID: 30246667. 
  1. Berman RM, Cappiello A, Anand A, Oren DA, Heninger GR, Charney DS, Krystal JH. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry. 2000 Feb 15;47(4):351-4. doi: 10.1016/s0006-3223(99)00230-9. PMID: 10686270. 
  1. Zarate CA Jr, Singh JB, Carlson PJ, Brutsche NE, Ameli R, Luckenbaugh DA, Charney DS, Manji HK. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006 Aug;63(8):856-64. doi: 10.1001/archpsyc.63.8.856. PMID: 16894061. 

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