Daily Archives: December 11, 2016

9 Startling Nutrient Deficiencies That Can Cause Depression

Pretty interesting! How wonderful it would be if one or more of these nutrients could alleviate one’s depression! If only it could be so easy, maybe it is…

http://www.curejoy.com/content/nutrient-deficiencies-cause-depression/

By Doug Cook

Deficiency of Omega-3 fats, Iodine, Zinc, Magnesium, Vitamin D, Selenium, Iron, B-complex and Vitamin C can trigger depression. The omega-3 fat DHA is critical for brain cell structure. Zinc improves digestive health promoting the release of serotonin and dopamine, magnesium helps produce vital enzymes and B-complex is required to maintain brain mass.

Working in Canada’s largest hospital for mental health and addiction, I absolutely appreciate the impact of lifestyle choices [diet/nutrition, stress reduction & leisure) on mental health including mood disorders like depression, seasonal effective disorder or SAD, anxiety and even bipolar disease.

As a nutrition educator, I routinely present on the topic of nutrition & brain health and food & mood. I review key nutrients that are absolutely vital for health brain; what we eat and drink directly affects the structure of the brain which, in turn, influences the brain’s function. This includes both the synthesis & function of neurotransmitters, as well as, the presence, or absence of inflammation.

The clients I work with are in recovery for drug [prescription & illicit] and alcohol addiction but essentially all of them are also dealing with mood disorders. It’s amazing to me how psychiatrists fail to appreciate the role of nutrition in mental health, including depression. It’s not only common sense but backed up by research that no amount of medication can make up for a crappy diet. The human body needs nutrients such as vitamins, minerals, essentially fats & antioxidants for vibrant health.

There is no biological or physiological need for Pristiq, Cymbalta, Wellbutrin, etc but there is for vitamin D, magnesium, iron and zinc for example.

It’s naive and unreasonable for anyone, doctor or patient, to think that one can be their best self, have optimal psychological and emotional health without addressing their underlying biology. Whether a person is using talk therapy, medication, or both to manage their mental health, there will be greater returns on investment, more bang for one’s buck if the physical health is addressed as well. Before anyone thinks I’m saying that medication don’t have a time and place in mental health is dead wrong. They do, but it’s important not to see the forest for the trees as they saying goes.

No amount of Paxil, Celexa, Lexapro or Viibryd will make up for an inadequate intake of iodine, B12, B3, folate or omega-3 fats or other nutrients.

Feeding Your Brain. Food and Mood

While there are dozens of neurotransmitters, many of which are produced in the gut as well as the brain, the three main ones that are talked about in mental health are serotonin, dopamine, and norepinepherine. The building blocks for these guys are amino acids derived from protein; a nutrient that most of use easily get in adequate amounts although they’re are exceptions [homeless, elderly, those with addiction]. The critical players in the synthesis and function of neurotransmitters however are vitamins & minerals. The analogy I like to use is a factory that needs a certain number of employees to show up for maximum output/production; if half call in sick, production suffers. Likewise for neurotransmitter production and function; we need optimal amounts of nutrients on a daily basis. If they are lacking in the diet, mood disorders, like depression, are more common and/or aggravated.

Optimize intake by improving diet and using targeted supplements, mood can improve and medication use reduced and sometimes eliminated according to loads of studies.

The star nutrient line-up includes

Omega-3 fats

The omega-3 fat DHA is critical for brain cell [neuron] structure. If the diet doesn’t have enough of it, other fats have to take its place. If it’s trans fat, that spells trouble. Trans fat increase inflammation and this increases the risk for depression. The other main omega-3 fat EPA helps with neuron function, as well as, reduces inflammation which is why research supports the role of omega-3 fats in improving symptoms of depression [and other mood disorders]. Food sources are fatty fish, omega-3 fortified eggs and supplements.

Iodine can be thought of as the new vitamin D. It’s an up and coming nutrient but not in a good way because it’s one mineral that most of use are not getting enough of. Iodine is critical for a healthy thyroid, the master of metabolism [i.e. cellular fitness]. It has largely been removed from the food supply and whereas we used to get about 800 mcg per day, most are lucky to get between 138 to 350 mcg per day. While this can stave off an overt deficiency, it likely won’t be enough to move people into the functional range where physiological processes are optimal including mental health. Good food sources include seaweed, cod, iodized salt. Other moderate food sources include milk, yogurt, and eggs. Good quality supplements should provide the RDA of 150 mcg as a foundation.

Zinc

Zinc is tireless ally. It is involved in over 250 separate biochemical pathways, or reactions, that support just about every function needed for best health, not the least of which is a strong immune system and mental well-being. Zinc is critical for neurotransmitter production and function. It is also needed for healthy digestion and as I mentioned a strong immune system, most of which is found in the digestive tract. A healthy digestive tract = optimal mental health since 90% of serotonin and 50% of dopamine is produced in the small intestines. Best food sources include oysters, crab, beef, lamb, pork, dark meat, chicken, legumes, cashews and a good quality multivitamin with minerals will have some as well.

Magnesium

Like zinc, magnesium is required for over 300 separate biochemical pathways, or reactions, needed for healthy bones & teeth, reduced anxiety, lower blood pressure, reduced risk for diabetes to name a few. Most of us only get about half of the recommended amount and the reasons are numerous; see post here, and here. Magnesium is needed to activate the enzymes needed for serotonin, dopamine and norepinepherine production. Good food sources include nuts & seeds, dark green vegetables, whole grains, bran and dark chocolate. Supplements are typically needed to help people meet their minimum daily requirement on a consistent basis. Supplements will also help increase magnesium intake that moves people with depression into that functionally optimal range where depression can be improved versus just avoiding a magnesium deficiency.

Vitamin D

Anyone who knows me or is familiar with this blog knows that vitamin D is my baby and that we don’t get enough of this vitamin, especially in Canada from mid-October till mid-April. The brain loves vitamin D and have loads of vitamin D receptors just waiting for their payload. I’ve written about vitamin D here, here, here, here and here. Vitamin D deficiency has not only been linked to depression, but anxiety, SAD, and dementia as well. Supplementation is the only viable option to raise vitamin D levels to where they need to be for optimal overall health but as well to lower the risk for depression. There is little natural food sources save oil/fatty fish like salmon, sardines, mackerel, herring and trout and eggs to a lesser extent.

Selenium

Like iodine, selenium is needed for good thyroid function; often, just increasing selenium intake can improve early symptoms of low thyroid function. A healthy thyroid supports mental health including reducing the risk for depression. Selenium is needed to convert the inactive thyroid hormone T4 to the active form T3; this conversion primarily occurs in the liver. Selenium is needed to make the master antioxidant and detoxifying compound glutathione. Increasing glutathione has been shown to improve depression likely because glutathione reduces inflammation in the brain. Good food sources Brazil nuts, fish, ham, shrimp, liver and chicken.

Iron

Iron deficiency is more common in women than men due to losses via menstruation. The most common form of anemia is iron deficiency and it’s symptoms are similar to depression: fatigue, irritability, apathy, brain fog, lack of motivation & appetite. Having a broad range of symptoms can lead to a misdiagnosis and aggravate any existing legitimate depressive symptoms. Good food sources are beef, pork, lamb, dark meat chicken, eggs, liver, oysters and white beans. Eating vitamin C-rich foods along with iron-rich foods helps to increase the absorption of iron. For women, a multivtamin with minerals typically provides 8 to 12 mg of iron. Men should choose a multi that is iron-free.

B-complex

Typically includes about 11 B vitamins all of which are involved in neurotransmitter production and function. Some, like B12 are needed to help maintain brain mass, a.k.a. prevent brain shrinkage, a cause of dementia. A classic B12 deficiency symptom is depression. Other important B vitamins for mental health include B1, B6, B3, and folate. Folate, along with B12 and B6 help to lower levels of homocysteine, a by-product of protein metabolism. Elevated levels of homocysteine increase the risk for depression. In order for dietary folate to be effective, it needs to be converted to its active form 5-MTHR however about 66% of the population don’t do this effectively because they have a mutation in the gene [5-MTHF reductase] that metabolizes folate into 5-MTHF putting them at a 180% increased risk for folate deficiency. Luckily this gene mutation can be tested for using a simple saliva DNA test called Nutrigenonmix. B vitamins are found in whole grains, nuts & seeds, dark green vegetables and meat.

Vitamin C

Believe it or not, I encounter scurvy in my practice today and it’s 2014; bleeding, swollen and achy gums all of which resolve within a week after the initiation of vitamin C supplements. But you don’t have to have scurvy to have functional vitamin C deficiency; an intake that is enough to prevent an overt clinical deficiency but not enough to allow one to function at one’s best. One of the more common symptoms of obvious or functional vitamin C deficiency is depression. Good food sources include citrus, kiwi, bell peppers and strawberries. However 20% percentage of the population can be functionally vitamin C deficient not only because they don’t get enough vitamin C from their diet but because they have a gene mutation that doesn’t allow them to absorb and metabolize it properly; putting them at a 150% increased risk of vitamin C deficiency. Luckily this gene can be tested for using a simple saliva DNA test called Nutrigenonmix.

The Role of Nutrients in Protecting Mitochondrial Function and Neurotransmitter Signalling: Implications for the Treatment of Depression, PTSD, and Suicidal Behaviours

In a nutshell, food feeds the brain. As an organ that accounts for 25% of our metabolic demands, the brain is in need of constant nourishment that can’t be met with a diet of crappy food. Having optimal mental health cannot be realized if the underlying biology of mood regulation, the structure and function of the brain, isn’t addressed. This is where very building blocks of vitamins, minerals and essential fats come into play. No amount of medication can make up for a lack of nutrients. Feeding your brain and an optimal sense of well-being is as close as your grocery store.


Caregiving Can Wear You Down #RealTalkAboutCare

Since Thanksgiving weekend, I’ve been sick with an upper respiratory infection (URI). As an asthmatic, URI’s tend to go to my lungs. My son, too, is sick and in bed (no way for a teenager to spend the weekend). URI’s…

Penguins in the Dark

This is an edition from 2013

I mainly ride on the road.  I haven’t been out on my Mountain Bike for quite some time.  There are different skills involved in riding off – road, for sure.  And, yes, I am much, much less experienced riding off – road, but there’s another – ideological – reason that I ride a Touring bike.  Riding amongst the traffic – and sometimes dozy pedestrians – means that I am at the heart of society, part of the life of the place. I hold the road, communicate with drivers, acknowledge others, and they acknowledge me, my place in the world, their world.

One of the symptoms I find most difficult is the sheer speed at which my anger flares. There is nothing unusual about this.  Anger management courses abound in the treatment of disorders like mine, believe me.  But that doesn’t mean I can’t get angry with good reason.

I got pretty angry recently, as a matter of fact.  With good reason.  Yet another car driver was lecturing me  – finger wagging included – on the well-worn theme of How Dangerous Cyclists Are.  Don’t worry, dear reader, I barely so much as missed a beat, as I was told (yet again) how dangerous cyclists are.

Let’s crunch some numbers. According to The Royal Society for the Prevention of Accidents in the United Kingdom (sorry to all my readers across the globe, but to include international statistics here is beyond the scope of this particular post.  I will return to what happens elsewhere in a future post). 107 cyclists were killed and 3,085 were seriously injured. These men, women and children were all hit by motor vehicles.  Virtually every single one of these people were hit by vehicles driven by people who failed to have additional (optional) mirrors fitted. Most were killed or injured at road junctions.

How many drivers are killed by cyclists in the United Kingdom every year? I hear you ask. I know of two cases in 2011.  Both were deadly cases of physical violence on the part of cyclists against motorists. I knew one of the victims.  His name was Tony Magdi.

You can see what I’m driving at.

People like me are pilloried twice over.  Once for being cyclists, out amongst the traffic, and then again for being – well, mad.  Sorry, that’s a technical term, I meant mentally ill.  That’s better…because we’re ill, aren’t we?  Infectious.  It runs in families, you can catch it by, by…..being a man born and raised in the United Kingdom of Afro – Caribbean descent.  Just check out the in – patient statistics for men diagnosed with Paranoid Schizophrenia in hospitals here.

Or by being a gay man. Oh no, that’s an out – dated, discredited view…isn’t it?

But I digress. What’s all this about penguins?

The other night I was cycling home – lit up like a Christmas tree, I might add – when in the light of the headlamps of the car wheezing up the hill behind me I saw two King Penguins waddling along the pavement ahead of me.

A moment later I saw them for what they really were: litter bins. I smiled to myself as I passed the traffic island, and swung left to allow the car behind me to overtake.

We can all think we see things that turn out to be, well, rubbish.

We’re not all Stephen Fry or Spike Milligan.  Some of us – even the suicidally depressed among us – are just trying to stay alive.

Epithalamium

You’re beeswax and I’m bird shit
. I’m mostly harmless. You’re irrational.
If I’m iniquity then you’re theft.
One of us is supercalifragilistic.
If I’m the most insane disgusting filth
you’re hardly curiosa.
You’re bubble wrap to my fingertips.
You’re winter sleep and I’m the bee dance.
And I am menthol and you are eggshell.
When you’re atrocious I am Spellcheck.
You’re the yen. I’m the Nepalese pound.
If I’m homesteading you’re radical chic.
I’m carpet shock and you’re the rail.
I’m Memory Foam Day on Price-Drop TV
and you’re the Lord of Misrule who shrieks
when I surface in goggles through duckweed,
and I am Trafalgar, and you’re Waterloo, 
and frequently it seems to me that I am you,
and you are me. If I’m the rising incantation
you’re the charm, or I am, or you are.
Nick Laird (1975 – )

Immune System Maintains Brain Health

Amazing! There are many ways that the immune system helps the brain and central nervous system (CNS). It used to be thought that the immune system was not in touch with the CNS at all, that the brain and the spinal cord were immune privileged sites. However, now, it is known that they are intimately in contact and the immune system has profound effects on the nervous system. One such effect is shown below. May more are in the article below.

  1. Mouse without T cells (immune cells) do not perform cognitive functions well!
  2. T cells’ procognitive effect is mediated by IL-4, an immune mediating molecule.
  3. IL-4 prevents macrophages from generating a proinflammatory signals that inhibit the production of a protein that is important in learning!

Immune System Maintains Brain Health

Once thought only to attack neurons, immune cells turn out to be vital for central nervous system function.

By Amanda B. Keener | November 1, 2016

In a dark room in Charlottesville, Virginia, a mouse swims in a small pool, searching for a place to rest. In 12 previous swims, with the help of visual cues and training from an experimenter, the mouse eventually tracked down a platform near the center of the pool. But just a day after its last swim, the animal is spending nearly as much time searching for the platform as it did on its first swim. The discombobulated mouse’s problem? It has no T cells.

“Mice without functional T cells do not perform cognitive tasks as well as wild-type mice do,” says the University of Virginia’s Jonathan Kipnis, who first demonstrated a link between the immune system and cognitive function in 2004 as a member of Michal Schwartz’s lab at the Weizmann Institute in Rehovot, Israel.1 He later discovered that T cells’ pro-cognitive effect is mediated by the cytokine interleukin-4 (IL-4), which prevents macrophages from generating proinflammatory signals that inhibit a protein important for learning and memory.2

Kipnis’s work is part of a wave of research changing the way scientists view the relationship between the immune system and the central nervous system (CNS). Until recently, the brain and the spinal cord were considered immune-privileged sites, strictly cordoned off from immune cells unless something went terribly wrong. Researchers knew, for example, that multiple sclerosis (MS) was caused by T cells that breach the selective border called the blood-brain barrier (BBB), enter the CNS, and attack the myelin sheath covering neurons. Even microglia, specialized macrophage-like immune cells that scientists had recognized as normal CNS residents since the 1960s, were mainly studied in the context of disease.

Saying the immune system is always good for the brain, it’s wrong; saying it’s always bad for the brain, it’s wrong. It depends on the conditions.—Jonathan Kipnis,
University of Vir­ginia

But over the past two decades, researchers have recognized that the entire immune system is very much a part of a functional CNS, with vital roles in cognition, injury repair, neurodegenerative disease, and sensory systems. Microglia pervade the CNS, including the white and gray matter that constitute the organ’s parenchyma. Other immune cells, including T cells, monocytes, and mast cells, reside in the brain and spinal cord’s outer membranes, known as the meninges, and circulate in cerebrospinal fluid (CSF).

“Ten or 15 years ago, it was all bad,” Serge Rivest, a neuroscientist at Québec’s Centre Hospitalier de l’Université Laval (CHUL), says of the relationship between the brain and immune cells. These days, he says, researchers are focused on understanding the good in addition to the bad and the ugly.

Injury patrol

IMMUNITY IN THE BRAIN: Until recently, the central nervous system was thought to be cordoned off from the peripheral immune system, but researchers now know that diverse immune cells—possibly by the millions—circulate in the cerebral spinal fluid and live in the brain’s outer membranes even in healthy individuals.
See full infographic: WEB | PDF
© 2016 TERESE WINSLOW LLC
As early as the 1980s, researchers knew that immune cells infiltrated the CNS after injury, but such immune activity was viewed as something to be stymied, not encouraged. In fact, doctors used corticosteroids, which suppress immune-cell activity, to treat brain injuries for many decades. But Schwartz says it didn’t make sense to her that tissues as indispensable as the brain and spinal cord wouldn’t take advantage of the immune system’s ability to protect against pathogens and repair damaged tissues. In the mid-1990s, she began searching for a positive neurological role of the immune system.

After nicking the spinal cords of rats, her team demonstrated that injecting macrophages at the injury site restored the animals’ motor function. The macrophages facilitated healing, as they are known to do in other tissues such as liver and muscle.3 (See “Immune Cell–Stem Cell Cooperation,” The Scientist, July 2016.) Around the same time, other researchers were finding that eliminating macrophages improved recovery from spinal cord injury in mice and rats.4 Because of this, Schwartz recalls, her work “was met with a high degree of skepticism.”

But over the next decade, Schwartz and others continued to unveil more ways that the immune system promotes CNS repair after trauma. Macrophages, for example, can damage neurons by secreting cytokines, proteases, or reactive oxygen species, but in rat and mouse models of spinal cord injury, they also produce transforming growth factor-beta (TGFβ), which promotes wound healing,5 and interleukin 10 (IL-10) which helps resolve inflammation.6 By the late 2000s, researchers recognized that different subtypes of macrophages can benefit neuronal growth in rodents, and that some were critical to recovery.7 Views also began to change on the clinical side after the 2004 Corticosteroid Randomization After Significant Head Injury (CRASH) study showed that corticosteroids didn’t help brain injury patients recover, but increased their risk of disability and death.8

More recently, research has revealed that it’s not just macrophages and other components of the innate immune system that help maintain CNS health; cellular drivers of adaptive immunity also contribute. In 2013, Schwartz and her colleagues demonstrated in mice that the lining of each of the brain’s four ventricles harbors memory T cells whose receptors bind proteins found in the CNS.9 Although these T cells are specific for CNS proteins, they don’t cause autoimmune disease. Schwartz contends that their specificity allows them to respond to local CNS damage.

Her team also showed that T cells present in this lining, called the choroid plexus, secrete cytokines such as interferon gamma (IFNγ), which allows selective passage of CD4+ T cells and monocytes from the blood into CSF within the ventricles.10 In a model of spinal cord bruising, mice deficient for the IFNγ receptor had reduced immune cell trafficking across the choroid plexus and poor recovery of limb movement. And last year, Kipnis’s team reported that IL-4 produced by CD4+ T cells in the CNS signals neurons to regrow axons after spinal cord or optic nerve injury.11

IN SICKNESS AND IN HEALTH: The immune system is a critical part of a healthy central nervous system (CNS), as well as the CNS’s response to injury.
See full infographic: WEB | PDF
© 2016 TERESE WINSLOW LLC
To better understand how different immune cells contribute to injury repair, Dorian McGavern, an immunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, is tracking responses to CNS injury in real time. Using two-photon microscopy to image cells below the surface of brain tissue in living animals, he and his colleagues have found that minutes after injury, microglia clear up debris in the parenchyma. “They’ll look around the environment, and basically start street-sweeping and picking up all the dead material,” McGavern says. Meanwhile, other immune cells remain confined to the meninges and to the so-called perivascular spaces between larger cerebral blood vessels and their sheaths of pia mater, the innermost meningeal membrane.

“When we watch the anatomy [after injury], we see that the microglia will stay in the brain parenchyma, and the neutrophils and macrophages will come to the lining of the brain and the perivascular spaces,” says McGavern.

When he and his colleagues prevented macrophages from entering the CNS by blocking receptors that respond to nearby cell damage, mice fared worse within the first 24 hours after injury.12 “In every case, we have created more injury and more [neural] cell death.” His team also found that microglia reinforce the BBB, which is composed of endothelial cells, pericytes, and astrocytes. Microglia fill in spaces left by astrocytes killed or damaged during injury. Without a robust barrier, McGavern says, unwanted immune cells may flood the parenchyma and do more harm than good.

Balancing health and disease

When Rivest first presented his work at a meeting, practically the whole audience lined up behind the microphone to make skeptical comments, he recalls. “I was really not well received there.” He adds that he himself was an early skeptic. “At the beginning, we were convinced that very strongly activated [immune] cells were bad for the brain, [but] it turned out that [they] prevent circulation in the brain of proteins that are neurotoxic.”

HUNGRY PHAGOCYTES: Monocytes (green) from the blood are attracted to amyloid deposits (red) in cortical veins of the murine brain. These cells help clear the plaques, improving the mice’s cognitive performance.CELL REPORTS, 5:646-53, 2013Looking beyond immune cells’ negative roles in neurological diseases has led researchers to some unexpected immune functions in the CNS, including the role for T cells in learning and memory that Kipnis described. Initially, he and his colleagues observed that mice without T cells are slower to learn in a water maze-based test of memory.1 The researchers could restore normal cognitive abilities to these mice by injecting them with wild-type T cells.20

In 2013, Rivest used two-photon microscopy to monitor monocytes in blood vessels of living mouse brains, and he watched as the cells migrated toward and cleared amyloid-β deposits within veins. When the researchers selectively depleted monocytes, the mice developed more amyloid-β plaques in the cortex and hippocampus.14 And when they knocked out the innate immune signaling protein MyD88, which mediates signals from several monocyte-activating receptors, the mice also experienced more amyloid-β accumulation, accompanied by accelerated cognitive decline.15

More recently, Rivest’s team found that microglia-forming monocytes are beneficial in a model of MS, where microglia are found within the inflammatory lesions. Last year, the researchers reported that inhibiting monocytes from entering the CNS reduced the clearance of damaged myelin and impeded proper remyelination.16

Schwartz has similarly found evidence for the immune system’s ability to protect against neurodegeneration. Last year, she and her colleagues reported that the choroid plexus epithelium was less permissive to immune cell trafficking in a mouse model of Alzheimer’s disease than in wild-type mice, due to anti-inflammatory signals produced by regulatory T cells (Tregs). They found that depleting Tregs in Alzheimer’s mice allowed macrophages and CD4+ T cells into the brain, reduced the number of amyloid-β plaques, and improved cognition.17 Similarly, blocking the T-cell checkpoint protein PD1, which normally supports Treg survival while suppressing the activity of other T cells, reduced amyloid-β plaques in mouse brains and improved the animals’ scores in a learning and memory water maze test.18

In 1996, Schwartz cofounded Proneuron Biotechnologies, which plans to test antibodies that target PD-1 in Alzheimer’s patients. This, she says, would be the first proinflammatory approach to treating a neurodegenerative disease, where immune activation has long been seen as a contributor to neural damage.

In addition to repairing neural injury, immune cells appear to play a role in fighting neurodegenerative disease.

But there’s a reason that scientists have believed that immune activity contributes to Alzheimer’s damage: microglia, perhaps best known for trimming back synapses, have the potential to become overzealous, and excessive synapse pruning can cause neural damage in a variety of CNS diseases. By blocking the cells’ proliferation in mice, Diego Gomez-Nicola of the University of Southampton in the U.K. has successfully alleviated symptoms of Alzheimer’s disease, amyotrophic lateral sclerosis, and prion disease. And earlier this year, Beth Stevens of the Broad Institute and her colleagues reported that inhibiting a protein that tags synapses for microglial pruning halted over-pruning and loss of synapse signaling strength in two mouse models of Alzheimer’s disease.19

“You’ll probably find just as many papers saying that microglia are good as microglia are bad,” says Gomez-Nicola, “and neither one nor the other is true.”

Rivest says a fuller appreciation of the benefits of immunity in the CNS could open a lot more doors for potential treatments than simply looking for ways to block inflammation whole hog. “The field is really moving toward that direction,” he says.

Behavior modification

Kipnis says regulation of stress may be linked to T cells’ role in learning. Stress can signal macrophages to secrete proinflammatory cytokines, some of which block a protein called brain-derived neurotrophic factor (BDNF), which astrocytes need to support learning and memory. CD4+ T cells in the meninges make more IL-4 cytokine after mice have been trained in a water maze—a stressful exercise for the animals—suggesting the signaling molecule might let macrophages know when the brain is dealing with the stress of learning something new, not the stress of an infection. “They tell macrophages, ‘Don’t overshoot,’” says Kipnis. In mice whose meninges are depleted of CD4+ T cells and thus deficient for IL-4, macrophages secrete proinflammatory factors unchecked in times of stress, disrupting their ability to learn and form memories.2

Last July, Kipnis and his colleagues also reported that mice lacking B and T cells were less social: while control mice spent more time investigating other mice than inanimate objects, immune-deficient mice had no preference.21 The researchers observed the same behavior shift in immunocompetent mice when they blocked a protein on T cells that facilitates migration to the CNS, or when they knocked out IFNγ, which Schwartz’s work has shown facilitates immune-cell migration through the choroid plexus.

HELP OR HARM: Mast cells (shown here) and other immune cells can support the health of the central nervous system and aid in injury repair and pathogen defense, but overactivation can lead to neural damage.© CNRI/SCIENCE SOURCEKipnis speculates about an evolutionary link between immunity and social behavior; IFNγ both encourages social activity and protects animals from many communicable diseases. He and his colleagues observed that IFNγ levels are highest in the brain tissue of social animals, such as rodents and zebrafish, when the animals are wild or housed in captivity together rather than individually, suggesting that social interaction and T-cell immunity in the CNS reinforce each other.

Others have proposed a link between behavior and innate immune cells called mast cells. Best known for their involvement in allergic responses in the upper airway, skin, and gastrointestinal tract, mast cells have been found in the meninges as well as in perivascular spaces of the thalamus, hypothalamus, and amygdala. They are known to quickly recruit large numbers of other immune cell types to sites of inflammation, and to play a role in MS. But mast cells also release serotonin into the hippocampus, where the molecule aids neurogenesis, supports learning and memory, and regulates anxiety.

Mice deficient in mast cells display deficits in hippocampal neurogenesis as well as in spatial learning.22 The animals also appeared more anxious, taking more time to enter an open space, for example.23 And Tufts University pharmacologist Theoharis Theoharides has found that human mast cells in culture respond to stress signals by releasing a growth factor that increases blood vessel permeability.24

Thus, like microglia, mast cells are a double-edged sword when it comes to neural health. It’s a reflection of the entire immune system’s love-hate relationship with the CNS, Kipnis says. “Saying the immune system is always good for the brain, it’s wrong; saying it’s always bad for the brain, it’s wrong. It depends on the conditions.”

Amanda B. Keener is a freelance science writer living in Winston-Salem, North Carolina.


Bonus Post: Poor? Mentally Ill? Sorry, You’re on Your Own

This is a post I wrote for my Et Cetera, etc. blog (janetcobur.wordpress.com), but of course it’s relevant here as well.

__________________________________________

Poverty and mental illness have something in common.

There is a stigma attached to both.

Both are seen as moral failings. If only people tried harder, worked more, improved themselves, they could lift themselves out of poverty. Without relying on anyone else’s help, which would be shameful.

And if only people stopped being so negative, looked on the bright side, smiled more, thought more about others, their positive mental attitude would make all those shrinks and pills unnecessary. They wouldn’t be shooting people with assault rifles and sucking up tax dollars for disability payments, which is shameful.

Society can’t afford poverty and it can’t afford mental illness. Why should we make the effort when the poor and the mentally disturbed don’t?

Why should these two conditions both be associated with such stigma and for such similar reasons? It’s simple. People don’t want to think that poverty or mental illness could happen to them.

The truth, however, is that a vast number of Americans are living one paycheck or one illness away from poverty, and one in four or five Americans will face a mental or emotional disorder at some point in their lives. And they are afraid. So they tell themselves that the conditions only affect Other People. And those people must be stupid or lazy or unmotivated or something, or they wouldn’t be poor or mentally ill in the first place.

And that’s where stigma begins.

And what are the consequences of stigma?

Well, first of all, it means that no one wants to spend money alleviating either condition. If these Other People can’t pull themselves up by their bootstraps and improve, the thinking goes, why should we pay them not to? Job training programs, child care, higher minimum wage, insurance coverage, community mental health centers, treatment programs for addiction, need to be paid for some way, but not with our tax dollars, by God!

And it means we don’t want to look at the Other People for fear of seeing ourselves. Don’t put halfway houses, group homes, unemployment offices, treatment centers, psychiatric hospitals, and other reminders in our neighborhoods. Not In My Backyard!

It’s not just a failure of compassion, though it’s that too. It’s not just a failure of the social “safety net,” though it certainly is that as well. It’s also a failure of the imagination – what would it be like if poverty or mental illness should happen to me? The reality is too unpleasant to think about, so don’t.

And while we’re talking about unpleasant, let’s mention the place where poverty and mental illness intersect – homelessness. Don’t we assume that homeless people are both poor and mentally ill? As such, spending money on them is doubly wasted. Why bother? It’s not like it’s going to help. Poverty, homelessness, and mental illness are incurable, after all. (Unless a person can cure their problems without outside help, of course.)

So what’s my stake in all this? Am I a bleeding-heart liberal do-gooder who wants to cure society’s ills and make us all foot the bill for it?

Well, yeah.

But I’m also living month to month on my income. My husband makes only a bit over minimum wage. We have both, at one time or another during our lives, been on unemployment and/or food stamps. We have no nest egg or emergency fund. It wouldn’t take much in the way of reversals to wipe us out. Even at that, we’re relatively privileged.

And I have a mental illness – bipolar disorder 2. Without insurance, I could not afford to see a psychiatrist, or buy medication (one of mine costs $800 per month), or get inpatient treatment if I ever need it. Right now my condition is moderately well controlled, but if I should suffer a setback, I might not be able to work at all. And there we are, back at poverty.

These two unfortunate conditions – poverty and mental illness – affect me directly, so I can’t look away and say they only happen to Other People. I know that they affect others more severely than they do me, and I don’t know how those people make it through.

But I do know that stigma isn’t helping any of us.


Filed under: Mental Health Tagged: mental illness in the news, news stories, public perception

More than a good ol College try

I’m trying my hand at art. I hesitate to call it that. Maybe it’s more like I’m trying to explore a creative outlet. I seem to be drawn to collage and mixed media. My loving husband often suggests it’s about the process, not so much the outcome. My perfectionism can get in the way of my enjoyment of things. I’m practicing letting go. Anything I’m doing, and I mean anything…laundry, washing my face, remembering medication, attempt at creativity..is more than I was doing pre-hospital.
I return to work tomorrow after 3 weeks off at one of the busiest times. I’m going to practice letting go. I can only do what I can do. One thing st a time. Whatever damn Mantra i can carry through the day. I want to return. I just want my response to the return to be healthy and productive. Fingers crossed!


Bipolar Robbed Me of Reading

I don’t remember a time when I couldn’t read.

Except when bipolar disorder took it away from me.

I was what they call a “natural reader” – someone who learns to read without being taught. Someone who just picks it up out of the air. And for me, reading was like breathing. It kept me going, kept me alive. Reading was part and parcel of my identity. I was never without a book within reach. I read while eating, walking down the hall, going to sleep, riding in a car.

Throughout my undiagnosed childhood years, reading was a way for me and my brain to play nicely together. If I was depressed, I could lose myself in escapist fantasy. If I was hypomanic, I could soar on adventures. And during the in-between times, I had access to unlimited worlds – places, people, situations, ideas, conversations – both familiar and strangely new. Reading was my joy and my solace.

For many years, reading was therapeutic. I could not only lose myself and escape the unpleasantness of my disorder for a time, I could learn more about depression and bipolar disorder, compare my experiences with those of others who struggled with mental illness, discover how medicine and law and psychology and sociology could shine a light on my experiences. I could even (God help me!) read self-help books, which were popular at the time, and learn all sorts of theories and techniques that didn’t improve what was wrong with me.

Books and words were my life. I got degrees in English language and literature. I read for work and for fun. I edited magazines, wrote articles and (occasionally) children’s stories, worked on textbooks.

Then my brain broke and reading went away.

I had a major depressive episode, which lasted literally years, and during that time I found it nearly impossible to read.

Why? My old companions, depression and hypomania.

Depression made me dull. I didn’t care about anything and found no happiness even in the books that had always been my refuge. I remember picking up a book that I more than loved and had returned to dozens of times, that had shaped my life in many ways, thinking that the familiar words would touch something still buried inside me. But this time there was no magic. Not even interest. The words were flat and dull, mere ink on the page. Reading – engaging with an author’s ideas, imagining characters, following plots and dialogue, discovering facts – was beyond me.

And hypomania? My version, instead of bringing euphoria, brought anxiety – an overwhelming twitchiness and fear of the unknown, jumping not just at shadows, but at the idea of shadows, things that had never happened. My attention span shrank to nearly nothing. I could barely read a few pages, not even a chapter, and when I was finally able to get back to a book, I was lost, disconnected.

Now that I am recovering from that episode, I am glad to say, I can read again. I read myself to sleep at night once again instead of crying myself to sleep. I devour entire chapters, keep at least two books going at once (one fiction, one nonfiction), delight in revisiting old favorites and seeking out new authors and genres (YA fiction and steampunk) and topics.

Not everything I read is uplifting. At the moment I’m deep in Octavia Butler’s Parable of the Talents, a post-apocalyptic science fiction dystopia that is eerily prescient for a book published in 1998. But I can tell when it’s getting too deep and frightening and switch off to Jasper Fforde’s Thursday Next literary fantasy Lost in a Good Book before the strife and struggle can drag me down.

And I can tell you this: It’s better to be lost in a good book than lost in your own broken brain.

 


Filed under: Mental Health Tagged: anxiety, bipolar disorder, bipolar type 2, books, childhood depression, depression, hypomania, my experiences, reading