Don’t Let Foot Cramps and Charley Horses Slow You Down

Sort of a banal post, but probably helpful as well. These cramps in my feet happen to me all the time as a result of being on Lithium. Lithium dehydrates you and if you don’t rehydrate enough, you can get muscle cramps. Also lithium changes your electrolyte balance and that can also cause muscle cramps. I try, always, to drink a lot of fluids, sometimes, I don’t hydrate enough and I get cramps. I saw this article and thought i am surely not the only one that that happens to, so I’m posting it. Pretty informational 🙂

You’re sound asleep, and then, without warning, you wake up with a paralyzing stiffness in your calf or foot.

Whether you call it a foot or leg cramp (aka “charley horse”), it’s a common, somewhat mysterious pain that happens when a muscle gets involuntarily stiff and can’t relax.

“They tend to happen more frequently as we age,” says sports and exercise medicine physician Kim Gladden, MD. “While they can be uncomfortable, they are rarely harmful.”

Here’s what causes these cramps, as well as tips to help prevent them.

7 common causes for cramps

Whether day or night, your foot and calf muscles can spasm or cramp. This can happen to various muscles — not just in the legs or feet — though these cramps are often most uncomfortable.

Causes for muscle cramps include:


  1. Lack of hydration.“If you are experiencing cramping, it’s important to look at your hydration first,” Dr. Gladden says. You want to make sure you are drinking enough water throughout the day.
  2. Problems with nutrition. While a balance of electrolytes (calcium, sodium, potassium, and magnesium) is essential for the contraction and relaxation of a muscle, it’s best not to simply self-treat with supplements. “Taking excess supplements if you don’t need them can be harmful,” Dr. Gladden says. Instead, she suggests eating a variety of foods with plenty of colorful fruits and vegetables. This includes leafy greens and fruits, including bananas, to add a balance of electrolytes to you diet.
  3. Side effect of medication. Some medications such as statins and furosemide (Lasix®) can also cause muscle cramps. A tip-off is when cramps start suddenly after you begin taking a new medication. If this happens, see your practitioner.
  4. Not stretching enough. Taking time to stretch each day, including after a brief warm up or after a shower can help. “You want your muscles to be as strong and supple as they can be. Adequate stretching after a brief warm-up period is key to this,” Dr. Gladden says.
  5. Overexertion. If you exercise harder than usual or experience muscle fatigue, this can cause cramps. Pace yourself.
  6. Poor circulation. If you have cramping that increases when you walk, it could be a problem with your circulation. “Some circulation problems cause pain that feels like cramping. If it gets worse when you walk, or if you have cramps that just don’t stop, definitely see your doctor,” Dr. Gladden says.
  7. The wrong shoes. A less-known cause for muscle cramping: your shoes. “You want to look at your shoes, especially if you changed from flats to heels. This also can cause cramps,” Dr. Gladden says.
  8. How to stop leg and foot cramps

    There are some simple ways to respond to leg and foot cramps:

    • If it happens while you are lying down or in bed, try to simply stand up and put some weight on the affected leg or foot. This can sometimes be enough to stop that tender stiffness.
    • Use warmth/heating pads to increase blood circulation to the muscle and to relax it. Soaking in a warm tub of Epsom salt can also help ease the tension.
    • For more stubborn pain, you can try a non-steroidal anti-inflammatory medication, such as ibuprofen.

    Easy stretches to keep calves and feet happy

    Here are some simple stretches that can help stop pain and prevent it.

    Basic calf stretch

    This calf stretch is commonly used by runners. Here’s how to do it:

    1. Stand with your palms placed against a wall, with arms stretched out
    2. Step back with leg of affected calf
    3. Lean forward on the other leg and push against the wall

    You should feel a stretch in your calf muscle and the back of the leg.

    Towel stretch

    Do this stretch while you sit:

    1. Keep legs outstretched in front of you
    2. Point the toes of your affected foot at the ceiling so that the leg is engaged
    3. Take a towel or neck tie and wrap it around your foot, holding it with both hands
    4. Lift the leg slightly until you feel a good stretch
    5. Keep cramps from happening again

      Here are some tips to prevent leg cramps:

      • Stay well hydrated
      • Stretch each day, especially before you exercise
      • Limit or avoid alcohol
      • Eat a balanced diet that includes natural sources of calcium, potassium and magnesium
      • Increase your activity level gradually

      If leg or foot cramps are occasional occurrences, you can generally manage them yourself. However, if they happen frequently, are severe, or if you are concerned any of your medications are the culprit, talk to your doctor. They could signal a medical problem that requires treatment.

“Fracture risk from psychotropic medications: a population-based analysis.” Aka Lithium cuts your risk of fractures by almost half!

Whereas other psychoactive drugs and even SSRI’s may increase the risk of fractures, “Lithium was associated with lower fracture risk (OR = 0.63; 95% CI, 0.43-0.93)”

This is great news, and another reason, besides controlling my bipolar disorder, that I am so very  glad I’m on Lithium.



Selective serotonin reuptake inhibitors (SSRIs), benzodiazepines, and antipsychotics have each been associated with an increased risk of fracture in older individuals. The aim of this study was to better define the magnitude of fracture risk with psychotropic medications and to determine whether a dose-effect relationship exists.


Population-based administrative databases were used to examine psychotropic medication exposure and fractures in persons aged 50 years and older in Manitoba between 1996 and 2004. Persons with osteoporotic fractures (vertebral, wrist, or hip [n = 15,792]) were compared with controls (3 controls for each case matched for age, sex, ethnicity, and comorbidity [n = 47,289]). Medications examined included antidepressants (SSRIs vs other monoamines), antipsychotics, lithium, and benzodiazepines.


Selective serotonin reuptake inhibitors were associated with the highest adjusted odds of osteoporotic fractures (odds ratio [OR] = 1.45; 95% confidence interval [CI], 1.32-1.59). Other monoamine antidepressants (OR = 1.15; 95% CI, 1.07-1.24) and benzodiazepines (OR = 1.10; 95% CI, 1.04-1.16) were also associated with greater fracture risk, although the relationship was weaker. Lithium was associated with lower fracture risk (OR = 0.63; 95% CI, 0.43-0.93), whereas the relationship with antipsychotics was not significant in the models that adjusted for diagnoses. A dose-effect relationship was seen with SSRIs and benzodiazepines.


This study provides novel insight into the relationship between fractures and psychotropic medications in the elderly. Selective serotonin reuptake inhibitors seem to have a greater risk than other psychotropic classes, and higher doses may further increase that risk. Lithium seems to be protective against fractures.

Significant Number Of Young People With Undiagnosed Bipolar Disorder

img_6229This article talks about giving antidepressants to depressed people who actually have bipolar disorder. This is a very dangerous thing to do as you can push someone who has bipolar disorder into full blown mania by giving them antidepressants without a mood stabilizer. The 10% stats are for the UK, but I am sure it’s the same here in the US. In fact, I was just such a “casualty.” I went into a severe depression in the end of 1985, I was then prescribed antidepressants without any mood stabilizer, and in February of 1986, I started becoming manic, not knowing what was happening to me, I didn’t report my symptoms to my doctor. In the end of February, 1986, I started becoming full blown manic, out of touch with reality, and in the beginning of March, I was hospitalized. This was in New Orleans, LA, in Touro Infirmary. I was in the hospital for a month, finally being discharged when my psychotic (out of touch with reality) symptoms were gone. I will wonder forever what would have happened if i had not been put on just antidepressants. What if my doctor had put me on Lithium along with the antidepressants, would I then never have manifested bipolar disorder? What if… can’t live there. Must live in what is in this very moment and live as well as I can, because what ifs are a waste of time. The only thing that matters is the reality of what is happening now and we must come face to face with it and live with it with strength and equanimity. I may never know why somethings happened, and there’s no point in blame or anger… they did, and I simply have to accept that they happened and go on from here to make as good a life as I can for myself.

Around 10% of UK primary care patients prescribed antidepressants for depression or anxiety have undiagnosed bipolar disorder, a study has found.

Researchers from Leeds and York Partnership NHS Foundation Trust and the School of Medicine at the University of Leeds interviewed young adults from general practices in a study1 published in the British Journal of General Practice(BJGP).

Bipolar disorder often presents with depression and can be difficult to diagnose. People who have had periods of symptoms of high mood (such as increased energy and activity, increased confidence, over-talkativeness or being easily distracted) often don’t recognise these as significant and don’t tell their doctor about them.

This can lead to inappropriate treatment, such as the prescription of antidepressants without mood-stabilising medication, which might increase the risk of mood remaining unstable.

The study found that among people aged 16-40 years prescribed antidepressants for depression or anxiety, around 10% had unrecognised bipolar disorder. This was more common among younger patients and those who reported more severe episodes of depression. The study recommends that healthcare professionals should review the life histories of patients with anxiety or depression, particularly younger patients and those who are not doing well, for evidence of bipolar disorder.

Dr Tom Hughes, Consultant Psychiatrist at Leeds and York Partnership NHS Foundation Trust and the University of Leeds, said: “Bipolar disorder is a serious problem, with high levels of disability and the risk of suicide. When it is present in depressed patients it can easily be overlooked. Under-diagnosis and over-diagnosis of illnesses bring problems. Our General Practitioners are the greatest part of the best nationwide health service in the world. We hope this study will be of some help to them and to their patients in helping the better recognition of this important and disabling condition.”

Professor Roger Jones, Editor of the BJGP, said: “Dr Tom Hughes and his colleagues from Leeds and York Partnership NHS Foundation Trust recommend that general practitioners look carefully at patients with depression and anxiety disorders, particularly younger patients and those who are not doing well with their treatment. By reviewing life histories for evidence of symptoms this could provide people with better treatment and quicker recovery.”

Ebselen, a mimic of Lithium may be able to be used as a treatment for bipolar disorder: Effect of the Putative Lithium Mimetic Ebselen on Brain myo-Inositol, Sleep and Emotional Processing in Humans

Lithium remains the gold standard in treating bipolar disorder but has unwanted toxicity and side effects. We previously reported that ebselen inhibits inositol monophosphatase (IMPase) and exhibits lithium-like effects in animal models through lowering of inositol. Ebselen has been tested in clinical trials for other disorders, enabling us to determine for the first time the effect of a blood-brain barrier penetrant IMPase inhibitor on human central nervous system (CNS) function. We now report that in a double-blind, placebo-controlled trial with healthy participants, acute oral ebselen reduced brain myo-inositol in the anterior cingulate cortex, consistent with CNS target engagement. Ebselen decreased slow-wave sleep and affected emotional processing by increasing recognition of some emotions, decreasing latency time in the acoustic startle paradigm and decreasing the reinforcement of rewarding stimuli. In summary, ebselen affects the phosphoinositide cycle and has CNS effects on surrogate markers that may be relevant to the treatment of bipolar disorder, which can be tested in future clinical trials.

Bipolar Disorder Treatment: Brain Cells May Reveal Why Lithium Doesn’t Work For Everyone

There it is in a nutshell, folks: “Neurons are normally activated by a stimuli and respond. The cells we have from all six (bipolar) patients are much more sensitive in that you don’t need to activate them very strongly to see a response.”

Researchers took skin cells from 6 people with bipolar d/o. They made them turn into stem cells, which then differentiated into neurons. When they activated these neurons, they saw that neurons from people with bipolar d/o didn’t need a very strong stimulus to become activated. So our neurons can be activated by very weak stimuli. In other words we react much more strongly to things than people who don’t have bipolar d/o! Hunh! I think I already knew that! I do it all the time. I have extreme reactions to small stimuli! And now here is the reason, in black and white, our neurons fire at stimuli that wouldn’t make the neurons of people without bipolar d/o.

“Mitochondria — the energy producing powerhouse of the cell — were more active in the bipolar neurons.” This means that bipolar neurons also produce more, therefore have more energy.

“Cells from the patients who responded to lithium showed weakened excitability after growing in the lithium bath, while cells from patients who hadn’t been helped by the drug remained hyperexcitable. The findings didn’t explain why exactly lithium works in certain patients but not others, but it provided a great starting point for probing at what those differences are.”

So cells from people who respond to lithium show weakened excitability in response to lithium, whereas cells of people who don’t respond to lithium keep being hyperexcitable. Again a difference at the cellular level.

This is so amazing, because now for lithium resistant patients, they can test other medications to see which will decrease the hyperexcitability.

In one of the first studies to show how bipolar disorder affects the brain at a cellular level, researchers have discovered that the brains of people with the disorder are more sensitive to stimuli than those in people without it.

The findings, published in the journal Nature, also suggested the reason why some bipolar patients respond to treatment with lithium while others do not. “Researchers hadn’t all agreed that there was a cellular cause to bipolar disorder,” said Rusty Gage, a professor in Salk’s Laboratory of Genetics and senior author of the study, in a press release. “So our study is important validation that the cells of these patients really are different.”

Bipolar disorder, which affects over five million Americans, is characterized by severe mood swings between depression and elation. The disorder can be challenging to treat because when lithium doesn’t improve the mood swings, mental health professionals must piece together a unique treatment plan with antipsychotic drugs, antidepressants, and mood stabilizers. Oftentimes, though, these treatments only affect one of the mood extremes, not both.

For the study, Gage and his team recruited six bipolar patients and collected skin cell samples. They reprogrammed the cell samples into stem cells, then coaxed the stem cells into becoming neurons. These induced bipolar neurons were then compared to the normal neurons of healthy people.

“Neurons are normally activated by a stimuli and respond,” said Jerome Mertens, a postdoctoral research fellow and first author of the new paper. “The cells we have from all six patients are much more sensitive in that you don’t need to activate them very strongly to see a response.”

Mertens also noted that the mitochondria — the energy producing powerhouse of the cell — were more active in the bipolar neurons.

Three of the bipolar patients’ cells responded to lithium treatment, while the three others’ did not. The scientists tested how the cells reacted to growing in a liquid with lithium, and then remeasured how sensitive they were. Though all of the bipolar patients’ neurons had been more sensitive than healthy ones in the first test, this test showed they behaved differently after lithium exposure.

Cells from the patients who responded to lithium showed weakened excitability after growing in the lithium bath, while cells from patients who hadn’t been helped by the drug remained hyperexcitable. The findings didn’t explain why exactly lithium works in certain patients but not others, but it provided a great starting point for probing at what those differences are.

“Now that we have neurons that show differences in excitability, we can use them to screen for better drugs,” Mertens said.

For example, a new drug that reverses the hyperexcitability at a cellular level would likely be able to treat bipolar disorder in patients. The team plans to study the affected cells for longer periods to determine whether the hyperexcitability it measured is simply an initial manic phase or more long-lasting.

“After a few months, it’s possible that this hyperexcitability becomes too much for the cell to handle and it crashes into a less excitable state,” Gage said. “That could signal the shift between the depression and mania that patients experience.”

Source: Gage R, Mertens J, Yongsung K, Yu D, Pham S, Diffenderfer K, et al. Bipolar patients’ brain cells predict response to lithium. Nature. 2015.

“Could Depression Be Caused By An Infection?” I would say Inflammation…

More accurately, could depression be caused by inflammation? People with mental illnesses often experience autoimmune illnesses, meaning their immune systems are over reactive, so much so that they are reacting against their own bodies. I am a case in point, I have food “allergies”, where my immune system reacts to certain foods and then epitopes that look similar to it in my joints and I suffer from joint pain, especially if I eat dairy. Also my thyroid has been knocked out by my own immune system. I have antibodies (autoantibodies) against my own thyroid in my blood, this is called Hashimoto’s thyroiditis. Normally TSH (thyroid stimulating hormone) levels are 0.5 – 4 mIU/L, when I found out that my thyroid had stopped working, my TSH level was 102! Which meant that my pituitary gland kept making TSH to try to make my thyroid work, but unfortunately my thyroid had been disabled by my own immune cells and couldn’t “wake up”! I also have eczema, an autoimmune disease of the skin, thank goodness it’s not too severe. The composer Robert Schumann’s sister suffered from severe eczema and eventually committed suicide. I wonder how much depression played a part in this? I suspect it played a big part.

Another case in point, my mother, who suffered from drug resistant depression with bipolar II, also suffered from rheumatoid arthritis and lupus, both autoimmune illnesses. Same gene pool you say, well look at this article called “Autoimmune Diseases and Severe Infections as Risk Factors for Mood DisordersA Nationwide Study” from: In this study, Danish researches “found a strong correlation between infection, autoimmune disorders, and mood disorders, strengthening the hypothesis that depression is directly linked to inflammation.” Also from the same study “In a population-based study, Eaton et al found a 70% increased risk of developing bipolar disorder (n = 9920) within 4 years of an autoimmune disease diagnosis and a 20% increased risk in the time span from 5 years onward after the diagnosis compared with the background population.” This pretty significant. Why aren’t drug companies investigating this? A drug that is used widely called Lamictal, a treatment for bipolar II, actually increases the activity of the immune system, making people more prone to “the deadly rash” aka Stevens-Johnson syndrome, an immunologically induced rash which can be deadly if not treated. When I was on it (disastrously, I might add) between 2002 -2008, that was when my joint ache, tendonitis, bursitis problems started. And my mood became worse and worse until I had myself hospitalized at Columbia Presbyterian, and Lithium saved the day!

Moods, autoimmunity and inflammation, definitely related, I actually wrote a long discourse on this very thing in late 2008 in a manic phase, if I can find it and if it makes sense, I will post it here, In the meantime, pharmaceutical companies seriously need to start doing some research on autoimmunity, inflammation and mood disorders. Perhaps an email to my new friends at Astra Zeneca is in order 🙂


Could Depression Be Caused By An Infection?

OCTOBER 25, 2015 6:01 AM ET
Katherine Streeter for NPR

Katherine Streeter for NPR

Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn’t work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons.

Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer’s idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations.

Cotton ran with the idea, scalpel in hand.

Pulled Teeth Eliminate Hallucinations

This 1920 newspaper clipping from The Washington Herald highlights Dr. Henry Cotton’s practice of removing infected teeth to treat mental health problems.

A 1920 newspaper clipping from The Washington Herald.

Library of Congress

In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, “eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill.” Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society.

Following his death in 1933, interest in Cotton’s cures waned. His mortality rates hovered at a troubling 45 percent, and in all likelihood his treatments didn’t work. But though his rogue surgeries were dreadfully misguided and disfiguring, a growing body of research suggests that there might be something to his belief that infection – and with it inflammation – is involved in some forms of mental illness.

Symptoms Of Mental And Physical Illness Can Overlap

Late last year Turhan Canli, an associate professor of psychology and radiology at Stony Brook University, published a paper in the journal Biology of Mood and Anxiety Disorders asserting that depression should be thought of as an infectious disease. “Depressed patients act physically sick,” says Canli. “They’re tired, they lose their appetite, they don’t want to get out of bed.” He notes that while Western medicine practitioners tend to focus on the psychological symptoms of depression, in many non-Western cultures patients who would qualify for a depression diagnosis report primarily physical symptoms, in part because of the stigmatization of mental illness.

“The idea that depression is caused simply by changes in serotonin is not panning out. We need to think about other possible causes and treatments for psychiatric disorders,” says Canli.

His assertion that depression results from infection might seem far-fetched, or at least premature, but there are some data to bolster his claim.

Harkening back to Adolph Meyer’s early 20th century theory, Canli notes how certain infections of the brain – perhaps most notably Toxoplasma gondii — can result in emotional disturbances that mimic psychiatric conditions. He also notes that numerous pathogens have been associated with mental illnesses, including Borna disease virus, Epstein-Barr and certain strains of herpes, including varicella zoster, the virus that causes chickenpox and shingles.

Toxoplasma gondii, a parasitic protozoan, afflicts cats and other mammals. Acute toxoplasmosis produces flu-like symptoms and has been linked to behavioral changes in humans.

Toxoplasma gondii, a parasitic protozoan, afflicts cats and other mammals. Acute toxoplasmosis produces flu-like symptoms and has been linked to behavioral changes in humans.

Eye of Science/Science Source

A Danish study published in JAMA Psychiatry in 2013 looked at the medical records of over three million people and found that any history of hospitalization for infection was associated with a 62 percent increased risk of later developing a mood disorder, including depression and bipolar disorder.

Canli believes that pathogens acting directly on the brain may result in psychiatric symptoms; but also that autoimmune activity — or the body’s immune system attacking itself — triggered by infection may also contribute. The Danish study also reported that a past history of an autoimmune disorder increases the risk of a future mood disorder by 45 percent.

Antibodies Provide A Clue

The idea there could be a relationship between the immune system and brain disease isn’t new. Autoantibodies were reported in schizophrenia patients in the 1930s. Subsequent work has detected antibodies to various neurotransmitter receptors in the brains of psychiatric patients, while a number of brain disorders, including multiple sclerosis, are known to involve abnormal immune system activity. Researchers at the University of Virginia recently identified a previously undiscovered network of vessels directly connecting the brain with the immune system; the authors concluded that an interplay between the two could significantly contribute to certain neurologic and psychiatric conditions.

Both infection and autoimmune activity result in inflammation, our body’s response to harmful stimuli, which in part involves a surge in immune system activity. And it’sthought by many in the psychiatric research community that inflammation is somehow involved in depression and perhaps other mental illnesses.

Multiple studies have linked depression with elevated markers of inflammation, including two analyses from 2010 and 2012 that collectively reviewed data from 53 studies, as well as several post-mortem studies. A large body of related research confirms that autoimmune and inflammatory activity in the brain is linked with psychiatric symptoms.

Still, for the most part the research so far finds associations but doesn’t prove cause and effect between inflammation and mental health issues. The apparent links could be a matter of chance or there might be some another factor that hasn’t been identified.

Dr. Roger McIntyre, a professor of psychiatry and pharmacology at the University of Toronto, tells Shots that he believes an upset in the “immune-inflammatory system” is at the core of mental illness and that psychiatric disorders might be an unfortunate cost of our powerful immune defenses. “Throughout evolution our enemy up until vaccines and antibiotics were developed was infection,” he says, “Our immune system evolved to fight infections so we could survive and pass our genes to the next generation. However our immune-inflammatory system doesn’t distinguish between what’s provoking it.” McIntyre explains how stressors of any kind – physical or sexual abuse, sleep deprivation, grief – can activate our immune alarms. “For reasons other than fighting infection our immune-inflammatory response can stay activated for weeks, months or years and result in collateral damage,” he says.

Unlike Canli, McIntyre implicates inflammation in general, not exclusively inflammation caused by infection or direct effects of infection itself, as a major contributor to mental maladies. “It’s unlikely that most people with a mental illness have it as a result of infection,” he says, “But it would be reasonable to hypothesize that a subpopulation of people with depression or bipolar disorder or schizophrenia ended up that way because an infection activated their immune-inflammatory system.” McIntyre says that infection, particularly in the womb, could work in concert with genetics, psychosocial factors and our diet and microbiome to influence immune and inflammatory activity and, in turn, our risk of psychiatric disease.

Trying Drugs Against Inflammation For Mental Illness

The idea that inflammation – whether stirred up by infection or other factors — contributes to or causes mental illness comes with caveats, at least in terms of potential treatments. Trials testing anti-inflammatory drugs have been overall mixed or underwhelming.

A recent meta-analysis reported that supplementing SSRIs like Prozac with regular low-dose aspirin use is associated with a reduced risk of depression and ibuprofen supplementation is linked with lower chances of obtaining psychiatric care. However concomitant treatment with SSRIs and diclofenac or celecoxib – two other anti-inflammatories often used to treat arthritis – was associated with increased risk of needing hospital care due to psychiatric symptoms.

A 2013 study explored the antidepressant potential of Remicade, an drug used in rheumatoid arthritis. Overall, three infusions of the medication were found to be no more effective than a placebo, but patients whose blood had higher levels of an inflammatory marker called C-reactive protein did experience modest benefit.

“The truth of the matter is that there is probably a subset of people who get depressed in response to inflammation,” says lead author Dr. Charles Raison, a psychiatry professor at the University of Arizona. “Maybe their bodies generate more inflammation, or maybe they’re more sensitive to it.”

How infection and other causes of inflammation and overly-aggressive immune activity may contribute to depression and other mental illnesses – and whether or not it’s actually depression driving the inflammation — is still being investigated, and likely will be for some time. But plenty of leading psychiatrists agree that the search for alternative pathologic explanations and treatments for psychiatric disorders is could help jump-start the field.

“I’m not convinced that anti-inflammatory strategies are going to turn out to be the most powerful treatments around,” cautions Raison. “But I think if we really want to understand depression, we definitely have to understand how the immune system talks to the brain. I just don’t think we’ve identified immune-based or anti-inflammatory treatments yet that are going to have big effects in depression.”

But the University of Toronto’s McIntyre has a slightly brighter outlook. “Is depression due to infection, or is it due to something else?” he asks. “The answer is yes and yes. The bottom line is inflammation appears to contribute to depression, and we have interventions to address this.”

McIntyre notes that while the science of psychiatry has a long way to go, and that these interventions haven’t been proved effective, numerous approaches with minimal side effects exist that appear to be generally anti-inflammatory, including exercise, meditation and healthy sleep habits.

He also finds promise in the work of his colleague: “Like most cases in medicine, Charles Raison showed that anti-inflammatory approaches may benefit some people with depression, but not everybody. If you try on your friend’s eyeglasses, chances are they won’t help your vision very much.”

Have Hope

I am reposting this due to some technical difficulties with the original post.

This, my first video blog post, is for people who have been newly diagnosed  with bipolar disorder. Just know that there is hope. And if I can do it so can you. And yes, meditation, yoga, relaxation, all that is great for you but it can not take the place of medication, specifically a mood stabilizer.i mean if you had kidney disease, would you think yoga, meditation, and relaxation would make you all better? No, you would not, you would take medication for it. Well bipolar disorder is a disease and you need to take medication for that as well. So remember, mood stabilizers and Hope are what you need.

Research identifies biomarkers of suicide across psychiatric disorders

The ability to predict suicidal ideation by looking at the amount of expression of certain genes is quite amazing in and of itself, but what is really amazing is that lithium alters sodium transport and may interfere with ion exchange mechanisms and nerve conduction. Fluid and electrolyte metabolism are believed to be altered in affective disorders and this may be related to the therapeutic action of lithium. SLC4A4 is involved in sodium transport, and it is this protein which is a biomarker for suicidal ideation. Could this also be one of the key proteins involved in mental illness? Why isn’t anyone but me asking this question? Oh my goodness, I’m going to call my psychiatrist and run this by him. These relationships are not random, there is something quite important going on here. Na+ transporter protein predicts chances of suicide, Na+ influx and outflux, possibly the pumps that do this, are affected by lithium which treats bipolar d/o!  Read on please!

Researchers identified biomarkers of suicidal ideation across multiple psychiatric disorders and developed an application to help clinicians accurately screen for suicide risk. These researchers looked at the expression of different genes and changes in their expression between a no suicidal state to a high suicidal state, to see if one of them would signal suicidal ideation in bipolar d/o, major depressive d/o, schizoaffective d/o and schizophrenia. They looked at 217 males with bipolar d/o, major depressive d/o, schizoaffective d/o or schizophrenia.

What they found was that SLC4A4 was the best biomarker for suicidal ideation across all illnesses! This gene encodes a membrane protein transporter which transports sodium bicarbonate across cell membranes. Sodium bicarbonate cotransporters, like SLC4A4, mediate the coupled movement of sodium and bicarbonate ions across the plasma membrane of many cells. This is an electrogenic process with an apparent stoichiometry of 3 bicarbonate ions per sodium ion. SLC4A4 predicted suicidal ideation among participants with bipolar disorder with an area under the curve (AUC) of 93% and future hospitalizations with an AUC of 70%. Using questionnaires such as the simplified affective state scale (SASS) and Convergent Functional Information for Suicide (CFI-S) which measure suicidal ideation along with the biomarker SLC4A4, the AUC was 92% for all psychiatric diagnoses, 98% for bipolar disorder and 94% for future hospitalizations.

Understanding and predicting suicidality using a combined genomic and clinical risk assessment approach.

Worldwide, one person dies every 40 seconds by suicide, a potentially preventable tragedy. A limiting step in our ability to intervene is the lack of objective, reliable predictors. We have previously provided proof of principle for the use of blood gene expression biomarkers to predict future hospitalizations due to suicidality, in male bipolar disorder participants. We now generalize the discovery, prioritization, validation, and testing of such markers across major psychiatric disorders (bipolar disorder, major depressive disorder, schizoaffective disorder, and schizophrenia) in male participants, to understand commonalities and differences. We used a powerful within-participant discovery approach to identify genes that change in expression between no suicidal ideation and high suicidal ideation states (n=37 participants out of a cohort of 217 psychiatric participants followed longitudinally). We then used a convergent functional genomics (CFG) approach with existing prior evidence in the field to prioritize the candidate biomarkers identified in the discovery step. Next, we validated the top biomarkers from the prioritization step for relevance to suicidal behavior, in a demographically matched cohort of suicide completers from the coroner’s office (n=26). The biomarkers for suicidal ideation only are enriched for genes involved in neuronal connectivity and schizophrenia, the biomarkers also validated for suicidal behavior are enriched for genes involved in neuronal activity and mood. The 76 biomarkers that survived Bonferroni correction after validation for suicidal behavior map to biological pathways involved in immune and inflammatory response, mTOR signaling and growth factor regulation. mTOR signaling is necessary for the effects of the rapid-acting antidepressant agent ketamine, providing a novel biological rationale for its possible use in treating acute suicidality. Similarly, MAOB, a target of antidepressant inhibitors, was one of the increased biomarkers for suicidality. We also identified other potential therapeutic targets or biomarkers for drugs known to mitigate suicidality, such as omega-3 fatty acids, lithium and clozapine. Overall, 14% of the top candidate biomarkers also had evidence for involvement in psychological stress response, and 19% for involvement in programmed cell death/cellular suicide (apoptosis). It may be that in the face of adversity (stress), death mechanisms are turned on at a cellular (apoptosis) and organismal level. Finally, we tested the top increased and decreased biomarkers from the discovery for suicidal ideation (CADM1, CLIP4, DTNA, KIF2C), prioritization with CFG for prior evidence (SAT1, SKA2, SLC4A4), and validation for behavior in suicide completers (IL6, MBP, JUN, KLHDC3) steps in a completely independent test cohort of psychiatric participants for prediction of suicidal ideation (n=108), and in a future follow-up cohort of psychiatric participants (n=157) for prediction of psychiatric hospitalizations due to suicidality. The best individual biomarker across psychiatric diagnoses for predicting suicidal ideation was SLC4A4, with a receiver operating characteristic (ROC) area under the curve (AUC) of 72%. For bipolar disorder in particular, SLC4A4 predicted suicidal ideation with an AUC of 93%, and future hospitalizations with an AUC of 70%. SLC4A4 is involved in brain extracellular space pH regulation. Brain pH has been implicated in the pathophysiology of acute panic attacks. We also describe two new clinical information apps, one for affective state (simplified affective state scale, SASS) and one for suicide risk factors (Convergent Functional Information for Suicide, CFI-S), and how well they predict suicidal ideation across psychiatric diagnoses (AUC of 85% for SASS, AUC of 89% for CFI-S). We hypothesized a priori, based on our previous work, that the integration of the top biomarkers and the clinical information into a universal predictive measure (UP-Suicide) would show broad-spectrum predictive ability across psychiatric diagnoses. Indeed, the UP-Suicide was able to predict suicidal ideation across psychiatric diagnoses with an AUC of 92%. For bipolar disorder, it predicted suicidal ideation with an AUC of 98%, and future hospitalizations with an AUC of 94%. Of note, both types of tests we developed (blood biomarkers and clinical information apps) do not require asking the individual assessed if they have thoughts of suicide, as individuals who are truly suicidal often do not share that information with clinicians. We propose that the widespread use of such risk prediction tests as part of routine or targeted healthcare assessments will lead to early disease interception followed by preventive lifestyle modifications and proactive treatment.Molecular Psychiatry advance online publication, 18 August 2015; doi:10.1038/mp.2015.112.

My last post, definitely PTSD


Ok, my last post, definitely PTSD. I react just as wildly as my son does to his problems. I react with the unbridled fear of losing him. There I said it, that is truly what I am terrified of, losing my beautiful, super intelligent, loving, compassionate son. I am terrified of the unknown. And the PTSD comes from the past, from the known, from losing my brother to bipolar 1. From the biggest tragedy in mine and my family’s life. Is it going to happen again? Unknown. And the unknown, mixed with a terrible, fearsome known, the past, is not easy to live with.

But although my son has an initially extreme reaction, he calms down and takes care of the troubling issue perfectly. And he has NOT been diagnosed with any illness 🙂 But that’s the thing with PTSD, it is not based on the present, it is based on the past and the fearful phantoms that memories and past thoughts conjure up. How do you get over this? Talking to my ecounselor about this pronto, no prontissimo! Life is really short, half or more of mine is over. I want to live it in peace and enjoying all the positive, fun things it has to offer, not in the black dungeon of fear.


My mood may also be kicking up. From the season, the increase in Synthroid, not enough Lithium, don’t know, but knowing that my mood IS getting too elevated is half the battle already won and I’ll take care of it. Do i have this? Yes, I think I really do. Breathe…