Borderline Personality Disorder (BPD) is often categorized – in short – as a mental illness where the survivor exhibits explosive anger, impulsive behaviors, and unstable relationships – with romantic partners, as well as friends and family.


Borderline Personality Disorder


Due to the destructive nature of these symptoms, BPD has almost become a bad word in the mental health community. As an MSW, I have come across professionals who won’t work with individuals who have been diagnosed with BPD due to the stereotypical “abusive” nature of the disease.

However, the symptoms listed above provide an overgeneralized assumption of the disorder based on only three out of nine possible symptoms – and all symptoms are frequently linked to trauma.

This overgeneralization of BPD marginalizes survivors of the illness by belittling or oversimplifying their experience – particularly those who don’t fall under the assumed criteria.

Furthermore, it makes finding help extremely difficult, let alone receiving an appropriate diagnosis. There are four types of Borderline Personality Disorder that all exhibit differently, and to be diagnosed with BPD, one must exhibit five out of nine possible criteria.

My Experience as a Professional Mental Health Worker with BPD

via Borderline Personality Disorder and Me — Thrive Global


Ps. For you to understand better and have a real help, Im leaving you a book link for Borderline Personality Disorder Workbook: An Integrative Program to Understand and Manage Your BPD (A New Harbinger Self-Help Workbook)




mental health professionls

Mental Health Professionals


This article can help you if you need help, but you’re not sure about the type of mental health professional to see.



If you want more information about what different mental health professionals do and if you want to know how to get help from a mental health professional.


Learn about mental health professionals and the differences between doctors, counsellors, psychologists, psychiatrists, youth workers and social workers here :


  • Psychologist (Ph.D or Psy.D) – Earn doctorate in psychology and go through special training to provide mental health and assessment services. They are your go-to for diagnostic assessments (like ADD or Bi-Polar), but they can also provide counselling one-on-one or in a group setting.
  • Psychiatrist (M.D. or D.O.) – The only mental health professional who can prescribe medication. They go to medical school and an additional 4 years of residency training in psychiatry. They can run assessments but typically don’t work exclusively as counsellors.
  • Social Worker (LMSW) – Earn master’s degree or Ph.D in social work and receive training in community and social welfare. They often work as counsellors focusing on areas like finances, housing, and access to government benefits.
  • Marriage & Family Therapist (LMFT) – Earn master’s degree or Ph.D in marriage and family therapy and focus on family systems. They do counselling with families, couples, and individuals and treat problems as relational issues.
  • Counselor (LPC, LHMC) – Earn master’s degree or Ph.D in counselling and focus on individual and group therapy. They treat problems as individual issues and may get additional training in specific areas like trauma, child counselling etc.
  • Life Coach – Does not require any credentials or license. Anyone can be a life coach regardless of training or education, but often coaches will seek out certification of some kind. Look for a coach that has a specialty and education.

Learn about mental health professionals and […]

Mental Health Professionals — Be Inspired..!!

So tomorrow is Christmas day. If you’re anything like me you’re feeling a bit of excitement, a bit of dread and very overwhelmed.

The amount of emotional energy alone that Christmas involves means that anyone with a mental illness tomorrow is going to find some aspects of it hard.

I thought I’d write a Christmas survival guide for all the others out there like me!


  • Set boundaries. If possible, lets the people you’ll be spending Christmas with know in advance what you will and will not be doing on the day.


  • As most conditions fluctuate, this might be difficult but remember you can change your mind and decide you are no longer willing or able to do something you said you could. This is okay and perfectly valid.


  • Remember that it’s your Christmas too. You should get some enjoyment out of the day, even if you have to achieve that by doing some ‘non-festive’ type things. (I will definitely be napping at some point!)


  • Reach out to your loved ones if you’re not feeling great. If this isn’t possible, most major helplines, such as The Samaritans (116 123) in the UK, are open on Christmas day.




Hopefully some of this is helpful to someone out there struggling. I’m wishing everyone a good holiday time and if you have any tips yourself, please add them in the comments!


via How to survive Christmas with a mental illness — schizowhatnow


What Schizophrenia Is

First of all, let’s talk about what is not schizophrenia.

People with schizophrenia do not have multiple personalities. In 1911, Eugen Bleuler was the first to use the term “schizophrenia.” Although the term “schizophrenia” comes from the Greek words “split” and “mind,” people with schizophrenia do not suffer from personality splitting.

This misunderstanding has led to the misuse of the term by many people. The “split mind” refers to the way people with schizophrenia are broken by reality; they can not say what is real and what is not real.


Who has schizophrenia?

Schizophrenia is one of the most common mental illnesses. Approximately 1 in 100 people (1% of the population) is affected by schizophrenia. This disorder is found all over the world and in all races and cultures.

Schizophrenia also affects men and women, although on average men develop schizophrenia earlier than women. Generally, men show the first signs of schizophrenia around the age of 20, and women show the first signs later than 20 years. Schizophrenia represents a huge cost to society, estimated at $ 32.5 billion a year in the US (according to statistics by Brain Facts, Society for Neuroscience in 2002).


What are the symptoms of schizophrenia?

The behavior of schizophrenic people is often very strange and shocking. This change in behavior, when people can not make the difference between what is real and what is not, is called “psychosis” or “psychotic episode.” The American Psychiatric Association has published guidelines that are used in the classification of people with mental disorders.

The most recent milestones are contained in the book called “Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition” (known as DSM-IV as an abbreviation). DSM-IV describes some symptoms that a person needs to have to be diagnosed as having schizophrenia. These symptoms include two or more of the following behaviors lasting at least one month:

  • Delirium – strange, false beliefs. This beliefs seem real to the schizophrenic person, but they are not real. For example, a person may think that aliens or spies control her or her behavior, mind and thoughts. Sometimes this delusion may be by nature paranoid.

People with paranoia have an unreal fear or suspicion that someone “wants to catch them.” Delusion can also be of grandeur. In these cases, people think they are important people, such as the president, the king, or the prime minister.

  • Hallucinations – oddities, unreal perceptions of the environment.


These hallucinations can be:

  • A. Auditive (I hear voices) – sometimes the voice tells the person to do something
    Visual (see lights, objects or faces)
    Olfactory (smell all kinds of things)
    Tactile (for example, feel that cockroaches are crawling on or under the skin)


  • Disordered thinking / speechUnnatural thoughts are usually measured by disorganized speech. Schizophrenic people speak very little; when they do, the speech is incoherent. Sometimes the person changes the theme of a sentence at her half.


  •  Symptoms negative – no normal behaviorDelusions, hallucinations and incoherent speech indicate the presence of abnormal behavior. Negative symptoms include social withdrawal, lack of emotions and expressions, energy, motivation and reduced activity. Sometimes schizophrenic people have hygiene and poor care habits.


  • Catatonia – immobility and “wax flexibility”Catatonia is a negative symptom by which the person remains fixed in one position for a long time. “Wax flexibility” describes the situation where the person’s arms remain stuck in a certain position even if they are moved by someone.When people show any of these five symptoms they are considered to be in the “active phase” of the disorder. Typically, schizophrenics exhibit lighter symptoms before and after this active phase.There are three basic types of schizophrenia. All those who suffer from schizophrenia have lost contact with reality.


The three types of schizophrenia are:

  1. Disorganized schizophrenia (formerly called hebephrenic schizophrenia) – lack of emotion, disordered speech.
  2. Catatonic schizophrenia – wax flexibility, low movements, rigid posture, sometimes excess movement.
  3. Paranoid schizophrenia – strong delirium or hallucinations.


What happens in the brain?

A common finding about a schizophrenic brain is that the lateral ventricles are larger. The lateral ventricles are part of the ventricular system containing the cerebrospinal fluid.

The picture below shows the magnetic resonance imaging (MRI) image of two twins: one with schizophrenia, the other not. Note that cerebral ventricles (red arrows) are larger in the case of schizophrenia glaucoma. (Image courtesy of NIMH Clinical Brain Disorders Branch)

A small hippocampus, a larger basal ganglion, and anomalies in the prefrontal cortex are present in some schizophrenics. However, these changes are not present in all schizophrenic patients and may occur in people who do not have this disease.



What are the causes of schizophrenia?

Probably there are multiple causes of schizophrenia, and researchers do not know all the factors that cause this mental illness.


Schizophrenia “is inherited from the family”. In other words, schizophrenia has an important genetic component.

Evidence of the genetic component comes from the study of twins. Monozygotic twins (identical twins) are those that have exactly the same genetic fingerprint; twin zigzag twins (fraternal twins) are those that have only half the same genetic fingerprint. If genetic factors were the only cause in the development of schizophrenia, then both monozygotic twins should have always developed this disease.


Trials on twins

Studies on twins show that the probability that both monozygotic (identical) twins develop schizophrenia is between 30-50%. The probability that both twins (fraternal) twins develop schizophrenia is 15%. This probability for non-twin siblings (like brothers of different ages) is also about 15%.

Do not forget that the rate at which we find schizophrenia in the population is about 1%. Therefore, because the probability of monozygotic twins is not 100%, genetic factors can not be the only cause. However, since the probability of monozygotic twins to make schizophrenia is much higher than in the case of dizzy twins, genetic factors play an important role.


Adoption studies

Some studies have focused on the history of families of children who were adopted at an early age and who developed schizophrenia later. One of the studies (Kety et al., 1968) showed that 13% of the biological relatives of Schizophrenia adopters also had schizophrenia, but only 2% of the “normal” adoptive relatives had schizophrenia. These studies support the role of genetic factors in triggering schizophrenia.

To learn more about the role of genetic factors in schizophrenia, see the Genetics and Mental Disorders page of the National Institute of Mental Health.



Among the non-genetic factors that can influence the development of schizophrenia are: family stress, weak social interactions, infections or viruses contracted at an early age, or traumas produced at infancy. In one way or another, the genetic fingerprint of individuals is combined with non-genetic (environmental) factors to trigger schizophrenia.



Many studies have investigated the possible role of brain neurotransmitters in the development of schizophrenia. Most of them focused on the neurotransmitter called dopamine. “Dopamine Theory in Schizophrenia” states that schizophrenia is caused by a superactive dopamine system in the brain. There is strong evidence that supports dopamine theory, but also a number of other data that do not support it:


Evidence for Dopamine Theory in Schizophrenia:

  1. Dopamine-blocking medication reduces schizophrenic symptoms.
  2. Dopamine-blocking medication has side effects similar to Parkinson’s syndrome.
  3. Parkinson’s syndrome is caused by the lack of dopamine in a part of the brain called the basal ganglion.
  4. The best drugs in the treatment of schizophrenia resemble dopamine and completely block dopamine receptors.
  5. High doses of amphetamines trigger schizophrenic symptoms – such as those in the “amphetamine psychosis” disorder.Amphetamine psychosis is a model for schizophrenia because medication that blocks amphetamine psychosis also reduces the symptoms of schizophrenia. Also, amphetamines worsen the symptoms of schizophrenia.
  6. Children at risk of schizophrenia exhibit the same pattern of brain waves as adults with schizophrenia. This abnormal pattern of brain waves in children can be reduced by drugs that block dopamine receptors.

Evidence against dopamine theory in schizophrenia:

  1. Amphetamines do more than just increase dopamine levels. They also change the level for other neurotransmitters.
  2. Drugs that block dopamine receptors act rapidly on the receptors. However, sometimes it takes many days to change the behavior of people with schizophrenia.
  3. The effect of drugs that block dopamine may be indirect. They could actually influence other systems that have a greater impact on the symptoms of schizophrenia.
  4. New drugs for schizophrenia, such as clozapine, block receptors for both serotonin and dopamine.

Treatment in schizophrenia



Medications that treat schizophrenia are called antipsychotic medications. This type of medicine was introduced for the first time in 1950. It has proven to be a great success in treating the symptoms of schizophrenia. Different types of antipsychotics work well on various disease symptoms and do not add dependency. The medicine is not a remedy for the disease but to reduce the


Possible side effects of antipsychotic medicines

1. Parkinson’s disease – as symptoms – tremor, muscle rigidity, loss of facial expressio
2. Dystonia – the contraction of the muscles
3. Do not worry
4. Tardive dyskinesia – involuntary gestures, abnormal movements of the face, mouth and / or body. These include licking the lips and the chewing movement. Approximately 25-40% of patients taking antipsychotic medication for several years develop these side effects.
5. Weight gain
6. Skin problems



Often antipsychotic medication does not reduce all the symptoms of schizophrenia. Also, since schizophrenic sufferers may become ill when they have to develop professional skills and careers, they may not have the ability to become useful members of society.

Therefore, psychological therapy, family and occupational
therapy can be used in conjunction with antipsychotic medication to help these people return to the community.

Recommendations :

The published material is the author’s opinion and meets the accepted scientific standards at the time of publication, but science is constantly changing and therefore can not guarantee that the information is complete, current, or error-free; the material is not and does not substitute for medical and psychological consultation; so use this material for information only and not for self-diagnosis or self-treatment – if you have any doubts about your health – contact your doctor and psychologist.
*For other questions – ask the author.
*The material presented may be further modified.

Inflammation And Mental Illness

Inflammation: The New Way To Understand Mental Illness

Highlights of Research


  1. How we began to understand the link between immune response and mental illness
  2. High levels of inflammation and the links with Depression and Mental Illness
  3. New anti-inflammatory therapies & how to access them


A Nobel Prize winning discovery

            A curious discovery made in an Austrian asylum 136 years ago is making an impact today in shaping our understanding of depression and mental illness. The finding, made by the Austrian neuro-psychiatrist Julius Wagner-Jauregg, was so groundbreaking it earned Wagner-Jauregg a Nobel Prize.

           The story started in the winter of 1883, at the First Psychiatry Clinic of the Asylum of Lower Austria. Wagner-Jauregg was first starting his psychiatry position at the clinic and was tasked to look after a wide variety of mentally ill patients. He came across a woman with psychotic delusions who also suffered from a high fever induced by acute bacterial skin infection. As the fever subsided, the patient became coherent and was cured of her psychosis. This perplexing discovery stuck with Wagner-Jauregg, and he began his decades-long quest to replicate that observation. [1,2]

          During the late 19th century, syphilis was still a dangerous health threat in Europe. Neurosyphilis (or general paresis of the insane, GPI), marked by grand delusions, paralysis, and dementia, was the manifestation of the tertiary stage of syphilis. [1] For many patients, death was a welcomed escape from the horrible disease. Ironically, GPI would also be the disease that propelled Wagner-Jauregg to international fame.

         Since his encounter with the woman in the Austrian Asylum, he had been experimenting with different types of infection to induce fever but to no avail. It was until the end of World War I that Wagner-Jauregg had the serendipitous opportunity to inject a malaria-infected blood sample from a soldier into several patients with GPI. The malarial inoculations were proven to be successful. This treatment, known as malariotherapy thereafter, was then widely used around the world.

         In 1927, Wagner-Jauregg was awarded the Nobel Prize for his contribution in developing malariotherapy.


The missing link between fever and the remission of mental illness

Wagner-Jauregg’s work with malariotherapy had not only made him the first psychiatrist to be awarded a Nobel Prize, but it also broke the “therapeutic nihilism” surrounding psychosis, which he believed to have a natural cause. However, he admitted that he had no clear understanding of the underlying mechanism that made malariotherapy worked in his Nobel Lecture. [4]

           Nonetheless, his work had produced an important nuance in understanding GPI – that there was a specific, organic root rather than universal, non-specific cause. In other words, induced fever was a targeted therapy for an illness caused by an anomaly or anomalies in the brain. In his concluding remarks during the Nobel Lecture, he said: “…… malaria besides a non-specific action against the syphilitic infection, also exerts a specific elective action on the cerebral process of progressive paralysis, including advanced infection of the cerebro-spinal fluid.” [4]

           It was not until the past decade that scientists began to understand the role of inflammation in mental illnesses such as depression. In a recently published study, scientists found as many as 90 genes over-expressed in individuals with major depressive disorders that were associated with the body’s immune response towards infection. [5]

         Additionally, there was some evidence that suggested physiological changes in response to depression. Inflammatory molecules such as interleukin-6 (IL-6), tumour necrosis factor (TNF)-alpha and interleukin 1-beta (IL-1β) could cross the blood-brain barrier to enter the brain and disrupt the functions of neurotransmitters such as serotonin. [6] It was previously thought that the blood-brain barrier was impenetrable to inflammatory molecules and, therefore, could not significantly influence any functions of the brain.

          Such a discovery had shifted the paradigm of our understanding of depression pathogenesis and opened new possibilities for novel treatment avenues.

The interleukin-6 molecule, a prominent pro-inflammatory protein that could unlock a new treatment of depression.

           The effect of inflammation on depression was particularly prominent in patients who were given interferon-alpha treatment for cancer. Interferons are a group of naturally-occurring proteins that are secreted by the immune system. Interferon-alpha has been shown to elicit inflammatory responses in the body and was intimately linked to depressive symptoms in patients who received infusions of the medicine.

           In the late 1990s, physicians began to realise that anxiety and depressed mood that arose from interferon-alpha treatment could not be entirely attributed to toxicity but could due to a more complex pathophysiological mechanism. It was also postulated that by reducing inflammation through alternations of the immune system, depression symptoms could be alleviated or, at least, reduced. [2]

Stimulation of the vagus nerve


       The cumulative evidence from these studies has strongly supported the hypothesis that reducing inflammation is beneficial for depression. As the production of pro-inflammatory signals is largely controlled by the central nervous system, much attention has been given to the role of the vagus nerve in regulating the inflammatory response.

         Simulations of the vagus nerve had shown to reduce pro-inflammatory cytokines such as IL-6, TNF-alpha, high mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF), which were closely linked to the relief of depression symptoms. [7] Acetylcholine, a major neurotransmitter of the vagus nerve, also demonstrated promising results in suppressing pro-inflammatory cytokines including IL-1β and IL-18. [8]

         It is also important to note that both the invasive (surgical) vagus nerve stimulation and the safer, transcutaneous alternative have shown a similar capability to suppress pro-inflammatory cytokines. Thus, these treatments could provide a viable treatment option to patients especially those who are non-responsive to standard antidepressant treatment due to high levels of inflammation. [9]



From Wagner-Jauregg’s malariotherapy to today’s vagus nerve stimulation, the medical community has gained substantial insights into the instrumental role of inflammation in depression. These discoveries have helped us to better manage depression and could possibly lead to safer more effective treatments and benefit to those who are not responding to traditional therapy which doesn’t address inflammation.



1       Tsay CJ. Julius Wagner-Jauregg and the legacy of malarial therapy for the treatment of general paresis of the insane. Yale J Biol Med 2013;86:245–54.

2         Wetsman N. Inflammatory illness: Why the next wave of antidepressants may target the immune system. Nat Med2017;23:1009–11. doi:10.1038/nm0917-1009

3 Julius Wagner-Jauregg – Biographical. Nobel Media AB. 2019. (accessed 3 Mar 2019).

4 Julius Wagner-Jauregg – Nobel Lecture. Nobel Media AB. 2019.

jauregg/lecture/ (accessed 7 Mar 2019).

5         Leday GGR, Vértes PE, Richardson S, et al. Replicable and Coupled Changes in Innate and Adaptive Immune Gene Expression in Two Case-Control Studies of Blood Microarrays in Major Depressive Disorder. Biol Psychiatry 2018;83:70–80. doi:10.1016/j.biopsych.2017.01.021

6         Zhu C-B, Blakely RD, Hewlett WA. The Proinflammatory Cytokines Interleukin-1beta and Tumor Necrosis Factor-Alpha Activate Serotonin Transporters. NeuropsychopharmacologyPublished Online First: 1 February 2006. doi:10.1038/sj.npp.1301029

7         Das UN. Vagus Nerve Stimulation, Depression and Inflammation. Neuropsychopharmacology2007;32:2053–4. doi:10.1038/sj.npp.1301286

8         Borovikova L V., Ivanova S, Zhang M, et al. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature2000;405:458–62. doi:10.1038/35013070

9         Cattaneo A, Ferrari C, Uher R, et al.Absolute Measurements of Macrophage Migration Inhibitory Factor and Interleukin-1-β mRNA Levels Accurately Predict Treatment Response in Depressed Patients. Int J Neuropsychopharmacol 2016;e. 19 pyw045. doi:10.1093/ijnp/pyw045