Online treatment for Depression and Anxiety

29 Jun

Lately,a few new programmes (linked below) have been developed offering online cognitive treatments for Mental Health Disorders.
These programmes are attractive due to being cost effective and bypassing often long waiting times to see a Psychologist.
So,do you think online treatment programmes can help with mild depression or anxiety?

http://www.mindspot.org.au/?gclid=COX5joSwibgCFWVKpgodBHwALg
http://ecentreclinic.org/index.php/our-courses/ecentreclinic-courses

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Micronutrients for Brain Health

24 Jun

Excellent article written by Victoria J Drake and reblogged from the Linus Pauling Institute at
http://lpi.oregonstate.edu/infocenter/glossary.html#peripheral%20neuropathy

Micronutrients and Cognitive Function

Summary

The brain requires a constant supply of micronutrients for energy metabolism of neurons and glial cells, neurotransmitter synthesis and action, nerve impulse propagation, and homocysteine metabolism. (More Information)
Deficiencies in various micronutrients, especially the B vitamins, have adverse effects on cognition. (More Information)
The developing brain may be particularly vulnerable to deficiencies in choline and essential fatty acids. (More Information)
Due to conflicting studies, more research in needed to determine whether micronutrient supplementation affects attention-related cognitive functions. (More Information)
Presently, there is little evidence that supplementation with B vitamins, antioxidant vitamins, choline, or omega-3 fatty acids will improve memory performance. (More Information)
More research is needed to determine whether micronutrient supplementation has any effects on executive functioning (i.e., higher-order cognitive processes). (More Information)
Some, but not all, studies have reported that micronutrient supplementation improves overall mood and psychological well-being. (More Information)
It is not yet clear whether supplementation with B vitamins, antioxidants, or omega-3 fatty acids protects against age-related cognitive decline. (More Information)
Several methodological issues (e.g., tests used to assess cognition, choice of study population, nature of the supplementation, study duration, etc.) may have contributed to the conflicting results observed in intervention studies. (More Information)

Good nutritional status is important for proper brain development and maintenance of normal cognitive function (1). Through unique biological functions, various micronutrients affect brain function. This article discusses the roles of key micronutrients, including the B vitamins, antioxidant vitamins, and certain essential minerals, in cognitive function. When appropriate, research on the role of other compounds, such as essential fatty acids and choline, is also presented. The cognitive effects of micronutrient deficiencies are discussed, and the effects of micronutrient supplementation on the broad areas of attention, memory, executive functions, mood, as well as age-related cognitive decline are covered.

Basic Needs for Cognitive Performance

Energy Metabolism of Neurons and Glial Cells

The human brain is a highly metabolically active tissue that depends on a constant supply of glucose to meet its energy needs. In fact, the brain accounts for approximately 25% of total body glucose utilization at rest, despite representing only 2% of adult body weight (2, 3). Blood glucose levels must be maintained at all times to avoid hypoglycemia and to supply the brain with its preferential fuel. During the initial stages of fasting, blood glucose levels are maintained through the breakdown of liver glycogen and then through the process of gluconeogenesis—the production of glucose from non-carbohydrate precursors, such as amino acids. The B vitamin biotin is required for a key enzyme in the gluconeogenic pathway (4). While glucose is the obligatory fuel, ketone bodies can also be used by the brain when glucose supply is inadequate, such as during prolonged fasting or starvation. However, ketone bodies are acidic, and very high levels of these compounds in the blood are toxic and may result in ketoacidosis (5). Thus, glucose is the preferred and normal energy substrate of the brain.

Glucose oxidation in the brain requires certain micronutrients as cofactors. For instance, forms of several B vitamins, including thiamin, riboflavin, niacin, and pantothenic acid, as well as the compound lipoic acid, are utilized in reactions that completely metabolize glucose to carbon dioxide and water (3). Additionally, the nutritionally essential minerals, magnesium, iron, and manganese are required for the complete metabolism of glucose; these micronutrients are utilized as cofactors, substrates, or components of enzymes in glycolysis and the citric acid cycle (6, 7). Moreover, generation of cellular energy in the form of ATP by the electron transport chain requires the vitamins, riboflavin and niacin; iron contained in iron-sulfur clusters; and the endogenously synthesized compound, coenzyme Q10 (8).

Cerebral Blood Supply

At rest, the brain receives approximately 15% of cardiac output (9). Proper cerebral blood supply is necessary to deliver oxygen, glucose and other macronutrients, and the required micronutrients for proper cognitive function. Nutrition has a role in maintaining optimal blood supply to the brain. For instance, insufficiency of several dietary components increases the risk of developing stroke, a pathological condition that results from impaired cerebral blood supply; see the Disease Index for examples.

Neurotransmitter Synthesis

A neurotransmitter is a chemical released from a nerve cell that transmits an impulse to another nerve cell or an effector cell, such as a muscle cell. Neurotransmitters have either excitatory or inhibitory effects; the type of effect is dependent on the receptor on the receiving cell (10). Neurotransmitters can be broadly divided into two main classes: small amino acids (e.g., gamma aminobutyric acid [GABA], glutamate, aspartate, and glycine) and biogenic amines (e.g., dopamine, epinephrine, norepinephrine, serotonin, histamine, and acetylcholine) (11).

In addition to various amino acids, several B vitamins, including thiamin, riboflavin, niacin, vitamin B6, folate, and vitamin B12, are needed as cofactors for the synthesis of neurotransmitters. Moreover, vitamin C is required for synthesis of norepinephrine (3), and the mineral zinc is important for proper function of GABA, aspartate, and norepinephrine (12). Further, choline is a precursor for the neurotransmitter acetylcholine (13).

Neurotransmitter Binding to Receptors

Neurotransmitters function by binding to receptors on the cell membrane of the neuron releasing the neurotransmitter (i.e., presynaptic neuron) or to receptors on the cell membrane of the receiving cell (i.e., the postsynaptic neuron). Receptor binding can either mediate the opening of ion channels or cause metabolic changes within the cell (3, 14). Specifically, direct action on ion channels results from neurotransmitter binding to receptor sites on the membrane of postsynaptic neurons. This binding causes the gate-like ion channels to open, which allows ions to flow into the cell (10). Influx of positively charged ions into the postsynaptic neuron can have excitatory effects by depolarizing the membrane; membrane depolarization can cause a nerve impulse or action potential if a certain threshold is reached within the neuron. This is commonly referred to as “neuronal firing.” In contrast, influx of negatively charged ions can have inhibitory effects by hyperpolarizing the membrane and thus preventing neuronal firing (15). In addition to direct effects on ion channels, neurotransmitters may bind to G-protein coupled receptors, thereby eliciting cell-signaling effects that could result in metabolic changes (e.g., alterations in activity of various enzymes) within a postsynaptic cell (14).

Vitamins could possibly influence binding of neurotransmitters to postsynaptic receptors. For instance, an in vitro study showed that two forms of vitamin B6, pyridoxal and pyridoxal phosphate, inhibited the binding of GABA to postsynaptic receptors (16). Also, a rat study associated vitamin B6 deficiency during fetal development and lactation with changes in the number and binding of dopamine receptors (17).

Nerve Impulse Propagation

The speed at which nerve impulses (action potentials) are propagated is influenced by the myelination of the nerve (18). Myelination refers to the process in which nerves acquire a myelin sheath—the insulating layer of tissue made up of lipids and proteins that surrounds nerve fibers. This sheath acts as a conduit in an electrical system, allowing rapid and efficient transmission of nerve impulses (10).

Certain micronutrients can affect the propagation of nerve impulses. In particular, adequate intake of both folate and vitamin B12 is important in maintaining the integrity of the myelin sheath, and thiamin is needed for maintenance of the nerve’s membrane potential and for proper nerve conductance (3). Additionally, iron has an important role in the development of oligodendrocytes, the cells in the brain that produce myelin (19).

Homocysteine Metabolism

Homocysteine is a sulfur-containing amino acid that is an intermediate in the metabolism of another sulfur-containing amino acid, methionine. Elevated homocysteine levels in the blood (i.e., hyperhomocysteinemia) may be a risk factor for cardiovascular diseases and could also be linked to dementia and Alzheimer’s disease (20, 21). The amount of homocysteine in the blood is regulated by at least three vitamins: folate, vitamin B6, and vitamin B12 (see diagram). Additionally, the nutrient choline is also involved in homocysteine metabolism. The choline metabolite, betaine, can also provide a methyl group for the conversion of homocysteine to methionine.

Why Mentally Ill are having their Physical Health neglected by Doctors

24 Jun

Patients with severe mental illnesses tragically die approximately 20 years earlier then the average citizen.
There are numerous causes for this as detailed below.

Reblogged from http://mentalhealthconnect.com.au/wordpress/summer-forum-2013-john-allan-putting-practice-in-place-for-healthy-living-for-people-with-mental-illness/

Summer Forum 2013 – John Allan – Putting practice in place for healthy living for people with mental illness
Feb 25th, 2013 by HamishH
John Allan is the Chief Psychiatrist of NSW and presented on the topic of implementing healthy living practices with people with mental illness.

John argued for the importance of setting clear and simple targets which are achievable and relevant to people with mental health problems.

John looked back the history of psychiatry and asked how far have we actually come? For example, life expectancy for people with serious mental illness was about the same as the life expectancy of the general population in 1910, now it is over 20 years less than the life expectancy for the general Australian population.

John reflected on the policy/practice divide… so what are the barriers for mental health consumers accessing physical health care?

Practicalities:

Inaccessibility of services and distance to services
Mistrust
Homelessness
Social isolation
Interpersonal barriers

Mental health care providers often do not ask about physical health care
Lack of information
An attitude from  service providers that it’s “not my problem”
Participants in studies in this area had a good awareness of the range of options in the community but clinicians often didn’t
Other barriers

Poor coordination between physical and mental health care providers
Diagnostic overshadowing: patients are “seen to be faking” – people feel they have to hide mental illness to get service, or act in ways that do get them service but that have them labelled as “attention seeking”
Lack of engagement is often seen by clinicians as being due to mental illness when it may be practical everyday things that get in the way
Symptoms of mental health disorders themselves make communication difficult
Disrespectful, non-caring behaviour by both mental health and general clinicians
Having no advocate
Feeling powerless
Ambivalence – too often we accept the persons view that they are stigmatised and the result is that we don’t meet their health needs met
What tools to we have to address these issues?

Recovery-oriented practice: the National recovery-oriented mental health practice framework

“Starting with the initial assumption that personal recovery is different for everyone, ‘personal recovery’ is defined within this Framework as being able to live well and to build and live the life one chooses in the presence or absence of mental ill health”

http://www.crazelateralsolutions.com

John also argued that clinicians will have more influence by “giving up” coercive power-assertive tactics, both over colleagues and consumers/patients.

John suggested making people with severe mental illness a special target for all governments, with specific, hard indicators of success. With these few simple indicators, practice and policy will shift to meet them.

Reduce smoking rates to general population levels
Reductions in average HBA1C concentrations to less than 7% among consumers with severe mental illness (HBA1C is a form of haemoglobin that gives a measure of the average concentration of glucose in the blood over a long period of time)
Increase of cancer treatment rates to the level in the general population
Education and awareness and training: for example enabling all psychiatrists to prescribe statins
 John suggested a number of steps that will help:

Adopt a recovery paradigm
Target for peer support workers
Equal go for people with severe mental illness in the NDIS
Self-management, life coaching, advocacy
Further information and resources 

The Concord Centre for Cardiometabolic Health in Psychosis

http://ccchip.com.au/

The National recovery-oriented mental health practice framework

 www.crazelateralsolutions.com

People with Schizophrenia have faulty Immune Systems

24 Jun

Diagnosis and treatment of Schizophrenia has generally been thought of to be under the specialty of Psychiatry,however it may be time that people diagnosed with Schizophrenia or psychosis be seen by Immunologists as well.

A 2012 Australian study by Professor Cyndi Shannon Weikert  and team from
http://www.neura.edu.au/research/themes/shannon-weickert-group
showed that approximately 40% of people with a Schizophrenia diagnosis have Immune System abnormalities.
This is a very significant finding.

http://www.medicalnewstoday.com/articles/248848.php

Catatonia: from subtype of schizophrenia to specifier for many disorders: J Clin Psychopharmacol.June 2013

24 Jun

Reblogged from Psychiatrist:update

Psychiatrist:Update

04.06.2013

Catatonia is a motor dysregulation syndrome.It is characterised by acute onset of stupor, mutism, negativism,  posturing, rigidity, and repetitive speech and  movement. Historically, catatonia was considered as a sub type  of schizophrenia. Sedative and seizure treatments were dramatically effective for catatonia though they offered little benefit for schizophrenia as such. Being understood only as a sub type of schizophrenia was a limitation, as it  prevented other catatonic patients from effective treatments. Giving antipsychotics to patients with catatonic symptoms had the risk of precipitating malignant catatonia (NMS).

Max Fink’s guest editorial welcome the changes made In DSM 5. DSM-5  deletes the catatonia type of schizophrenia (295.2), adds a new class of ‘‘Catatonia Not Elsewhere Classified (299.89),’’ retains the medical disease association of catatonia introduced in DSM-IV (293.89), and accepts catatonia as a specifier of 10 psychiatric diagnoses.  Catatonia is now completely divorced from schizophrenia.

When German psychiatrist Karl Kahlbaum described catatonia, he didn’t…

View original post 300 more words

Causes of Psychosis

23 Jun

Psychosis is often assumed to be caused by Schizophrenia,and when a patient presents to their Doctor or Emergency Room with symptoms of hallucinations,delusions, agitated or bizarre behaviour,the assumption and diagnosis is often of Schizophrenia.
However,many other illnesses can cause behaviour changes or paranoia,and it’s important for the physician to be aware of them,as often the treatment is different for what would be used in Schizophrenia.
In addition,some of these disorders are time critical in nature.
Often,these disorders involve physical symptoms too,however psychosis as the primary symptom has been reported in some cases.

Some other causes of psychosis are:

-Hyperhomocystinemia
-Vitamin B12 deficiency
-Autoimmune Disorder with NMDAR Antibodies or GAD Antibodies
-Sjogren Syndrome
-Temporal Lobe Epilepsy
-Gluten Intolerance
-Paraneoplastic Disorder
-Crohns Disease
-NMDA Receptor Encephalitis
-Lupus
-Lead Toxicity
-Multiple Sclerosis
-Neurosyphillis
-Frontal Temporal Dementia
-Huntington’s Disease
-Chromosomal Disorders
-Porphyria
-Lymes Disease
-Homocystinuria
-Thyroid conditions such as Graves Disease and Hashimoto’s Encephalopathy
-Toxoplasmosis Infection
-Brain Tumour

References:
http://www.ncbi.nlm.nih.gov/m/pubmed/23091569/?i=11&from=psychosis%20antibodies
http://bestpractice.bmj.com/best-practice/monograph/1066/overview/aetiology.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619167/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688330/
http://www.japi.org/february2008/CR-115.htm
http://www.m.webmd.com/a-to-z-guides/news/20040219/gluten-intolerance-linked-to-schizophrenia
http://www.ncbi.nlm.nih.gov/m/pubmed/23032251/?i=14&from=psychosis%20antibodies

Schizophrenia as an Autoimmune Disease

18 Jun

Evolutionarypsychiatry.com has a great blogpost regarding Autoimmune Brain Antibodies found in Schizophrenia.
There is growing evidence that Schizophrenia is likely an Autoimmune Disease in at least a subset of patients,with antibodies to NMDAR receptors found.

http://evolutionarypsychiatry.blogspot.com.au/2013/01/is-schizophrenia-autoimmune-disease.html?m=1