‘Caroline’s doctor prescribed her Prozac, which her psychologist supported. She was reassured – but once she started taking it she felt worse, with more extreme panic.’
Caroline was always someone who ran on nervous energy. But when a man began stalking her last year, harassing her for 10 months, the lawyer and mother of two developed a new kind of cell-deep fear that took over her mind.
“It has sucked so bad. More than anything,” she says, referring to the nine months of anxiety that followed. “I didn’t even know things could suck as bad as it sucked.”
It came on in stages. She’d have a day where she suddenly felt very disoriented, as though someone had put something in her drink. The next day she’d be fine.
“I felt my throat tightening, so I went to the doctor, and then to the ENT surgeon, but there was nothing.
Julia Rucklidge’s team is currently conducting a trial to see if micronutrients can improve depression and anxiety pregnancy. Register your interest at bit.ly/pregnancy-study.
“It was terrifying and strange and then it all fell apart and I got this crippling panic disorder: rolling panic, panic attack followed by panic attack, that went on for six weeks. When it came on it was like full alert: it was front line of the Iraqi special forces in Mosul. It was like that, but you’re just in your house.”
The stalker has stopped now, but he left behind a full-blown generalised anxiety disorder, something Caroline* now realises she’d caught glimpses of throughout her life. She says the symptoms are hard to describe – a staticky crackling in her ears, for one.
“It’s a terrible, unnerving, unending fear, something every molecule in your body experiences. My brain is fried.
“It’s not like just being nervous about exams – it’s a very powerful inability to calm down,” she says. “But it’s a difficult illness to communicate to the world. The number of times that people popped in and said: ‘You look fine! You look great!'”
Anxiety is a growing modern affliction. Although, whether that’s due to greater awareness, or because we really are experiencing a higher incidence of clinical-level panic than usual, is uncertain. Anxiety New Zealand estimates that a whopping one in four New Zealanders experience anxiety, panic attacks, and phobias every day.
Alongside that has come a well-documented rise in demand on a struggling national mental health system, as well as an international increase in pharmaceutical treatment. One in 10 adults in the developed world now takes an antidepressant. In June it was reported that the number of New Zealand children and teens on them has doubled over the past 10 years, with nearly 15,000 prescribed them last year.
Psychiatric medication can be lifesaving, but medication can be tough on the body and mind, writes Naomi Arnold.
Psychiatric medication can be lifesaving. Ruby*, in her early 30s, says it saved her life. Diagnosed with anxiety, depression, obsessive compulsive disorder, and post-traumatic stress disorder, she had reached desperation point. She’s tried about a dozen on the anti-psychotic, anti-depressant, and anti-anxiety spectrum, and says they’re a tool you use in tandem with a host of other approaches to mental health.
“I have no doubt that I wouldn’t be here without them,” she says. “They saved my life.”
But medication can be tough on the body and mind – and it can be hard to get right. Caroline’s doctor prescribed her Prozac, which her psychologist supported. She was reassured – but once she started taking it she felt worse, with more extreme panic.
Her doctor doubled the dose, which she says was “a whole new type of hell”.
After six weeks she stopped taking it – which medical professionals agree is highly inadvisable – but in Caroline’s case the panic subsided. Later, she went on Mirtazapine, but the side effects were “extraordinary”. (Think weight gain, foggy thinking, memory loss, erratic periods, loss of libido and all the while the anxiety appeared to increase.) Again, she went against her doctor’s advice and stopped taking it.
“One week off that now and I’m almost back to normal,” she says.
She’s been told she’s one of a handful of people who react badly to the happy pills, but there is growing evidence that they’re not the only solution.
The Mental Health and Nutrition Research Group in the Psychology Department at the University of Canterbury has been investigating the link between micronutrients and mental health, and has stacked up a pile of research to demonstrate the benefits in children and adults, including earthquake victims.
Since 2010, when the group’s first study was published, UC clinical psychologist Julia Rucklidge has been a frequent face in the media, including presenting a TEDxChristchurch talk, The Surprisingly Dramatic Role of Nutrition in Mental Health, which had more than 600,000 views online.
One of the research group’s most recent publications, in the Journal of Child and Family Studies, investigated anxiety and stress in children following the Christchurch earthquakes. It found symptoms of anxiety improved when they were supplemented with specialist formulations of micronutrients (see sidebar).
Neil McNaughton needs participants for his study and would like to hear from people either with anxiety or those who are curious about EEGs. Contact anxiety@otago.ac.nz.
“We saw such robust changes in the anxiety levels of the children in that study,” Rucklidge says. “Certainly the research is suggesting it’s a viable way forward, with virtually no side effects.”
The children’s sleep improved. They were less anxious about going to school. They seemed easier to reason with, and were better self-regulated.
“In our studies with kids, they often have multiple problems, not just anxiety. We see kids with encopresis [soiling themselves], bedwetting, a lot of irritability, oppositional behaviour, temper tantrums; and we have found with our research that those types of behaviours can also be well managed with the nutrients.
“Our experience of the nutrients over 10 years is that when it works – and I have to always be careful to say it doesn’t work for everyone – but when it does work we see a broad range of symptoms getting better.”
When 10-year-old Sam joined one of UC’s micronutrient studies, he wasn’t taking them for his tics and anxiety; he was taking them to see what effect they’d have on his ADHD. But a couple of weeks after he started on the specialist vitamins and minerals, his parents began to notice a difference.
“His anxiety had gone down and his tics had reduced, which go hand in hand,” his mother Karen says. “When he finished the programme, we took him off the micronutrients and we noticed within two days it all came back. He was quite anxious and had his head shake going on, clicking his fingers, doing all the things he used to do.”
They put him back on the pills. Six months on, Sam is still taking them, his parents buying the product direct from the distributor in Auckland when the study supply ran out.
“My message to other parents would be: don’t be scared to try them,” Karen says. “Even the smallest changes can make all the difference.”
The positive effect of nutrition on mental health is hardly a new idea. There are multiple studies showing the brain benefits of a better diet, but much of the discussion around junk and processed foods has been centred on obesity, not brain health.
Rucklidge believes that our current approach to mental health isn’t working very well. Many people don’t improve, even if they can access treatment, which would be a cause for outcry in any other field of medicine, she says.
“When it comes to mental health there’s this assumption that what we are actually offering, if everyone could get it, works. And that’s the wrong assumption,” she says.
“There’s this talk that we just need more resources. I would say we need to change what we’re doing, not just add more of the same.
“Even if you get the best treatment, many people don’t get better. That’s a hard thing for me to say, but the message has to get through.”
Pharmaceutical medication and psychotherapy certainly have their place, she says. But micronutrients have no side effects, and no street value. Why not try them before drugs, which can knock around already vulnerable people?
“We’re fine about all the people being on antidepressants, even though the long-term evidence for that approach is questionable and the side-effect profile can be concerning.”
But she says there’s difficulty getting buy-in from professionals. “There’s a lack of saying: ‘Why don’t you try some B vitamins first? Or change your diet?'”
She has lobbied for UC’s research to be considered in national care plans, but says there’s frustrating inertia.
Medsafe general manager Chris James says he’s aware of Rucklidge’s work and the organisation has approved the use of the micronutrient products in her clinical trials only.
“Due to the inclusion of certain ingredients or levels of certain ingredients and the conditions for which the products are used in Prof Rucklidge’s work, these products are currently considered to be unapproved medicines,” he says.
But after the trials that UC runs, the families have often found such relief with the products that they want to keep using them. In a convoluted workaround, they’re able to buy the micronutrients with the permission of their GP or prescriber, which essentially means they are sold as an off-label medicine.
For the treatment to enter the mainstream and be prescribed as easily as Prozac, these micronutrients would need to become approved medications. Rucklidge would prefer they be approved as part of the Natural Health Products Bill and allowed to be sold as such.
But that’s difficult, as the vitamins and minerals in the products Rucklidge and her team use to achieve therapeutic results differ vastly from your standard supermarket multivitamin. They are sometimes present in high amounts many times over the recommended daily intake (RDI), and are therefore declared to be medicinal – but the cost and difficulty of registering them as medicine would put most natural health companies out of business.
The RDI is not an upper limit of safety, Rucklidge says. A handful of Brazil nuts can put you over the RDI for selenium, for example… “We have lots of evidence that there are very minimal safety issues, if any.”
The entire issue of what natural health products can be sold, and what they can claim, is currently before the Government as the Natural Health Products Bill, and Rucklidge has been lobbying against some of its wide-ranging restrictions.
The process for bringing a product into clinical care is extensive, and James says the Ministry of Health hasn’t received any application – including from Rucklidge – for consent to distribute the micronutrient products in New Zealand.
Rucklidge says that’s not her role, and she needs to stay at a distance from the products. It’s why she’s reluctant to mention brands.
“I am a researcher, not a salesperson or distributor of medicines,” she says.
“I find it frustrating as I need to stay impartial to do the research but also feel I have to advocate for people we have helped and for the vulnerable, people who are mentally ill.
“It would be nice if the Ministry recognised the benefits of the nutrients and actively worked with me and others involved to make access to them for New Zealanders simpler and affordable.”
She did apply to Pharmac to have them funded, but was turned down.
“I only did that because I am saddened when we help someone get better through our trials and they switch to medications because they can’t afford the nutrients. If the Ministry of Health really had the health of New Zealanders at heart, they would be proactive about it, they would find a way.”
James says the Ministry is considering the ingredients and conditions to determine their suitability under the upcoming Natural Health Products regime, and the work is ongoing.
In the meantime, Rucklidge finds herself sought out by thousands of people looking for help when everything else has failed. She replies with a form email, outlining the nature of her work and from where the micronutrients can be obtained.
Otherwise, her basic advice to improve mental health is, of course, to eat less processed food and more fruits and vegetables. But in the lab, she and her team don’t talk much about diet at all. Besides, basic lifestyle changes involving brisk walks in the fresh air and carrot sticks can seem impossible to someone in the clutch of depression or anxiety. It’s only when the dark moods lift that they become simple.
“We give nutrients to people and they get better,” she says.
“When people who aren’t eating very well start to feel better when getting additional nutrients in pill form, they start to make dietary changes. They don’t crave sugar and carbs as much, and we start to see improvements down the road.
“Once they see the simple effect of the pill and the impact it can have on their behaviour, a light bulb goes on.”
WHAT ARE MICRONUTRIENTS?
Micronutrients – as opposed to macronutrients carbohydrate, protein, and fats – are the regular vitamins and minerals that the body needs in trace amounts: B-complex vitamins, selenium, iodine, zinc, magnesium, iron, copper, etc. The World Health Organisation calls them “magic wands”, enabling the body to produce enzymes, hormones and other substances essential for proper growth and development.
We should be able to get enough from a healthy diet, but that’s in increasingly short supply these days because of an increased intake of processed foods, soil deficiencies, and certain farming practices.
GETTING THE MEDS RIGHT
Diagnosing and prescribing for psychiatric illness isn’t an exact science; people slip through the cracks and struggle to access help but they can also struggle with treatment itself.
However, there might soon be a better treatment answer than trial and error. University of Otago neuroscientist Neil McNaughton is developing one of the first methods to biologically test for any mental disorder, by measuring the brain response in a special test. The project, which has $1 million in funding from the Health Research Council, will run until the end of 2018, and investigates a particular brain rhythm that is reduced by anti-anxiety medication.
The study tests if the brain response is high in subjects with anxiety disorders. If it is successful, it should allow development of clinical tests that will be able to show who is more likely to have success with some types of medication and who is more likely to respond to others.
“This should help, particularly with the problem that – even when medication works – it can take weeks to have its full therapeutic effects, and so finding the right treatment can be a very long, drawn-out process,” he says.
The work should also lead to development of other biomarkers for mental illness, which means that multiple diagnoses at once will be possible.
* Names have been changed.
Anxiety New Zealand: anxiety.org.nz. Helpline 0800 ANXIETY (0800 269 4389)
– Sunday Magazine
Next Teach Me story:
Think yourself fit: How a healthy mindset can add years to your life
The National Alliance on Mental Illness will present a free 12-week course for anyone with a relative, significant other or close friend who has a mental health issue. The course is taught by trained NAMI family members. All course materials are furnished at no cost to you.
The curriculum focuses on Schizophrenia, Major Depression, Mania, Schizoaffective Disorder, Mood Disorders, Borderline Personality Disorder, Anxiety Disorders, Bipolar Disorder, Obsessive-Compulsive Disorder (OCD), and Post Traumatic Stress Disorder (PTSD). The course discusses the clinical treatment of these illnesses and teaches the knowledge and skills that family members need to cope more effectively as caregivers, including communication skills, problem solving, self-care and much more.
The course starts Thursday, Sept. 14 from 7 to 9:30 p.m. at 52 East Main St., Flemington. Registration is required.
For more information, contact Doug at 908-304-4048 or dhwilliams02@yahoo.com, or Katie at 609-240-8072, or ktblooms@gmail.com
The National Alliance on Mental Illness will present a free 12-week course for anyone with a relative, significant other or close friend who has a mental health issue. The course is taught by trained NAMI family members. All course materials are furnished at no cost to you.
The curriculum focuses on Schizophrenia, Major Depression, Mania, Schizoaffective Disorder, Mood Disorders, Borderline Personality Disorder, Anxiety Disorders, Bipolar Disorder, Obsessive-Compulsive Disorder (OCD), and Post Traumatic Stress Disorder (PTSD). The course discusses the clinical treatment of these illnesses and teaches the knowledge and skills that family members need to cope more effectively as caregivers, including communication skills, problem solving, self-care and much more.
The course starts Thursday, Sept. 14 from 7 to 9:30 p.m. at 52 East Main St., Flemington. Registration is required.
For more information, contact Doug at 908-304-4048 or dhwilliams02@yahoo.com, or Katie at 609-240-8072, or ktblooms@gmail.com
Obsessive-compulsive symptoms may be unnoticed or unreported by patients because the focus of attention is on the primary diagnoses.
Obsessive-compulsive symptoms (OCS) predict both the presence and severity of anxiety and depressive disorders and may also affect the trajectory of these disorders, making OCS a potential course specifier signaling unfavorable outcomes, new research shows.
A team of researchers headed by Mieke Klein Hofmeijer-Sevink MD, PhD, of the Mental Health Care Institute GGZ Central, Amersfoort, The Netherlands, examined 2- and 4-year data collected in a prior longitudinal cohort study, the Netherlands Study of Anxiety and Depression (NESDA). The study consisted of 2981 adults (age 18 to 65) at baseline, including subjects with anxiety and depressive disorders and healthy controls.
For the current study, the researchers used the 2-year follow-up (wave 3) data as the baseline measurement and the 4-year data (wave 4) as 2-year follow-up. They analyzed data from healthy controls (n=469), participants with a remitted disorder (n=909), and participants with a current anxiety/or depressive disorder (n=747). Of these, 205 patients had a current depressive disorder, 270 had a current anxiety disorder, and 272 had a current comorbid anxiety and depressive disorder.
To assess OCs, the researchers used the Young Adult Self-Report Obsessive-Compulsive Scale (YASR-OCS) and to diagnose anxiety and depressive disorders they used the Composite International Diagnosis Interview (CIDI), version 2.1, using the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) criteria. The Beck Anxiety Inventory (BAI) was used to assess the severity of anxiety symptoms and the Inventory of Depressive Symptomatology (IDS) was used to determine the severity of depressive symptoms.
Based on a predefined threshold on the YASR-OCS, 76.4% of the sample (n=1624) did not have OCS (YASR-OCS ≤7), while OCS (YASR-OCS 7) were present in the remaining 23.6% (n=501).
Male sex, younger age, and fewer years of education were associated with OCS. Moreover, the presence of OCS was associated with higher levels of anxiety and depressive symptoms.
OCS were predominantly present in participants with current anxiety and/or depressive disorders (χ2: 473.74 (df 4), P .001), in contrast to being “hardly” or “infrequently” present in healthy controls and remitted patients, respectively.
In participants with a current disorder, the presence of OCS was associated with the severity of the disorder. Participants with OCS and a current depressive disorder had higher mean IDS scores than participants without OCS (IDS 26.4 [SD, 11.0] vs 20.3 [SD, 10.8]; F 15.07 [df 1], P .001).
Similarly, patients with OCS and a current anxiety disorder had higher mean BAI scores, as compared with those without OCS (BAI 14.5 [SD, 8.5] vs 11.8 [SD, 8.7]; F 5.95 [df 1], P =.02).
In participants with a comorbid anxiety and depressive disorder, IDS and BAI scores were both significantly higher in patients with OCS vs patients without OCS (IDS: 33.7 [SD, 11.5] vs 24.7 [SD, 10.7]; F 39.86 [df 1], P .001, and BAI: 20.3 [SD, 10.0] vs 13.4 [SD, 8.4]; F 31.22 [df 1], P .001).
At 2-year follow-up, 4.5% of healthy controls developed first onset anxiety and depressive disorders, which were associated with the presence of OCS. Of individuals who had a remitted disorder at baseline, relapse within 2 years occurred in 19.5% and was also significantly associated with OCS.
Persistence of the baseline disorder at 2-year follow-up was significantly associated with the presence of OCS above the cut-point in participants with a comorbid anxiety and depressive disorder (76.6%, χ2 15.06 (df 1), P .0001). However, persistence of a single baseline disorder (depression or anxiety) was not significantly associated with the presence of OCS.
OCS in healthy controls were associated with the development of anxiety or depressive disorders at the 2-year follow-up, while in participants with a remitted disorder, OCS were significantly associated with relapse. However, the association lost significance after adjusting for severity of anxiety and depressive symptoms.
“OCs frequently co-occur in populations with anxiety and depressive disorders as a primary diagnosis,” the researchers observed. However, although present, they “might be unnoticed or unreported by patients because the focus of attention is on the primary diagnoses.”
In light of the high relapse rate of participants (one-fifth of the sample), “identifying patients at high risk for relapse is of utmost importance,” the researchers emphasized, noting that “it seems important to treat these symptoms from the early treatment stages on.”
They suggested a transdiagnostic treatment form of cognitive behavioral therapy (CBT) that “targets more than one diagnosis by, for example, focusing on regulating emotions.”
Calming yourself down is easier than you think. Buzz60
In last week’s column, I shared the four successive clinical stages of anxiety: a perceived threat, the feeling of fear and worry, the attempt at avoidance and the final long-term, ingrained anxiety disorder.
Today, I would like to describe what happens to our bodies and our brains when anxiety hits us. If last week’s column was the “why,” today’s column is the “how” of anxiety.
The human body has an excellent “fight or flight” response when confronted by a threat. I would add a third response: fight, flight or freeze, since anxiety can also make us become socially isolated and emotionally frozen.
The specific brain structure that determines that something is fearful and a threat is called the amygdala. It also interacts with the motor aspects of the periaqueductal area of the brain, telling us we should flee.
At the same time, parts of our endocrine hormone system (the hypothalamus, pituitary and adrenal glands) release cortisol, called the “stress hormone.” Continued activation of cortisol has negative short- and long-term effects. These include impaired cognitive functioning, increased blood pressure and a decreased life expectancy.
Anxiety disorders with a strong “worry” component, such as an obsessive-compulsive disorder, may have a slightly different brain circuit of action than other anxiety disorders.
It is interesting to note that the section for “obsessive-compulsive and related disorders” is separate from, and follows, the section on “anxiety disorders” in psychiatry’s latest edition of its diagnostic manual, the DSM-V. In everyday clinical practice, an anxiety disorder is often diagnosed with depression and/or a second anxiety disorder.
What are some of the brain’s neurotransmitters that are involved with anxiety?
GABA (gamma-aminobutyric acid) is an important neurotransmitter that inhibits and regulates the amygdala. GABA is also an important ingredient in medications, such as benzodiazepines, used to treat anxiety.
Benzodiazepines are used by 5 percent of the general population and by 10 percent of elderly females to calm the feelings of anxiety. They include such well-known drugs as Xanax, Klonopin, Valium and Ativan.
Anti-depressants are also used to reduce anxiety/fear symptoms in disorders as general anxiety disorder, panic disorder, social anxiety disorder and PTSD. Buspar, SSRI’s, such as Prozac and Luvox, and SNRI’s, such as Cymbalta, are commonly prescribed. Beta blockers, commonly used for hypertension, are also used for “stage fright,” and are often used by many professional musicians before a concert.
Psychotherapy and cognitive behavioral therapies are also used in conjunction with medication to treat anxiety disorders. Certain anxiety disorders, such as specific phobias, are best treated by cognitive behavioral therapy and exposure therapy, for more effective, long-term results. These treatment techniques are also used for individuals with social phobias and agoraphobia (a fear of public places and crowds).
In next week’s column, I will address what aspects of society and culture can make a person anxious.
Philip Kronk, M.S., Ph.D. is a semi-retired child and adult clinical psychologist and clinical neuropsychologist. Dr. Kronk has a doctorate in clinical psychology and a post-doctoral degree in clinical psychopharmacology. His year-long internship in clinical psychology was served at The University of Colorado Medical School. Dr. Kronk writes a weekly, Friday online column for the Knoxville News Sentinel’s online website, knoxnews.com. He can be reached at (865) 330-3633.
Curiously, and perhaps eagerly, I am looking at a bull terrier named Sputnik, searching for a resemblance.
He is a stocky three-year-old, mostly slate grey, with a white stripe on his head and a pink splotch on his elongated, bull-terrier nose. So far, our only similarity is we’re both waiting in a trailer that is serving as his examination room at Tufts University’s veterinary school in North Grafton, Massachusetts.
Sputnik has canine compulsive disorder and is at Tufts for a checkup with Nicholas Dodman, a veterinarian who has been studying CCD for over two decades. I am shadowing this visit to learn about Dodman’s work and, selfishly, to learn something about myself; I was diagnosed with obsessive–compulsive disorder a few months ago.
When Dodman first started seeing these dogs, he realised he had been handed a potentially ideal animal model to study human OCD. But in 20 years of studying dogs, discovering genes that may be involved and new neural pathways, one problem has continually clouded his research: the debate over whether CCD can truly be compared to human OCD. “When it comes to problems of the mind, people have a mental block,” he says. “The mind is thought of as uniquely human.”
I try to see into Sputnik’s eyes. He stays close to his owner, Dan Schmuck, giving me an occasional glance. Sputnik was a tail chaser, and would spin for hours on end. At the moment, he is completely still. Like me, it seems he keeps that kind of behaviour away from the public eye.
Two years ago, after rescuing Sputnik from a shelter, Schmuck went on a business trip. His mother called him to say that their new dog had started chasing his tail, and she could not get him to stop. At first, Schmuck and his wife thought it was funny. They took a video of their young puppy spinning, and you could hear them laughing in the background. But soon, the humour faded.
“It was as if I didn’t exist,” Schmuck explains. “His head will lurch all the way against his shoulder, and stare at his tail, as if his nemesis is staring right back at him. He will slowly start working up to chasing, and it will get faster and faster until his head is hitting whatever wall he bangs into. Even though he’s getting hit so hard that you think he’s getting a concussion, he will keep doing it until his teeth and his tail start hitting the wall and he’s shooting blood all over the place.”
Schmuck had to take time off work to stay home and physically restrain him. He held Sputnik’s head in one hand, and wrapped his arm around his rear until he calmed down or fell asleep. “Then he would wake up and I could just feel him… you could feel his head start lurching like he’s thinking about it. It was an unsustainable situation.”
Schmuck drove from his home in Baltimore to see Dodman in Massachusetts. Dodman had seen this kind of spinning many times before. Tail chasing is a common compulsive behaviour for dogs, and for bull terriers specifically. Particular breeds have particular behaviours they exhibit with CCD. Bull terriers spin, Dobermans lick their limbs and suck their flanks, Labradors hold objects or chew rocks, and King Charles spaniels snap at imaginary flies.
Like human OCD, which is commonly focused on washing, hoarding, counting or checking, canine compulsions fit into neat categories. And while these behaviours may sound trivial, they are performed to the extreme. They take over eating, sleeping and all basic functioning. In some cases, they can be fatal.
Sputnik steps out from the safety of Dodman’s shadow, timidly eating treats. His tail hangs innocently between his legs, and I am having a hard time imagining him whirling, manic, out of control in a pool of his own blood. “Over the last two years, he has gone from being a dog that was going to have to be put down, to being a normal dog,” says Schmuck. “He maybe looks at his tail once a day. It’s a miracle.”
Sputnik is on Prozac now, along with a few other medications to temper his behaviour. Could Sputnik be like me, a person with OCD? Was he thinking about his tail right now, somewhere in the recesses of his doggy mind?
“You can’t access an animal’s thoughts, so the purists call it only canine compulsive disorder, not obsessive–compulsive disorder,” Dodman says. “But it looks for all the world, when Dan is holding Sputnik back, that he’s constantly thinking about it. That’s an obsession.”
I was seven, maybe six, when I realised that my hands were dirty. I could wash them, and then they would be clean. But if I touched something – the banister, my clothes, the sofa, a door handle – they would be dirty again. That was easy enough to fix, just wash again. Until I touched something else, and the process would repeat.
At home, it was not an issue. I could wash my hands whenever I felt my hands were not clean. But at school, snack time, field trips – there was not always a place I could wash my hands. Or, the catch-22, the public bathroom at school or the cinema was not clean enough. I could not really be sure that my hands were clean.
I devised a whole bunch of techniques to maintain my hands’ cleanliness. When I went out for lunch on the weekends with my parents, I would wash before we left, close my fists tightly, and hide them in my sleeves until we got to the restaurant. Or I would not eat the parts of my food that I had held with my hands. I left the bottom halves of French fries and discarded the corners of sandwiches.
I invented a game that I played with my friends at the movies: bobbing for popcorn with our tongues. When the lights dimmed, they returned to eating their popcorn normally; I continued to bob.
This went on for a couple years, until the fourth grade. I still remember the first food I ate without washing my hands. They were fruit gummy snacks handed out at an after-school programme I went to. I opened the plastic bag, reached in with my fingers and put them straight into my mouth. I may have even licked the tip of my index finger a bit. I did not know why I was suddenly different, but I felt exhilarated. I was free, normal. I did not know what had kept me chained those past few years, but I was glad it was over. I had seconds that day, in my favourite flavour, grape.
In 1989, a popular science book called The Boy Who Couldn’t Stop Washing was published. Its author, Judith Rapoport, then chief of the Child Psychiatry Branch at the National Institute of Mental Health, had studied and treated all kinds of neuropsychiatric illness, but a fascination with OCD grabbed hold of her. People with OCD had to participate in detailed rituals and compulsions to assuage strange beliefs: that they had just killed someone, that everything was contaminated, that they had sinned in some way, that things had to be just right.
Before her book came out, OCD was thought to be rare. We now know it affects 1–3 per cent of the population. Rapoport’s book was one of OCD’s first steps into the spotlight – she went on Oprah and Larry King Live. Millions of people began to understand something about their own odd behaviours, or those of their friends and family members. Soon, Rapoport started to get letters and phone calls – including some with questions she had not expected.
“A whole bunch of them talked about their dogs,” she says.
People wrote that their dogs did these behaviours too, especially excessive washing. Did she think they had OCD? It was an interesting idea. “If people ask one weird question, you shrug it off,” she says. “But if 20 of them ask it, you pay attention.”
A dog owner herself, she went to her vet to ask about acral lick, a common CCD behaviour when a dog licks or sucks at its paw or leg until the fur and flesh are worn through, leading to infection, amputation and sometimes death. Her vet told her yes, acral lick was a huge problem with no good treatment options, and his dog suffered from it. She asked if he would be willing to try medication – the same medication given to people with OCD, which increases levels of the brain chemical serotonin.
“We put his dog on a dose that we guessed at, given the weight of dogs and the weight of people, and the dog had a remarkable response,” she said. “You could say this all started when I cured my vet’s dog.”
Encouraged, Rapoport designed a double-blind controlled study. Dogs with acral lick received one of two drugs for OCD that targeted serotonin, or a placebo, or an antidepressant that worked for depression but not OCD and would not alter serotonin levels. The results were “dramatic”: the only group that improved was the group that got the serotonin drugs.
Still, Rapoport took her findings with a grain of salt. As a psychiatrist, she says she usually needs to know what her patients think of their compulsions to give them a true OCD diagnosis: “Patients with OCD have insight and they say, ‘Look, this is very embarrassing, I think this is crazy what I’m doing, but I can’t stop,’” she explains. “Well, you can’t get that sort of information from animals, so animal models are often very limited for psychiatry.”
After publishing her findings, she moved back to human patients. But her work caught the attention of a veterinary anaesthesiologist with an interest in behaviour: Nicholas Dodman.
Turning behaviour “on” and “off”
After an injection of morphine, a small black horse named Knightly Night began to repetitively paw at the ground.
It was the 1980s, and Dodman had noticed that by using different drugs he could change the way animals behaved. In horses, he could “turn on” certain repetitive disorders that in the equestrian world were called stall walking or cribbing. Together with Louis Shuster, a professor of biochemistry and pharmacology at Tufts School of Medicine, he asked the question that would launch his career in animal behaviour: if they could turn a behaviour on, could they also turn it off?
Dodman and Shuster gathered horses with severe problems, who would pace and bite at guardrails, and gave them narcotic antagonists – the opposite of morphine. They all stopped.
“This behaviour has been going on for two thousand years of horses in captivity and nobody knew why,” says Dodman. “We were able to show that somehow you can turn it on and turn it off; that it was caused by some neurotransmitter imbalance.”
Dodman and Shuster’s initial hypothesis was that the drugs were blocking the brain’s natural opiates, stopping the behaviour because the animal no longer felt good while doing it. In further experiments, that theory did not hold up. So then they theorised that the on–off switch they had discovered actually lay in the drugs’ effects on NMDA receptors, which interact with a brain chemical called glutamate. Dodman and Shuster thought maybe cutting the line to glutamate was somehow stopping the behaviour.
To test their theory, Shuster went to a local store and bought a bottle of Delsym, a cough suppressant containing dextromethorphan, which also blocks NMDA. They fed it to a pony named Cinnamon Bun, a severe crib biter.
“He glugged it down and it stopped his cribbing behaviour,” Shuster says. “The cough medicine made his lips all pink, he looked rather strange, but it worked.”
Dodman opened an animal behaviour clinic at Tufts to expand his research to other kinds of animals, and the patients began to crawl in. He saw all kinds of pets: more horses, cats and birds, but he began to narrow his focus to dogs.
“The reason canine genetics are so cool is one word,” Elaine Ostrander tells me. “Breeds.”
Ostrander is the chief of the Cancer Genetics and Comparative Genomics Branch at the National Human Genome Research Institute, and has been working in dog genetics for 25 years. Her lab develops dog genome databases to look for genes that could be important for animal health or translate to humans. She says they have explored everything from infectious disease to cancer, including diabetes, kidney failure, retinitis pigmentosa and gout.
“If you want to understand the genetic underpinning of a complex disease, we know there’s lots of genes involved,” she says. “In human populations, there are dozens of genes that contribute. Every family is a little bit different. Some genes seem hereditary, some seem not to be, it’s a very complex mosaic. In dogs, you simplify that mosaic.”
Within breeds, dogs are genetically very similar. But also between breeds of related dogs, Ostrander can see commonalities. By looking for disease genes in sick dogs in closely related breeds, she can exclude false positives; if four similar breeds with a disease all carry the same gene, one that unaffected dogs do not have, she knows she’s got a strong candidate.
In 1994, Dodman teamed up with Alice Moon-Fanelli, an animal-behaviour geneticist, to help him begin to explore the genetics of his dog patients. Ostrander had the genetic data and Moon-Fanelli started to gather phenotypes, the expression of those genes: including the details of each dog’s behaviour, along with its breed, pedigree, age of onset, and anything else that might be useful.
Moon-Fanelli says when they started their project, the idea of CCD – not even as a model, just as a standalone disorder – was not widely accepted. Animal repetitive behaviours were considered “stereotypies” – mindless actions that were a result of poor environment or boredom, like tigers pacing in a cage at the zoo. “I came into it asking, ‘Why is this any different?’” she says. “And looking at almost 400 bull terriers over the years, and all the Dobermans and cats, it became clear that it wasn’t because of a suboptimal environment. These animals were pets, they had great lives in wonderful homes.”
The dogs’ symptoms usually started around puberty, as is often the case in people. Compulsive behaviours ran in family lines, just like people. And just as human psychology had to realise that human OCD was not a result of upbringing, animal medicine was doing the same.
“One living species to another, you know that they are obsessing and that they are possessed by demons that they cannot control,” says Moon-Fanelli. “And it’s the same thing with people. It’s just that people speak the same language so they can tell us what they’re thinking. We have to develop our interpretation, and try to be objective, based on what we see in its behaviour.”
Pamela Perry, a behaviourist at Cornell University’s College of Veterinary Medicine, is not involved in Dodman’s work. She treats animals that have a variety of behaviour problems, and says that while stereotypies and compulsions can often overlap, she does recognise a distinction. She agrees that we do not know for sure if animals are obsessing. But she has seen dogs who do not just compulsively chase light and shadows: they even get up before dawn and wait for the sun to cast shadows that they can then chase. Another client had bought a new washing machine, and their dog would wait for it to turn on and spin along with the whole cycle. As soon as it stopped, he would stop.
“If they’re waiting and anticipating, personally I think we can presume that they’re obsessing to some degree,” Perry says.
Control, and the loss of it
Despite having one of the classic presentations of OCD, handwashing, it never occurred to me or anyone who knew me that I had OCD. I have always been anxious, enough so that I sought out talk therapy several years ago and considered myself a person with generalised anxiety disorder.
My anxieties were always around a common theme: cleanliness, disease, health, germs. I also have a phobia of vomiting, which I obsess about daily. I think about throwing up probably 10–14 hours out of the day, and actively avoid situations that I think will cause me to feel sick or be sick. I thought this was what anxiety was – to be concerned about a specific set of things.
In psychotherapy, we discussed the “reasons” for my anxieties. My parents are scientists and I learned about germs at a very early age. My father was also concerned with germs and cleanliness, food poisoning and food safety. I liked to be in control, and throwing up was a total loss of control, a window into vulnerability. These sessions made me feel better, and I do think my obsessions diminished a little bit as a result. I felt that knowing their origins and roots would help me manage them, help me talk them down.
Looking back, I think my inability to recognise that I had OCD was rooted in the belief that, as a human, I had control over my behaviours and thoughts. Or that, if I did not, it was because of deeper human thoughts – if I could just uncover them, I would regain control.
But in situations where I was challenged, I quickly saw how little control I had. When I accidentally ate something that had gone rotten, I descended into total and utter panic for days. When my boyfriend got the stomach flu, I fled our apartment, staying in a hotel for three nights. When I got home, I bought hospital-grade cleaner and bleached and cleaned our home. I did not feel safe for weeks; every day I thought obsessively about the germs that were still present, waiting to infect me.
Some of this may sound understandable, albeit a little over the top. But like the dogs, or others with OCD, it is the amount of disruption of daily life that determines a disorder. I was spending hours upon hours thinking, cleaning, worrying, obsessing.
Throughout all this, I still did not think I had OCD, and it was not until my physical compulsions returned, at the end of last year, that I finally thought it might be more than anxiety. I travelled for work from May to December of last year, and dealt with some very minor health problems. Whether through those triggers, stress, isolation, or some combination, the compulsions began to creep back up on me.
Like my childhood handwashing, I do not know when exactly they began. Now that I am doing them, it is as if they are permanent fixtures, though I can look back six months ago and recognise that I was free of them. My current rituals mostly centre on eating, swallowing and food safety.
Right now, when I eat, I have to eat completely alone, and if someone else is in the room, I cannot eat. I just… can’t. When I do eat, if the food needs to be heated in the microwave, I have to set it to an odd number, usually 4 minutes and 37 seconds. Then, I have to stop the microwave at 37 seconds, though 27 or 17 are acceptable also. (While doing this, I recall with an odd fondness that in my childhood the number on the microwave always had to be 29. It is like remembering an imaginary friend.) As I am eating, each time I swallow, I have to lightly touch or grasp the tip of my nose and look up to the far-left corner of my field of vision.
In addition to the eating rituals, my other obsessions got much worse. I started to throw away food compulsively, food I knew – logically – was okay to eat. But fears of contamination take hold: what if it’s gone bad? What if the refrigerator isn’t cold enough? What if this bag of frozen berries was in a place in the freezer where the air didn’t circulate properly?
The fear and obsession with vomiting became extreme. Anything that looked or reminded me of throw-up could cause panic. Spilled coffee, splatters of water, soup, anything creamy, the words “chunk” or “throw”. Even writing this single paragraph, using these words, has taken me hours. Each time I write “throw-up” or “vomit”, I have to take a break.
Last year, when I was travelling, I wasn’t having any kind of treatment, not even talk therapy. When I got back to New York in January, I enrolled in a clinical trial for people with anxiety at Columbia University. While being evaluated, my interviewers casually asked, “Do you have any phobias or anxieties that aren’t related to your OCD?”
The question stopped me in my tracks. I have OCD?
We don’t know exactly what goes wrong in the brain to cause OCD. We do know that a group of drugs known as SSRIs (like Prozac), which increase serotonin levels, seem to help – but only for some people. About half of people see a response to the SSRIs, and a “successful” response can mean as little as a 35 per cent reduction of symptoms. As a recent review of OCD treatments said: “This means that even treatment-responsive patients may continue to have levels of symptoms in the mild-to-moderate range and spend hours daily preoccupied with their obsessions and compulsions.”
Looking for causes
Whether you believe in a dog model or not, one thing is becoming clearer in human OCD research: serotonin is not the complete story.
As Dodman had noticed, glutamate seems to be important. Recent neuroimaging of people with OCD has shown higher blood flow and activation in the cortico-striato-thalamocortical circuits, a network that loops from the deep centres of the brain to the prefrontal cortex. This area is dominated by glutamate pathways that are believed to generate controlled movement and thought, and to modulate behavioural routines. Some OCD researchers now hypothesise that SSRIs work not because of serotonin, but because they stop the release of glutamate. Further work, testing the cerebral spinal fluid levels of people with OCD, found that they had significantly higher levels of glutamate.
Still, knowing that glutamate plays a role, in dogs or in people, doesn’t help discover the genes that cause this disorder in humans, which is where an accurate animal model could be extremely helpful.
“The problem with the large number of behavioural disorders is that we don’t really have a good clue as to what the underlying molecular change is,” says Ed Ginns, a neurologist and geneticist who works with Dodman. “If we can at least get that, we’re confident that, with further molecular and clinical studies, pathways and even potential targets for treatment can be identified.”
When he first met Dodman, Ginns had been studying diseases like bipolar disorder and depression in genetically closed populations like the Amish. For him, it was never an issue that Dodman’s sample was built of Dobermans and terriers. He says it was compelling because, like the conditions of those Amish – and unlike other animal models – the dogs’ disorder had arisen naturally.
“These are not artificial constructs,” he says. “These are patients walking into his office with a real behavioural issue. It doesn’t rely on us guessing what we think might be the gene or the change in a mouse that might model a disease.”
Ginns and Dodman’s first collaboration was a genome-wide analysis, comparing 92 flank- and blanket-sucking Doberman pinschers with 68 control Dobermans. They got one strong statistical hit in what Dodman calls a “genetic oasis” – there was only one large gene there for them to look at, called neural cadherin or CDH2. In the brain, CDH2 is involved in the development of glutamate receptors.
“It was a great gene,” Dodman says. “Everyone basically took a big breath and stepped back. This was the first behavioural gene that had ever had anything to do with OCD, and one of the few behavioural genes that have been discovered.”
The next step was to look for CDH2 in people. Dodman and Ginns took their research to the National Institutes of Health, and a group there analysed data they had from people with OCD. The results were inconclusive. They found a suggestion that some CDH2 variants might be associated with Tourette syndrome, but that picture was fuzzy as well.
“We didn’t find something earth-shattering,” says Jens Wendland, a physician and psychiatrist who co-authored the study. “But to be fair, we know now that the cohort would have needed to be much, much larger, at least an order of magnitude larger, to be properly powered to do that. And we tried the best we could with the means we had available at the time.”
Wendland thinks that sequencing has advanced enough that it’s more beneficial to study humans than to redo any dog studies. He is sceptical whether we can ever really be sure that a dog’s symptoms can correspond to humans’. “We will never really know that for sure, so you could argue why should we take this leap of faith in the first place?” he says.
“I would much rather start to work on the biology of genes identified from human studies, however challenging that may be. As opposed to starting with a gene mapped to a behaviour in nonhumans where I can never be certain that this is really affective of the condition that I want to treat.”
In 2008, Dodman decided to take the initiative and move his theories to a clinical setting. For many years, he had been discussing his work with Michael Jenike, founder of the Obsessive Compulsive Disorder Institute at McLean Hospital in Belmont, Massachusetts. Jenike enjoyed his talks with Dodman but wasn’t convinced. Like Judith Rapoport, he says that the trouble with dogs and birds and mice is that unless he can talk to them, he can’t properly diagnose OCD. Still, he was willing to try giving some of his patients memantine, a glutamate-targeting drug normally used to treat Alzheimer’s, which Dodman had started giving to dogs with severe CCD.
In a group of 44 patients, everyone got a drug to increase serotonin levels, but half were given memantine as well – and it worked. For those who also got the glutamate drug, symptoms reduced by 27 per cent on average, compared to 16.5 per cent for the others. It isn’t perfect, but Jenike continues to use this combination of drugs with patients who aren’t responding well to SSRIs. Dodman and Shuster had already patented the combination of drugs as a treatment for OCD, but their tech transfer office at Tufts couldn’t get any pharmaceutical companies interested. However, subsequent research has supported the idea that both serotonin and glutamate pathways need to be addressed when treating OCD.
In brain imaging of his compulsive Dobermans, Dodman found that they had structural abnormalities associated with OCD in humans. In February 2016, a group led by Dan Stein, head of the Department of Psychiatry and Mental Health at the University of Cape Town, published the results of a re-examination of the CDH2 gene in humans. Their sample was made of 234 people with OCD and 180 healthy controls, and their findings were more conclusive than the previous study: they found two differences in the CDH2 gene that seemed to be correlated with OCD, though Stein says more work is needed to fully understand the connection.
Dodman’s latest work, published in 2016, compares dogs that have severe and mild cases of CCD. He found two areas of interest in the genome. The first has a human counterpart that is associated with an increased risk of schizophrenia, and the other harbours serotonin receptor genes.
From these most recent findings and their connection with serotonin, Dodman has a new theory. He thinks that the CDH2 gene, which involves glutamate, is required for a dog to be genetically predisposed to CCD in the first place. A human might have a different predisposition gene, but Dodman guesses it involves glutamate too. Serotonin genes, he thinks, are modifiers that control to what degree a dog has CCD (or a person has OCD). He now hopes that someone will look for similar modifier genes in humans, or expand standard OCD treatment to include both serotonin and glutamate pathways.
Dodman still thinks that any hesitation to accept research based on a dog model of human OCD doesn’t lie in specific doubts about the validity of the model, but in a greater philosophical problem: the difficulty in accepting that our minds might be closer than we want to believe to the minds of dogs.
“It really helps to be a veterinarian,” he says. “Because one of the things people say when you’re a vet is, they say: ‘It must be so difficult because you have to learn all these differences between the various species.’ The answer is, actually you don’t. What you learn to do is appreciate the sameness.”
As my evaluations at Columbia have continued, I’ve come face to face with another kind of sameness. It’s unsettling, almost spooky – as if someone has entered the most private, most anxious parts of my brain, written down my personal thoughts, and then put them on a questionnaire to be read out loud by a bored psychiatrist. Every worry, every obsession, the things I have to do in secret are standardised and stereotypical enough to be on these general evaluation forms.
Soon after I was officially enrolled in the clinical trial, I began cognitive behavioural therapy. It is the exact opposite of my past therapy sessions. I loved my psychodynamic therapist. We would meet once a week in her pleasant office, with bookcases and Asian artwork hanging on the wall. She was achingly smart and well read, and as we talked about my feelings and childhood, we often discussed theories and psychoanalytic texts. It felt like an intellectual exchange, something human of the highest order. Deconstructing, understanding, breaking down symbols and metaphor into meaning.
At CBT, I am meeting twice a week on a hard plastic chair in a tiny office with no windows. But we are not here for my feelings; actually the opposite. I am here to provoke my anxieties, confront them and, hopefully, neutralise them. I’m beginning exposure therapy and response prevention. We will not be discussing my dreams. CBT feels as close to dog training as any human activity can get.
We meticulously go through all my phobias, obsessions and rituals and rate them on a hierarchy. Now my job is to attempt to cease the rituals, and expose myself to increasingly upsetting stimuli for an hour a day, and 90 minutes twice a week in session.
After my first exposure session, I was stunned the whole subway ride home. It was upsetting, but more because it was the first time I realised how sick I was. I had looked at photos of spilled orange juice, something I haven’t been able to do because it reminds me of throw-up. First I looked at a cartoon, then more and more difficult photos (difficulty being based on how similar the colour and texture were to actual vomit).
I was so distressed by these photos I could barely glance at them before breaking out into my touching-and-looking swallowing ritual. There was a part of me that thought: this is ridiculous. It felt as if I was being tortured, but I was simply seeing a cup of juice overturned. How could this be making me so upset? I knew it was a cup of juice, and yet when I looked at it, the obsessions flowed in, thinking about being sick, thinking about if the image would make me sick, imagery of me or others getting sick, on and on.
Alice Moon-Fanelli said that the spinning dogs seemed like they had been taken over by demons. These were my demons. I didn’t expect them to look like spilled juice.
I picked up a copy of Rapoport’s book, now over 25 years old, and the same Twilight Zone-esque feelings from my evaluation interviews came back. The young boy who “couldn’t stop washing” also hid his fists in his sleeves and had a complicated swallowing ritual that involved touching and blinking. If the name had been removed, I could have easily believed someone wrote it about me.
In her book, Rapoport wrote that she was amazed at the sameness of OCD behaviours. Though she remains unconvinced how much animal models will ultimately help, she did say that psychiatrists could learn from the work of ethologists, who study inborn behaviour patterns in animals. Rapoport’s collie dog turned in circles – not compulsively, but before it lay down to sleep. In the dog’s ancestors, that behaviour was conserved to trample down grass or ward off hiding snakes or insects. But in her suburban home, it remained.
“The highly selective nature of OCD behaviors is just as remarkable,” she wrote. “Washing, grooming, hoarding – any theory of this disease must account for the incredible selectivity of these behaviors, which could be action patterns from an ethologist’s field book. As psychiatrists, we need to be field observers much more often than we are.”
Forcing myself to see myself as an animal, one that could be overtaken by innate behaviours, helps me make sense of what it means to have OCD. The endless thoughts of vomiting and cleanliness, and my eating rituals, are the same as a dog spinning round and round. The spinning even provided me an apt visual metaphor to latch on to. When the thoughts or fears begin, it is like a whirlpool: swirling, spinning, gaining momentum and sucking all logic or reason into the bottom, out of sight. As a human, I am enraged when I can’t stop my obsessive thoughts. As an animal, it makes sense that I can’t talk my way out of compulsions or fears. It is easy to accept that a dog’s broken neural circuitry was causing their tail chasing. I’m working on lending myself that kind of compassion.
The day after Sputnik, I meet Bella, another bull terrier who used to spin but after treatment has stopped almost completely. Bella’s owner, Linda Rowe-Varone, has a similar tale to Sputnik’s owners: one day her sweet puppy started to spin, and nothing she could do could stop her. Like Dan Schmuck, she tells me she almost reached breaking point.
“There was a time I really thought she was spinning so much that I could not keep her in my home anymore,” she says with tears in her eyes. “And Dr Dodman just kept telling me, ‘Just wait it out, wait it out, you’ve got to give her a little more time.’ And I’m really glad I did.”
Bella is active, playing and running around the examination room. Rowe-Varone tells us that Bella is also obsessed with balls, and she has to limit what kinds of toys she is exposed to. I wonder where the vets draw the line? All dogs have a favourite toy, one they love to play with. When can they call it an obsession? (When did I go from being a person who liked to be clean, to becoming obsessed with cleanliness?) Rowe-Varone says that she has to keep balls hidden in the garage, and if Bella sees them, she will sit outside the garage door for hours.
The debate about whether dogs can truly obsess doesn’t enter this room. The consensus here is that Bella knew her balls were in the garage and couldn’t get them off her mind. I’m struck by how accepting dogs as an animal model for human OCD required two shifts in thinking: not only did we have to become more animal, but we had to grant them a bit more humanity as well.
Dodman remembers a dog that was obsessed with water. It lived mostly in New York City but when it went to the owner’s Hamptons home it would jump into the pool and do laps for seven hours a day, whining in anxiety the whole time.
Stephanie Borns-Weil, who took over from Dodman as programme director at the Animal Behavior Clinic at Tufts last year, has seen a golden retriever obsessed with water too: it would get into the bathtub with the kids, or stand in puddles on its walks and refuse to move. Another dog she saw a few months ago would go into a lake by its house, take out five rocks and put them by a tree. If the owner removed them, it would return to the lake and get the rocks back.
One Doberman needed to cover her food before she ate. When her owner fed her, she put some paper towels next to her food. The dog would take a paper towel very delicately in her mouth, cover the food, and then uncover the food to eat it. If she couldn’t perform this ritual she wouldn’t eat. Dodman remembers another odd eating ritual: a dog who would take individual pellets of food and place them in the button compressions in the couch cushion in the next room. Only when he had put seven pellets into seven button holes could he eat the rest of the food out of his bowl.
I look back at Bella, who has bored of our chatting and is resting underneath a desk. The eating rituals that Dodman and Borns-Weil are describing are hitting a bit close to home, and maybe that’s why, for the first time, I do recognise a bit of myself in Bella. There is a big container of balls above her head, which we hurriedly covered when we came in. Is she thinking about them now, just like I’m thinking about my own obsessions?
When I leave Tufts that day, my boyfriend, Zach, picks me up and we head back to our hotel, tired and hungry. I don’t have a driver’s licence, and I needed Zach to drive me the three hours to rural Massachusetts. The drive up from Brooklyn was fraught with anxiety. Being in the car is one of my triggers. Obsessions about car sickness began weeks ago, when I first booked the rental. The whole drive I was tense and white-knuckled.
I know that I need to eat the moment we get back to our room. Zach jumps on the bed, settling in with a book. Nervously, I ask him: can you leave, so I can eat? The ritual needs to happen alone. He’s frustrated. Now? He will have to go sit in the lobby. Fine. Annoyed, he grabs his coat and heads towards the door.
Now I’m upset. Upset I have to do the ritual, upset he can’t be more understanding, mad at myself for having so little control. “You think I want to do this?” I yell defensively. “I just need a little time.”
“Whatever,” he says, slamming the door.
I realise I’ve made the same plea Dodman made to Rowe-Varone when she was about to give up on Bella: “You’ve got to give her a little more time.”
I’m in tears as I set up for lunch. Three napkins, an odd number, and I warm up the soup stopping on 37. I eat, with the ritualised looking and touching, trying to not think about how my soup kind of looks like throw-up.
“It’s not that they’re dogs and it’s not that we’re humans,” Ginns said to me. “It’s that both groups are suffering from this same clinical presentation that disrupts their development and lives. And it’s that description that for me defines compulsive behaviour.”
I take a deep breath. Just wait it out, wait it out, you’ve got to give yourself a little more time.
A breakthrough discovery related to the physical underpinning of obsessive-compulsive disorder (OCD) shows that brain inflammation is significantly elevated in OCD sufferers.
“Our research showed a strong relationship between brain inflammation and OCD, particularly in the parts of the brain known to function differently in OCD,” said senior author Dr. Jeffrey Meyer, head of the Neuroimaging Program in Mood Anxiety with the Center for Addiction and Mental Health’s Campbell Family Mental Health Research Institute.
“This finding represents one of the biggest breakthroughs in understanding the biology of OCD, and may lead to the development of new treatments,” added Meyer.
That’s significant because currently available medications are ineffective for about one in three individuals with OCD, note the researchers. About 2.2 million Americans suffer from OCD, according to the Anxiety and Depression Association of America (ADAA). Like other behavioral disorders, the condition can result in mental anguish for those affected by it.
“In general, those who have OCD suffer from unwanted and intrusive thoughts that they can’t seem to get out of their heads (obsessions), often compelling them to repeatedly perform ritualistic behaviors and routines (compulsions) to try and ease their anxiety,” describes the ADAA.
For the current study, the Canadian researchers assessed 40 individuals — 20 with a history of OCD and 20 without the condition. They conducted a positron emission tomography (PET) scan that allowed them to assess inflammation levels in the brain. Looking at six brain areas that are linked to OCD behavior, the researchers found inflammation rates that were 32 percent higher in those areas among people with the condition.
The study also found that people with OCD who attempted to ignore feelings of compulsion and not act on them showed higher levels of inflammation than those who followed through on their obsessions. With the greater sense of the physical symptoms of OCD, the study may give scientists more ammunition to develop more effective treatment options.
“Medications developed to target brain inflammation in other disorders could be useful in treating OCD,” said Meyer. “Work needs to be done to uncover the specific factors that contribute to brain inflammation, but finding a way to reduce inflammation’s harmful effects and increase its helpful effects could enable us to develop a new treatment much more quickly.”
Already, the researchers have opened up an investigation into which individuals specifically show the highest signs of inflammation, which could help steer treatment methods.
Most people with OCD are unable to bring their obsessions to a halt and “untreated OCD can be detrimental to all aspects of life,” notes the ADAA.
The NHS prescribed a record number of antidepressants last year, fuelling an upward trend that has seen the number of pills given to patients more than double over the last decade.
The figures raised questions over whether the rise shows doctors are handing out the drugs out too freely or whether it means more people are getting help to tackle their anxiety, depression and panic attacks.
Prescriptions for 64.7m items of antidepressants – an all-time high – were dispensed in England in 2016, the most recent annual data from NHS Digital showed. That was 3.7m more than the 61m items dispensed during 2015.
It also represents a massive 108.5% increase on the 31m antidepressants which pharmacies dispensed in 2006.
There are no figures for how many people are being given antidepressants, though, as NHS Digital do not record that. The 64.7m items were used to treat depressive illness, generalised anxiety disorder, obsessive compulsive disorder and panic attacks, NHS Digital said.
The 64.7m items dispensed in 2016 cost the NHS £4.12 each on average, or £266.6m of its overall £9.2bn annual spend on medication of all types. However, that is less than the £291.5m the drugs cost in 2006, because antidepressants have more than halved in cost from the £9.39 items typically cost a decade ago.
Leading doctors defended the sharp increase in the use of drugs which have been accused of fostering dependency in some patients, their potential side-effects and not always relieving symptoms.
“While at face value the rise might seem alarming, it could also be indicative of better identification and diagnosis of mental health conditions across healthcare, and reducing stigma associated with mental health in society, leading to more people with mental health conditions seeking medical assistance,” said Dr Helen Stokes-Lampard, the chair of the Royal College of GPs.
“Both would be positive steps forward as we strive for parity of esteem between physical and mental health.”
The drugs can be of real value to patients, Stokes-Lampard added.
“Antidepressants can be effective drugs when used appropriately and they do help a lot of patients. Nevertheless, no doctor wants their patients to be reliant on medication, and where possible we will always explore alternative treatments, such as talking therapies.”
However, she added, “there is a severe lack of these services available in the community, where they could be of great benefit to patients”. Patients and GPs need more such services to exist, she said. And she urged NHS England to deliver on its commitment of 3,000 new mental health therapists, to be based in GP surgeries, as a matter of urgency in order to help improve care for the mentally unwell.
The Royal College of Psychiatrists also endorsed the value of the drugs. While mild depression can be treated with talking therapies, “there is evidence that for people who have recurrent episodes of depression longer use of antidepressants reduces incidence of relapse and in certain situations this will be clinically appropriate,” said Dr Kate Lovett, dean of the college.
“Antidepressants are used in the treatment of both depression and anxiety disorders. They are an evidence-based treatment for moderate to severe depression and their prescription should be reviewed regularly in line with clear national guidance,” she added.
NHS Digital’s annual report on the prescription of all drugs in England paints a picture of ever increasing intake of pharmaceutical products. The total number of prescriptions dispensed has risen 46.8% in the last 10 years, from 752m items in 2006 to 1.1bn last year. The average number of items prescribed for each person has gone up over that time from 14.8 to 20.
Drugs for diabetes cost the NHS the most: £984.2m or £2.7m per day. The cost of those rose by £47.6m (5.1%) between 2015 and 2016 alone.
But more drugs are prescribed for high blood pressure and heart failure – 71.5m items last year, up 50% since 2006 – than any other medical condition.
The greatest increase in cost for any type of medication over the last decade has come with anticoagulants and blood-thinning drugs. Costs have gone up by £76.6m (34.5%) over that time to £298.7m last year.
The £9.2bn the NHS spent on drugs overall last year was slightly – £61.8m (0.7%) – less than it spent in 2015, probably because doctors are prescribing more generic medication. But the total annual bill has risen by 12.3% since 2006.
Repetitive hand-washing is a common OCD symptom. Credit: Lars Klintwall Malmqvist/public domain
While most people have heard of obsessive compulsive disorder (OCD), there are many misconceptions about what it truly means to have it. A Baylor College of Medicine expert discusses these common misconceptions and gives her advice on the best treatment options for OCD.
“OCD is characterized by having compulsions and obsessions that are caused by unwanted, intrusive thoughts. Individuals don’t want these thoughts, and it causes anxiety and they engage in repetitive rituals, which don’t bring them any joy or pleasure. It’s something that they do because they feel like they have to in order to get rid of that thought,” said Dr. Elizabeth McIngvale, assistant professor in the Menninger Department of Psychiatry and Behavioral Sciences at Baylor.
She explained that one of the misconceptions about OCD is that there is just one, general type but in reality, there are many different categories of the disorder. Some of the main categories are:
Contamination OCD: This often includes the fear of germs, the fear of blood-borne illnesses and the fear of household or environmental contaminants.
Scrupulosity OCD: This is a form of OCD where individuals find themselves engaging in repetitive rituals around prayer, morals or beliefs. They get stuck in these types of behaviors and do them with a moral or religious base.
Checking OCD: Individuals with this type of OCD may repetitively check their locks or their household appliances and engage in a lot of checking rituals to prevent something bad from happening.
Symptomatic OCD: This can be very similar to hypochondriasis where individuals have intrusive thoughts that they have contracted an illness of some type and get sucked into engaging in compulsions around fears of having a disease.
Perfectionism OCD: This form of OCD can involve rereading or rewriting documents for hours, checking to make sure that everything is done right even though the individual knows it is done correctly.
Sexual intrusive thoughts: These are unwanted, intrusive thoughts around sexual behaviors that individuals often find grotesque, appalling or repulsive, and they engage in different rituals to get rid of the thought.
Harming intrusive thoughts: Individuals fear that they might violently harm somebody or act out even though there is no history and/or intent to do so. A compulsion for individuals with this type of OCD is often to get rid of all the sharp objects in their house or remove all of the items that could be used as weapons.
Another big misconception about OCD is that it is a personality disorder, said McIngvale. There is a personality disorder called obsessive compulsive personality disorder (OCPD) but it is much different than OCD, she said.
“Obsessive compulsive personality disorder, in my opinion, is often what society thinks OCD is. People with OCPD might organize their closet perfectly, have all of their items color-coded and organized by type or category, or if you open their fridge all of their labels are lined up perfectly and everything has a place. However, individuals with OCPD often talk about the fact that there’s not an unwanted, intrusive thought and there’s no fear attached to these behaviors. They just organize things a certain way or do these kind of compulsive behaviors because it makes them feel better,” McIngvale said. “However, with OCD, it is something that individuals don’t enjoy – there’s nothing they like about it, they are doing it because they feel like they have to in order to get rid of the intrusive thought or fear. It is debilitating and draining and not something that makes the individual feel better and more productive when they are done.”
McIngvale also emphasized that it is incorrect to use OCD as an adjective. She gave the example of the improper use of the term as when someone says, “My co-worker is so OCD.”
For individuals who think that they have OCD, McIngvale recommends finding a behavioral therapist who specializes in exposure with response prevention therapy, which is a specific form of cognitive behavioral therapy that is offered for OCD. It is the most researched, effective and well-known treatment for OCD. She added that the individual also meet with a psychiatrist who specializes in OCD for medication options for OCD.
“Unfortunately, OCD is one of the disorders that takes, on average, about 25 years for people to get a diagnosis and proper treatment, but I really want to make sure that everybody with OCD knows that there is hope and there is help available,” McIngvale said.
Intrusive thoughts are insignificant or irrelevant thoughts that occur to a person in any situation. These thoughts usually do not have any meaning, but are frightening and scary. Frequent or excessively intense occurrence of these thoughts may result in obsessive-compulsive disorder (OCD).
Obsessive compulsive disorder
OCD is a neurobiological anxiety disorder. This disorder comprises of extraneous thoughts (obsession) and repetitive behavior (compulsion).
Obsession: Obsessions are intrusive thoughts, ideas, images, or visuals that pop up in the mind without one’s control. Obsessive thoughts are inappropriate and are capable of making a person feel scared, guilty, anxious, or as if their thoughts are reflecting reality. Persons affected with intrusive OCD often find it disturbing and troublesome, as the thoughts usually involve things that are considered important or valuable.
Compulsions: These are the repetitive behaviors of a person, as a result of the fear created by intrusive thoughts. The behaviors might be visible (like washing and cleaning) or invisible behaviors such as counting, praying, and repeating certain words for a long time. People with intrusive OCD thoughts repeatedly perform these behaviors until they are convinced that the danger is over.
The behaviors found in intrusive OCD often include frequent cleaning of a body part, storing unwanted objects, arranging objects in a particular manner, counting some items repeatedly, making several confirmations that the door is locked, checking numerous times that the stove is turned off, and seeking reassurance from a person frequently. These disorders are caused by a variety of conditions that may be genetic, neurobiologic, or environmental, and sometimes a result of medications and/or psychotherapy.
Types of Intrusive OCD thoughts
Innumerable types of intrusive thoughts may arise in affected individuals. Some common and frequently occurring thoughts leading to repetitive and compulsive behaviors relate to repetitive checking of one’s actions to avoid contamination, home security systems, avoiding house fires, violent fantasies, avoiding harm to family and loved ones, and arranging things in order to avoid very bad consequences.
Impact of Intrusive Thoughts on OCD
Dr. Debra Kissen, from “the Light on Anxiety Treatment Center” of Chicago, prepared a checklist of the common intrusive thoughts. She chose a set of people not having OCD as a sample, and provided them with a series of questions. The questions were related to violent, sexual, unwanted actions and loss of control. The overall sampled population revealed only a small percentage of them had intrusive thoughts.
However, when the same set of questions was shown to people diagnosed with OCD, about 90% of them reported that they were heavily impacted by intrusive thoughts, and a very high level of distress.
OCD is not only dangerous because of intrusive thoughts, but because one’s responses to those thoughts make it complicated. When a person tries to fight intrusive thoughts that arise in him, the inevitable consequence is that the frequency of the thoughts increases. In other words, the more a person avoids them, the worse it gets.
Causes of Intrusive OCD
Studies of OCD show that it is sometimes caused by the damage to a particular part of the brain known as the basal ganglia. Insufficient supply of oxygen to the brain, neurotoxic agents, and infections caused by bacteria are some reasons for such damage. Repetitive intrusive thoughts can be defined as a state of brain lock that happens to the four parts of the brain. In patients with OCD, these parts are ‘locked together’ due to their overstimulation.
In imaging studies, it has been found that two brain structures that interact with basal ganglia are more expressive in OCD patients. These structures are called the anterior cingulate gyrus (ACG) and the orbitofrontal cortex (OFC). They act to identify errors in the brain circuit. Their coordination with the basal ganglia sheds light on the genesis of OCD.
Formally, there are two theories proposed to explain the interaction of basal ganglia and ACG/OFC. According to the first theory, the damage in the ACG or OFC paves the way for loss of error-detection capability, which allows the brain to increase recurrence of thoughts that lead to OCD. This theory fails to elaborate the reason why people have the feeling of worry and insecurity. The second theory speculates that the occurrence of OCD is due to the result of pressurization of the ACG/ OFC complex leading to the relay of false error messages of to the basal ganglia, producing the feeling of something having gone wrong.
A common symptom of OCD is an obsession with cleanliness.
Obsessive-compulsive disorder is an intrusive condition that remains difficult to treat. This is due, in part, to the causes behind the disorder remaining hidden. Recent research, however, points the finger at brain inflammation.
Obsessive-compulsive disorder (OCD) is characterized by uncontrollable obsessions and compulsions. Individuals with OCD may experience intrusive thoughts that produce anxiety or a need to repeat certain actions to relieve pent-up anxiety.
Common obsessions in OCD revolve around cleanliness, sexual taboos, aggressive thoughts, and symmetry.
Affecting an estimated 1 percent of people in the United States, around half of OCD cases are classed as severe.
OCD is generally treated with talking therapies – in particular, a type of cognitive behavior therapy called exposure and response prevention is recommended. There are also some medications available, with selective serotonin reuptake inhibitors being the most commonly prescribed. Currently, however, therapies only work for around 70 percent of OCD-affected individuals.
One of the biggest stumbling blocks to finding good treatments is that the physical causes of OCD are not known.
Inflammation and OCD
Breaking research published this week in JAMA Psychiatry takes a look at the role of brain inflammation in OCD. The senior author of the study is Dr. Jeffrey Meyer, head of the Neuroimaging Program in Mood Anxiety at the Centre for Addiction and Mental Health in Toronto, Canada.
Inflammation is a natural process; it is a normal component of the immune response and a standard reaction to injury. However, if the level of inflammation is inappropriate or continues for too long, it can have negative consequences. For instance, in a number of diseases including rheumatoid arthritis and atherosclerosis, inflammation is heavily involved.
Growing evidence suggests that certain psychiatric conditions may involve neuroinflammation, some of which include major depressive disorder, schizophrenia, and bipolar.
Dr. Meyer and his team set out to understand whether inflammation in the brain could play a role in the development of OCD. To this end, they recruited 40 participants, comprising 20 with OCD and 20 without. Each was scanned using positron emission tomography that had been adapted to pinpoint and measure inflammation in the brain.
Specifically, the researchers were able to selectively dye microglia, which are cells that act as the nervous system’s most prominent immune defense and which are activated during inflammation. The researchers measured levels of microglia in six brain regions known to be important in OCD, including the orbitofrontal cortex and anterior cingulate cortex.
The results were clear: in the brain regions associated with OCD, individuals with the disorder had 32 percent more inflammation when compared with people without the condition.
“This finding represents one of the biggest breakthroughs in understanding the biology of OCD, and may lead to the development of new treatments.”
Dr. Jeffrey Meyer
From inflammation to treatment
Another interesting finding was that individuals who reported the highest levels of stress when trying to stop themselves from acting on compulsions also had the highest levels of inflammation in a particular brain region.
As so many diseases involve inflammation, there are already a range of drugs designed to tackle it. Because these drugs already exist on the market, it may be a fruitful avenue of research in the hunt for more effective treatments for OCD.
“Medications developed to target brain inflammation in other disorders could be useful in treating OCD,” Dr. Meyer says. “Work needs to be done to uncover the specific factors that contribute to brain inflammation, but finding a way to reduce inflammation’s harmful effects and increase its helpful effects could enable us to develop a new treatment much more quickly.”
Studies are now under way that examine the possibility of designing a blood marker test that could distinguish which patients would benefit most from anti-inflammatory drugs.
Although, as ever, more research is needed, this finding could mark a significant move forward in understanding and treating OCD.
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