Sniffles and Suicide

Let's revisit the basic premise, my hypothesis we are searching to disprove.  Humans are not broken, but we are not optimized for our current environment, whether it be modern stress, modern social structure, modern diet, modern sleep, or modern activity.  Perturbations from the homo sapiens "norm" of paleolithic life (minus the few adaptations we have accumulated in the recent years) lead to modern human disease, mental and physical.  


In a broad stroke, pathology in the human body is mediated via abnormal immune response - thus autoimmunity and inflammation.  This piece of the theory has mounting evidence both for physical and mental health diseases.  Inflammation in the brain can lead to disturbances of human behavior - to anxiety, extreme depression, and even suicide.

Today an interesting paper newly out in the Journal of Clinical Psychiatry, Suicide and Prescription Rates of Antiallergy Medications: An Ecological Study.

I know.  That sort of a title will make any Evolutionary Psychiatrist's ears prick up.

First, though, suicide.  With any human condition, sometimes the best place to look for clarity and understanding is Steinbeck, who won the Nobel and Pulitzer prizes for literature.  And, like many men of the 20th century, John Steinbeck died of heart disease in his 60s.  

He wrote a sympathetic portrayal of a suicidal man in what I consider to be his best work, East of Eden:

On another sheet he wrote, "Dear Will, No matter what you youself may think -- please help me now. For Mother's sake -- please.  I was killed by a horse -- thrown and kicked in the head -- Please!  Your brother, Tom."

...In his bedroom he broke open a new box of shells and put one of them in the cylinder of his well-called Smith and Wessen .38 and he set the loaded chamber one space to the left of the firing pin.  His horse standing sleepily near the fence came to his whistle and stood drowsing while he saddled up.

It was three o�clock in the morning when he dropped the letters in the post-office at King City and mounted and turned his horse south toward the unproductive hills of the old Hamilton place.

He was a gallant gentlemen.

Certainly many suicides are planned -- often if family members get letters or phone calls ahead of time, it can be prevented.  Sometimes though, suicidal urges come on in an unbearable wave, and if someone has access to lethal means (typically firearms, hanging, or jumping), the urge becomes deadly.  A very interesting examination of people who survived jumping from the Golden Gate Bridge showed that only 10% of people who survived went on to complete suicide later.  Most of the time, the urge to kill oneself is impulsive.  Often there are biological markers - increased inflammation and low serotonin, among others. 

Allergies, of course, are very common.  And if suicide is in part an inflammatory issue, then one would suspect that people inflamed with allergies are more likely to commit suicide.  There are, indeed, correlations between allergy and suicide.  And while I tend to think of spring and fall as suicide seasons (spring in particular)  due to rapid change of sunlight during those times, spring and fall are also allergy seasons, with spring being the peak of hospitalizations for those with severe allergy problems.  It turns out that the link between suicide and seasons (particularly the springtime) is stronger in those with allergies.

The authors of the allergy medicine and suicide paper had an interesting premise.  They looked at the theory between the connectedness of allergy and suicide in a very biological way.  They looked a data showing increased gene expression of cytokines that mediate the activity of a  of a certain type of immune cell, Th2 (T-helper cells type 2) in the prefrontal cortex of postmortem suicide victims.  Then they looked at the main treatments for allergies/asthma - antihistamines (like claritin) and intranasal steroids (like rhinocort).   An antihistamine won't change Th2 helper cell activity.  A steroid will decrease it via direct means.  The authors went county by county in the US comparing non-sedating antihistamine prescription data and inhaled corticosteroid data with reported suicides, antidepressant prescription data, availability of psychiatrists, urban vs. rural, demographics, within-country vs. intra-county and crunched numbers.  And man, they crunched numbers to a degree that is way beyond my ken.  They used logarithms and differential equations and basically took the huge amount of data and crunched the heck out of it.  I can't speak to the veracity of the crunchedness as I am no statistician.  It sounds reasonable but any mathematical skeptic who wants to look at the paper and pull it apart, feel free to get in touch.  

They found that antihistamine prescriptions (and they excluded sedating antihistamines such benadryl or vistaril which are often prescribed for sleep, not allergies) were positively correlated with suicide rates (p=.0001) and that intranasal corticosteroids prescription rates were inversely associated with suicide rates (p=.0004).  So if prescriptions for inhaled corticosteroids were to increase by 1%, the suicide rate should decrease by 0.16% (0.04 suicides per 100,000 people).  The use of decongestants was neutral with respect to suicide risk.

The discussion in the paper is complex, noting that systemic steroids are known to cause problematic psychiatric side effects (which is certainly true) but that intranasal steroids (for the most part) seem to bypass this problem and have minimal systemic effects, merely decreasing inflammation in the nose, where it counts.  Some data suggesting that intranasal steroids do cause jitteriness, anxiety, agitation, insomnia, and depression in certain people makes the findings of this study even more interesting.  Could Th2 suppression in certain cases more than compensate for the negative psychological effects of nasal corticosteroids, at least with respect to suicide? 

In East of Eden, Tom knew what his mother felt about suicide:

[She] had a strong distaste for suicide feeling that it combined three things of which she strongly disapproved -- bad manners, cowardice, and sin.

Inflammation is, indeed, unmannerly, but I think we go too far to call it cowardice or sin.  We should look closer, look further, and truly delineate this pathology.  Suicide is the 10th leading cause of death in the world, and the 11th in the United States.  Inflammation is the number one cause of death in the modern world.

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Is Postpartum Psychosis an Autoimmune Disease?

Here's an article for the "everything is connected" file.  Also for "yes, psychiatric disease has biologic underpinnings and is medical illness" file.  Also the "inflammation in the wrong place at the wrong time is super-bad" file.  And it may be of interest to anyone who has had symptoms of autoimmune disease helped by an anti-inflammatory (paleo-type) diet.

Postpartum psychosis is rare and scary.  About 1 in 1000 women become psychotic in the first months after having a baby (though anything up to 12 months after is considered "postpartum" the greatest risk is in the first month).   The most typical presentation is one of manic psychosis, with prominent insomnia, irritability, and delusions of grandeur.  However, some women will also be depressed and be delusional and suicidal, or even with delusions that lead a women to kill her baby.

Not surprisingly, a prior diagnosis of bipolar disorder is the greatest risk factor for developing postpartum psychosis.  However, most women with postpartum psychosis have no history of psychiatric illness at all (1). Often the illness requires hospitalization, and though there are no "consensus treatment guidelines," in almost all cases benzodiazepines (sedative, anti-anxiety meds, such as lorazepam) are used to help stabilize sleep-wake cycles, and in most cases antipsychotics are also used, typically with good effect.  If those aren't helping, lithium is added.

Here's another bit of info about pregnancy.  The fetus is obviously genetically different than mom, so women develop a depressed immune system during pregnancy, in order to protect the growing beastie from mom's antibodies and killer cells.  This is why I was told to studiously avoid unpasturized cheese and raw eggs and deli meat during pregnancy, and why healthy women in the third trimester are much more likely to develop severe complications and die from the flu than women who are not pregnant.

It is well known that in women with a dysfunctional immune system (the autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and autoimmune thyroiditis), the autoimmune symptoms are generally greatly ameliorated during pregnancy.  However, this time of relatively low autoimmune symptoms is followed in the post-partum period by a "rebound" with greatly increased symptoms and greater autoantibody titers measured in the serum.

So is post-partum psychosis a symptom of autoimmune disease?  Specifically autoimmune thyroid disease, as thyroid disease (both hyper- and hypothyroidism) is well known to cause psychiatric symptoms, even psychosis?

Well, those societies with socialized medicine were able to gather data in such a way as to start to give us an answer to that question.  In the Netherlands, all the women in a certain area of the country who developed post-partum psychosis and ended up in the hospital were checked for autoimmune thyroid antibodies and thyroid function upon admission to the hospital.  A larger control group of other post-partum women were also checked.  Critically, women who were medicated at admission (particularly with lithium) were excluded from the study, as lithium is known to depress thyroid function.  All women with a previous history of thyroid disease, bipolar disorder, schizophrenia, or psychosis were excluded.  That left a group of 29 women with new-onset post-partum psychosis and 117 controls.

Here is what the researchers found.  5% of post-partum women in the control group had measurable autoimmune thyroid autoantibodies at 4 weeks after delivery, a sign of autoimmune thyroid disease.  This is comparable to surveys of a general population of women in the Netherlands.  None of them had measurable abnormalities in thyroid function or any symptoms.  In contrast, 19% of the post-partum psychosis patients had measurable thyroid autoantibodies at admission (again, prior to receiving any lithium or antipsychotic medication treatment), and half of those women also had measurable thyroid abnormalities.  In the following 9 months, 67% of the postpartum psychosis women with autoimmune thyroid antibodies went on to develop measurable thyroid problems (abnormal TSH or free thyroxine).  None of the control women did.  The odds ratios for these findings were all >2, some as large as 9, which is quite significant, especially considering the size of the sample).

Even though patients with previous bipolar disorder were excluded from this study, the researchers note that the 19% prevalence of autoimmune thyroid antibodies in these psychotic women is similar to the prevalence in women with bipolar disorder (2).  And, to really get your noggins going, twin studies of bipolar disorder show that the presence of autoimmune thyroid antibodies are correlated not only to the illness itself, but to the genetic vulnerability to the illness (3).

The researchers in this study strongly recommended that all women with postpartum psychosis be monitored for thyroperoxidase antibodies and thyroid function abnormalities, and furthermore that all women at high risk for postpartum psychosis be monitored before and throughout pregnancy and the postpartum period.  Though this was a small observational study, the advice seems very reasonable.

And, as always, we find that "post-partum psychosis" like many psychiatric symptoms is the equivalent of a fever - signaling underlying abnormalities, but not always caused by the flu.  Sometimes fevers are caused by different bugs, or cancer, or autoimmune disease.  Differentiating the underlying pathology will go a long way to informing our treatments (and helping in prevention) in the future.

Psychiatrists and other doctors reading this article will be interested in one directed more to healthcare professionals about the same study at the MGH Center for Women's Mental Health blog by Ruta Nonacs, MD PhD.  Thanks to Dr. Trevisan for the link to the blog post!

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Evolutionary Psychiatry and Bipolar Disorder

A couple of papers came to my attention this week that relate to what I consider "real" evolutionary psychiatry.  That is, what are some evolutionary reasons we might have genes that make us vulnerable to psychiatric disorders.  The "real" evolutionary psychology academics consider this discussion to be "Abnormal Psychology,"  and like all evolutionary psychology, it is somewhat controversial.  I actually don't think about the disorders much as evolving in an evolutionary light� I tend to think in terms of the human body and gut and neurons working outside design specs, thus breaking down (that is "my" version of evolutionary psychiatry).  But the overlap between one ev psych and another deserves some scrutiny, because certainly I can make the case (and often do, to patients, particularly those with bipolar and ADHD and OCD) that there are elements of these disorders that are quite adaptive to certain situations, as long as the maladaptive parts don't derail everything.

Part of my major hypothesis is that the industrial/digital age and processed, low-nutrient food has brought out more severe and different phenotypes of underlying vulnerabilities, and has also brought out seemingly new illnesses ("atypical depression").  Thus a less destructive phenotype (a mildly paranoid schizotypal person, for example, who will be more creative than the average person, as compared to full-blown schizophrenia, which impairs functioning to a terrible extent) will persist in the population due to selective advantage for certain traits.

My only previous article on "real" evolutionary psychiatry can be found here: The Creative Advantage.

Well.  It is fitting the first of the two papers today comes from Medical Hypothesis.  Melissa McEwen sent it to me - I think she likes that journal because it is crazy and it makes her laugh.  (Here is advice for those aspiring to be published there:  The purpose of Medical Hypotheses is to publish interesting theoretical papers. The journal will consider radical, speculative and non-mainstream scientific ideas provided they are coherently expressed.) 

I have no publications, myself, though I have assisted in some research efforts.  My mentor would like me to cobble something together from all the research I've done for the blog on affective disorders, or something.  I never did fancy myself much of an academic� thus never felt the motivation to write anything boring enough to be published in a journal ;-)� however, it would certainly add to my street cred.  I don't know that I can write the exotic papers for Medical Hypothesis, however (Melissa sent me a paper previously about some sort of reptile origin theory of illness?  I can't remember, but it was hysterical, and it must have slipped through part of the editorial process as it was also mostly incoherent).  Back to evolutionary psychiatry!

Evolutionary origin of bipolar disorder - revised (EOBD-R) is the paper in question, by one Julia A. Sherman of Madison, Wisconsin.  A quick google search brings up her original EOBD (sans R) from 2002.  And as much as I make light of Medical Hypothesis, I do have to admire the originality of the paper, noting that it is wildly speculative and the basic premise is most likely incorrect.

Ms. Sherman connects the dots between the circadian rhythm issues and vulnerability to bipolar disorder (manic episodes are known to peak in the spring time, when the light increases exponentially day by day in extremely northern or southern latitudes.)  In a nutshell, the EOBD suggests that bipolar disorder developed as an adaptive trait in the northern temperate zones which had more extreme winters during the ice age.  If you were hypomanic all spring and summer, you got a lot of stuff done, and then you could slow down and "hibernate" (be depressed) during the winter and not use much energy.  The "R" or revision in question actually brings in the interesting bit of Neanderthal DNA that all of us non-San Bushmen (or otherwise directly derived from Africa without side-stepping through Europe or Asia and coming up close and very personal with other hominids) seem to have.  Ms. Sherman thinks that bipolar disorder is a Neanderthal trait.

Hmmm.  She brings in the observations of a German psychiatrist from the early 20th century, E. Kretchmer, who noted that folks with bipolar disorder tended to be of a certain "pyknic" constitutional type.  They have a "thick trunk, relatively short limbs, and a big head on a short, thick neck."  Apparently, several other researchers in the early 20th century, when they were really into measuring heads and body sizes and making silly claims based on the measurements found that manic-depressive patients were more likely to be pyknic (endomorphs),  and schizophrenics were more likely to be "leptosomic" (ectomorphs).  A much newer study in 2003 also confirmed this finding. Sherman believes it is striking that Neanderthals are also described as having big bellies and short limbs.  Interesting.   In addition, people of African descent apparently have lower incidence of bipolar disorder in some studies Sherman cites.  However, there is no reliable data among truly purely African populations such as the San.

There is more to the paper, but I hit the highlights.  I'm not entirely sure what to think.  There is no question that bipolar disorder has a seasonal component and that light and dark therapies can be useful. Hypomania, with the extended bursts of drive, energy, and creativity can also be very adaptive.  And one can imagine being moderately depressed during a cold, dark winter might keep a small tribe of Neanderthal out of each other's hair, when there might have been nothing much to do anyway.  I think the pyknik bit is a little ridiculous - as we know, actually, both schizophrenia and bipolar disorder are related to metabolic syndrome, even in people who have never been on medicines.  I also would bet a poodle that there are San bushmen with some bipolar disorder out there, but symptoms might be attenuated by their latitude and hunter-gatherer lifestyle with plenty of socialization and exercise (though they do like those omega 6-filled mongongo nuts), according to my own wildly speculative theorizing�

The second paper is far less... imaginative and was published in the much more staid Journal of Affective Disorders.  Creativity and affective temperaments in non-clinical professional artists:  An empirical psychometric investigation.  These researchers looked at 152 undergraduates in art school (or other creative majors) vs. 152 undergraduates who were in majors predicted to lead to professions "mostly requiring the application of learned rules" (like accounting, I suspect).  The students were tested with several standard measures to detect subclinical and clinical manifestation of cyclothymia (a mild variation of bipolar disorder), and also other scales of general health and demographic data.  I don't think it will surprise anyone to know that the creative students were significantly more likely to score into the cyclothymic range on these scales.

An interesting quote from the paper:

Positive mood, and happiness in particular, was postulated to fuel creativity. Enhanced positive affect is a feature of both hypomania and mania, which are core symptoms of bipolar disorder and may predispose people within the manic-depression/bipolar disorder spectrum to creativity. By contrast, postulated that depression might provide fresh insights which can be executed into the artistic oeuvre during the energized phases of cyclothymia.

 So it appears that bipolar disorder is linked to creativity, which may have an adaptive advantage.  I don't think that is particularly controversial, but it is nice to see more studies on the subject.  Now were Neanderthals more creative than homo sapiens?  At least in the springtime?  That might help Julia Sherman's hypothesis!

Edited to add - a Neanderthal winter love song? By Primitive Radio Gods (right click to open in new tab).

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Offline

Hi all! A snowstorm took out my
home Internet service a week ago, and it is still not repaired. I have a post written for when service is restored, but in the mean time, be sure to check out the "map" at the upper right for some pertinent archives.



- Posted using BlogPress from my iPhone

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Brain Shrinkage and B Vitamins

As we discussed before, humans are rather unique among primates in that our brains appear to shrink as we age.  When I first posted the article, Steve Parker, M.D.* noted that there was a recent article on PLOS1 about B vitamins decreasing brain shrinkage, so I thought I would investigate the matter further.  Recently I've been going through this years' issues of The Carlat Report** to get some CMEs, and they mentioned the B vitamins and that study too.

Snow Patrol:  Called Out in the Dark (right click in new tab to open)

But before we get to that study, let's look at an older one, from 2002:  Homocysteine and Brain Atrophy

(I KNOW.  Homocysteine.  That bad boy of the folate cycle.  Always hanging out when everyone wants him to be recycled and go home.  Possibly cleaving your disulfide bridges and leaving your arteries and cartilage all crispy and brittle.  Maybe just a sign that you aren't eating all your B vitamins, amino acids, and various co-factors that you need.)

Homocysteine (Hcy) has been implicated as a risk factor for vascular disease as well as brain atrophy.  There is evidence to implicate Hcy in increased oxidative stress, DNA damage, the triggering of apoptosis and excitotoxicity, all important mechanisms in neurodegeneration.  Hcy� also causes damage to the vessel wall� the high prevalence of hyperhomocysteinemia in the population and its easy treatability [via B vitamin supplementation - ED] make Hcy an interesting amino acid for future intervention studies in the prevention of degenerative brain disorders.

  So if we want to break it down, homocysteine is part of the one-carbon metabolism cycle.  B12 and folate are also an important part of this cycle, and deficiencies in these are clearly related to nerve damage and neural tube defects in infants.  Deficiencies in either of these vitamins will lead to an increase in homocysteine, which is also apparently directly neurotoxic.

The brain might be particularly vulnerable to higher levels of homocysteine because it lacks two major metabolic pathways for eliminating it (biochem nerds, hold on to your hats), remethylation and transsulfuration.

All right.  There's theory, and lots of it.  What about the observational evidence?  Well, a number of cross-sectional studies have examined a relationship between too much homocysteine and brain atrophy.  In an Australian study of stroke patients, high homocysteine was related to increased brain atrophy, and the OPTIMA and Rotterdam studies replicated this finding in healthy elderly.    Other observational studies have shown a correlation between higher homocysteine level and Alzheimer's disease, to the point where homocysteine levels seemed to be able to predict the speed of progression of the disease.

If we look at specific cognitive impairment trials, higher homocysteine levels have been shown to correlate with poorer performance on a number of cognitive tests - story recall, spacial coping, etc.  In fact, homocysteine levels accounted for "7-8% of the variance in late-life cognitive ability."

In a prospective observational study (the Framingham heart study), higher homocysteine at baseline was related to an increased risk of developing Alzheimer's later on.  Several other smaller studies have repeated this finding.

Moving onto trials - B vitamins lower homocysteine levels.  Folic acid supplementation can lower homocysteine by 25%, B12 by a further 7%.  Betaine is somewhat less effective.  These B vitamins have been used in mild cognitive impairment and dementia.  In small, open-label trials, B vitamin supplementation (typically folate and B12) have been helpful in some tests of cognitive impairment and homocysteine levels�

Fast forward to 2010, when the freely available study at PLOSone came out:  Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in  Mild Cognitive Impairment: A Randomized Controlled Trial

Sounds cool, right?  Well, turns out the first author has a patent for a folate or B vitamin something or other in the treatment of Alzheimer's so keep that in mind.  But still cool.  168 folks with mild cognitive impairment were randomized to placebo or B vitamin supplementation (0.8 mg/d folic acid, 0.5mg/d vitamin B12, and 20 mg/d vitamin B6).  Both groups of people underwent baseline and serial follow up MRIs and cognitive testing.

In the end, the B vitamin supplementation seemed to slow the brain atrophy compared to the control group.  The treatment response was related to baseline homocysteine levels - the rate of atrophy in patients with a homocysteine level at baseline of >13 micromol/L was 53% lower in the active treatment group than in placebo.  A faster rate of atrophy was associated with lower cognitive testing scores.

So, pretty interesting.  And certainly treating our elders with B vitamin supplementation seems to have few downsides.  A lifetime of offal eating might leave us well-served in that regard.

* Steve Parker MD is the go-to person where I send my patients leery of my wild and wooly evolutionary approach who are looking for something a bit more� conservative.  He has a great set of evidenced-based blogs and books on the Mediterranean Diet, with some ketogenic options, and has recently started up a Paleo Diabetic blog as well.

** The Carlat Psychiatry Report is my go-to source for unbiased, evidence-based round-ups of everything in psychopharmacology and beyond.

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Quick Talk Update

Just a quick reminder that I will be speaking to the Harvard Law School Food Law Society at Noon on Monday, October 31, 2001.  Further details about the event are here:  http://hlsfoodsociety.weebly.com/events.html

I am told it is open to the public.

I've been deluged at work, but have managed to pull a few interesting papers today, so cross fingers that I will get a moment to blog about them later tonight or tomorrow.

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Conventional Wisdom and the Lunatic Fringe

This weekend I had a terrific opportunity.  Nathan Rosenberg is an exceptional fellow who is co-president of the Harvard Food Law Society and a key organizer of next year's Ancestral Health Symposium.  He found me at AHS11 and asked me if I might be interested in speaking at Harvard Law School - I said sure, though I wondered what I would say, seeing as how doctors and lawyers are natural enemies. (Kidding.  Sort of.  Actually I have a GREAT lawyer.  He probably sleeps better not knowing about this blog.)

My talk is next week, on Halloween - the link is here.  I'm really looking forward to it.  My focus will be on how diet is likely a large actionable component of our mental health problems, and how mental health is both expensive and disabling.

However, on October 21st, the Harvard Food Law Society sponsored a great event - TEDx talks on obesity, with some of the foremost obesity researchers in the country (including Willet, Ludwig, Lustig, and Guyenet) along with many lawyers and policy makers talking about their efforts to encourage local agriculture and vegetable consumption over promotion of the commodities crops and CAFO operations.

The talks will be freely available some time - maybe follow the TEDx website?  They were fascinating - I was, frankly, shocked by Willet's dietary prescription based, for the most part, on epidemiologic evidence.   He advocates cereal fiber and polyunsaturated fats as a major portion of a "prudent" diet.  He was very pro-Mediterranean diet and whole foods, but was quick to say "it's all digested to the components" - so does he think a whole grain cracker fried in seed oil and sprayed with some vitamins is equivalent to nuts and legumes?  He was anti-saturated fat and red meat, but pro-poultry and fish.  He mostly stuck to obesity and heart disease, but used epidemiology and small, short randomized controlled trials as evidence.  Willet is, apparently, the 2nd (or 6th?  I forget) most cited person in the scientific literature.  He is HUGE.  He is conventional wisdom, in a nutshell, though Stephan Guyenet told me Willet is pro-egg, and Willet himself says that the food pyramid, demonizing fats and, in effect, promoting low-fat processed carbohydrates in favor of whole foods, was a public health disaster.

If we rely on epidemiology alone we would still have 90 y/o women taking hormone replacement therapy.  But Willet seemed convinced that confounders are easy to account for.  His confidence was� breathtaking.  Willet also dismissed anecdotes of traditional diets as the weakest form of evidence (which isn't entirely wrong, but ignores the compelling congruence of these healthy human diets across many cultures).  Willet also said that ancestral diets are not useful because "those people only lived to 50-55 and we don't want that."  Sigh.  Willet eats kashi grains for breakfast, apparently.

Ludwig's talk began, very promisingly, with an evolutionary history, but ended with the basic Harvard School of Public Health prescription for a healthy diet.  (Ludwig got a lot of media flack recently for suggesting that obese kids should be taken from their parents - the actual editorial he wrote suggests that foster care could be an option in intractable cases and I feel was taken out of context).  I was puzzled how we got to cereal fiber (how do we have cereal fiber, on a viable level, without processed foods?) and seed oils, but that's epidemiology for you.  He was quick to point out that if we substitute nuts and legumes for a big mac, once a week, we would have a measurable difference in obesity over time.  Okay - Stephan Guyenet was quick to point out the sleight of hand.  The substitution does not mean that red meat is bad for you.  Well - Ludwig looked great (very slender, not-inflamed looking at all) and apparently might be interested in speaking at AHS12.  It seems he is thinking in evolutionary health ways, but has not strayed from the conventional wisdom fold as of yet.  Very interesting.

Stephan's talk was excellent; it was mostly a historical review of the changes in the American diet over the past 150 years.  He pointedly showed the increases in fat (primarily polyunsaturated), poultry consumption, and linoleic acid over the last 50 years, coinciding with the obesity and diabetes epidemics.  His major point was that we have gone from all home-cooked foods to a high level of fast food, restaurant food, and pre-prepared convenience foods at home.  Does convenience kill?  Most likely...

(An important note - heart disease has been in decline for the past 30-40 years, though it might be leveling off now.  It is unclear if that is due to aggressive control of high blood pressure, dietary changes, or even statins.  But don't make the false proclamation that heart disease is increasing lately, because it is not).

Lustig did his anti-sugar talk (which also pointed out the problems with epidemiology as a prescription, I am told) on Thursday night, when I could not attend.  He did attend the panel discussion, when he came out as neutral on sat fats, pro-omega3, anti-omega6, anti branched chain amino acids, and anti MCTs.  And, of course, anti frucrose, and while he would not come out against whole fruit whole hog, he did discuss the anecdote of the "fruit orgy" of orangoutangs where they seasonally develop insulin resistance and put on fat.  Lustig seems to feel that fructose, MCTs, and BCAAs are damaging to the mitochondria and lead to insulin resistance (thus he is anti-corn fed beef, as corn-fed beef is higher in BCAAs than grassfed, apparently.  I don't know enough to say whether that is wacky or not.)  Ludwig was quick to point out that there is no evidence linking fruit consumption to any chronic illness.  I'm quick to point out that I eat 1-2 bananas a day, and I rely on 1/2 banana before and after crossfit for happy lifting.

What we can all agree on - eat "real" food, and from a policy and preventative perspective, perhaps the most important, simple message is to eliminate sugar-sweetened drinks in the diet.  I think everyone would pretty much agree on that one too.

The policy/lawyer talks were terrific -- they were very interesting, and exciting, as these lawyers and seasoned politicians are going forth to help farmer's markets and soil preservation, water preservation, sustainable agriculture and align government policy incentives with the supply and availability of local, real foods.  Some of the real initiatives include penning legislation to abolish state sales tax at local farmer's markets (just as most states do not charge sales tax for staple food items at the grocery store), and streamlining state and local regulations to allow for farmer's market and production and sale of homemade low-risk specialty items (such as jams or apple pies). As the current farm bill heavily supports the commodity crops (corn, wheat, soybeans, etc.) and downgrades vegetables to "specialty crops," some changes would be nice!

I left the talks a little shaken.  I felt (as always) the standard anti-obesity message is not practical for a non-Mediterranean culture and likely to be a terrible failure here in the U.S., land of the processed health food,  and the pro-egg, fat-is-okay (albeit *cough* polyunsaturated) message has certainly not been carried to clinicians, nutritionists, and doctors in the field.   That Willet and Ludwig were not willing to support whole dairy or red meat/pigs was unfortunate.  The "whole foods" message gets really lost when we are parsing out red meat and even dairy.  Forget the "nuts and legumes" (seriously, legumes?  The only beans worth eating are refried in lard, amirite? - to clarify, this is my little joke, as beans upset my tummy) - how to we kick red meat and dairy to the curb without eating a crapload of disgusting kashi?  I can't fathom it - Stephan I think would advise in consideration of sustainability and a large scale policy level for us to add potatoes (not fried, but whole, baked or boiled potatoes) and use traditional methods to prepare grains.

However, today I was fortunate enough to be invited to a lunch with Stephan Guyenet, Mat Lalonde, and friends and significant others.  It was very refreshing to be with Mat and Stephan, who seem to be aligned with me about not supporting the some paleo fringe extremes (meaning acceptable carb levels vary, gluten and dairy levels vary in tolerance on an individual basis, etc.).  We were also concerned about ideologues who seem to support one aspect of a diet as the end all, be all to ill health (fructose, or wheat, or carbohydrate), when the scientific truth is far more complex.

One of the most interesting aspects of the discussion was reflection upon genetic adaptations to agriculture - hemochromatosis (a disorder where humans can't properly get rid of iron, which was likely protective in grain-eating, low iron situations but which would make a classic low-carb, ruminant heavy, offal heavy diet dangerous), lactose tolerance in adulthood, and variations in folate metabolism.  Evolution did not end with the paleolithic, of course, and while the generalities of "eat real food" are true for everyone, the specifics can vary a great deal depending on context - insulin resistance, obesity, large exercise volume, etc.

I don't have a specific prescription on this blog for a very important reason, but let me be explicit  - for the most part, go archevore, exercise, tighten up the sleep, learn stress reduction, and that will help a great deal, and if all those things aren't in order, meds and strict ketogenic diets and supplements may well be shoveling sand against the tide.   This all doesn't mean I'm entirely anti-meds or anti-ketogenic diets - indeed, if the issues are substantial and significantly impair functioning, I want to help in whatever rational and evidenced-based way possible� but don't look for magic.  For the most part, it fails us.

How You Like Me Now?  The Heavy

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