You Are What You Eat

Did you know that diet could affect mental health?  Okay, that is, perhaps, putting it too strongly.  Diet is correlated with mental health, especially in Australia.

Mental health disorders tend to be pretty chronic and can be debilitating.  And, unlike many chronic diseases of Western Civilization, they tend to strike young.  Autism in babyhood, anxiety disorders often before age 10, mood disorder in the teens, schizophrenia in the late teens and early adulthood� psychiatric disorders cost us so much in terms of productivity and health.

Y'all already know what I think.  (Donnie Darko, Mad World right click to open in new tab).

There is every reason to believe a modern, processed, nutrient-poor diet could have a lot of influence on mental health.  Of course, no one knows what to tell anyone to eat except for "fruits and vegetables." And that is what PLOS1 tells us today�

A Prospective Study of Diet Quality and Mental Health in Adolescents

In this study, several thousand Australian adolescents filled out surveys about diet, health, and mental health several years apart.

Here is how diet quality was assessed:

 As such, a point was allotted for each of the following: eating breakfast at home on school days; eating lunch brought from home; consuming two or more fruit serves per day; four or more vegetable serves per day; fruit and/or sandwiches as after school snacks; generally avoiding biscuits, potato chips, pies, hot chips, fried foods, chocolate, sweets, ice-creams as after school snacks; and, finally, both consuming healthy after school snacks and avoiding unhealthy after school snacks. 

(Chocolate????)

It is not terribly surprising that an unhealthy diet score in the first survey correlated with a poorer rating of mental health in the second survey several years later.  Covariates were assessed for but can never really be extinguished completely� interestingly, mental health at baseline did not predict diet several years later, strengthening the findings of the study.

But I rather love these researchers, and will quote some of the interpretation in full here:

...the prevalence of emotional and conduct problems in adolescents increased in the period between the mid 1970's and 1999, while a new meta-analysis, reporting on data collected at many time points and, thus, free of confounding by age and/or recall bias, has reported large generational increases in self-reported psychopathology in American high school and college students between the 1930s and 2007. These increases did not appear to be explained by social response biases, economic cycles or changes in student populations, and the authors concluded that changes in unidentified cultural factors have resulted in increased rates of psychopathology among American youth.

 Paralleling this possible increase in the rates of psychological illness among young people are data indicating a reduction in the quality of adolescents' diets over recent decades. A report based on trends in adolescent food consumption in the US identified a reduction in the consumption of raw fruits, high-nutrient vegetables and dairy foods, which are important sources of fibre and essential nutrients, between 1965 and 1996, with an associated increase in the consumption of fast food, snacks and sweetened beverages. Concurrently, population surveys demonstrate a substantial increase in overweight and obesity among children and adolescents over recent decades. Obesity does not necessarily indicate nutritional repletion, as high-energy foods typically have poor nutrient content.

Could it all be connected?  Increasing muffin tops and increasing psych hospitalizations in children and increasing psychopathology?  And how expensive is it to society when a lean cuisine is the epitome of healthy eating?

A very very mad world indeed.

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More on Infections at Psychology Today

Updated another post (with some new research findings) at Psychology Today that is pertinent to my most recent post here:

Could Alzheimer's Dementia be Caused by a Virus?

Also new(ish) at Psych Today:

Parkinson's, CoQ10, and Creatine

Brain Energy

More new posts soon!

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Infections and Schizophrenia Risk

Whew.  Quite a response over my disappointment in Wheat Belly.  And Melissa gives us an informed and reasoned review (mine was more of a visceral reaction).  It's hard for me to see the merit in a book just because the idea of wheat not being ideal for human consumption agrees with my own views.

On the interesting papers front, a couple of new articles shine more light on the relationship between infections and mental disorders.  I consider this type of thing "evolutionary psychiatry" as it brings us closer to finding the true pathology of illness, inflammation, and disease.  In addition, the typical evolutionary prescription of nutrient-rich and anti-inflammatory diets and appropriate amounts of vitamin D ought to increase resistance to infection and resilience to the inflammation and autoimmune issues that may be spurred on by such infections.

The first paper is from Denmark, Toxoplasma Infection and Later Development of Schizophrenia in Mothers, from August's American Journal of Psychiatry.  There is also an enlightening editorial in the same issue.

Toxoplasma gondii is a parasite that one can pick up from contaminated cat feces, from eating undercooked meat containing the infectious cysts or contaminated vegetables, and from being a fetus whose mother is infected.  Infection in pregnant women can cause major birth defects in offspring, and this fact is the origin of the common advice for pregnant women not to clean litter boxes.  Studies have linked infection with toxoplasma with schizophrenia since the 1950s.  More recently the association was confirmed in a 2008 study of the US military.  All these early studies were retrospective and observational, which is the weakest sort of experimental data this side of the anecdote.  Meaning folks with schizophrenia were compared with normal controls, and it turned out that people with schizophrenia have a higher rate of previous exposure to toxoplasma.

A step up from the retrospective, after the fact sort of study is the observational cohort study.  In this type of study, a group of people are followed for many years to see what develops.  This type of experiment presumably takes away what sorts of bias can be introduced by finding cases after the fact. (For example, do people with prodromal symptoms of schizophrenia engage in behavior that makes it more likely for them to be infected with toxoplasma - washing hands less, or not cooking meat as thoroughly?)  Scandinavian countries are hotbeds of these studies, as they've collected all sorts of medical data on pretty much all of their citizens for a generation now.

In Denmark, 45,609 women were followed from childbirth, when antibodies indicating prior prenatal exposure (or not) to toxoplasma in their babies were measured by heel-stick 5-10 days after being born.   All these antibodies circulating in the baby's bloodstream were made by the mother, not the baby, as a baby won't make too much in the way of these sorts of antibodies (IgG) until the immune system is a bit more mature, by 3-6 months.  Therefore mothers with babies who were positive for T gondii exposure were presumed infected themselves.  Some, but not all, of the mothers had been tested for IgG levels in the first trimester of pregnancy - these levels correlated with the newborn levels that were available for all the mothers.

Over the following years (the women were followed from 1992-2008), 80 of the mothers developed schizophrenia.  The ones whose babies had the highest IgG levels had a higher risk of developing schizophrenia than those who had babies with the lowest levels (the risk was increased by 1.73-fold, which was statistically significant - though with a population risk of approximately 1%, toxoplasma seems to increase the risk to about 1.7%).   Other meta-analysis have shown odds ratios of around 2.54-2.73 (odds ratios above two are considered a significant finding).  In the Danish study, adjustments were made for confounders (such as age, urban or rural, and other known risk factors), and women already diagnosed with schizophrenia at the beginning of the study were obviously excluded.

Why would infection with T gondii increase the risk of schizophrenia?  Active infection in the central nervous system can certainly cause huge problems (such as seizures) and inflammation.  In addition, our immune reactions to these infections can cause problems, especially if something on the infectious particle looks a bit like something in our own cells.  The classic example of this type of problem is rheumatic heart disease, most likely caused by our own antibodies attacking heart tissue after a strep infection.  It is also thought that neurological symptoms of lupus are caused by these neuro-specific auto-antibodies.  In the case of toxoplasma, it is a possibility that the anti-toxo IgG antibodies react with neural tissue and might help the immune system attack the NMDA receptors in particular.

The paper Progressive Gray Matter Loss and Changes in Cognitive Functioning Associated With Exposure to Herpes Simplex Virus 1 in Schizophrenia: A Longitudinal Study appeared in the same August, 2011 issue of the American Journal of Psychiatry.  In this study, there were four groups of folks - schizophrenic patients (none of whom were on antipsychotic medication) who were seropositive for HSV1 infection or not positive, and normal healthy controls who were also positive for HSV1 infection or not.  All these folks were followed with some cognitive testing and neuroimaging at the beginning of the study and at one year.  It was found that the schizophrenic folks with HSV1 infection had significant worsening of certain measures of cognitive functioning and shrinking of gray matter in certain regions (meaning the brain cells are dying off).  The other three groups of people didn't have these changes.

Here is what the researchers had to say about the possibilities:

There are several plausible explanations for the observed changes. In the rodent and rabbit models of CNS HSV1 exposure, latent infection and reactivation directly affected functioning through neuronal death or dysfunction. Neuronal death resulted from apoptosis. Neuronal dysfunction during reactivation and latency resulted from modulation of apoptosis and autophagy, host cell translational shutoff, oxidative damage, and/ or neurotransmitter alterations. Even with peripheral infections, HSV1 could alter neurotransmission through release of cytokines, especially chemokines, which may be elevated in HSV1-exposed individuals. Human studies support some of these observations. These processes occur throughout the life of an infected person.

In short, infection (even a smoldering latent infection without obvious active signs) in the brain or periphery can lead to all sorts of changes in the way the cell handles energy and self-destruction and general inflammatory badness.

Monitoring, modulating, and avoiding these infections seem like different ways to decrease the risk of central nervous system symptoms.

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Slam-dunked and Wheat Belly

All right.  Work has been really, well, working me lately, so I've barely had time to sleep, much less to review papers, keep up with the blogosphere, and write.

I do like this song, though (right click to open in new tab):  Days are Forgotten (and it is getting very difficult to find songs on youtube that will play without ads upfront - sorry if there is an ad on this one!  It had a glitch and skipped the ad but might not work for everyone :()

Despite the time crunch, I did manage to squeeze in Wheat Belly over the weekend (most of it), and read the rest last night.

No, I don't like it.

No, I don't eat wheat as a rule, and I am not a grain industry shill.

But I don't feel I have to put my name out in support of a shoddy, sloppy book just because the overall message "wheat sux" agrees with my thoughts that wheat gluten and other wheat proteins likely are inflammatory in many people and cause problems for more than just those with celiac disease.  I think most physicians and researchers with critical thinking skills will find this book useless and full of hyperbole.  For those not taken in by the confident tone, it may do more harm than good.

Why don't I like Wheat Belly?  In short, it is the carelessness and simplicity of the message.  Hyperbole and poorly supported, confident claims.  Obesity and chronic illness is a complicated subject.  It doesn't come down to wheat.  Wheat isn't responsible (entirely) for "moobs" or the other too-cute phrases Dr. Davis churns out ad nauseum throughout the book.

An example?  In chapter 4, Dr. Davis spends a bit of time discussing the evidence linking wheat to schizophrenia and addiction.  I've discussed this issue at some length and noted the obvious circumstantiality of the evidence and the need for more research.  (see Wheat and Schizophrenia and Wheat and Serious Mental Illness).  And while Dr. Dohan (who was the major researcher who championed the wheat causes schizophrenia meme) felt he had evidence that schizophrenia has increased incidence in wheat-eating populations, most modern schizophrenia researchers make note that schizophrenia is pretty consistent in incidence across many populations - around 1%-1.3% incidence, in the developing world and in the Western world, in rice eating Chinese areas and the wheat-eating American Midwest.

Dr. Davis says:  "while it seems unlikely that wheat exposure caused schizophrenia in the first place, the observations of Dr. Dohan and others suggest that wheat is associated with measurable worsening of symptoms."  I don't get that quote at all.  Is the incidence of schizophrenia higher in non-wheat eating countries or not?  Do exorphins cause psychotic symptoms or not?  Schizophrenia, after all, is defined by the symptoms.  Something that "worsens" schizophrenia will cause schizophrenia, a symptomatically defined illness, as I've discussed earlier in my posts on cannabis.

But where I find the book to be critically annoying is in the discussion of addiction and opiates.  Wheat, as we know, has break-down components that are exorphins, which activate the opiate receptors in the brain and nervous system (the same receptors that are activated by our natural endorphins, opium, morphine, heroin, percocet, and other opiate painkillers).  The opiate pathway is part of the reward pathway in the brain, and is actually activated by anything "rewarding" - such as sex, exercise, drugs, gambling, and rock and roll.

Where I agree with Dr. Davis is that I have seen clinical evidence that some people seem to be "addicted" to wheat.  Particularly night bread binge-eaters.  They talk about bread much like one of my opiate addict patients would talk about oxycontin.  They can't stop eating it even after they are full, and even when they desperately want to lose weight.  They will leave their cozy house and pick up crackers, pretzels, fast food with fluffy bread, or a fresh loaf to eat at night. Critically, in certain cases (where more evidence-based methods have been tried), I've managed to stop these cravings and binge behaviors with naltrexone, which blocks the opiate receptors and short-circuits reward.  The problem is, ALL reward is mediated through opiate and dopamine, so using naltrexone doesn't tell you that you've blocked specific wheat exorphins - maybe the person has a real jones for fresh steaming lovely bread for simple reward sake - like some people love chocolate, Pringles, or cocaine.

It's a good message, though, and something that should be researched.  But then Dr. Davis comes up with this sentence (and also states he has seen the withdrawal and "brain fog" from wheat in "thousands of people"then later "I've personally witnessed hundreds of people�"), which is incredibly jarring and ruins the credibility of the message: "Let's pretend you're an inner-city heroin addict.  You get knifed during a drug deal gone sour and get carted to the nearest trauma emergency room.  Because you're high on heroin, you kick and scream at the ER staff trying to help you.  So these nice people strap you down and inject you with a drug called naloxone, and you are instantly not high."

Naloxone (and it's orally administered cousin, naltrexone), is an opiate blocker, or "opiate antagonist."  It will immediately knock opiates off the opiate receptor and put someone high on opiates into instant withdrawal.  This is not only extremely unpleasant, it tends to make people very agitated, unhappy, and even violent.  If you have to do it to save someone's life, you do it.  If someone is overdosing on opiates and loses the chemical signal to breathe, it will be lifesaving. If someone is alert and active and still high on heroin, injecting someone with naloxone would be a galactically stupid thing to do, particularly if you were just injured in a knife fight and needed some painkilling.  Injecting someone with naloxone will mean that the strong painkillers will not work in someone who will have a high tolerance to hospital painkillers.

Any emergency room physician, nurse, or doctor with a shred of ER experiecne will read that sentence in "Wheat Belly" and go, "huh?  What is this guy talking about, and is he galactically stupid?"

Honestly, I think it is a throwaway line that was carelessly written and carelessly published.  And other "paleo" books like  "The Vegetarian Myth" are full of lines like that.  But you know what, I have a much higher standard for a cardiologist than I do for a non-scientist like Lierre Keith.  I want real science, real risks, real data.  Not hyperbole and nonsense.

So no, I don't recommend Wheat Belly. And I don't recommend eating wheat either.

(Nor am I saying that Dr. Davis is stupid - far from it - just careless in his phrasing.  If you are going to take on Conventional Wisdom of Healthy Whole Wheat, you really have to "bring it."  It was not brought.)

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Of Like Minds

As you may recall from my AHS - The People Post, one of the best experiences from my visit to Los Angeles was meeting a few other like-minded psychiatrists there.  Evolutionary medicine, as sensible and evidenced-based as I try to make it, can feel very lonely and off the beaten path.  So it is lovely to meet people who see the innate reason of it all.   The northeastern US is both protective and stifling in its conservative medical atmosphere - so to have others thinking in ways apart from psychopharmacology and psychodynamic or behavior therapy as the end-all, be-all is, well, glorious.

Beethoven - Symphony No. 9, 4th Mvt (one of the finest pieces of music ever written, though choral music is not always my favorite, I make an exception for this one - right click to open in new tab)

Not long after I returned from AHS, I received an email from a psychiatrist I had seen on Jimmy Moore's low carb doctors list, Judy Tsafrir, M.D..  She works maybe 30 miles away and has a holistic psychiatry practice in Newton (a city just to the west of Boston, which, I'm told has the highest number of psychiatrists per capita in the world - and yet we could still all be working 24/7 and turning people away.  Remarkable).  Dr. Tsafrir has extensive experience and training in both child psychiatry and psychoanalysis (unlike myself - I am a pretty run-of-the-mill adult psychiatrist).  In more recent years she has turned to dietary therapies and has become an expert in the GAPS diet.

I met Dr. Tsafrir for lunch a few weeks ago, and like most analysts she is a patient and serene sort of person - rather the opposite of myself in some ways (as I can be somewhat impatient and directive).  We talked a bit about our training and experiences and our frustration with the restrictive (and sometimes disastrous) mold that encompasses "evidenced-based medicine." And of course we are interested in the best data and best evidence for our patients, yet the money and the studies seem to be spent and performed with a different agenda.

Dr. Tsafrir has started a blog, and I am adding her to my "Of Like Minds" group to the right.  Her latest entry is about her thoughts on "Wheat Belly," entitled One Size Does Not Fit All. I encourage any readers with GAPS questions especially to take a peek, as I have only started reading the book and have no clinical expertise in that area.

People often ask me if I know of like-minded psychiatrists where they live.  There is Ann Childers, MD in Oregon, the two psychiatrists I met at AHS (I did not ask them about sharing their names or details so will not do so), and now Dr. Tsafrir!  And maybe more and more, every year.  We shall see.

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Happy Happy Coffee!

I'm really falling behind my stack of papers.  Fortunately, life is good and busy, and there are always new, catchy songs to listen to:

The Temper Trap:  Fader

That song really puts a spring in my step.  Rather like a strong cup of coffee.  Full disclosure - more of a tea person, but I've been known to drink a cup of joe every now and again.  Maybe I ought to drink a bit more� the evidence is mixed, frankly.  And certainly I can't tell you how many times I've had patients complain of insomnia, only to find out they are drinking 6 large iced coffees a day, or 12 Mountain Dews (no matter how much I exercise, I don't seem to be able to take this weight off, doctor�).

But what does the research say about, say, depression and coffee?  A brand spanking new piece of epidemiology from the Nurses' Health Study was published in the Archives of Internal Medicine this month - Coffee, Caffeine, and Risk of Depression Among Women.

Some facts from the article - 80% of the caffeine in the world is consumed as coffee.  Interesting.  Prospective studies of men and caffeine use showed a strong inverse association between coffee drinking and depression, with no association for tea or cola.  Three cohort studies showed an inverse relationship between coffee consumption and suicide (though in a Finish study, there was a J-shaped curve with both very high (>7 cups of coffee daily) and low consumption of coffee seemingly less protective than moderate amounts.)

So, in the Nurses' Health Study (following 121,700 American female nurses starting in 1976), women filled out questionnaires every two years.  97,000 filled out questionnaires in 1996, 98, or 2000, and those with no history of depression at that time (50,739 women) (those with unknown history were excluded) were followed over the next decade.

Regular coffee drinkers in this cohort were more likely to be smokers, drinkers, and not go to church!  They also tended to have lower rates of diabetes and obesity.  Average consumption for the whole group was about 1&1/2 cups of coffee a day.

Among the 51,000 women, about 2600 developed clinical depression in the 10 year period.  There was a dose dependent, inverse relationship between the amount of coffee consumed and the risk of developing depression over the years.  When covariates (such as age, health, smoking, divorces, etc. etc.) were all adjusted for, the inverse relationship became even stronger!  No associations were found between tea consumption, chocolate consumption, decaf coffee, or soda consumption and depression.

So what's up?  Is coffee an antidepressant?

I Know What I Am: Band of Skulls

Well, maybe.  This is no randomized controlled trial, so causation cannot be determined, but caffeine (1,3,7-trimethylxanthine) antagonizes the adenosine A2A receptor.  This is thought to have pro-dopamine effects.  By taking out adenosine, we might also be affecting the transmission of norepinephrine and serotonin, both known targets of antidepressant medicines.

Since coffee is known to cause insomnia and anxiety, both features of depression, a weakness of the study is that women prone to insomnia and anxiety might limit their intake of coffee, thus biasing the results so that women who can tolerate a truckload of coffee also happen to be the ones less prone to depression.

But� all told, it seems that this study is another notch in coffee's bedpost.  Though less than 8 cups a day seems prudent.  And I really can't recommend Mountain Dew :)

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Anger and Serotonin

My buddy Jamie Scott is a research machine.  It's all I can do to keep up with the interesting papers and links he emails my direction.  Today's article is yet another one we owe to his sharp eye.  He also has brand new digs at a wordpress blog (*brief moment of jealousy*) - so edit/add him to your blogroll and check it out:

That Paleo Guy

Some music - I rather adore the Yeah Yeah Yeahs.  Here's an oldie but a goodie:  Gold Lion (right click to open in new tab).  Favorite comment on youtube:  "i think I just got whiplash rocking out to this song" [sic].

Want something a bit more classical?  How about a Chopin Nocturne played by none other than Rachmaninoff from 1927?  (You will not be rocking out, but it is quite lovely).

The paper is in Biological Psychiatry: Effects of Acute Tryptophan Depletion on Prefrontal-Amygdala Connectivity While Viewing Facial Signals of

Aggression

It's kinda cool.  Involves humans, which is always a plus.  It is one of those "view angry faces whilst in a functional MRI machine" which has some limitations, but it is pretty much the only way to see what's going on in real time in the old noggin, seeing as how it's rather awkward to test gene expression and neurotransmitter levels other ways without decapitation (not likely to pass the institutional review board any time soon, unless you were unfortunate enough to be born as a research rodent).  (Random aside - Andrew tweeted this REAL MIND READING finding yesterday.  Wow.) 

How many segues is that?  Welcome to my left-handed, small child-raising brain.  As we know, depletions in serotonin, especially in a particular communication circuit between the frontal lobes (the policeman) and the amygdala (the emotional/rage center of the brain) leads to anger and aggressive behaviors.  Now, there are some people who are just aggressive altogether - I'm thinking Drew Barrymore's boyfriend in one of the Charlie's Angels movies.  We're not talking about that.  We're talking about impulsive aggression.  All the sudden, you just want to jump out of your car and strangle the other driver who cut you off (please don't do this).  Impulsive aggression can be unexpected and very scary, and can certainly ruin lives.  

So what if it happens just because you forgot to eat your banana this morning???  Oh, don't worry, we are likely more resilient than all that� but in an experimental setting, one can pretty much abolish serotonin via a weird laboratory tryptophan-depleting drink.  Then you get into an MRI machine.  Then you look at pictures of angry faces (if I were running this experiment, I would pipe in some hard core metal, and not one of Chopin's Nocturnes).  Of course, I read A Clockwork Orange in high school.  The tryptophan-depleting drink significantly reduced both plasma tryptophan levels (remember, tryptophan is the precursor to serotonin) and the ratio of tryptophan to other long-chain neutral amino acids  (remember, tryptophan competes with these other amino acids for entrance into the brain).  

In the end, the reactions of the tryptophan-depleted individuals to the angry faces vs. controls was statistically significant.  Tryptophan-depleted folks had a higher response to the angry faces within the amygdala (the rage/anger part of the brain) compared to controls, and compared to the response to neutral faces.  These findings would suggest that, as suspected, serotonin helps you chill out and assess the situation when faced with an angry hoarde.  

Between the mind reading and the availability of a rapid acting tryptophan-depleting anger drink that will affect our aggressive reactions, I'm a little worried about the future of our free will.  But I'll try to eat some protein, micronutrients, a banana, and put my trust in the incompetence of bureaucracy in order to be less paranoid.

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