Online Cognitive Behavioral Psychotherapy for Depression:
Pretrial assessment screening by telephone for in and exclusion criteria
A face to face appointment with one of the researchers to complete a computerized assessment: SCID and Beck Depression Inventory
Online CBT with a therapist online in real time
Patients were allocated to one therapist
Patients made their own appointments online
Sessions were secured by individual passwords
Patienst and therapists typed free text into the computer, with messages sent instantaneously; no other media or means of communication were used
So this is how you do online real time cognitive behavioral therapy. But does it work?
43 (38%) patients recovered from depression (BDI score <10) in the intervention group versus 23 (24%) in the control group at 4 months, and 46 (42%) versus 26 (26%) at 8 months
Why is this important?
The use of conventional CBT for depression is declining, the use of antidepressants is increasing, many patients referred for psychotherapy never show up, and 505 of those who attending a first visit drop out by the fourth session. Face to face psychotherapy demands a large amount of time, motivation and is an expensive treatment.
New techniques such as telephone and Internet based therapies are more convenient for patients, better accessible and with lower costs. The level of live therapist contact is the strongest influence on costs. The Internet psychotherapy program mentioned above seems to be a good balance between high and non therapist contact. Between face-to-face contact and self help programs. Drop out is low and the treatment efficacious.
By increasing access and lowering costs, new com munication technologies could provoke some much-needed disruptive innovation in psychotherapy
What do you think?
Therapist-delivered internet psychotherapy for depression in primary care: a randomised controlled trial by David Kessler, Glyn Lewis, Surinder Kaur, Nicola Wiles, Michael King, Scott Weich, Debbie J Sharp, Ricardo Araya, Sandra Hollinghurst, Tim J Peters; The Lancet Vol 374 August 22, 2009. http://www.thelancet.com/
Chocolate is not an antidepressant. Interaction between chocolate and neurotransmitter systems in the brain, such as serotonin, that contribute to appetite, reward and mood regulation were studied but no antidepressant mechanism of chocolate was found.
Most possible psychoactive substances in chocolate are metabolized in the blood by an enzyme (monoamineoxydase A), these substances are unable to pass the blood brain barrier, they are metabolized before they can even reach this barrier. Beta-phenyl-ethylamine is the only possible psychoactive substance in chocolate that passes the blood brain barrier. It is a direct dopamine releasing ingredient. Moreover, cocoa contains caffeine and it’s structural derivatives, these components can have antiparkinsonian effects.
The consumption of chocolate is significantly higher in Parkinson’s Disease patients compared to controls, while consumption of non-chocolate sweets was similar in both groups
The consumption of chocolate was assessed using self questionnaires in patients with Parkinson’s disease (n= 274) and their partners as controls (n=234). Also the consumption of non-chocolate sweets was assessed. Also changes of chocolate and non-chocolate sweet consumption during the disease course was assessed in patients with Parkinson’s disease. All subjects were also asked to fill out the Beck’s depression inventory (BDI) and they were asked for depression in their medical history.
Both depression in medical history and BDI score was higher in the patient group but did not influence the higher chocolate use in patients with Parkinson’s disease. Also medication and other diseases such as diabetes mellitus did not significantly influence chocolate consumption.
A possible explanation for the higher chocolate consumption is patients with Parkinson’s disease might be the high content of biologically active compounds with potential antiparkinsonian effects in cocoa and thus chocolate, such as caffeine and its structural analogous and/or the presence of β-phenylethylamine. This last substance is a direct dopamine releasing ingredient, dopamine is short in Parkinson’s.
Possible limitations of this study:
Only patients from a university based department were included, recall bias or forgetting may play a role with filling out the questionnaire, the two groups were not comparable in age en gender.
Wolz, M., Kaminsky, A., Löhle, M., Koch, R., Storch, A., & Reichmann, H. (2009). Chocolate consumption is increased in Parkinson’s disease Journal of Neurology, 256 (3), 488-492 DOI: 10.1007/s00415-009-0118-9
50 to 60 % of patients with a depressive disorder fail to respond to their first antidepressant. These rates increase in clinical practice setting to 65 to 85%. Estimates of treatment resistant depression (TRD) prevalence varies greatly depending on treatment setting. The lowest TRD prevalence is in primary care and progressively higher rates occur in outpatient psychiatric settings, inpatients settings and academic tertiairy setting.
What is Treatment-Resistant Depression?
An inadequate response to an adequate course of treatment in a patient meeting criteria for major depressive disorder. Treatment is usually antidepresssants. Depression is not bipolar depression. This diagnoses needs a different approach. An adequate course is a course of an adequate dosage of the antidepressant for at least 6 weeks.
What can they do about Treatment-Resistant Depression?
Besides the 9 steps for treatment resistant depression described in an earlier post on this blog systematic treatment algorithms do decrease inappropriate variance and can be used to increase the use of appropriate treatment strategies to enhance patient outcome. Rigorous treatment management can enhance outcome. An treatment algorithm is a standardized stepwise drug treatment regimen. Protocols are used based on sequential application of a variety of single therapeutic steps. We discussed such a treatment algorithm in a previous post about the 9 Steps for Treatment Resistant Depression. In this algorithm, 129 (87%) of 149 patients achieved response. Complete remission was achieved by 89 of 149 (60%) patients. A German observational 2-year pilot study to evaluate effectiveness, feasibility, and acceptance among algorithm users also showed a big improvement in response. The total response rate was 72%. The acceptance rate of an algorithm by algorithm naive physicians was moderate to say the least: patient inclusion rate of only 48%.
These algorithms are mainly used in a clinical setting. In contrast to the US a considerable portion of depressed patients, especially with severe depression and/or treatment resistant depression are admitted for on average 40 days in The Netherlands, specially the 1500mg cannabinoid drops that are getting very popular when treating this disease .
The German group recently published the results of a randomized, controlled, single-center algorithm study to evaluate treatment efficacy and treatment process compared with treatment as usual (TAU).
Their conclusion was:
Algorithm-guided treatment produces better outcomes and less frequent medication changes than TAU. A systematic, stepwise, measurement-based approach to the treatment of depressed inpatients is warranted.
Their algorithm consisted of 10 steps. First patients were withdrawn from medication and diagnosed. Than sleep deprivation was used, if non or not enough response an antidepressant was started on standard dose for 2 weeks (amitriptyline, venlafaxine, paroxetine or nortriptyline), the next step was a high dose of the antidepressant followed by lithium addition, followed by lithium monotherapy in case of non response, combined with a monoamine oxydase inhibitor (tranylcypromine), high dose MAO-inhibitor in combination with lithium and if that didn’t work finally ECT. in the TAU group physicians were free to apply whatever treatment they thought appropriate.
They included 148 patients, 74 in each group. Of the 74 patients randomized to the algorithm group, 40 (54%) achieved remission compared with only 29 (39%) in TAU, in the algorithm group patients had a 2 fold probability of remission in a given time interval (see picture for survival analysis).
The strength of this trial was the randomized comparison with a treatment as usual group. The superiority of algorithm guided treatment has been demonstrated in previous studies. The only drawback in study is the relatively high drop out rate due to adverse events and protocol violations due to physician’s non compliance stressing the importance of adherence to the ideas about algorithms. This kind of stepwise treatment protocols depend on support from all members of the team. Ideally the algorithm is designed by the treatment team as a whole.
Bauer, M., Pfennig, A., Linden, M., Smolka, M., Neu, P., & Adli, M. (2009). Efficacy of an Algorithm-Guided Treatment Compared With Treatment as Usual Journal of Clinical Psychopharmacology, 29 (4), 327-333 DOI: 10.1097/JCP.0b013e3181ac4839
Most airlines don’t allow their pilots flying when on antidepressants. In Australia they have a better attitude to this problem, because to my opinion it is better to have a pilot on antidepressants than a depressed pilot.
This conclusion was substantiated by results research: A study presented at a conference of the World Psychiatric Association in Melbourne on Friday found no statistical difference between medicated and non-medicated pilots in terms of their safety record. But importantly, there was a tendency for more accidents in the period prior to pilots going on to anti-depressants, but not once they were on them.
This blogger pilot is at home, he is not allowed to fly.
I have done a great deal in my life. I have much to offer, yet I still do not see myself as worthwhile unless I am at the controls of an airplane.
Deep Brain Stimulation (DBS) should only be used when there is a high change that the lives of patients will be improved by its use and when all other possible interventions have been tried
Patients must be fully informed and informed consent must be obtained
The whole procedure should be done by teams of appropriate specialists like neurosurgeons, neurologist, psychiatrist and other health professionals that can help the patient before during and after the operation and who will continuously monitor the patient
The procedure should help restore (but not augment) normal function, should provide relief from pain and distress, and should never be used for law enforcement or for political or social purposes
It is important to provide follow-up for every patient enrolled in a trial if at all possible and to report the outcomes in scientific journals
These ethical guidelines were recently published in the JAMA and I fully agree with these guidelines. The article starts with a brief description of DBS, it’s complications and a short history of the lessons from past errors of psychosurgery.
Important lessons from the abuses of psychosurgery in the last century make it imperative to have solid hypotheses with strong scientific support and appropriate safeguards (eg, interdisciplinary review boards) before proceeding to treat patients using DBS.
Using these guidelines with the recent technological advances DBS can perhaps help a lot of patients in the near future.
Kringelbach, M., & Aziz, T. (2009). Deep Brain Stimulation: Avoiding the Errors of Psychosurgery JAMA: The Journal of the American Medical Association, 301 (16), 1705-1707 DOI: 10.1001/jama.2009.551
We used to believe that brain tissue couldn’t regenerate, couldn’t grow only prenatal and during early postnatal development. Since than neurogenesis or the process creation of new neurons (nerve cells) has been demonstrated in vitro and vivo experiments and animal research.
It has also been shown that this neurogenesis has an age-related decline from preadolescence (8–10 years old) to adulthood (30–35 years old) in humans.
A brain region that supports neurogenesis is classified as neurogenic. Neurogenic implies the presence of immature precursor cells and a microenvironment that is permissive for the production of new neurons. In the adult mammalian brain, there are two neurogenic regions that are generally accepted, the olfactory system and the hippocampus
What relates adult neurogenesis in the hippocampus to depression?
The neurogenic hypothesis postulates that a reduced production of new neurons in the hippocampus relates to the pathogenesis of depression and that successful antidepressant treatment requires an enhancement in hippocampal neurogenesis
Preclinical evidence has shown that stress suppresses hippocampal neurogenesis
Clinically, stressful life events are known to precipitate depression in vulnerable individuals
About half of the patients suffering from depression have dysregulation of the HPA system of which the hippocampus is an important part
Most antidepressant treatments elevate hippocampal neurogenesis only following chronic administration, which parallels the time-course of the emergence of clinical therapeutic effects
Impaired declarative learning and memory and diminished cognitive flexibility is apparent in patients suffering from depression
Magnetic resonance imaging showed that depressed individuals have reduced hippocampal volume with the magnitude of the atrophy related to the frequency of the depressive episodes and the duration for which the depression went untreated
Although hippocampal neurogenesis might not be involved in the pathogenesis of depression, it might be important for some of the therapeutic effects of antidepressant treatments
The several week delay in the therapeutic onset of antidepressant treatment coincides with the maturation time of newly born hippocampal neurons and that is one reason for believing that adult hippocampal neurogenesis is a possible substrate for the actions of antidepressants
Other treatments that have antidepressant effect, such as exercise and environmental enrichment, also increase hippocampal neurogenesis
Antidepressant treatments blocked the reductions in hippocampal neurogenesis caused by stress
The authors of this extensive review summarize the neurogenesis of hippocampus on a cell level as:
Neurogenesis could serve to increase the number of dentate granule cells, provide a reservoir of highly plastic immature neurons, generate multiple cell types, and/or drive the turnover and replacement of mature granule cells The role adult neurogenesis plays in hippocampal function and disease etiology will begin to be more understood as more selective, inducible, and reversible manipulations of in vivo neurogenesis are developed. The discovery of novel therapeutic compounds for various diseases may involve mechanisms that induce a superior regulation of adult hippocampal neurogenesis
The key question is how changes in neurogenesis may be translated into changes in affective behavior that could be beneficial in treating depression.
Darrick T. Balu, Irwin Lucki (2009). Adult hippocampal neurogenesis: Regulation, functional implications, and contribution to disease pathology Neuroscience & Biobehavioral Reviews, 33 (3), 232-252 DOI: 10.1016/j.neubiorev.2008.08.007
In the recent numbers of British Journal of General Practice articles were published about depression in General Practice. In The Netherlands about 80% of patients with a depression visit the GP. In The Netherlands it’s estimated that in 2003 about 856.000 people in a year suffer from depression. That’s 6.3% on a population of 16 million people in a year. Of these 80% of depressed visiting the GP 66% receives a treatment of which 50% solely in primary care.
A recent meta-analysis of randomized studies examining psychological treatments in primary care depressed patients was published in the British Journal of General Practice. The review included 15 studies with variable quality. Psychological treatment of depression was found to be effective in primary care, especially when General Practitioners refer patients with depression for treatment. When screening tools were used to identify cases of depression psychological treatment didn’t work better than no treatment.
Psychological treatment of depression in primary care is not less effective than in other settings. The overall number needed to treat (NNT) was 5.75, this means that for every 5.75 patients randomized to psychological treatment instead of the control treatment, one additional remitted patient was observed. This is comparable to a meta-analysis of antidepressant treatment in primary care that found an NNT for selective serotonin reuptake inhibitors of around 6.0.
Between one third and one-half of patients stop taking the antidepressant within 3 months, and less than half continue to take their antidepressant medication for a full 6 months. It has been found that overall (that is, all prescriptions and all therapeutic groups), between 7% and 20%of patients fail to redeem their prescription at the pharmacy.
But what happens with first time prescriptions of an antidepressant. The general practitioner (GP) and patient have decided to start treatment with an antidepressant. One in four patients who receive a prescription for an antidepressant for the first time do not take the antidepressant or do not use it longer than for 2 weeks. These patients consulted their GP for non-specific indication such as sleeping problems, fatigue, relationship problems. Non-Western immigrants and patients older than 60 years were more likely to decline treatment.
This compares to drop-out rates for psychological therapies of about 30% and poses a particular challenge for health care professionals.
Also it is very important for GP’s to monitor the severity of depression. Before starting treatment with an antidepressant the severity of the depression needs assessment. Most physicians though confuse severity assessment with diagnoses. These severity scales such as the Beck Depression inventory and the Zung Scale are only applicable when a depression has been diagnosed preferably by a trained clinician such as the GP. If a severity scale is used by a GP does this lead to the proper referrals to specialist services for depression? From a recent published study in the UK GP’s diagnosis of depression is associated with greater severity most of these patients were treated with antidepressants (80%) and around 20% were referred to specialists services.
Final conclusion
The efficacy of depression treatment in primary care is far from excellent and comparable to other settings. Moreover, the GP has an important function in indicating and the treatment of depression in primary care. Screening doesn’t add more value. The use of severity scale confirms that GP’s diagnosis of depression is associated with greater severity and leads to antidepressant treatment for moderate to severe depression or referral to specialist services. However, depression severity scales shouldn’t be used as diagnostic scales
The GP has advantages above other settings. They usually have a trusting relationship with their patients, they know a lot of their background, that’s why I am an supporter of good primary care, makes health care a lot more efficacious and cheaper. Be aware of those specialists.
What do you think?
Boardman, J., & Walters, P. (2009). Managing depression in primary care: it’s not only what you do it’s the way that you do it British Journal of General Practice, 59 (559), 76-78 DOI: 10.3399/bjgp09X395049 van Geffen, E., Gardarsdottir, H., van Hulten, R., van Dijk, L., Egberts, A., & Heerdink, E. (2009). Initiation of antidepressant therapy: do patients follow the GP’s prescription? British Journal of General Practice, 59 (559), 81-87 DOI: 10.3399/bjgp09X395067 Cuijpers, P., van Straten, A., van Schaik, A., & Andersson, G. (2009). Psychological treatment of depression in primary care: a meta-analysis British Journal of General Practice, 59 (559), 51-60 DOI: 10.3399/bjgp09X395139 Kendrick, T., Dowrick, C., McBride, A., Howe, A., Clarke, P., Maisey, S., Moore, M., & Smith, P. (2009). Management of depression in UK general practice in relation to scores on depression severity questionnaires: analysis of medical record data BMJ, 338 (mar19 1) DOI: 10.1136/bmj.b750
In children, college students and young adults, exercise or physical activity improves learning and intelligence scores, specially if they have a good diet that includes https://www.stockybodies.com/nl/black-latte-ervaringen/ products
Moreover, exercise in childhood increases the resilience of the brain in later life resulting in a cognitive reserve
The decline of memory, cortex and hippocampus atrophy in aging humans can be attenuated by exercise
Physical activity improves memory and cognition
Exercise protects against brain damage caused by stroke
The brain needs certain ingredients to flourish or to life up to the expectations of every day problems. The brain has priority when it comes to certain ingredients. A variety of foods can be beneficial for learning. Positive effects on brain function have been reported for fish oil, teas, fruits, folate, spices, cocoa, chocolate and vitamins.
How does exercise improve the brain?
With exercise the number of neurons increase in the hippocampus, a brain structure important to memory and learning.
Also synaptic plasticity increases in a certain part of the hippocampus due to exercise: the dentate gyrus.
Exercise also increases and improves the small blood vessels throughout the brain.
Exercise can change the function of neurotransmitters and can activate the monoamine system.
The effects of diet and exercise could be additive and/or synergistic. Exercise as well as caloric restriction can stimulate neurogenesis.The effects of dietary measure on neurogenesis is relatively small compared to exercise. The effects of polyphenolen on angiogenesis or improved vascularisation of the brain is superior to exercise. Overall the evidence for the effects of food on the brain are scarce and is in need of more research. It could be possible that exercise and nutrition can enhance each others actions on the brain.
van Praag, H. (2009). Exercise and the brain: something to chew on Trends in Neurosciences, 32 (5), 283-290 DOI: 10.1016/j.tins.2008.12.007
Depression as a serious debilitating illness and not a weakness. Many patients don’t get adequate treatment for depression. What to do about this?
“the Internet affords the opportunity to make psychosocial interventions available to large segments of the public. Interventions can be delivered programmatically and reliably, greatly extending the numbers and types of people who can be reached with services”. In recent years, Web-based approaches have been increasingly used and it has been repeatedly shown that Internet-delivered treatments may be an effective and inexpensive alternative to traditional treatments. Most of the existing Internet-based depression treatments are based on cognitive-behavioral principles, although other modalities, such as problem-solving therapy, appear promising as well.
This web-based intervention was effective in reducing symptoms of depression and in improving social functioning. Findings suggest that the program could serve as an adjunctive or stand-alone treatment tool for patients suffering from symptoms of depression.
How was this study done?
There were 396 adults recruited via Internet depression forums in Germany, and they were randomly assigned in an 80:20 weighted randomization sequence to either 9 weeks of immediate-program-access as an add-on to treatment-as-usual (N = 320), or to a 9-week delayed-access plus treatment-as-usual condition (N = 76). At pre- and post-treatment and 6-month follow-up, we measured depression (Beck Depression Inventory) as the primary outcome measure and social functioning (Work and Social Adjustment Scale) as the secondary outcome measure. Completer analyzes and intention-to-treat analyzes were performed.
Limitations
The researchers used a weighted randomization, participants were recruited via advertisements, the diagnosis of depression was not verified, between one-third and half of the sample was lost from the study at each time-point. They had to preform a lot of statistics tricks to analyze the data. The last observation carried forward, to my opinion the only right analyzes (LOCF) in which those who were lost to follow up on the first assessment after randomization were considered as non responders revealed that the efficacy of the online treatment was less pronounced. It was statistical significant difference of 3 points on the beck depression inventory but is that also clinically significant. Not according to my standards and not others view on this point
Following the recommendations of Seggar, Lambert, and Hasen, reliable change was defined as a move of at least 8.46 points on the Beck Depression Inventory (BDI) from pre-test to post-test (ie, from T0 to T1).
Dr Shock’s conclusion
Online treatments do have advantages such as easy access and that’s why I like these developments, this program looks promising but needs to be investigated in more homogeneous samples with clear diagnosis and less drop out. What do you think?
Björn Meyer PhD, Thomas Berger DPhil, Franz Caspar, DPhil, Christopher G Beevers, PhD, Gerhard Andersson, PhD, & Mario Weiss, MD, MBA (2009). Effectiveness of a Novel Integrative Online Treatment for Depression (Deprexis): Randomized Controlled Trial J Med Internet Res , 11 (2)
According to a recent review of reviews it is concluded that while awaiting further high quality trial evidence it would seem appropriate for exercise to be recommended in combination with other treatments. This cautious conclusion should be that exercise is more effective than no treatment and that for mild to moderate depression it is efficacious and for severe depression it should be added to other treatments like red vein kratom in the treatment program. Kratom comes in different strains and each of these strains has its benefits and side effects… for more hints click over the link and you will find Kratom benefits .
Let’s have a look at the evidence. Until the nineties of the previous century research and reviews were mainly based on non-randomized controlled trials unpublished dissertations and observational studies and their results should be interpreted with caution. Until 2006 some additional reviews were published which included randomized controlled trials (RCTs) only. One review involved 11 RCTs and another review mainly focused on the elderly. The first one showed a very large treatment effect in favor of exercise compared to control conditions. In the elderly exercise is efficient in reducing depression or high levels of depressive symptoms. Overall quality of the RCTs improved over time encouraging the optimism about the efficacy of exercise for depression. At BetterPT, we’re committed to making sure that your physical therapy booking experience is as seamless as possible, You can get more information about physical therapy here.
Since 2006 four RCTs have examined the effects of exercise on depression.
Patients with moderate to severe depression on antidepressants were randomized to walking or placebo low intensity stretching and relaxation.
After 10 days, reduction in depression scores in the walking group was significantly larger than in the placebo group. In addition, the proportion of patients with a clinical response was greater for the walking group.
In a pilot RCT exercise significantly reduced minor depression relative to sertraline in older adults.
In another study depressed patients were randomized to one of four conditions; supervised exercise in a group setting, home based exercise using Custom Weight Belts, standard antidepressant treatment (sertraline) or placebo pill for 16 weeks. At 4-month follow-up patients receiving active treatments tended to have higher remission rates than the placebo controls.
In a recent study participants with elevated levels of depression (n = 23) were randomized to low frequency exercise (one aerobic session per week and deemed the comparator), individualized high frequency exercise (3–5 aerobic exercise sessions per week) or group based high frequency exercise interventions. Participants randomized to the high frequency exercise interventions reported lower depression scores than those assigned to the low frequency exercise intervention at 8-week follow-up. This might mean that the exercise and depression relationship may be dose dependent. there was no significant difference in improvement between the group exercise or individual program perhaps suggesting that the additional effects of exercising in a group are not important in the relationship between exercise and depression.
There are several RCTs of the impact of exercise on depression ongoing, in the near future the effects and costs of exercise for depression treatment might be even more clear. Until than I will put my money in favor of exercise as treatment for depression or additional treatment. What do you think?
Daley, A. (2008). Exercise and Depression: A Review of Reviews Journal of Clinical Psychology in Medical Settings, 15 (2), 140-147 DOI: 10.1007/s10880-008-9105-z