Friday, November 1, 2013

Gluten and Schizophrenia Again (with an added splash of Toxo!)

Researchers have been chasing the elusive links between gluten and major mental illness for decades. Despite some hyperbolic coverage in Wheat Belly and slightly more convincing coverage in Grain Brain, there is, so far, quite a bit of smoke, but no fire outside a few case studies. Curt Dohan had quite a few papers back in the day (including this one), and much more recently Faith Dickerson, now armed with antibody titres, could be more precise (including in this paper).

In the last couple years the rather stunning data from the CATIE trial (a very large multi-center study of schizophrenia treatment run by NIMH in the last decade) that schizophrenics were 5X as likely to have anti-tTG antibodies as healthy controls and over 7X the likelihood of having high AGA (antibodies to gliadin) compared to normal controls has made more researchers take notice. Yet on face, all we could really say is, wow, a certain subset of people with schizophrenia sure do have some suspicious antibodies to different wheat proteins, and it is pretty clear that devastating neurological illness can be caused by gluten (dystonias in some people, for example) without the classic celiac gut findings, but is the issue in schizophrenia a leaky gut (thus higher antibody titres to certain food moieties) or the wheat itself, or both? I covered these questions in a bit more detail here.

One major issue with the theory that wheat causes schizophrenia is that schizophrenia seems to have a similar prevalence in gluten and non-gluten eating areas, but since "schizophrenia"is pretty clearly recognized as a final common pathway for a number of different genetic and environmental pathologies, it wouldn't necessarily torpedo the gluten theory. Now, finally, we can test whether gluten-free diets help symptoms in the subset of schizophrenics who have suspicious wheat antibodies. The newest round of researchers, led by Jessica Jackson (along with Alessio Fasano) at the University of Maryland and Emily Severance at Johns Hopkins, are following these leads.

Come A Little Closer: Cage the Elephant

First off, we have "A gluten-free diet in people with schizophrenia and anti-tissue transglutaminase or anti-gliadin antibodies." This paper starts off with discussing the mixed results of previous trials (7 in all) of gluten-free diets in schizophrenia, showing a subset with real improvement (and some with remission, which is an astonishing finding), but many without improvement whatsoever. None of these studies tried to differentiate schizophrenics with or without anti-tTG and AGA, mostly because they were done before these titres were available. The paper makes the distinction that anti-tTG antibodies are more likely to signify celiac disease, whereas AGA is more likely to signify non-celiac gluten sensitivity. In the current paper, exactly two patients with schizophrenia (one woman symptomatic since 1976 and a man symptomatic for the past 8 years) and positive antibody titres (one for anti-tTG and one for AGA) who were stable on medicines but still symptomatic (pretty common) were put in an inpatient unit and observed on a gluten-free diet for two weeks.

The woman had improved concentration and attention (critical, because psychotic symptoms often respond relatively well to medication, but poor executive functioning, attention and concentration are not so responsive, and those deficits keep many people with schizophrenia from being able to function independently). The man had some reduction in psychotic symptoms and increased insight into his condition. Since schizophrenia is a progressive neurodegenerative disease, seeing improvement, particularly in the woman who had been sick since 1976 from a non-medicine intervention in two weeks' time is at the least interesting.

The limitations of this study are profound. Open label, about as tiny as you can get, and obviously taking someone and sticking him or her in an inpatient unit with structure and observation is an intervention all on its own. But the level of improvement was enough that Schizophrenia Research (not the topmost tier of psychiatry journals, but certainly no Medical Hypothesis) published the paper, and it is available free full text on pubmed if you care to click the link above.

The second paper was sent to me by the amazing Victoria Prince (who just finished her last rotations in medical school. Woo hoo!) I love this paper, and I want to give Emily Severance a hug just for the ideas it brings together. She already deserves a hug for the previous paper I discussed in this article: Schizophrenia and the Gut. We know schizophrenia is multitudes, it's complex, it's genetic and environmental and immune-mediated. Ergo: Anti-Gluten Immune Response following Toxoplasma gondii Infection in Mice. (I know, mice.) It's also available free full text over at PLOSone.

Anyway, we already know that folks with schizophrenia have higher levels of gut inflammation (measured by checking antibodies to known infections that get into the system when there is gut inflammation or infections that actively cause gut inflammation, such as our old friend Toxoplasma gondii), and the newer the onset of illness, the more likely you are to find gut inflammation, AND the more antibodies to gluten and casein you have, the more likely you are to have these signs of gut inflammation. So Dr. Severance sought to answer some of the questions raised by this finding. Did the infection cause a gut pathology that allowed neurotoxic food fragments to attack the brain of the genetically susceptible? Were the infections themselves the problem in the brain, and the food antibodies just secondary to the infections? Well, it is difficult (not to say unethical) to do the sorts of experiments you need to answer these questions in humans, but mice can be housed and infected and their little immune systems examined in greater numbers over several generations more readily.

So the researchers took mice and gave them delicious T gondii infected rodent chow (via infected ground up mouse brains!!). They infected some adult mice and a subset of female mice who were then knocked up so they could check the pups for gut inflammation as well…there are a lot of mini-experiments in this paper and I won't explain them all to death here, as the paper is freely available. Anyway, after infection with T gondii, serum antibodies to wheat proteins and complement activation (not a sign of well-bred mice but rather a measure of inflammation) increased in the infected groups but not in the mock-infected or uninfected groups. The anti-wheat antibodies in mouse pups born to the infected moms were also significantly higher than in those born to uninfected mouse moms.

So here we have proof, in mice, that infection with Toxoplasma, a known risk factor for schizophrenia in humans, leads to the generation of anti-gluten antibodies, presumably via a gut inflammatory mechanism. Most importantly, in the mouse pups, the anti-gluten antibodies and infection happen at a time of critical neurodevelopment. Thus the combination of infection and, perhaps, a dietary enhancer (such as, possibly, gluten) could be working in concert to make someone vulnerable to developing schizophrenia later on. The "gut inflammatory" mechanism is vague at this point. In celiac disease in humans (more associated with the anti-tTG antibodies), there is definitely gut damage and permeability. In non-celiac gluten sensitivity (more associated with AGA), there doesn't seem to be frank leakage, but apparently large gluten peptides can cross the border via transcytosis and this may happen more readily if the gut is infected and the immune system is on the case and things…frankly the exact details of gluten and the gut continue to elude us. Check out the last paragraph of this paper (BIG HUGS):

In summary, the models described in this paper provide appropriate experimental tools to examine the impacts of gluten peptides, T. gondii and associated immune activation on brain physiology. As we accumulate more information from analyses of clinical biomarkers, we can adapt these animal models to test the effects of dietary modifications and other types of infections on behavioral endpoints, the pharmacological outcomes of specific antipsychotics on immune system parameters, and the autoimmune response responses triggered by T. gondii infection. Ultimately, we envision a translational system by which we can fully evaluate the interface of environmental perturbation and genetic predisposition as it relates to serious neurodevelopmental disorders such as schizophrenia, bipolar disorder, and autism.

I've never been a very linear person; I tend to absorb and think about things all at once. That's part of what I like about my so-called Evolutionary Psychiatry. We can think about lots of things at once as they impact physiology, immune activation, and genetics. The researchers who also seem to think this way, but can also break down these questions and not leave gaping holes (Severance's previous experiment where she took the trouble to go across the ocean to study gut and immune activation in medication naiive and medicated schizophrenics, taking out a major confounder in most schizophrenia research in the US) are the kinds of thinkers we need who can do good science to work out these big complex tangles. I can't wait for the next papers to come out. In the mean time, there is no clinical guidance. Is it worth checking your schizophrenics for anti-tTG and AGA? What are the risks of recommending a gluten-free diet and what is the likelihood it will be strictly followed in an outpatient setting?

Always, more questions than answers.

Thursday, October 31, 2013

Get Your Sleep On

New post over at Psychology Today about the possible benefits of sleep flushing the brain like a cranberry bog harvest. And some gluten and psychosis and toxoplasma mash-up here in the next couple of days, once I clean the house and get all the candy and mouldering pumpkins put away.

Even Michael Stipe thinks sleep is important in this odd homage to the 7th interval…

Happy Halloween! Don't let the goblins bite.

Sunday, October 6, 2013

Heart Rate Variability, Pig Roasts, and Other Randomness

Brand new post is up at Psychology Today:

Depression and a Broken Heart

It is an introduction to the concept of healthy heart rate variability, about which Grayson Wheatley had a featured talk on the first day of AHS13, and he graciously helped me with research for the article. I'm hoping to do a little series on it with some more technical articles here if I have the time.

I just noticed the Psychology Today Evolutionary Psychiatry Blog has been viewed over a million times, which is heartening. Both Your Brain on Ketones and Magnesium: The Original Chill Pill have over 100,000 views. In fact all the older posts have several thousands of views, except A Case of Scratchy Mice, so click on that and give that post some love too.

Sleigh Bells: Bitter Rivals

What has been keeping me busy besides kids, teaching, and paying the bills? Well, I'm working on an academic chapter for an ancestral health textbook, running 5Ks in the dark (fun but very strange, like a fitness rave), and attending pig roasts (another special thanks to Diana Rogers for inviting my family to the amazing Clark Farm, and I can't wait for her next book to come out!). All usually live-tweeted for the psychoanalysts out there.

Electric Run, Gillette Stadium, Boston

The mobile chicken coop at Clark Farm.

The pig. Now in my belly.

Other stuff: The Paleo Manifesto is out, at last. I was able to read a pre-release copy in July and loved it. John Durant makes his journey personal, likable, and pertinent to any modern Western human. He shines new light on the long historical path that we took to get to the here and now, and how we can use those lessons to be healthier, saner, and live a little more naturally wild. It isn't another diet book and is definitely worth a spot on the bookshelf.

Also reading Grain Brain, which is aptly named and seems like it would be just my sort of thing, but so far, I'm not all that happy with it. I will post more if it turns around and by no means is this little blurb to be considered a full review. Dr. Pearlmutter is a neurologist with extensive training and clinical experience in nutrition, but he is militantly anti-carb and suggests everyone keep to less than 60 grams of carbohydrate a day. He states this amount is "one serving of fruit" daily though my nutrition trackers will put a banana at 30 grams and an apple at 34 grams. I'm all for the therapeutic benefit of ketogenic diets and very low carb diets for those who thrive on them, but not everyone will, particularly those who participate in certain types of athletics (like myself) that require a lot of glycolytic work (CrossFit, ahem). I don't think 100 grams of carbs a day, for example, will actively rot your brain in most circumstances. I'm crossing my fingers the book will get better and there has got to be some useful information in there.

The other books I'm looking forward to: Well Fed 2 and Chris Kresser's Personal Paleo Code.

Here come the sheep at a real farm to table experience:

Sunday, September 22, 2013

More Zinc Nitty Gritty

On the personal front we are going full speed ahead into fall, school, apple picking, corn mazes, and sweater weather. I also decided to participate in a little n=1 experiment of caffeine elimination for 24 days along with Dallas Hartwig, who apparently does an elimination of this sort at least once a year. He drinks quite a bit of coffee and the occasional detox seems prudent. For me, I figured there wouldn't be much difference in my life with or without caffeine. I rarely drink coffee, and a typical day will see me drinking 0-3 cups of tea, most days one. Since I could skip a day of caffeine without even noticing, I imagined there wouldn't be caffeine withdrawal.

I was surprised about 52 hours after my last dose when the classic headache and a combination of irritability and cognitive fog set in. (Withdrawal can begin as early as 12 hours, typically peaks at 48 hours, and can last 2-9 days total). Mine lasted about 6 hours until I went to bed, and it was gone the next morning. Over the next three weeks, I noticed my sleep was improved, muscle tension was noticeably decreased at the end of a clinic day, and I missed caffeine the most on Monday mornings, Wednesday afternoons (not surprising, my longer clinic day), and, unexpectedly, Sunday mornings. For the first week and even into the second I still didn't feel quite as "sharp," though that feeling began to pass a little by the third week. The experiment ends in a couple of days, and I have plans to moderate my caffeine intake a little more than I did before. Maybe 3 days a week instead of most days a week (thinking of those "most missed" times), and probably won't exceed a single cup of tea. All told, I learned some things, and I'm glad I did the experiment. Probably a worthy one for most people to do, as long as the withdrawal isn't too debilitating.

Last week we left off with some review of zinc, before that a bit of a review of the pathophysiology of depressive disorders in the brain. Today I would like to tie that together from the most recent review article and then discuss the overall human clinical data about zinc as an antidepressant.

Damage to the brain in major depression in the hippocampus seems to occur in part due to overstimulation of the NMDA receptors (by glutamate or similar substances). The overstimulation leads to a large influx of calcium molecules into the cells which results in damage to the neurons and can stimulate programmed cell death. Zinc can turn off this cascade to some extent, because it is a non-competitive inhibitor of the NMDA receptor, which means it keeps the receptor from being quite as easily activated. Thus it could potentially decrease the amount of damage done during a period of high stress.

In addition, zinc spurs the production of the brain fertilizer, BDNF, in the hipocampus, leading to recovery, nerve regeneration, and repair. Below is a modified diagram from the review similar to the ones I posted a couple of weeks ago with much of the zinc penciled in (IN COLOR. hah). For more step by step explanation, please go back to my previous post. Click the diagram to make it larger.

So now, the human data, which works better as a list:

1) In healthy humans, zinc levels in the central nervous system and in the serum tend to be equivalent with free passage through the blood brain barrier.
2) A post-mortum study of schizophrenic patients showed 50% reduction in brain zinc (particularly in the hippocampus) compared to controls.
3) In neurodegenerative diseases, reductions in brain zinc tend to be higher than reductions in serum zinc.
4) Numerous studies link lower serum zinc levels to increased depression scores on a rating scale (there is even some linear correlation, making zinc a reasonable candidate as a biomarker for depression).
5) Zinc levels are lower in treatment resistant patients (in some but not all studies).
6) Patients whose depression improves also have recovery of zinc levels.
7) People who are depressed tend to have lower zinc levels and lower zinc intake (eating less meat, fish, and legumes, and I'm assuming oysters), but hospitalized depressed patients fed the same diet as controls also had lower zinc levels than the controls.
8) Intense, competitive, anxious "Type A" personalities tend to excrete more zinc under stress than the more laid back, "Type B" sort of person.
9) Zinc is excreted in hyperactive kids exposed to artificial food dyes but not in kids who weren't hyperactive in a small study.
10) Zinc supplementation can increase testosterone in zinc-deficient men, and low testosterone is associated with depression.
11) In several (small) randomized trials, zinc (25mg) plus an antidepressant elicited a more robust recovery than antidepressnt alone. Similar results have consistently been found in animal models.

Still, more data is needed, and more information is needed about the genetic differences in people in zinc absorption, sequestration, and secretion in healthy and unhealthy states. The upper limit of recommended zinc intake is 40mg daily, the recommended daily allowance is around 11-12. Temporary supplementation of less than the upper limit during a stressful period seems low-risk, but there is still much to learn.

Sunday, September 15, 2013

Zinc at Psych Today

Terribly busy between back to school (both kids now have homework!) and my sister getting married last weekend (which required me to be a bridesmaid and also to supply a few adorable flower girls and some quick cross-country flying and jetlag). Also trying to get in our American Psychiatric Association Annual Meeting abstracts on time…my medical school class starts next week panic yet?

I'm still working on the nitty-gritty of zinc and depression from the last paper, but for a review: Zinc! An Antidepressant? at Psychology Today, so each click supports my research, writing, and the blog.

Appropriate new (amazing) song: Hurricane.

Trying to keep active and getting the girls out of doors as much as possible before the winter closes in. Not enough time for writing and thinking, but as always, those are luxuries, particularly in modern times. Doesn't that seem backwards? It seems to me there should be more time for leisure.

Keep eyes peeled for more on zinc and the pathophysiology of depression.

Friday, August 30, 2013

Pathophysiology of Depression and Happiness

I'll be on the Creative Live video podcast later today (3pm pacific, 6pm eastern) on the topic of happiness (Dave Asprey invited me to participate, and while he is going into some of the technology he uses to monitor his brain and functioning, I'll be talking about some of the research about happiness and different Eastern and Western perspectives.)

Just going through an amazing review from Neuroscience and Biobehavioral Reviews: Potential roles of zinc in the pathophysiology and treatment of major depressive disorder. I'm going to do an updated zinc post (which is why I pulled the paper), but it does have a terrific and concise review of the biology of depression and, as it happens, happiness. Though this biochemistry will not be part of the talk later today. Suffice it to say (click the diagrams to make them bigger if you like):

So diet provides the amino acid tryptophan, but circumstances can push the metabolism in two directions, toward the neuroprotective, neurogenerative and repair pathway (via serotonin and melatonin) or to the neurotoxic pathway. Stress and inflammation tend to favor the production of kynurenine, which can become quinolinic acid (a potent oxidative agent and neurotoxin) or kynurenic acid (which can go both ways, more on that in a bit).

On the neurotoxic pathway, quinolinic acid triggers the release of glutamate via alpha 7 nicotinic acetylcholine receptors and may also directly stimulate the NMDA receptors. High levels are associated with reduced neuronal growth and repair in the hippocampus of the brain along with markers of neuronal injury. Kynurenic acid, also made from kynurenine, can ameliorate this pathway somewhat by modulating the activity of these alpha 7 nicotinic receptors, but in the wrong amounts kynurenic acid can be neurotoxic as well. In layman's terms you get depressed mood, irritability, suicidal thoughts, memory problems, poor resistance to stress, dysregulated energy metabolism, poor sleep or unrestorative sleep. Poor motivation and reduced concentration. The brain just doesn't function well.

On the bright side you get serotonin and melatonin supporting sleep, appropriate circadian rhythms, appetite and hormonal regulation, and then the effects of reduced excitotoxicity via various receptors and components including 5-HT1A, leading to good memory, good neuronal plasticity (which permits adaptation to new experiences and stimuli), and appropriate levels of brain derived neurotrophic factor and dopamine (some of these are mediated by insulin growth factor 1 by the way) toward neurogenesis and neuroprotection. So here we have good memory, good sleep, regulated energy metabolism, positive outlook, motivation, serenity, and appropriate resiliency to stress.

My apologies for the low tech diagrams, but hey, this is a free blog after all…zinc, by the way, plays a role at almost every level in these pathways. But more on that in a bit!

Sunday, August 25, 2013

Does Soda Rot Your Brains Along With Your Teeth?

This study made big news last week, but I was in the midst of AHS13 in Atlanta, and besides the normal conference exhausting insanity, I also had either food poisoning or some sort of gastroenteritis. Only now I'm recovered enough to unbury myself (more or less) from the usual home and work chores.

U2 Some Days Are Better Than Others

I'll do a companion post on AHS13 and my talk there in a bit, but I did want to do a quick review of the horrifying study tracking soda consumption in 5 year-olds. The study was part of a Fragile Families and Child Wellbeing cohort of about 3000 urban US children and their mothers from 20 different cities. The sample is 51% African American, 28% Hispanic, and unmarried mothers outnumber the married ones 3:1. In this cohort,  43% of the 5 year old children consumed at least one soda per day, and 8.2% drank three or more servings a day. Those who did drink 4 or more sodas daily were over twice as likely to destroy things belonging to others, get into fights, and physically attack people, and violence across the cohort linearly correlated with the amount of soda consumed. We've seen a similar pattern in a previous study of adolescents. No one has measured it in young children before.

Covariates included violence in the home, fruit juice and candy consumption, obesity, maternal education, and hours of TV watching, and when the statisticians took these confounders out, the correlations between violence and soda consumption still held. Perhaps the most interesting bit of the study is that fruit juice consumption was correlated with less aggression and candy with mildly increased aggression, so sugar itself is clearly not the whole story here. The authors had all sorts of guesses as to what might be going on, but with the observational nature of the study they are only hypotheses. The main theory is the magical combo of preservatives, caramel coloring, caffeine, and sugar is a quick ticket to aggression and wild swings of blood sugar (though blood sugar wasn't measured). Since soda consumption is also correlated with depression in adults, and depression in parents is correlated to behavioral problems in offspring, high soda-drinking moms might be depressed with high soda-drinking aggressive kids.

Regardless of the whys and wherefores, one doesn't have to go too far out on a limb to say that giving kids soda is a lousy idea, and that the sugar alone is not the problem or only a piece of it (despite my fondness for the fructose malabsorption theory).

Times have changed… (from Gene Simmons Twitter feed) via Mark D. White

Friday, August 9, 2013

Sunshine and Sad Hamsters

First off, I can't believe this blog is over three years old. Figured that out when I linked an old zinc post, because I completely missed the three year anniversary a few months ago. In any event over the past three years I have seen a greater acceptance of employing grain-free diet interventions along with avoiding processed food, and some more skepticism of the "vegetable oils are heart-healthy" meme.

For example, I missed the December 2011 of Prostaglandins, Leukotrienes, and Essential Fatty Acids (I must admit, not on my regular reading list), but there was an interesting back and forth over a study and a few letters to the editor that were pro modulating the omega3/6 ratio over dumping massive amounts of omega 6 into the diet and making up for that by supplementing with omega 3. The main gist of the editorials was that we don't really know what the heck we are doing when it comes to downstream regulation of omega 6 fatty acids and maybe we should be cautious about eating so much of it. It's nice to see lipid researchers admit that, though letters to the editor are all about some cranky academics espousing their objections to some of the status quo out there.*


In addition, the University of Maryland is trying to put together a study to test gluten-free diets in schizophrenia, following on the interesting findings from the CATIE trial that showed folks with schizophrenia were so much more likely to have antibodies to wheat proteins than the general population. Worth a shout out.

But enough about nutrition for now. I really did intend to have more about other evolutionarily appropriate common sense interventions for mental health in this blog, and this week a study came out that fits the bill, at least for hamsters: Nocturnal Light Exposure Impairs Affective Responses in a Wavelength-Dependent Manner.

Flickr Creative Commons
In order to make sense of this study we have to know a little bit about the retina of the eye. Most people are aware that we have light receptor cells in the retina called rods and cones. There is a third set of light receptors in the retina as well called the photosensitive ganglion cells (otherwise known as the intrinsically photosensitive retinal ganglion cells, or ipRGCs), and these cells have the specific job of sending light information back to the suprachiasmatic nucleus in the brain, where circadian rhythms are controlled. The photopigment in these cells, melanopsin, is particularly excited by blue light, of wavelengths around 480 nm. That means that blue light, above other light, is the most likely to send the signal to the brain that it is daytime. Since blue light is nice and bright and makes for nice contrast with cheap LEDs, it is one of the colors of choice for computer screens, tablets, and smartphones. It's also one of the key wavelengths in light from compact fluorescent bulbs that are all the eco-rage nowadays. 

So, as we probably know by now, picking up that phone to send a tweet in the middle of the night is also telling your circadian rhythm part of the brain GOOD MORNING, which the suprachiasmatic nucleus finds confusing, in humans and in hamsters. The ipRGCs not only send signals to the hypothalamus to regulate sleep, appetite, fertility, etc., but also to the limbic areas of the brain, wherein lives anxiety and fear.

In the paper, hamsters were exposed to white, blue or red light (red does not activate the suprachiasmatic nucleus) or left in the dark at nighttime. It is important to know that hamsters are nocturnal, but behavioral changes have been observed in diurnal rodents as well when exposed to white or blue light after dark. The hamsters who were exposed to the white and blue lights seemed more depressed. And by depressed, they actually ate less sugar water than the dark and or red-light hamsters, and there seemed to be reduced neuroplasticity in the hippocampus of the white and blue-exposed hamsters, which is an ominous sign. A fully neuroplastic hippocampus is important to maintaining positive mood and being resilient to stress. Other rodents exposed to nighttime light had reduced performance in learning and memory tasks. Circadian disruption is bad news.

No after dinner iPad for you
But enough about rodents. In August's Current Biology, some scientists took 8 people camping in the Rocky Mountains in July (sign me up!). No computers, smartphones, or flashlights allowed, though campfires were de rigueur. In one week of monitoring the participants in their normal modern environments, they noticed that average melatonin onset occurred 2 hours before sleep start time, which was typically at 12:30am, and melatonin offset occurred after the natural average wake time of 8am. After a week of camping, melatonin onset occurred just after sunset, and bedtime and awake time was moved two hours earlier. While camping the folks also got a lot more bright natural light exposure than in their ordinary lives.

Morning light exposure and early rising are both used as treatments for depression, by the way.

The gist of the study: "Increased exposure to sunlight may help to reduce the physiological, cognitive, and health consequences of circadian disruption.

*describes my blog exactly. Except the "academic" part…

Thanks to Jamie, Victoria, Dallas, and Stephan for emails and or tweets alerting me to the above papers.

Sunday, August 4, 2013

Love and Darkness and my Sidearm

I rather liked The Bourne Legacy, though it is certainly formulaic and silly in parts, but Jeremy Renner is amazing. He's not the most ripped or handsome action hero out there (most of them are comically ripped and/or handsome), but there's something about his acting that is very emotionally appealing. I also have a soft spot for parkour stunts and Moby.

The movie raises some philosphical questions about the morality tweaking human chemistry, for what purpose, and how much do we know…which is the main reason I write this blog. I like to look through the evidence for low-risk, common sense prevention and symptom help for mental health conditions. Going down into the labyrinth of medications for mental health can get very complicated and beyond a lot of evidence base too fast for comfort. The vast majority of the people I see for an intake have already started medications. I'd like to be able to reach some people before that point, when it is reasonable to try a better sleep plan, better food, exercise, and stress reduction.

First off a new post at Psychology Today about a study released last week linking consumption of coffee (with or without grassfed butter, I imagine) to lower rates of suicide. Hardly evolutionary, but certainly low risk, unless you have bad insomnia or anxiety.

Still my favorite Moby song with bonus Gwen Stefani: Southside

A powerful tool to change our biochemistry is to eat good, whole, natural, unprocessed food. Those definitions get muddled enough to be frustrating…but I really mean industrial processing, not the processing of fermentation or sprouting or rinsing, etc. Here are two new cookbooks out to give you some more ideas about how to incorporate convenience into a whole foods diet. Both these books were sent to me free of charge by the publishers for review.

First up is Paleo Lunches (and Breakfasts) On the Go by Diana Rodgers, who is a practicing nutritionist and farmer in the process of getting her RD.  She hosted the amazing farm to table dinner at AHS12 that I'm rather sorry to have missed (already had plans…).

Diana's book is (as advertised) filled with plenty of quick and easy options for lunches and breakfasts. I still admit to eating two poached eggs every single morning, though maybe once a month I change it up with some gluten-free pancakes or a smoothie. Today I made some egg muffins (basically an omelet in a muffin tin), based on a recipe from the book and they were delicious, and the kids ate them with very few threats, even though I added green peppers.

As a working mom, Diana has some of the same time constraints I do. I need fuss-free food that will keep, be easily packed for camp or school, and I don't have time to make special, different meals for the kids. Her recipes (so far) are flavorful, easy, but interesting. I have a special talent for taking great ingredients, throwing them together, and making horrible food (particularly in the crock pot), so cookbooks like this one are essential reading in my house. Diana also told me, "I hate baking," and there is a minimum of mixing and baking in this book, fortunately.

Second up is a book sent to me by Primal Blueprint publishing, Primal Cravings, Your Favorite Foods Made Paleo. I got it in the mail at a particularly busy time and didn't have a moment to review it until now.

I must admit, I was predisposed not to like it. The whole idea of whole, real foods to me is to get people used to eating nose to tail food that isn't dressed up or hidden. The road to nirvana and good health is paved with basic, healthy foods, not paleo cheesecakes. But within the book are a whole lot of easy, basic recipes like broccoli salad, baked eggs, pork cabbage cups. There is a dessert section, and a bread recipe, and fortunately these have a minimum of coconut flour which, in my experience, is rather like getting a mouthful of chalk with your food. I still would almost always rather have a real brownie every now and again than some frankenstein version of it, but then I can get away with a bit of gluten as long as it's not too much. (But you just said above that you eat gluten-free pancakes…yes, I do, because I find pancakes when made from rice flour or tapioca flour or almond flour taste pretty much exactly the same as normal pancakes, and the kids love them.) There are a few kids in the neighborhood now with gluten sensitivity, so if I were to have a birthday party at my house, I would probably make up a batch of one of these recipes, or if I were requested to make a batch of cookies for school or something. More often now, the school asks for fruit which is fine by me. So I suppose there is a use for paleo baking, it's just not a common need for me. And there are even some recipes that will make it easy to use up the supply of beef gelatin I got from amazon (a few tablespoons go a long way when it comes to gelatin, so I have a lot of gelatin to use up!) 

I do like Primal Cravings, and it does have a place on the shelf now growing heavy with paleo cookbooks. Just remember my bias is for easy recipes with not too many ingredients because I can't be too fancy or fussy even for a family get-together (my family usually gets a roast or roasted chicken for those sorts of occasions).

In a couple of weeks I will be giving a talk on disordered eating in the modern world at AHS13 in Atlanta. They rented out a much bigger venue this time, so I believe there are still tickets available. Looking forward to seeing my paleo buddies again! I'm working to make my talk both interesting, evidenced-based and practical so we'll see. Be sure to say hi if I'll see you there.

Sunday, July 28, 2013

Minerals, OCD, ADHD, and Questions

None other than the amazing Dallas Hartwig sent me a link to this paper about OCD and serum mineral levels a while back. It's hard to know what to make of the paper. In Bangladesh, 48 folks with OCD (mostly men) and matched controls had serum measures of minerals zinc, copper, magnesium, manganese, iron, and calcium taken. And, low and behold, the serum levels of those anti-anxiety metals zinc and magnesium (along with iron) were significantly lower than controls, and calcium and manganese were significantly higher. Copper levels were not significantly different.

And that's all we have. One small study, just an observation, a single measurement. Just a blood measurement too, not cellular or other tissue.


The main thing I take away from this study is that we still know so very little about nutritional status, minerals, and psychopathology. There are any number of fMRI and other expensive studies looking at the brain in OCD trying to peer into the metabolism of the brain in OCD, and we can learn from those sorts of studies, but we do tend to forget that these are full-body disorders mediated in part by the stress response, so there are some other systemic and measurable clues as to what is going on in the body.

Zinc, magnesium, and iron do tend to be low in people with certain psychopathology. In ADHD and autism, for example, there are several studies showing increased zinc excretion and decreased zinc levels in the body in kids. If you search individually for iron and OCD links in pubmed, you tend to find case studies of kids with pica (obsessively eating sponges, clay, or the padding from couches or other non-nutrative substances) who turn out to have iron deficiency (typically from previously undiagnosed celiac disease). When the gluten is stopped and the iron is repleted, the pica goes away. Iron also tends to be on the low side in kids with ADHD who have ferritin tested, though this larger study showed no association between iron status in the general population of children and symptoms of ADHD.

Are these cause or effect? Do certain variations in mineral metabolism leave you more vulnerable to psychopathology, or do the symptoms expose you to greater stress so your mineral status is different compared to healthy controls? Certainly in the particular cases of the pica "OCD," there is a clear arrow of causation from celiac disease to iron deficiency to pica symptoms. But in other cases the stress will cause people to excrete more magnesium and zinc, which if they are not repleted could amp up the stress response in general and be a self-perpetuating cycle. In the modern world where we get many minerals from our grains and don't tend to drink mineral water, if soils are depleted of certain minerals (and perhaps higher in others due to different agricultural practices) and the phytates in grains, legumes, and nuts bind some of the minerals, all the sudden it is a lot harder to replete minerals than if our intake was more like the ancestral picture prior to agriculture. Combine chronic modern stress with mineral deficiency with a certain genetic vulnerability to ADHD symptoms, OCD symptoms, other anxiety symptoms, etc. and you now have a lot more psychopathology popping up.

One side of the mineral story is the decreased zinc, magnesium, and iron. The other side is the increase in serum manganese and calcium. At this point it is a bit hard to know what to make of that. In certain folks with schizophrenia, there is a certain type of antioxidant-assisting enzyme called manganese superoxide dismutase that has lower activity, leading to poorer ability to clear the toxic metabolic byproducts and presumably cell damage and neurotoxicity. In ADHD (once again), high serum manganese is fairly consistently seen in children with the disorder when it is measured. The same is also true of children with cognitive disorders and other learning problems. Manganese is found in high concentrations in soybeans, rice, and black beans (in which case the associated phytates would protect one somewhat from absorption…but our modern tendency to eat a lot of different processed "foods" made from the same few grains might make us more vulnerable to certain deficiencies and excesses).  Manganese seems to interfere with cell energy metabolism, making it hard to make enough ATP to power the cell.

ADHD is associated with issues with dopamine neurotransmission, and manganese can accumulate in the presynaptic dopaminergic neurons via the dopamine transporter. In high enough concentrations, manganese is absolutely neurotoxic and leads to symptoms similar to Parkinson's disease. Brazilian children with ADHD tended to have high serum manganese prior to being treated with ritalin, which blocks the presynaptic dopamine transporter (therefore increasing dopamine in the synapse). After treatment, the serum manganese levels in these children dropped and presumably there was decreased uptake of manganese into those dopamine neurons.

Calcium's link is even trickier to figure out. Certainly on a synaptic level, calcium flux through membranes is a major "on" switch for neurotransmission. If there is too much calcium flux, you get "excitatory neurotoxicity," and this mechanism is related to migraines, seizures, and probably bipolar disorder. Whether or not higher (but still normal) serum levels of calcium (which, like magnesium, is very tightly hormonally regulated because you can get heart arrhythmias and sudden death if the levels are off) is associated with higher excitatory neurotransmission is unknown to me…hypercalcemia is definitely associated with fatigue, cognitive dysfunction, and irritability, but are high-ish but still normal levels, particularly in certain vulnerable people? I've not seen studies or anything about that, but it is plausible.

Once again, more questions than answers. Typical.

More on minerals

Magnesium and the Brain, The Original Chill Pill

Thursday, July 4, 2013

Zoo Humans

A brand new post is up at Psychology Today:

Zoo Humans

Hat tip to John Durant for the idea and to Erwan Le Corre for the name (and also to the originator, of course, published in 1969 of which I was unaware…The Human Zoo by Desmond Morris which I have now ordered from Amazon. John tells me his new book, The Paleo Manifesto has quite a bit more about primates and zoos in the second chapter. I got a preview copy of the book a few days ago but haven't had a chance to look at it yet.*

Lots still going on! Finishing up the draft of the book, working on chapters and articles for other publications, and (eventually) prepping for my presentation at AHS13. There are a number of interesting papers being published nearly all the time, and I will try to squeeze out more moments to write about them.

*Having read it now, John even has a visit to the Cleveland Zoo! I really enjoyed The Paleo Manifesto and will have a review up closer to the publication date. In short, it is a fascinating foray into one man's discovery of what it means to be human in the Industrial Age. From zoos to religious hygiene practices sex cults to monasteries to skulls to sleep to swimming in the ocean on New Year's Day, John brings together culture and biology to explain the quirks of modern human life.

Tuesday, June 18, 2013

Infection and Psychosis in Schizophrenia

Last year the daughter of one of my patients called me. "Mom is acting really strange. She's being aggressive, and she thinks my Dad is still alive. I don't think she slept last night. Do you think she needs an increase in her medication?"

My patient was a sweet 70 year old woman with a psychosis-heavy bipolar disorder who could get paranoid from time to time, but was never violent, and had been stable on a low dose of medicine for many years. I told her daughter, "If she didn't fall down and hit her head somehow, I think she has a urinary tract infection (UTI). You should take her in to see her primary care doctor if she'll let you. Otherwise, you might need to take her to the ER."

A few hours later, the daughter called me back, quite amazed. "You were right! Her doctor says she has a bad UTI. How did you diagnose that over the phone?"

I'm sure all my psychiatrist/doctor readers were guessing the outcome right away. UTIs rather famously turn into strange behavior in the elderly, particularly in those with dementia. One time when I was on call in the emergency room, we got a consult for new-onset obsessive compulsive disorder in  77 year old. My fellow resident and I exchanged looks and told the emergency room intern to wait for the results of the urinalysis before we were consulted. 77 year olds don't develop OCD out of the blue without something else medical going on. We were correct…she had a urinary tract infection. The "OCD" resolved with antibiotics. The tricky part for doctors is that these UTIs can occur without any of the usual symptoms we are used to hearing about. No incontinence, fever, or urinary urgency. Or sometimes the patient can't tell us about these symptoms.

So we already know that urinary tract infections can cause pretty weird behavior in vulnerable people. Recently Brian Miller, MD from Georgia Health Sciences University wrote an article in Psychiatric Times about his recent study in the Journal of Clinical Psychiatry: "A Prevalence Study of Urinary Tract Infections in Acute Relapse of Schizophrenia." Not only do I have a subscription to JCP, but my academic access should grant me full access, but on a Sunday morning I was unable to get a copy of the full text because JCP's website is HORRIBLE. In desperation I emailed Dr. Miller, and on Monday morning he very kindly sent me not only a copy of the full text article, but also his letter to the editor in Schizophrenia Research. Thank you!

Schizophrenia is associated with hugely increased mortality, and those afflicted die in increased numbers and earlier from almost every major leading cause of death. Heart disease is most famous (blamed on the increased schizophrenic tendency to smoke and to the effects of the medications), but schizophrenics have an 8-fold increased risk of death by pneumonia. Is it from lack of self-care and not being organized enough to go to the doctor for serious medical symptoms? Maybe. That has been the assumption. But recent studies have shown what is no surprise to followers of Evolutionary Psychiatry. Schizophrenia is not just a brain disease, it is a disease of immune function. Schizophrenics have major abnormalities in levels of inflammatory cytokines, C-reactive protein, and reduced neutrophil activity. Neutrophils are a first-line response to inflammation and are vital to keeping us safe from bacterial infection. 

Despite all these abnormalities, Dr. Miller notes in his paper that there are NO studies of the prevalence of infection at the time of infection of hospitalization for acute illness relapse in patient with schizophrenia. As all clinical psychiatrists will know, schizophrenics can remain relatively stable for many years, then have terrible relapses of psychotic behavior. Often going off medication or substance abuse is blamed (and may well be responsible). But sometimes something else is going on… and it may well be a bacterial infection. Dr. Miller studied healthy controls and some long-term schizophrenics admitted with acute psychotic relapse. He found that those hospitalized with schizophrenia, men and women, were 29 times as likely as controls to have a urinary tract infection. 35% of subjects in the acute relapse group had serologic/urinalysis evidence of a UTI as opposed to 5% of stable outpatient and 3% of controls. 

There are reports of certain antibiotic treatment associate with increased risk of psychosis (cipro and gatifloaxin are known)… is it the antibiotics, or the UTI they were treating? It is well-known that elderly and particularly demented patients are vulnerable to odd behavior caused by urinary tract infections. It is not beyond the realm of possibility that people with schizophrenia are vulnerable to the same pathology. 

The time is coming that schizophrenia is recognized as a full-body immune dysregulation disorder, from the gut to the brain to the neutrophils. At that point are the psychiatrists going to be removed from the picture and the allergists and rheumatologists to step forward? We'll see. 

Sunday, June 2, 2013

Gut and Brain Again

A long time ago, when I was an intern, I would drive into the hospital for ultra long shifts. Day went into night into the next day. You might be lucky to get one day off in a month. It's illegal now to work interns as much as we were worked, and I understand the sleep science behind the laws. But at the same time, you learn something about yourself and your patients in the long march over a day and a night and a day.

Bono says this song is about a hangover. I used to listen to it on repeat during that sleep-deprived drive into work for those long, long days. In A Little While. I would close my eyes on the elevator in the hospital and hear it playing in my head. Right now I am working a great deal on various projects and of course with my clinical practice. I hope to get a little bit of a break before too long…and have time to do more fun and interesting reading and blogging.

When we are born, we are colonized by the first generation of those eventual 100 trillion bacteria from nearly 1000 differenct species that makes up 90% of the cells of our body. These cells communicate with our brain and likely affect our behavior. The organisms help us to break down complex polysaccharides and they are critical to the normal development of the immune system. A relatively new paper reviews how they might influence anxiety and depression (1).

The mircobiome is influenced by age, diet, stress, metabolism, antibiotics, geography, and genetics. As regards stres reponse, mice lacking a microbiome have an exaggerated hypothalamic-pituitary-adrenal response to stress compared to mice normally colonized. The mircobiome seems to play a role in programming stress response from the very beginning. Stress will also increase intestinal permeability, which gives the bacteria of the microbiome greater access to communicate via inflammation and the enteric nervous system. Microbes can communicate with the human brain via various neurotransmitters, such as GABA, and there is also evidence that different gut bacteria have different effects on serotonin signalling in the central nervous sysem (at least in mice).

When pathogenic bacteria are introduced into the gut of mice, a robust central nervous system response is evident via the vagus nerve, followed by a systemic inflammatory response. Friendlier bacteria (such as lactobacilli) also elicit a central nervous system response, but not the systemic inflammation. Also in mice, certain neurons of the enteric nervous system change how excitable they are (or how easily they signal) depending upon the species of bacteria in the gut. Now repeated in many studies, the infection of mice with pathogenic bacteria increases anxiety-like behavior and treatment with friendly gut bacteria reverses the change in behavior. In some of these studies, changes in the production of nerve fertilizer (so to speak), brain-derived neurotrophic factor, matched the increases and decreases in anxiety-like behavior. The friendly bacteria are associated with greater nerve plasticity and repair, whereas the pathogenic bacteria showed the opposite.

In humans, there are few studies, and none in people diagnosed with clinical anxiety or depression. However, in a double-blind placebo controlled trial of probiotics given for 30 days (2), healthy volunteers who took the probiotic showed significantly less psychological distress than those who didn't. Another three week study showed the healthy volunteers with the most depression-like symptoms had significant improvement on a probiotic while those who took placebo had no benefit (3). There are also positive studies showing probiotics impacting anxiety symptoms in people with Chronic Fatigue Syndrome and undergoing cancer treatment.

Many questions remain that must be further studied. There are differences in how easily the gut microbiome is changed in different life periods, with childhood perhaps showing more amenability to change. In adults it is likely that fecal transplants and the introduction of chronic parasitic infection are the only practical way to permanently affect the microbiome. Childhood exopsure to antibiotics and probiotics may have different consequences than adult exposure to the same.

(2) Messaoudi, M. et al. (2011) Beneficial psychological effects of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in healthy human volunteers. Gut Microbes 2, 256–261

(3) Benton, D. et al. (2007) Impact of consuming a milk drink containing a probiotic on mood and cognition. Eur. J. Clin. Nutr. 61, 355–361

Thursday, May 23, 2013

APA Annual Meeting 2013

Many months ago, psychiatrist extraordinairre Drew Ramsey, MD of Columbia University asked if I would be part of a group to present information in a workshop format at the American Psychiatric Association annual meeting in San Francisco. He submitted an abstract, rounded up a reputable mentor on the scientific advisory board and collected not only myself but also Mala Nimalasuriya, MS and Roger McIntyre, MD to present.

Leagues: Spotlight

I must admit I've been a very bad academic up until this point. I keep the tip of my little finger in the academic world by teaching the clinical section of the introduction to psychiatry course at Harvard Medical School and have given a few Grand Rounds and other CME talks around town, but I haven't published or done any research besides serving as a psychiatrist for a project in the first couple years after residency. So for me, the opportunity to present at the largest annual meeting of psychiatrists in the world seemed, well, amazing. I do try for the blog to be honest and based on common sense and evidence and practicality, but at the end of the day, it is just a blog, and there are probably 10,000 new blogs on the Internet every single day.

Writing articles for the blog entertains me, helps me to learn, and is a lot more fun than toning it down for the interminable language of scientific papers, which tend to be interesting yet hideous unless written by the best (such as Gabbard or Rook). I do admire those who do publish, like Dr. McIntyre, whose resume is about 80 times as long as mine.

But I never look a gift horse in the mouth, and if they wanted me to present at the APA, I would help deliver…

Drew began the presentation with a brief overview of some important brain nutrients and the concept of whole foods versus the ubiquitous bastardization of wholesome living food we call "processed food." Drew's example: "I went to the store to buy some ham, and it was advertised as 'gluten-free.' When did gluten get into my ham?" He also reviewed some of the dietary pattern studies and elimination diet studies I've mentioned on my blog from time to time. Drew is both an expert at the various nutrients in whole foods, but also anti-"nutritionism," highlighting the importance of combinations of nutrients and their availability in whole foods that is quite different from the stripped down nutrients replenished with salt, industrial fats, and synthetic vitamins so prevalent in processed foods. Drew is the author of The Happiness Diet and the upcoming 50 Shades of Kale (he did indeed order the kale salad at the Split Bread in San Francisco).  I'm going to review The Happiness Diet soon, once I get a minute…

Maya continued the talk with information from her master's thesis on nutrition, the brain, and brain derived neurotrophic factor (BDNF). BDNF is brain fertilizer that helps with neurogenesis and repair, and good nutrition is associated with goodly amounts of BDNF.

Roger followed up with his vast body of work on obesity and mood disorders, noting the effects of weight loss, obesity, and active mood disorders on particular inflammatory cytokines. He highlights the point that the success I see with some of my folks on a paleo-style diet may be a result from an anti-inflammatory state that comes along with weight loss rather than from any particular diet per se.

I was the closer for the presentation with a very brief overview of the evolutionary medicine hypothesis, its pluses and pitfalls, the commonalities of a paleo-style diet and some evidence (including the evidence on fructose malabsoprtion) linking modern diets to poor mental health. I gave a few case studies and my clinical pearls for helping introduce a whole foods diet to people as part of a holistic model for health care in addition to more traditional therapies. I also discussed the theoretical applications of ketogenic diets in psychiatric disorders, the available evidence (almost nil: all pilot trials or case studies), and advised folks to keep an eye out for more research.

We had a number of questions and interest in the ideas of celiac disease masking as major mental illness, coconut and MCT oil, tofu and the poor performance of so called "modern diets" in the dietary pattern studies and depression, and interesting tracks for research and some practical questions about implementing recommendations. At the end we were approached by a number of psychiatrists wanting more information.

Did I mention our room was completely packed with people sitting in the front and aisles and lined up out the door?

All in all, a great success.

The remainder of the APA was, as always, interesting. 15,000 psychiatrists and the launch of the DSMV meant a continuous Scientology protest outside, plus a number of men with bushy eyebrows and bow ties. I attended a number of lectures, the most notable being a 4 hour seminar on giving better lectures. The APA attracts psychiatrists from all over the world, and I would estimate the number of international attendees at 1/5-1/4 in the lectures I attended.

I happen to be friends with the son of a former president of the APA, and as such was able to finagle my way into the APA Presidential Reception at the Palace hotel, which was great fun. My friend's father and his wife very kindly introduced me to everyone, and I can't express my appreciation enough.

It was also great to hang out with Drew Ramsey; food-minded and sensible psychiatrists are always a pleasure to talk to, crossing fingers we'll be invited to the next APA, and I'm going to get his 50 Shades of Kale to help me cope with the mountains of kale I get from my CSA, which starts up next week.

Sunday, May 5, 2013

A Bit of Hiatus

Hi there. Yes, it has been a while. I am spending several hours each day working on the book, so other writing has taken a back seat for the moment. In addition, I am preparing for the upcoming American Psychiatric Association Annual Meeting in San Francisco, where I will be presenting as part of a group on food and the brain (on Sunday afternoon, before the Clinton speech, for anyone who will be there). My next talk after that will be in Arlington, VA, as I have graciously been asked to be a (far less glamorous and much shorter) speaking substitute for the Melissa half of Whole9Life for the summer of Melissa's maternity leave. You can get tickets for the talk here. I'll be adding a bit on the psychology of change and sleep cycles to the general Whole9 information.

Sometime in the next week or so I will have a new (or new-ish) post on Psychology Today. And you never know what will happen if a white-hot paper comes to my attention.

In the meantime, have a lovely spring. Keep checking back, and as always I'm still far too talkative on twitter.

Sunday, April 21, 2013

Marathon Monday

I've always worked on Marathon Monday until this year, when we went to California to visit my sister for the week. Otherwise, since my oldest is now in school and had the day off, we may well have been downtown to see the festivities. For four years I lived about a half mile from where the bombings took place. I've walked down Boylston Street hundreds of times.

Two things folks who have not spent time in Boston may not understand about the events in Boston and Watertown this week: Marathon Monday, Patriot's Day, is a family event. I personally knew hundreds of people who went down to the race, because nearly everyone seems to go. My niece and nephew had watched a bit just down the block, though they had left by the time of the bombing. My sister-in-law knew a woman, a nurse, and her new husband who both lost limbs from the bomb, but so far I've not heard from other friends, family, or patients who were hurt. The "could have been" is sobering.

The second thing to understand is that Boston proper is a very small city. One could walk across it in a few hours. It is just a bit of a walk across the river to Cambridge, more of a hike over to Watertown. Closing down the city to do a confined manhunt in Watertown might seem unimaginable in Manhattan or Dallas or Los Angeles, but it is not so terribly far-fetched in Boston.

I mostly know the medical community, and some people in the law enforcement community. Atul Gawande wrote a good post for The New Yorker online about why so many survived the initial blast despite critical injuries. Today there are more than 50 people still hospitalized. And of course the five who died (including the MIT officer who was shot by the alleged bombers on Thursday night/Friday morning and the older bombing suspect himself). We will go back to work tomorrow and see how people are handling what happened, though I was on call for the practice and spoke with a few people who were very shaken up, particularly on Friday.

It was a good week to have been away, but I am glad to be home. My family is safe and sound, and it is so terrible that so many families were maimed and wounded this week. Thank you to those who reached out to me via social media and email, concerned about us.


Friday, April 12, 2013

Sunlight, ADHD, and Current Events

First off, a brand new post is up on Psychology Today (one never before seen on this blog):

Sunlight and ADHD

Secondly, the blog has been a bit quiet of late because I am busy trying to get some real work done on the book. The deadline for a solid first draft is fast approaching.

In light of some shake-up in the blogosphere and the recent paleo debunking fad, I do plan a little post about what I think of the "paleo-style" diet (though long-time readers probably know my opinion already).

Also, for any of you who speak Polish, many of my articles have been translated…here is the link from Joanna Satula-McGirr:,emily_deans_m_d/

Stay tuned!

Tuesday, April 2, 2013

PaleoFx13 and BA Training

Last weekend I went down to Austin for the PaleoFx13 conference. While I enjoyed PaleoFx12, I had a bit of trepidation at the idea of going back, mostly because the science talks were exceptionally fringe. However, I really enjoyed the people, and since I’m originally from Austin, it’s a nice excuse to get down for a few days and see my family and old friends and escape the horrendous early spring in the Northeast.

Muse: Panic Station (really digging the 21st century Stevie Wonder vibe of this song)

PaleoFx13 was a blast. The venue at the Palmer event center was terrific. Keith and Michelle Norris and all their help (including Corben Thomas among others) organized things very well, and the focus was drawn away from the sketchy science of yesteryear and more towards functional fitness and practical applications. For all the recent acrimony and problems in the paleoblogosphere, PaleoFx manages to make ancestral health a lot of fun. And we definitely needed the fun.

My contribution as a presenter was not fringe at all, but rather the evidenced-based application of behavior theory and stages of change and motivational interviewing on lifestyle changes in general. I use these techniques pretty much every day in my clinical practice in coping with addiction and other lifestyle changes, so it was both straightforward for me and rewarding. Several physicians came up to me after the presentation and spoke to me about their need to really tailor interventions to the particular stage of change of the patient to reduce frustration and prevent wasted energy. My friend, Jacob Egbert DO used the second half of our presentation to talk about his interventions in the gym, his success stories, and the idea of a gym (or any community) as a primary care center for wellness and prevention of chronic disease. He has struggled a great deal with the paradigm of modern medicine and the push for more procedures, more billing, and less holistic care.

I spent a lot of time with my online coach, Clifton Harski of BA training and his amazing girlfriend, Amy. She is a gymnast and he a kinesiology major and former MovNat master trainer along with a ton of experience with other forms of functional fitness. 

The term “functional” merely refers to full body, useful movement, such as getting up from the floor or climbing trees or Olympic weightlifting. I’ve been doing a program designed by Clif for about two months, and my general strength and movement has increased a great deal, even after two years of CrossFit. His BA training “Bootycamp” uses a lot of bodyweight movement and kettlebells to increase lower body stength. It’s high volume and intense, and beneficial, though he backed off and lightened my workouts when I was having a stressful week. Despite an injured shoulder, I’ve been able to do some legit chin-ups since I started his program. Between that and the heavy deadlifts, I can draw a lot of eyes in the globogym.

In person training (with an excellent trainer)  is always best, but with my time constraints and boredom with the standard fare (and the fact that I am just a psychiatrist who can do chin-ups rather than some sort of athlete), the online training keeps things interesting as well as challenges me in a way that local trainers probably wouldn’t. In person, Clif helped me perfect my two-kettlebell swing while Amy helped me achieve the one-armed handstand (against the wall!). Clif, like many of the folks I admired at PaleoFx loves perfecting human movement. It turns out I have an issue with my hip adductors, which my CrossFit trainer had noticed, and kept ordering me to keep my knees out on squats, but that wasn’t enough to fix the problem. 

Clif’s programming of one-legged deadlifts helped me to isolate the problem and start to work on it. He also respected the limitations of my shoulder and programmed specific strength exercises with that in mind. He is thoughtful about movement and functional training, but also recognizes that fitness should not be so deadly serious that we can’t enjoy it (just like paleo food…fun healthy delicious food as opposed to quinoa and textured soy protein? Sign me up!)

At PaleoFx I was fortunate enough to hang out with all the folks who goof off and do stupid human tricks between conference sessions, including Amy, Skyler Tanner (my favorite efficient exercise trainer) and Jacob Egbert. (Photo taken from A Jolly's twitter stream.)

I won’t be able to post before and after pictures of my bootycamp derriere, but rest assured I’m stronger and more shapely after the introduction to Clifton’s program. His brilliant tagline is “turn that applesauce into apples.” I’m going to hire him to give me some extra workouts in the future along with 2X  a week CrossFit training (nothing like the social crew at CrossFit to keep me motivated and coming back for more early morning gym time). 

Hopefully I will be able to attend PaleoFx14 and beyond! Life is becoming incredibly busy…today I presented at Psychiatry Grand Rounds at a hospital in Cambridge and it was very well received. Last week I presented at UT Austin, and flubbed the talk a bit as I am used to presenting a lower-level talk, or to clinical medical audiences. All the criticism and experience is very welcome. My wish is that a medical student and his or her eager mentor will latch hold of the idea of studying fructose malabsorption and depression. And if it is fecal transplants and depression instead, or magnesium and depression, or whatever, I will be a happy camper.