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Sleep Guide For Anxiety

Anxiety comes in many forms, from the general worry that comes from everyday life to the intense fear caused by major psychiatric disorders. As debilitating as anxiety can be to our mental and physical health, it’s also corrosive to our quality of sleep—whether you’re a college student pulling an all-nighter or a veteran jolted awake from a nightmare caused by PTSD.

This guide covers how anxiety and sleep are interrelated, change with age, and what you can do to improve both.

Anxiety and Sleep

Nearly 40 million people in the US experience an anxiety disorder in any given year. More than 40 million Americans also suffer from chronic, long-term sleep disorders. Those numbers aren’t a coincidence. Anxiety and sleep are intimately connected: The less sleep you get, the more anxious you feel. The more anxious you feel, the less sleep you get. It’s a cycle many insomnia and anxiety sufferers find hard to break.

Anxiety and sleep are intimately connected: The less sleep you get, the more anxious you feel.

Common anxiety symptoms like restlessness, increased heart rate, rapid breathing, and gastrointestinal (GI) problems make it difficult to fall asleep.

Because insomnia and anxiety are so closely linked, one of the first steps in treatment is to determine which is causing the other — that is, which is the primary cause and which is the secondary symptom. “Sometimes, insomnia is secondary,” says psychotherapist Brooke Sprowl, “in that it is caused by another primary disorder such as depression, anxiety, or a medical condition. In this case, usually treating the primary disorder [improves] the insomnia.”

Whether insomnia is the primary or secondary cause, natural remedies like magnesium glycinate and melatonin have been shown to help with sleep, says Sprowl. Non-medication treatments like cognitive behavior therapyalong with good sleep hygiene are also effective at combating insomnia and anxiety.

Health Risks of Insomnia

Insomnia affects cognitive functions and cripples school and work performance. According to one study, 70% of college students with lower GPAs also had difficulty falling asleep. Insomnia also slows reaction times, raising the risks of driving a car or operating heavy machinery.

Sleep deprivation is also bad for your physical health, increasing your risk for developing high blood pressure and heart disease. And long-term sleep disruptions may even raise the risk of some forms of cancer.

Common Sleep Disorders

There are many forms of sleep disorder besides insomnia. All interrupt sleep, threaten our health, and increase nervousness and stress. Here are a few common ones:

Delayed Sleep Phase Syndrome

Anyone who has changed time zones or experienced “jet lag” understands the effects of delayed sleep phase syndrome (DSPS). When your sleep and wake cycles don’t align with the current time zone, you feel groggy when you shouldn’t.

While these symptoms are temporary for most, people with DSPS stay out of sync for long stretches of time, negatively affecting their work and activities. Because people with DSPS are forced to conform to the external clock rather than their internal one, they suffer from lack of sleep and increased anxiety.

Obstructive Sleep Apnea

Obstructive sleep apnea is when a sleeper’s relaxed airways close and obstruct breathing. Interrupted breathing episodes occur numerous times during sleep and are usually accompanied by snoring.

Sleep apnea sufferers are often unaware they have the condition.

Obstructed airways result in lowered oxygen levels and increased carbon dioxide in the blood. Sufferers are often unaware they have the condition. Sleep apnea increases the risk of heart disease, stroke, diabetes, and cancer. Sleep studies are required to diagnose obstructive sleep apnea.

Forms of Anxiety

How do you know if you have garden-variety nervousness or a more serious anxiety disorder? Usually, the difference is how significantly your anxiety affects your life.

For someone at a party who doesn’t know anyone, a certain level of anxiety is normal. However, if their anxiety is interfering with daily activities (e.g. making friends, school work, job performance), they may have a serious anxiety disorder.

Every form of anxiety will affect your quality of sleep if it goes on long enough

Whether social nervousness or a serious phobia, every form of anxiety will affect your quality of sleep if it goes on long enough. Below are descriptions of the five major anxiety disorders. If you think you may have one, consult your physician or therapist about diagnosis and treatment.

Generalized Anxiety Disorder

People with generalized anxiety disorder (GAD) display excessive anxiety and worry most of the time. Instead of one source of anxiety, sufferers tend to worry about multiple things simultaneously. GAD symptoms will last at least six months and begin to negatively affect social interactions like school, work, and family life. GAD affects 6.8 million adults (3.1 percent of the U.S. population), yet only 43 percent of sufferers receive treatment.

Social Anxiety Disorder

The fear of public speaking (glassophobia) is still ranked alongside death as a the number one fear among 20 percent of Americans. Social phobias like public speaking apply to formal situations, but for people with social anxiety disorder, their fear extends into informal interactions like eating and drinking in front of others. People with social anxiety disorder struggle when meeting new people, making friends, interacting with teachers, or buying items at a checkout counter.

Obsessive-Compulsive Disorder (OCD)

Those with obsessive-compulsive disorder (OCD) have recurrent, unwanted thoughts (obsessions) and/or repetitive behaviors (compulsions). OCD sufferers often perform repetitive “rituals” like washing their hands, checking, counting, or cleaning. The rituals are intended to lower anxiety levels, but the result is temporary. Obsessive-compulsive disorder is often associated with poor sleep, especially if repetitive behaviors involve getting out of bed.

Panic Disorder

Panic attacks are unexpected episodes of intense fear followed by physical symptoms like chest pain, heart palpitations, and shortness of breath. These episodes of intense anxiety are the major result of panic disorder. Because panic attacks manifest without warning, the fear of having another one is a major source of fear itself.

Panic disorder makes insomnia worse for many sufferers. Most people will experience only one or two panic attacks in their lifetime. But anyone who has panic attacks frequently enough that they live in fear of having another one, probably has panic disorder.

Post-Traumatic Stress Disorder (PTSD)

Everyone who experiences a traumatic event feels a certain level of anxiety. Our fight-or-flight responses help protect us, whether from a physical attack or a natural disaster. Once the event is over, some residual anxiety is normal—but, eventually, anxiety levels return to normal.

For some people, however, this never happens. Instead, they develop post-traumatic stress disorder (PTSD)—an anxiety disorder where sufferers continually re-experience the fear of a traumatic event(s) long after it has passed. One of the most common symptoms of PTSD is intense nightmares, which are major sleep disruptors.

Although PTSD causes sleep disorders, the disorder also contributes to acquiring PTSD. One sleep study of National Guard members showed this causal relationship. The National Guard members were screened for sleep disturbances a few months before deployment to Iraq. A year later, they came back and were tested for PTSD. Researchers found that soldiers who had sleep disorders before they were deployed were more likely to have PTSD afterward.

Researchers found that soldiers who had sleep disorders before they were deployed were more likely to have PTSD afterward.

While PTSD is often associated with military veterans, anyone experiencing a traumatic event can develop symptoms. For example, one in eight heart attack survivors develop PTSD.

Sleep and Anxiety as We Age

In general, our anxiety levels lower as we get older—ramping up during our adolescence and slowly abating with old age. The difference in anxiety disorder rates for adolescents (32 percent) and adults (19 percent) is significant.

Prevalence of anxiety disorders by age

But while anxiety in general improves with age, our quality of sleep gets worse. One cause of this is that our sleep patterns change as we get older. We tend to sleep less—28 minutes per decade according to one sleep study of men.

Another cause comes from chronic age-related aches and pains that rouse us from sleep. Our brain chemistry also changes as we age. Levels of melatonin, the chemical responsible for beginning the sleep cycle, decline as we get older.

If we don’t take the steps to improve our sleep as we age, we can counteract the positive gains we get from lowered levels of anxiety. To do that, we need to understand how anxiety and sleep affect us at critical points in our life.

Children and Adolescents

For the first few decades of our lives, our sleep patterns change dramatically. Our bodies and brains grow, and our sleep needs change along with the sources of anxiety.

Infants need the most sleep and have frequent sleep-wake episodes throughout the day. Around six months, children begin sleeping through the night. By adolescence, they achieve the average adult sleep requirement of 7 to 10 hours per day. Sleep deprivation symptoms for children and adolescents include:

  • Irritability
  • Behavior problems
  • Poor academic performance
  • Automobile accidents
  • Napping (teenagers)
Normal sleep patterns in children and adolescents

Sleep Disorders

Sleep disorders like snoring and sleep apnea are rare in children and adolescents, while others like delayed sleep phase syndrome (DSPS) or behavior insomnia are more common.

Anxiety Disorders

The sleepless night after watching a scary movie is a familiar experience for most of us. But children with anxiety disorders feel an intense nervousness and fear during everyday activities.

One in eight children has an anxiety disorder, which is often accompanied by depression. Here are some common symptoms of childhood and adolescent anxiety that are possible sleep disruptors:

  • Change in eating habits
  • Anger or irritable mood
  • Clinginess
  • Nightmares
  • Substance abuse

College Students

The college years mark a time when we’re the most anxious and most sleep deprived. All-night cram sessions, midnight social gatherings, and 8:30 a.m. classes take their toll on the health and mental well-being of college-aged students. Sleep studies of college-aged students show up to 60 percent suffer from poor sleep quality, while almost 8 percent have insomnia disorder.

leep studies of college-aged students show up to 60 percent suffer from poor sleep quality

Poor sleep quality affects grades too. One study of student sleep patternsshowed those who got more than 9 hours sleep tend to have higher average GPAs (3.24) than those who got less than 6 hours sleep (2.74). Just getting 10 or 15 minutes less sleep every night can add up quickly over four years—making a significant dent in overall academic performance.

College students show high rates of anxiety disorders. In fact, anxiety for college students has surpassed depression as the most common mental health diagnosis—affecting about 1 in 5 students.

Navigating new surroundings, strange faces, and responsibilities during college are a necessary part of becoming an adult, but the transition comes with a healthy dose of anxiety. Much of that worry comes from performing well on exams.

Test Anxiety

Test anxiety is something most college students bring with them from primary and secondary school. But in college, the stakes are even higher for students who’ve taken on the responsibility for policing their own grades.

Test anxiety is particularly pernicious because it affects a large portion of students (around 17 percent) and is a common way for students to slip into bad sleeping habits.

Students with test anxiety are more susceptible to bad sleep hygiene from staying up late to cram for tests. And the general anxiety they feel weighs on their ability to fall asleep.

Test anxiety and fear of failure often set off a series of what-if hypotheticals. “What if I don’t pass this test? I’ll flunk this class. What if I flunk this class? I won’t graduate. What if …”. Students can lower their stress by following some common guidelines to overcome test anxiety, which include getting enough sleep.

Sleep Disorders

College students suffer from sleep disorders at about the same rate as older adults. It’s a statistic at odds with society’s view that a group of young, healthy people are vulnerable to “older” maladies. But sleep disorders like delayed sleep phase syndrome (DSPS) and sleep apnea affect up to 27 percent of students.

College students suffer from sleep disorders at about the same rate as older adults.

College students may be more likely to develop DSPS given their penchant for late-night study sessions and other activities. They’re awake more during the night time and may nap to “catch up” during the day.

Over time, their internal clocks (circadian rhythms) begin to slip out of sync with the regular day-and-night cycle. What results is a type of “academic jet lag” that can last for semesters and cause long-lasting physical and mental harm.

Getting Better Sleep in College

Here are some tips for changing your daily college routine to improve your quality of sleep and lower your anxiety levels.

  • Get out of your head. If you can’t fall asleep because you can’t turn off your thoughts, get out of bed and do something “mindless”. Go for a walk. Do push-ups. Doodle on paper. Try yoga. Turn your focus to your body and not your mind.
  • Get into the sunlight. Your circadian rhythm is sensitive to light and darkness. Get a good dose of sunlight every day. Walk around campus. Eat lunch on the lawn.
  • Don’t “catch up” on weekends. Keep a consistent sleep schedule. Don’t sleep in more than an hour on weekends.
  • Save your bed for sleeping. Don’t do anything else in bed but sleep. Watch TV and do homework somewhere else. Train your brain and body to expect sleep when you lay down. And don’t make a habit of sleeping anywhere else besides your bed (e.g. couch, recliners).
  • Don’t drink alcohol before bed. You may think alcohol helps you sleep, but it actually disrupts your sleep cycle throughout the night. Avoid alcohol at least 4 hours before bed.

Seniors

Diagnosing anxiety disorders in seniors is notoriously difficult. Factors like changes in medication and age-onset dementia make it hard to diagnose older folks, and social stigma around mental illness make seniors hesitant to report issues. A mental health screening is a quick and easy way to find out if anxiety symptoms are impacting your life enough to warrant medical attention.

Although aging usually involves a drop in anxiety levels, the stress and fears of adult life still pose a real barrier to getting a good night’s sleep. Over half of seniors report some problems with their sleep.

The elderly tend to have more interruptions during sleep and sleep fewer hours. The aches and pains of age-related physical problems like chronic pain, arthritis, and diabetes cut into our sleep quality. Fewer hours means the amount of quality sleep they get becomes even more important. Follow these sleep guidelines for seniors to make sure you’re getting a good night’s rest.

Tips for Sleeping With Anxiety

The nightly rituals and sleep habits you use make up your sleep hygiene. Having good sleep hygiene increases your chances of getting quality sleep and relieving anxiety. Bad sleep hygiene includes eating too late, sleeping on a bad mattress, or living near a noisy interstate.

Some changes to your sleep habits are relatively easy to make, others not so much. But each one you can address is another step towards getting a good night’s sleep and reducing anxiety.

Tips for sleeping with anxiety

Keep a Tight Sleep Schedule

The more you stick to a sleep routine, the faster you’ll fall asleep. Like any other habit, sleep is highly sensitive to change. Sleeping only in your bed (not the recliner) or waking up at the same time on weekends are both effective sleep rituals. They send strong signals to your brain when it’s time to sleep and wake. Alter your routine, and your sleep will suffer.

Sleep schedule consistency also helps lower anxiety levels. Anxiety is about the fear of the unknown. Adhering to a strict sleep schedule reinforces a strong sense of control and predictability into your life.

Exercise Regularly

Regular exercise is often touted as one of the best ways to get a good night’s sleep, relieve tension and eliminate stress. However, if you want to get the most benefit from exercise, do it at the right times.

Exercise releases endorphins and revs up your body and brain. Doing it too late in the evening or just before bedtime makes it harder to fall asleep. Plan your exercise regimen for morning or afternoon. Give your body time to come down and soak in the relaxing effects of physical exercise.

Meditate

Meditation is a treatment for insomnia that helps lower anxiety.

Mindfulness meditation brings your attention to the present experience by eliminating thoughts about the past and future. It helps you focus on the now by eliminating backward, revisionary thoughts and forward-looking worries. Since the past and future are the subject of most worries, mindfulness helps eliminate those anxiety-producing thoughts.

One study of middle-aged adults showed that six weeks of mindfulnessawareness meditation resulted in less insomnia, fatigue, and depression compared to a control group. Get started with meditation by choosing a mindfulness program that’s right for you.

Mindfulness meditation is only one technique in a larger sleep treatment strategy called cognitive behavior therapy, which helps you identify and change thoughts and behaviors that cause sleep problems.

Dampen Distracting Noises

We still have the high levels of alertness our early ancestors employed to stay alive for thousands of years. That’s why even sounds slightly above a whisper (30 decibels) can still disrupt our sleep. With sleep disruptors this quiet, you may not even know they’re affecting you. Here are a few ways to tamp down unwanted nightly noise:

  • Use a white noise machine to cover random sounds within your sleep space.
  • Try earplugs designed for sleeping.
  • Soften hard surfaces like floors and walls with rugs or acoustic foam.
  • Soundproof curtains for windows.
  • Don’t run dishwashers and washing machines at night.
  • Plant thick hedges outside your bedroom window to block exterior noises.

Turn Off Bad Lighting

Different lighting colors and intensities affect our circadian rhythms. Bright blue sunlight tells our brains it’s time to get up, dim amber-colored lighting signal that it’s almost time for sleep. That bright street lamp outside your bedroom window may be counteracting your brain’s signal to go to bed. But you can fight light pollution by following these tips:

Improve Sleep-Space Lighting

Use thick window covering to block out external light. Adjust your alarm clock to a lower intensity setting. Unplug non-essential electronics that contain bright LED indicator lights. Keep your sleep environment as dark as possible, and use strategically placed night lights for safe travels to the bathroom.

Block Blue Lighting Before Bed

There are also lights that disrupt your sleep before you lay down. Laptops, tablets, and cell phone screens all emit a blue light that tricks your brain into thinking the sun is still up. They also inhibit the release of melatonin.

Avoid staring into screens an hour or two before bedtime. If digital device abstinence isn’t an option, set your displays to “night mode”. This automatically changes screen colors from blue to amber at sunset—the longer wavelength light won’t disrupt your circadian rhythm. Also, try wearing blue light blocking glasses in the evening.

Get a Mattress and Pillow That Fits You

When we lay on an unsupportive mattress or overly stuffed pillow, pressure points build on our sides, back, and neck. These pressure points cause us to literally toss and turn in an attempt to find a comfortable position all night.

Relieve pressure points by getting a mattress and pillow that conforms to your body. Most modern memory foam, latex, and elastic polymer mattressesare designed to conform to your body while also supporting it—but tests show mixed results.

Your pillow should support the curves of your head and neck while keeping your head cool. Good air circulation keeps your head cool and comfortable. Look into getting a pillow that offers proper airflow.

Why Sleeping Well Is Getting More Difficult

The connection between sleep and anxiety is deep—primordial even. Our bodies and minds have evolved to be a search light for dangers. It’s a major reason humans still exist. But those ancient hazards that plagued the sleep of our ancestors—those predatory howls and snaps of twigs—are now the stresses and worries of a modern life. Our anxiety triggers are the same; it’s the environment that’s changed.

Our technological devices do more than emit a blue light that disrupts our circadian rhythms. They bombard us with sources of anxiety from every corner of the world every hour of the day.

Every war, famine, or natural disaster we hear about pushes our anxiety levels higher. And our sleep suffers. Nighttime rituals and blackout curtains help, but how we handle those stressors during the day may be the key to staying calm and well rested.

Recent studies are already looking into the effects of social media use and stress in adolescents, and news fatigue is a commonly reported phenomenon among Americans.

Being constantly “plugged in” to current events or monitoring the lives of family and friends keeps our fight or flight responses turned on. In a modern, technological world, turning inward for self-maintenance and tranquility is no longer a self-obsessed, “new age” idea, it’s a prerequisite to getting through life.

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Omega-3 Polyunsaturated Fatty Acids Are Associated with Healthy Aging

 

Plasma levels of seafood-derived long-chain ω-3s in elders predicted risk for various adverse conditions.

Although consuming long-chain ω-3 polyunsaturated fatty acids (PUFAs) has favorable physiological effects (e.g., on endothelial function), the relation between plasma PUFAs and healthy aging is unknown. In this prospective cohort study, researchers determined the longitudinal association between serial measures of summed and individual plasma PUFAs (i.e., eicosapentaenoic, docosapentaenoic, and docosahexaenoic acid) and α-linolenic acid and healthy aging.

Participants were 2622 elders (mean age, 74) with healthy aging at baseline. Healthy aging was defined as absence of cardiovascular disease, cancer, lung disease, severe chronic kidney disease, and cognitive and physical dysfunction. Plasma PUFA levels were measured three times during the study period (1992–2015), and participants were classified into quintiles based on their plasma PUFA concentrations. During the study, 89% of participants experienced unhealthy aging. In an analysis that was adjusted for multiple variables, risk for unhealthy aging was 18% lower in participants in the highest PUFA quintile compared with those in the lowest PUFA quintile. A significant dose-response trend was observed. Assessed individually, higher intake of eicosapentaenoic and docosapentaenoic acid (but not docosahexaenoic acid or α-linolenic acid) was associated with lower risk for unhealthy aging.

Higher plasma levels of PUFAs, especially seafood-derived eicosapentaenoic acid and endogenous and seafood-derived docosapentaenoic acid, were associated with higher likelihood of healthy aging. This study is unique in that actual plasma levels, not dietary intake histories, were used. However, given the study design, causality could not be established, residual confounding was possible, and the results might not be generalizable to younger people. Nonetheless, the results support guidelines for increased consumption of fish.

Lai HTM et al. Serial circulating omega 3 polyunsaturated fatty acids and healthy ageing among older adults in the Cardiovascular Health Study: Prospective cohort study. BMJ 2018 Oct 17; 363:k4067. (https://doi.org/10.1136/bmj.k4067)

Zhu Y et al. Omega 3 polyunsaturated fatty acids and healthy ageing: Fresh evidence provides clues to healthier, not just longer lives. BMJ 2018 Oct 17; 363:k4263. (https://doi.org/10.1136/bmj.k4263)

Serial circulating omega 3 polyunsaturated fatty acids and healthy ageing among older adults in the Cardiovascular Health Study

Fresh evidence provides clues to healthier, not just longer lives

Populations across the world are living longer.1 Between 2015 and 2050, the proportion of the population worldwide, who are aged over 60 will nearly double from 12% to 22%.2 Amid this rapid shift in the age distribution, increases in longevity bring opportunities but also challenges at both individual and societal levels. While recognising the great achievement of extended longevity, the evidence base for an improved healthspan (the length of time an individual is able to maintain good health)3 is less encouraging, highlighting the need for research on healthy ageing.4

In a linked paper in this issue, Lai and colleagues (doi:10.1136/bmj.k4067) investigate the association between circulating levels of omega 3 polyunsaturated fatty acids (n3-PUFAs) and healthy ageing in a sample of adults with a mean age of 74 years at baseline who were followed for up to 22 years in the Cardiovascular Health Study.5 Among the 5888 participants enrolled from Medicare (aged 65 or more or receiving social security disability insurance) at four communities in the United States, 2622 eligible participants were included in this analysis.

Plasma phospholipid n3-PUFAs levels were measured at baseline and at six and 13 years, providing an objective assessment of four individual n3-PUFAs: two derived largely from seafood (eicosapentaenoic acid and docosahexaenoic acid), one predominately endogenous (docosapentaenoic acid), and one derived largely from plants (α-linolenic acid).

Through review of medical records and diagnostic tests, the authors determined that 89% of participants experienced unhealthy ageing during follow-up, while 11% experienced healthy ageing—defined as survival without major chronic diseases and without cognitive or physical dysfunction. After adjustment for covariates, the group with the highest cumulative mean concentrations of eicosapentaenoic acid from seafood had a 24% lower risk of unhealthy ageing than the group with the lowest concentrations. For the predominantly endogenously metabolized docosapentaenoic acid, the top three groups had an 18% to 21% reduction in the risk of unhealthy ageing, relative to the lowest group. Docosahexaenoic acid from seafood and α-linolenic acid from plants were not associated with healthy ageing.

A rich body of literature suggests a protective role of n3-PUFAs in reducing cardiovascular risk,6 whereas mixed or inconclusive findings have been reported for the other components of the unhealthy ageing examined in this study: cancer, lung disease, severe chronic kidney disease, and cognitive and physical dysfunction.7891011 Self reported dietary data that are potentially subject to recall bias and measurement errors may partially contribute to these inconsistencies. This is where Lai and colleagues make a valuable contribution, by combining reported dietary data with repeated measurements of biomarkers to account for trends over time in individual n3-PUFAs.

A few other points are worth considering when interpreting this study’s findings. Firstly, biomarker concentrations are a function of both dietary intake and metabolism, influenced by the interplay of exogenous and genetic factors that are difficult to separate. Interestingly, after additional adjustment for fish intake, the association between higher docosahexaenoic acid concentration and healthy ageing became noticeable. This might suggest that metabolically determined levels of docosahexaenoic acid have a greater role in healthy ageing than dietary determined docosahexaenoic acid.

Primarily endogenously derived docosapentaenoic acid is a metabolic intermediary between eicosapentaenoic acid and docosahexaenoic acid.12 Investigation of the independent and combined effects of docosapentaenoic acid with other n3-PUFAs under controlled feeding conditions would contribute to our understanding of their specific roles in healthy ageing.

Secondly, associations between eicosapentaenoic acid and healthy ageing and between combined eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid and healthy ageing were only significant in the highest group. So who was in this top group, and could high n3-PUFA concentrations simply be a marker of some unmeasured confounding advantage through life? The study cohort was born in the 1910s and 1920s,13 a generation characterised by long term improvements in population level socioeconomic resources,14 which may influence longevity and health across the lifespan. Indeed, educational attainment was among the strongest covariates in this study. Therefore, we cannot rule out the possibility of differential exposures across the n3-PUFA quintiles to unmeasured chronic and acute stressors related to socioeconomic resources.

Thirdly, the median concentrations of α-linolenic acid across groups accounted for just 0.09% to 0.21% of total fatty acids, approximately one third of eicosapentaenoic acid, one fifth of docosapentaenoic acid, and one twentieth of docosahexaenoic acid circulating concentrations. The limited variation in α-linolenic acid concentrations and vegetable intakes in this predominantly white study population may have contributed to the null association between α-linolenic acid derived from plants and healthy ageing. Further research is needed in populations with more diverse dietary patterns.

Epidemiological associations cannot infer causality, so we caution against using these findings to inform public health policy or nutritional guidelines. We live in challenging times, when lifespans are increasing but healthy lifespans are not. Following the World Health Organization’s policy framework for healthy ageing,15 any evidence based clues to improve health in later life are welcome, but additional efforts to accelerate this area of research are essential

 

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What are the uses of ketamine?

Ketamine is a medication that is used to induce loss of consciousness, or anesthesia. It can produce relaxation and relieve pain in humans and animals.

It is a class III scheduled drug and is approved for use in hospitals and other medical settings as an anesthetic.

However, it is also a commonly abused “recreational” drug, due to its hallucinogenic, tranquilizing and dissociative effects.

Controversy has arisen about using ketamine “off-label” to treat depression. Off-label uses of drugs are uses that are not approved by the the United States, (U.S.) Food and Drug Administration (FDA).

Ketamine is safe to use in controled, medical practice, but it has abuse potential. Used outside the approved limits, its adverse mental and physical health effects can be hazardous. Prolonged use can lead to tolerance and psychological addiction.

Fast facts on ketamine:Here are some key points about ketamine. More detail is in the main article.

  • Ketamine is similar in structure to phencyclidine (PCP), and it causes a trance-like state and a sense of disconnection from the environment.
  • It is the most widely used anesthetic in veterinary medicine and is used for some surgical procedures in humans.
  • It is considered a “club drug,” like ecstasy, and it has been abused as a date-rape drug.
  • Ketamine should only be used as prescribed by a doctor.

 

What is ketamine?

ketamine and dissociation
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Ketamine can produce feelings of dissociation when used as a drug of abuse.

Ketamine belongs to a class of drugs known as dissociative anesthetics. It is also known as Ketalar, Ketanest, and Ketaset.

Other drugs in this category include the hallucinogen, phencyclidine (PCP), dextromethorphan (DXM), and nitrous oxide, or laughing gas.

These types of drugs can make a person feel detached from sensations and surroundings, as if they are floating outside their body.

 

Therapeutic uses

Ketamine is most often used in veterinary medicine. In humans, it can induce and maintain general anesthesia before, during, and after surgery.

For medical purposes, ketamine is either injected into a muscle or given through an intravenous (IV) line.

It is considered safe as an anesthetic, because it does not reduce blood pressure or lower the breathing rate.

The fact that it does not need an electricity supply, oxygen, or highly trained staff makes it a suitable option in less wealthy countries and in disaster zones.

In human medical practice, it is used in procedures such as:

  • cardiac catheterization
  • skin grafts
  • orthopedic procedures
  • diagnostic procedures on the eye, ear, nose, and throat
  • minor surgical interventions, such as dental extractions

It has been used in a hospital setting to control seizures in patients with status epilepticus (SE), a type of epilepsy that can lead to brain damage and death. However, researchers point out that ketamine is normally used for this purpose after 5 to 6 other options have proven ineffective. Ketamine for the treatment of refractory status epilepticus

It is also an analgesic, and, in lower doses, it can relieve pain.

In 2014, researchers found that a ketamine infusion significantly reduced symptoms of post-traumatic stress disorder (PTSD) in 41 patients who had undergone a range of traumas.

Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder

Researchers are looking into other possible medical uses of ketamine, particularly in the areas of treatment-resistant depression, suicide prevention, and substance use disorders. However, this use is controversial.

 

Treating depression

Researchers for the American Psychological Association (APA) noted in April 2017 that a number of doctors prescribe ketamine “off-label,” for people with treatment-resistant depression.

However, they caution:

While ketamine may be beneficial to some patients with mood disorders, it is important to consider the limitations of the available data and the potential risk associated with the drug when considering the treatment option.”

The FDA has not yet approved it for treating depression.

In a study published in BMC Medical Ethics, researchers urge doctors to “minimize the risk to patients” by considering carefully the evidence before prescribing ketamine off-label for patients to treat depression and prevent suicide.

Citing “questionable practice” regarding the prescription of ketamine, they point out that there is not enough evidence to prove that ketamine is safe, and that some studies supporting its use have not been sufficiently rigorous in terms of research ethics.

They call for open debate, more research, and for doctors to try all other options first, before prescribing ketamine.

The National Institutes of Health (NIH) are currently supporting research into whether ketamine may help people with treatment-resistant depression.

 

Effects

Ketamine use can have a wide variety of adverse effects, including:

  • drowsiness
  • changes in perceptions of color or sound
  • hallucinations, confusion, and delirium
  • dissociation from body or identity
  • agitation
  • difficulty thinking or learning
  • nausea
  • dilated pupils and changes in eyesight
  • inability to control eye movements
  • involuntary muscle movements and muscle stiffness
  • slurred speech
  • numbness
  • amnesia
  • slow heart beat
  • behavioral changes
  • increased pressure in the eyes and brain

It can also lead to a loss of appetite, upset stomach, and vomiting.

When used as an anesthetic in humans, doctors combine it with another drug to prevent hallucinations.

Risks

Ketamine is considered relatively safe in medical settings, because it does not affect the protective airway reflexes, and it does not depress the circulatory system, as other anesthetic medications do.

However, some patients have reported disturbing sensations when awakening from ketamine anesthesia.

Ketamine can cause an increase in blood pressure and intracranial pressure, or pressure in the brain.

People with the following conditions cannot receive ketamine for medical purposes:

  • brain swelling
  • glaucoma
  • brain lesion or tumor

It is used with caution in those with:

  • coronary artery disease
  • increased blood pressure
  • thyroid disease
  • chronic alcohol addiction
  • acute alcohol intoxication
  • aneurysm
  • chest pain
  • mental illness

These effects may be stronger in people aged over 65 years.

Some people may have an allergy to the ingredients. Patients with any type of allergy should tell their doctor before using any medication.

Anyone who is using this drug for therapeutic purposes on a regular basis should have regular blood pressure checks.

As a drug of abuse

Ketamine is most often used in the dance club setting as a party drug. It produces an abrupt high that lasts for about an hour. Users report euphoria, along with feelings of floating and other “out of body” sensations. Hallucinations, similar to those experienced with LSD, are common.

In 2014, 1.4 percent of 12th graders reported using ketamine for recreational purposes. This was down from 2002, when 2.6 percent reported using it.

Street names include:

  • Cat Valium
  • KitKat
  • Special K
  • Vitamin K
  • The horse tranquilizer
  • Ket
  • Purple
  • Super K
  • Jet

It is taken orally as a pill, snorted, smoked with tobacco or marijuana, or mixed into drinks. Most often, it is cooked into a white powder for snorting. Taken orally, it can cause severe nausea and vomiting.

Regardless of how it is ingested, its effects begin within a few minutes and last for less than an hour.

Higher doses can produce more intense effects known as being in the “K-hole,” where users become unable to move or communicate and feel very far away from their body.

Some users seek out this type of transcendental experience, while others find it terrifying and consider it an adverse effect.

Adverse effects

Unwanted effects include:

  • addiction
  • psychosis
  • amnesia
  • impaired motor function
  • high blood pressure
  • respiratory problems
  • seizures

As the user can become oblivious to their environment, ketamine abuse puts the person at risk of accidental injury to themselves and vulnerable to assault by others.

Problems with co-ordination, judgment, and the physical senses can continue for up to 24 hours. If an individual is using ketamine in a recreational setting, a sober friend should remain with them to ensure their safety.

Long-term effects include bladder and kidney problems, stomach pain, and memory loss.

If addiction and dependence develop, there is also a risk of depression.

Frequent, illegal use of ketamine can lead to serious mental disorders and major physical harm to the bladder, known as ketamine-induced ulcerative cystitis.

Ketamine and alcohol

Ketamine toxicity alone is unlikely to lead to death, according to the WHO. However, combining it with other substances, such as alcohol, can increase the sedative effects, possibly leading to a fatal overdose.

In the U.S., 1,550 emergency department (ED) visits were due to illegal ketamine use, and 71.5 percent of these also involved alcohol.

Overdose

The risk of overdose is high, because, for a recreational user, there is only a slight difference in dosage between obtaining the drug’s desired effects and an overdose.

Addiction

Ketamine is a Class III controlled substance. Prolonged use can cause dependence, tolerance, and withdrawal symptoms. Quitting can lead to depression, anxiety, insomnia, and flashbacks.

Chronic users have been known to “binge” their ketamine use in an attempt to experience again the dissociative, euphoric effects of their early first use.

The complications of long-term use can be fatal.

A final word

Ketamine is an anesthetic drug, used in human and veterinary medicine. It is important to distinguish the valid medical uses from the non-medical, recreational use of the drug.

When properly administered by a trained medical professional, ketamine is a safe and valuable medication.

Used in recreational settings, however, ketamine abuse can produce unpredictable physical and mental health results. In the long term, it can lead to psychological damage and, in some cases, death.

Any drug use should be prescribed by a doctor who knows the patient’s full medical history.

Intranasal Ketamine | 703-844-0184 | Ketamine Treatment Provider | Alexandria, Va 22306| Ketamine for deprssion | Psychedelics for depression | Ketamine for opioid use disorder | Ketamine doctor | Loudon, Va 22043 22046 22101 22102 22107 22108 22109 | IV Ketamine for depression | Ketamine for PTSD , OCD | Bipolar | Ketamine Infusion Center | 703-844-0184 | Loudon, Va | Ketamine IV Treatment Center | Ketamine Doctor | Intranasal Ketamine |Alexandria, Va 22306 | Ketamine for Depression | Intranasal Ketamine | OCD| CBD Center | Medical CBD | Medical THC Center | THC Doctor | Ketamine for Alcoholism | Intranasal Ketamine | 22043 22046 22101 22102 22106 22107 22108 22109 20175 20176 20147 20148 20151 22030 22031 22032 22034 22038 | IV Vitamin Therapy

 

 

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.

20160309_FactFile_Ketamine

Ketamine and Depression_ A Review

Psilocybin-occasioned mystical experiences in the treatment of tobacco addiction.

Psychedelic-Assisted Psychotherapy A Paradigm Shift in Psychiatric Research and Development.

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.

Intranasal Ketamine | 703-844-0184 | Ketamine Treatment Provider | Alexandria, Va 22306| Ketamine for deprssion | Ketamine doctor | Loudon, Va 22043 22046 22101 22102 22107 22108 22109 | IV Ketamine for depression | Ketamine for PTSD , OCD | Bipolar | Ketamine Infusion Center | 703-844-0184 | Loudon, Va | Ketamine IV Treatment Center | Ketamine Doctor | Intranasal Ketamine |Alexandria, Va 22306 | Ketamine for Depression | Intranasal Ketamine | OCD| CBD Center | Medical CBD | Medical THC Center | THC Doctor | Ketamine for Alcoholism | Intranasal Ketamine | 22043 22046 22101 22102 22106 22107 22108 22109 20175 20176 20147 20148 20151 22030 22031 22032 22034 22038 | IV Vitamin Therapy | Depression Linked to Atrial fibrillation

 

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One more reason to treat your depression rapidly with Ketamine:

 

Depression Linked to Increased Risk of Developing Atrial Fibrillation

NEW YORK—Depression appears to be a risk factor for atrial fibrillation, the most common arrhythmia in the U.S., according to new observational data from the national Multi-Ethnic Study of Atherosclerosis (MESA) study.

Considering that 20% of U.S. adults report depressive symptoms, “our findings identify a large portion of the U.S. population that is potentially at an increased risk of developing atrial fibrillation and who may benefit from more targeted efforts to prevent atrial fibrillation,” Dr. Parveen Garg, from the Keck School of Medicine at the University of Southern California in Los Angeles, told Reuters Health by email.

He presented the study March 22 at the American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions in New Orleans.

The analysis included 6,644 adults (mean age, 62; 53% women, 38% white, 28% black, 22% Hispanic, 12% Chinese-American) with no known heart disease at baseline who were followed for a median of 13 years as part of the MESA study.

In the fully adjusted model, individuals with a Centers for Epidemiologic Studies Depression Scale (CES-D) score of 16 or higher (indicating clinically relevant depressive symptoms) had a 34% (P=0.039) higher risk of developing atrial fibrillation during follow-up compared with those with a CES-D score of less than 2. Similarly, individuals reporting antidepressant use had a significant 36% increase in their risk of developing atrial fibrillation compared with those not on the drugs.

“An important next step is to confirm these results in other studies, especially those with more comprehensive and clinically validated assessments of depression. If confirmed, then it will be important to determine if treating individuals with depression actually reduces their risk of atrial fibrillation,” Dr. Garg said.

Several mechanisms have been proposed to explain a possible link between depression and atrial fibrillation, Dr. Garg explained. Depression can increase systemic inflammation and activate the autonomic nervous system, which increases catecholamine levels, and the hypothalamic-pituitary-adrenal axis, which increases cortisol levels. Depression may also activate the renin-angiotensin-aldosterone system.

“Taken together, these changes may induce atrial fibrillation susceptibility either directly by disrupting the electrophysiologic properties of the atria or indirectly by promoting atrial fibrosis, increasing the atrial pressure,” Dr. Garg said, adding that further research is needed to fully understand the mechanisms involved.

Dr. Gordon Tomaselli, a spokesman for the American Heart Association, said this study “affirms the association between depression and atrial fibrillation in a population that I think is important because it’s a mixed population and not just the standard Caucasian population.”

“There are some associated risk factors in people with depression that might increase their risk of atrial fibrillation, including an increased incidence of hypertension in some patients who have depression as well as other disorders that might be driven by activation of the sympathetic nervous system like anxiety disorder. So there are several reasons why people might have depression and atrial fibrillation,” Dr. Tomaselli, who was not involved in the research, told Reuters Health by phone.

“One question is what should we do about it, and I’m not sure we have an answer from this study except to make sure that we are looking for symptoms of depression,” he said. “We don’t know whether treatment of depression will reduce the incidence of atrial fibrillation. There is some reason to think that it might, but there are other reasons to think that antidepressant drugs actually have some effects on the heart, the ion channels that determine the rhythm of the heart.”

The study had no commercial funding and the authors have no relevant disclosures.

SOURCE: https://bit.ly/2pCdkOA

AHA Epidemiology and Prevention – Lifestyle and Cardiometabolic Health Scientific Sessions 2018.

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At NOVA Health recovery [703-844-0184 | Fairfax, Va 22306 ] we offer our patients cutting-edge treatment options for their depression, and one of our main stars is IV (intravenous) ketamine. But why does it have to be IV? “I don’t like needles, why can’t I just take this as a pill or as that nasal spray everyone is talking about?” you may be thinking. IV is the best route for your brain to receive ketamine because of something called bioavailability. In addition, it is also more effective, more precise, and safer for you.

What is bioavailability? It is the amount of medication that your body and brain is actually able to use, which is sometimes different than the amount of medication that your body receives. When you take any medication, parts of the active ingredients in them don’t go to your bloodstream; they get digested, altered into an unusable form, metabolized and excreted into your body. This is particularly prevalent in oral and intranasal medications. In fact, receiving a medication intravenously is the only way to have 100% bioavailability. Let’s take a look at the different bioavailability percentages based on what route you receive ketamine:

Intravenous: 100%

Intramuscular: 93%
Intranasal: 25-50%
Sublingual (under the tongue): 30%
Orally (by mouth): 16-24%

When we give ketamine intravenously, we know exactly where your entire dose is going: straight to your brain. The same cannot be said for other forms of ketamine. Intranasal ketamine has to bypass several layers of tissue before it can reach your brain, and too many things can happen that could cause you to lose some or most of your dose: sneezing, dripping, running down the back of your throat, etc. The same can be said for an oral pill and an intramuscular injection; these routes are just too unpredictable, and when it comes to treating your depression, we don’t want the results to be unpredictable.

When you receive IV ketamine in our office setting, it is given slowly over one hour. By doing this, we are able to monitor you closely, and if you experience any unpleasant side effects and want to stop the infusion, we are able to do that. By contrast, a dose of ketamine via intranasal spray would be done at home with no physician or nursing supervision, so side effects cannot be immediately addressed if they arise. The same is true for intramuscular or oral dosing – after you take the pill, or receive a shot of ketamine into your muscle, there is no way to stop the absorption of the medication into your bloodstream as the full dose is administered within seconds.

IV ketamine is by far the safest and most effective approach in using ketamine to treat depression. You are in a comfortable setting with healthcare providers with you the whole time, the potential for side effects is low, and you are certain that the dose you receive is the dose that is going to your brain, maximizing the benefits of this cutting-edge treatment.

However, we do offer the other routes of administration and take – home prescriptions for Ketamine therapies for those who are in our program. Contact us today at 703-844-0184 to get started on your treatment.

 

Neograft | 703-844-0184 | Fairfax, Va 22304 | Hair doctor | Hair replacement Center | Trichology | Hair Restoration

Fairfax Hair Loss Center | 703-844-0184 | Neograft | Hair FUE | Hair Loss Center | Trichology | Hair Doctor | Hair transplantation

 

Hair Loss

We recognize that hair loss is not only a complex medical condition, but one that affects every aspect of the hair loss sufferer’s life. Hair loss affects as many as 50 million people in the United States, men and women alike. If you’re experiencing hair loss and you and your doctor are looking for medication treatment options then contact us.

For male patients – Androgenetic alopecia (AGA) or common male pattern baldness (MPB) or hair loss due to hormonal causes, makes up 95% of male hair loss cases. By the age of thirty-five, two-thirds of American men will experience some degree of appreciable hair loss, and by the age of fifty approximately 85% of men have significantly thinning hair. Approximately twenty five percent of men who suffer with male pattern baldness begin the painful process before they reach the age of twenty-one.

Many women also experience female pattern hair loss. When androgenetic alopecia affects women it is called female pattern alopecia or female pattern baldness. Hair loss in women is different than that of men, with hair thinning tending to be more diffuse.

Although for both men and women androgenic alopecia is the most common form of hair loss, doctors also see many people with other forms of alopecia. Many medical conditions also have alopecia as a primary symptom.

We can get compounded unique formulas that may improve results. Many patients use topical treatments with one or multiple actives in topical solutions, foams, scalp lotions and shampoos. Call us to learn more about our compounded treatments for hair loss.

Some of the actives for hair loss treatments include:

  • Minoxidil
  • Finasteride
  • Latanoprost
  • Tretionoin
  • Azelaic Acid
  • Fluocinonide
  • Progesterone
  • Estradiol
  • Biotin
  • Ketoconazole
  • Saw Palmetto
  • Zinc Sulphate
  • Niacinamide
  • Many More

Sample Formula – latanoprost 0.01% and minoxidil 5%. Each drug acts on a different prostaglandin and synergize to restore the prostaglandin balance. One formula uses a special foam base, which is a creamy, drip free foam formulation with a light skin feel that work very well on the scalp. It is very easy to apply and skin friendly maximizing patient comfort and for optimal treatment results.

Biotin / Minoxidil / Niacinamide / Sodium Hyaluronic Acid Solution Compounded

Co-Enzyme Q10 / EGCG / Progesterone / Zinc Oxide Cream Compounded

Fluocinonide / Azelaic Acid / Minoxidil / Tretinoin Shampoo Compounded

Latanoprost / Finasteride Topical Foam / Solution Compounded

Latanoprost / Minoxidil / Finasteride Topical Foam / Solution Compounded

Minoxidil / Finasteride / Azelaic Acid / Progesterone / Tretinoin Topical Solution Compounded

Minoxidil / Finasteride / Tretinoin Topical Foam / Solution Compounded

Minoxidil / Spironolactone Topical Foam / Solution Compounded

 

Ketamine Infusion Center | 703-844-0184 | Loudon, Va | Ketamine IV Treatment Center | Ketamine Doctor | Intranasal Ketamine |Alexandria, Va 22306 | Ketamine for Depression | Intranasal Ketamine | OCD| CBD Center | Medical CBD | Medical THC Center | THC Doctor | Ketamine for Alcoholism | Intranasal Ketamine | 22043 22046 22101 22102 22106 22107 22108 22109 20175 20176 20147 20148 20151 22030 22031 22032 22034 22038 | IV Vitamin Therapy

703-844-0184 | Ketamine Treatment Center | Alexandria, Va 22306 | Call for Ketamine Doctor | Ketamine for depression, OCD, Chronic Pain

 

 

Ketamine Nasal Sprays for Depression – Alexandria, Va Ketamine Provider 

703-844-0184 

What is ketamine?

Ketamine Nasal SprayKetamine is a drug currently approved by the FDA for use as a general anesthetic during minor surgical procedures such as biopsies. It is widely known as a recreational drug because of its ability to induce cognitive-dissociative, hallucinogenic, and euphoric states in humans. Recently, it has been implicated in research as a potential therapeutic agent in depression especially in patients who have failed previous standard therapies.

Why ketamine?

Standard pharmacologic therapies for depression take several weeks of treatment before patients experience relief. Ketamine is different in that it has been shown to reduce depression symptoms and suicidal ideation in as little as forty minutes. This is considered a potentially lifesaving breakthrough in the treatment of depression because ketamine can rapidly reduce symptoms especially in emergency situations.

How does it work?

The most common medications used in depression affect serotonin in the brain. Ketamine works by a different mechanism. It has been shown to block the glutamate receptors in the brain resulting in its famous hallucinogenic effects. Ketamine has been shown to act on several other receptors, but it is theorized that at low doses, blocking glutamate receptors in the brain may be the reason for its anti-depressive effects.

Who should (and shouldn’t) take ketamine?

Ketamine has not been approved by the FDA for treatment of depression. Although, because of new studies, psychiatrists have been prescribing ketamine “off-label” for patients who did not respond to selective serotonin reuptake inhibitors (SSRIs) such has Celexa (citalopram), Zoloft (sertraline), or Prozac (fluoxetine) for immediate treatment of symptoms.

Ketamine has been shown to transiently yet significantly increase blood pressure following administration. Patients with high blood pressure should use caution when using ketamine. Ketamine has also been shown to be associated with increases in psychosis or dissociative properties.

Ketamine nasal sprays offer a quick and convenient way to administer ketamine for patients who need immediate relief, although they are currently not available commercially, so you will not find them at your local community pharmacy. Compounding pharmacies have the proper experience, equipment, and personnel to safely compound and customize this medication for you.

References

  1. Ketalar [package insert]. Chestnut Ridge, NY 10977: Par pharmaceutical; 2017 https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/016812s043lbl.pdf
  2. Browne CA, Lucki I. Antidepresssant effects of ketamine: mechanisms underlying fast-acting novel antidepressants. Front Pharmacol December 2013.
  3. Lapidus K, Levitch CF, Perez AM, et al. A randomized controlled trial of intranasal ketamine in major depressive disorder. Biol Psychology 2014;76:970–976
  4. Sanacora G, Frye MA, McDonald W, et al. A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA Psychiatry 2017;74(4):399-405.

Ketamine Infusion Center | 703-844-0184 | Loudon, Va | Ketamine IV Treatment Center | Alexandria, Va 22306 | Ketamine for Depression | OCD| CBD Center | Medical CBD | Medical THC Center | THC Doctor | Ketamine for Alcoholism | Intranasal Ketamine | 22043 22046 22101 22102 22106 22107 22108 22109 20175 20176 20147 20148 20151 22030 22031 22032 22034 22038 | IV Vitamin Therapy

 

703-844-0184 | Alexandria, Va 22306 | Ketamine Treatment | Call for an infusion | Ketamine for depression, pain, OCD, anxiety

 

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Ketamine for Delirium Tremens

This study suggests that ketamine can safely be used to avoid intubation and may decrease length of intensive care unit stay.

Severe alcohol withdrawal, or delirium tremens (DT), is a life-threatening condition that can require massive doses of benzodiazepines or barbiturates (GABA agonists), which can require intubation and prolonged intensive care unit (ICU) care. These authors studied a retrospective sample of adult patients admitted to a single ICU with DT to determine whether adjunctive therapy with ketamine improved outcomes.

They compared outcomes in 29 patients who received symptom-triggered therapy with GABA agonists with outcomes in 34 patients who were treated after initiation of a guideline that added an intravenous ketamine infusion (0.15–0.3 mg/kg/hour) to GABA agonist therapy. Using multivariable modeling that accounted for initial ethanol level and the total amount of GABA agonist required for treatment, patients who received ketamine had significantly lower rates of intubation (29% vs. 76% for patients who did not receive ketamine) and shorter ICU stay (5.7 days vs. 11.2 for patients who did not receive ketamine). There were no reported adverse events.

Adjunct Ketamine Use in the Management of Severe Ethanol Withdrawal

Adjunct Ketamine Use in the Management of Severe Ethanol Withdrawal

 

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Opiate addiction | 703-844-0184 | Suboxone doctors in Alexandria, Va 22306 | Fairfax, Va | Dr. Sendi | Alcohol Treatment | Addiction Treatment Center | Prazosin for Harm Reduction in Alcohol Use Disorder | CBD doctor | CBD center | Medical THC | THC | Ketamine Treatment Center | Ketamine Infusion Center | Mcclean, Va | 703-844-0184 | 22043 22046 22101 22102 22106 22107 22108 22109 20175 20176 20147 20148 20151 22030 22031 22032 22034 22038 | Alcohol Use Disorder | Alcohol treatment

703-844-0184 |  Alcohol treatment | Alexandria, Va 22306

 

Prazosin for Harm Reduction in Alcohol Use Disorder?

 

 

Double-Blind Randomized Clinical Trial of Prazosin for Alcohol Use Disorder

 

Increasing doses of prazosin reduced heavy drinking, but adverse effects were common.

In some patients with post-traumatic stress disorder (PTSD), the alpha-1 noradrenergic blocker prazosin has been helpful for nightmares and, in open-label studies, has decreased stress reactivity, alcohol craving, and alcohol use. The alpha-1 noradrenergic blocker doxazosin has also been found to be useful for alcohol and other substance use disorders. These investigators conducted a randomized, placebo-controlled, double-blind, 12-week study of prazosin for alcohol use disorder in 92 outpatients without PTSD (mean age, 48; 79% men).

Participants averaged >67% heavy drinking days and 12 drinks per drinking day in the prior 90 days. After two 1-mg bedtime test doses, prazosin and placebo were up-titrated, depending on adverse effects, over 2 weeks; prazosin targets were 4 mg in the morning, 4 mg in the afternoon, and 8 mg at bedtime. Twelve patients dropped out during titration; of the 80 completers, 70 reached the target dose. The prazosin group took ≥1 dose on a mean of 65% of days and all 3 doses on 55% of days.

Prazosin was associated with self-reported fewer heavy drinking days and fewer drinks per week (–8 vs. –1.5 with placebo); differences in drinks per week accelerated after 8 weeks. Drinking days per week and craving showed no group differences. Mean systolic blood pressure decreased by 3.5 mm Hg with prazosin. Frequent adverse effects with prazosin were drowsiness (64% vs. 31% with placebo) and edema (20% vs. 4%). Symptomatic (1 patient in each group) and asymptomatic orthostatic hypotension did not differ between groups.

 

 

Evidence suggests that elevated brain noradrenergic activity
appears to be involved in the initiation and maintenance of
alcohol use disorder (1, 2). A clinically feasible approach to
reducing brain noradrenergic activity is to reduce activation
by norepinephrine at the postsynaptic a-1 adrenoceptor.
Prazosin is a clinically available lipid-soluble a-1 adrenoceptor
antagonist that reduces brain a-1 adrenoceptor–
mediated signaling when administered peripherally (3). In
rodents, prazosin has been shown to decrease withdrawalinduced
alcohol intake (4), alcohol drinking by alcoholpreferring
(P) rats (2), and stress-induced alcohol seeking
(5), and it has been shown to block yohimbine-induced reinstatement
of alcohol seeking (6). In human alcohol use disorder
studies, prazosin has been shown to reduce reactivity
to stress and to result in reduced craving (7), reduced drinks
per week (8, 9), and reduced drinking days per week (8). In
persons with DSM-IV alcohol dependence and comorbid
posttraumatic stress disorder (PTSD), one study found that
prazosin reduced drinking but not PTSD outcomes (10), and
another study found no prazosin effect on either outcome (11).
Doxazosin, another a-1 adrenoceptor antagonist, did
not outperform placebo on drinking outcomes in a study of alcohol treatment seekers, but among those with a high family
history density of alcohol problems, the active medication
was associated with improved drinking outcomes (12). Across
the entire sample, alcohol treatment seekers with higher
standing diastolic blood pressure receiving active medication
had better outcomes than those receiving placebo (13).
After obtaining positive results in a pilot study (8), we
conducted a 12-week randomized controlled trial comparing
prazosin and matched placebo in 92 participants who met
diagnostic criteria for alcohol use disorder but not PTSD.
Individuals with PTSD were excluded because there is evidence
that prazosin reduces symptoms of PTSD (14), and we
were interested in isolating the effects of prazosin on drinking
alone in light of evidence linking excessive drinking to
stress and the adrenergic system. Both treatment arms included
medical management (15), and daily symptoms were
monitored via a telephone-based interactive voice response
system to obtain close to real-time data regarding alcohol
consumption. Our primary hypotheses were that prazosin
would lead to a decreased likelihood over time of any drinking
and of heavy drinking (i.e., $4 drinks for women, $5 drinks
for men) as well as a decrease in number of drinks consumed.

 

 

These results indicate that prazosin has the potential to
reduce the likelihood of heavy drinking and number of
drinks per week over time but not the number of drinking
days per week. They suggest that prazosin may be most
useful in reducing heavy drinking associated with negative
consequences (29), which is consistent with a harm reduction
approach characterized by safer consumption rather
than full abstinence.

 In addition to reducing rodent self-administration of
alcohol (33), prazosin compared with vehicle has also been
shown to reduce self-administration of cocaine (34), heroin
(35), and nicotine (36). In humans, the previous positive pilot
studies of prazosin for alcohol use disorder (8, 10) and the
present study provide preliminary support for an effect of
prazosin on heavy drinking and number of drinks per week.
Another a-1 antagonist, doxazosin, has shown a signal for
reducing drinking in alcohol-dependent individuals who
have a positive family history of alcohol problems (12).
Doxazosin has also been found to reduce cocaine use in
cocaine-dependent individuals compared with placebo (37)

 

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