Anorexia and Season of Birth

Quick post tonight.  I have been at a conference all day (and will be there all day tomorrow), and I'm swimming in a bit of information overload.  However, a bunch of new ideas are now simmering for future posts.  I have some more Diet and Violence papers to blog about also, but first a little paper sent to me (of course) by Evolutionary Psychiatry's dear friend, That Paleo Guy, Season of birth and anorexia nervosa from the British Journal of Psychiatry.

(Retriever, I think this post will also address some of your questions from your excellent comment on my last post!).

Previous studies of anorexia and birth month were too small to be of much use.  You need a lot of cases to detect differences between patients and controls if season increases risk marginally.  In this study, the researchers combined the results from several different UK studies, and then used some fancy statistical techniques such as "harmonic and spectral analysis" as opposed to the traditional chi squared test to wring as much out of the data as they could.

All told, 1293 cases of anorexia nervosa were compared to births in the general population from 1950-1980.  The results:

Here is the pertinent graph (reproduced here with permission) and the source: linked at the British Journal of Psychiatry.

You will see there is a bit of a spike of anorexia cases for people born in the springtime, and a yearly nadir in October.

The discussion is short but sweet (and as the paper is free full text, I encourage you to take a look from the link in the first paragraph).

What these sorts of results show us is that early life and the neonatal period can plausibly be a time when suboptimal environments can eventually show up as disease later in life.  Apparently there was a finding recently that an interaction between a dopamine receptor gene and season of birth influences body weight regulation in women with bulimia (1).   But here is a problem with season-of-birth research - pregnancy is 9 months long, and obviously development occurs during all of that time, with vulnerable developmental windows of different sorts opening at different times all during the gestation.  The environmental factors that could affect a seasonal change include maternal nutrition, sunlight, vitamin D, stress, temperature, and infectious disease (you can probably think of a few more).

Here is a quote from the study pertinent to Retriever's question and encapsulates my thoughts as well:

Interestingly, vitamin D levels have been shown to be associated with psychiatric disorders.  Although the presence of low vitamin D levels in people with psychiatric illness may be the consequence of reverse causation, further support for a role of vitamin D comes from functional studies showing that it is also involved in neuroprotection and brain development.

So low vitamin D during development could plausibly cause problems - or maybe low vitamin D in mom is a sign of some sort of illness or problem, and that illness is the issue… if the first part is true, vitamin D supplementation will be protective.  Otherwise, who really knows?    Vitamin D has SO many roles in the body that pinning down the whys, wherefores, and causation chicken-egg issues can be super tricky.

It would be nice if some vitamin D levels were measured - in the Netherlands they keep samples of neonate blood and have measured vitamin D levels for schizophrenia research - I bet someone could do the same comparison with anorexia.  It would still just be an association, but at least we could say vitamin D was definitely involved somehow if such a study were done.

Well, better get some shut eye as I have to be up early for the train into the city.  Good night!

Standing on the Sun Will Not Prevent Depression

Vitamin D. What a roller coaster. There's the Vitamin D Council telling you to aim for a level of 60-80 ng/ml, and then the Institutes of Medicine rather grumpily suggest 20 is sufficient with a monstrous report no one has time to read except Chris Masterjohn. Vitamin D Council says no risk of toxicity below 150 - Chris Kresser, Paul Jaminet, and Kurt Harris talk about lack of randomized controlled trials and suggest somewhere between 20-50 as a good range (depending on the expert and depending on your skin color), and there is risk of kidney stones, calcification, and premature aging at higher levels. As I am a (very) pale woman, and I have looked at a bit of the pregnancy and cancer literature, I tend to think, hey, pale pregnant women might do better a bit above 50, Caucasian women should aim for 40-50, and everyone else, 30-40 is probably a good range. But Kurt makes a good point in his podcast with Chris Kresser - the 25 (OH) Vitamin D3 level we al measure is still indirect. 1,25 OH Vitamin D is the active hormone, but its metabolism is tightly regulated and levels are rarely out of a narrow range no matter how deficient we are - so who knows what a low serum level of 25 (OH) Vitamin D3 actually means in local areas, such as the brain, or in scanning for cancer cells in other sequestered areas of the body.

I don't know if I really have much of a horse in this race, though, as the data for mental health is scanty, to say the least. But the theory is sound for vitamin D to play a prominent role in mental health, as it interacts with stress hormones and nerve growth and repair, and seems especially active in those areas of the brain associated with mood, appetite, and sleep (the hippocampus and hypothalamus).

Australian researchers have been valiantly paving the way in single megadoses in seniors for years now. In the Vital D Study, 2317 women over 70 living in the community were recruited from voting rolls (which is compulsory in Australia). Women were included in the study if they had a high risk of hip fracture or previous hip fracture, osteoporosis, or high risk of low vitamin D levels. For several years, they were given a single dose of 500,000 IU Vit D3 or placebo (in 10 easy to swallow capsules) once each year in the autumn or winter, and several measures were followed along the way.

One of the measures, more fractures, proved that standing on the sun once yearly is not a terrific way to prevent them. The active group getting the vitamin D had significantly more fractures and falls.

And then there is depression. It was a lot of people, so the typical short scales were used (the GHQ-12 questionnaire). I already blew the punch line in the title. The active group had no significant difference from the placebo group in the amount of depression or change of depression with the huge bolus of vitamin D3.

Let's look more closely. The average vitamin D level for all the women at the beginning of the study was about 50 nmol/L (1 ng/ml = about 2.5 nmol/l, so the more typical 25 OH vit D3 level measurement I'm used to seeing is 20 ng/ml.) For the most part, the women in the active arm had vitamin D levels 40% higher than the placebo arm, with a level of 120 nmol/l (48 ng/ml) after dosing, and 90 nmol/l (36 ng/ml) after 3 months.

And the discussion, which is (typically) the most interesting part. The association between vitamin D and mental health is inconsistent. Epidemiology shows a correlation between low levels of vitamin D and depression. In a small fibromyalgia study, mood and fibromyalgia symptoms were not related to vitamin D levels before or after supplementation, even in those with vitamin D deficiency. In another 6 month study of older women receiving 800 IU Vit D3 and 1000 mg calcium daily, depression scores did not improve compared to placebo. In another group of folks receiving 100,000 IU Vit D3 vs phototherapy for seasonal affective disorder, Vit D3 was a clear winner. In another study of obese individuals, 20,000-40,000 vit D3 per week for a year showed a beneficial effect on depressive symptoms, though those with a baseline level > 40 nmol/L (16 ng/ml) had no benefit.

How to pull it all together? Well, 1,25 OH Vitamin D, the active form, definitely has a role in the central nervous system in neurogeneration and repair. However, the CNS may have a separate conversion system from 25 OH Vit D3 than the rest of the body. Evidence from a study I blogged about earlier suggests maybe a u-shaped curve is applicable - neonates with the lowest and highest amounts of vitamin D had the highest risk of schizophrenia later in life.

It is probably safe to say that giving 70 year old women massive doses of vitamin D3 once a year is a bad idea - bones and mental state accounted for. "Clinical studies of vitamin D in clinical populations with documented insufficiency remain warranted." And, indeed, at no time in history would we ever have been exposed to 500,000 IU vitamin D3 in a single day.

My personal clinical experience? A LOT (I'd say 1/2 to 2/3) of people who come to see me have horrible vitamin D levels. I live in the far north of the US, but it is not uncommon for levels of 12-14 ng/ml to show up on my initial tests, with the lowest I have seen being 4. I would have to say, sunshine and/or vitamin D supplementation (depending upon the season) has perked up my clinical population over a timeframe of, say, 6 months. At the same time we have implemented other interventions (nutrition, therapy, medication), so who knows what made the difference.

Is Vitamin D the end-all, be-all missing link to the question of crappy modern health and modern disease? No. Does it play a role? Most likely. But you can't overdose on vitamin D via sunshine, and you sure can via megasupplements. Vitamin D is a hormone that sticks around for a while, not something to muck around with willy-nilly. I supplemented this winter, as I was low. I'll make every effort to soak up the rays all summer. Will I supplement next winter? Probably not.

Diet and Violence

Paul Whiteley*, I believe, originally posted to the comments concerning some very interesting studies on diets and violence. Over the past 10 years, several groups of researchers have done some decent work in this area, and (for once in the nutritional-type literature) I can actually look at a randomized controlled trial of good size and design that was actually replicated.

The modern era of good studies begins with Oxford nutrition and criminology researcher, Bernard Gesch (1). Back in 2002, he published a (full free text) study entitled "Influence of supplementary vitamins, minerals, and essential fatty acids on the antisocial behavior of young adult prisoners." In this study, 231 (young, male, adult, prisoner) volunteers agreed to receive a daily vitamin, mineral, and essential fatty acid supplementation or placebo. The average length of the supplementation was about 142 days, and a number of measures were taken before and during the active phase, including psychological testing, reports of violent acts, and reports of disciplinary action. Prisoners were randomized in part based on baseline disciplinary status and their progress in the "prison regime."

Here are the active ingredients of the multimineral, multivitamin, one of which the prisoners in the active arm received daily:

The prisoners also received a fatty acid supplement with 1260 mg linoleic acid (I know - we'll talk about that later), 160 mg gamma linolenic acid, 80 mg EPA and 44 mg DHA. The placebo fatty acid pill was made from vegetable oil.

The results? The average number of "disciplinary incidents per 1000 person-days" dropped from 16 to 10.4 in the active group (p<0.001), which is a 35% reduction, whereas the placebo group only dropped by 6.7%. Especially violent incidents in the active group dropped by 37%, and in the placebo group only 10.1%. That's a pretty impressive finding, really. Currently, Gesch is working on a study of 1000 prisoners in 3 different UK prisons for a 3 year trial, including blood chemistry analysis to see what the baseline levels of micronutrients are in the prisoners, and also more cognitive testing, designed to answer some questions the earlier study couldn't answer. However, luckily for us (as the newer Gesch results have yet to be published), a Dutch research team led by Zaalberg repeated the experiment (more or less) in "Effects of Nutritional Supplementation on Aggression, Rule-Breaking, and Psychopathology Among Young Adult Prisoners." The researchers note that behavior issues have been linked to deficiencies in omega 3 fatty acids, and that low levels of magnesium and zinc are also associated with hyperactive behavior, impaired brain development, and cognitive dysfunction. Check out the quote from the study:

The mechanisms underlying potential associations between nutrition and behavior, however, are not yet clearly established. Although a clear comprehensive theory is lacking, several findings do offer some clues on the plausibility of dietary interventions. Epidemiological research, for instance, shows that major changes in dietary patterns over time have taken place, especially in industrialized world during the last century [Cordain et al., 2005; Crawford et al., 1999; Muskiet, 2005; Simopoulos, 1999]. These changes resulted in (micro)nutrient intakes that are significantly lower than in the ancient, Paleolithic diet. Indeed, some ecological studies show correlations between diet and behavioral outcomes [Christensen and Christensen, 1988; Hibbeln, 2001; Peet, 2004], including criminal behavior [Hibbeln, 2001]. A major limitation of epidemiological studies is, however, the impossibility of making causal inferences. For this reason, the findings mentioned above must be judged with caution and experimental confirmation is needed.

(I love these researchers already!) They did this trial specifically to see if they could replicate Gesch's work. Only they made some very likeable modifications in their supplement - specifically leaving out linoleic acid "because of its abundance in the Dutch diet", and using larger capsules that could include more bioavailable forms of minerals, so there was more magnesium (300mg of Mg citrate vs 30mg (of ?) in the Gesch trial). They also halved the amount of vitamin D (from 400 IU to 200 IU) in the supplement (but did not specify why). And no one supplemented with micro doses of lithium :-).

Here is how they changed the omega 3 compared to Gesch:


In all, 221 young male prisoners completed the study. Many dropped out, often due to transfer to another prison or being released. Of the completers, numbers of violent events in the active group dropped 34%, whereas incidents in the control group increased 14%. The overall number of incidents was lower (11 per 1000 person-days) in the Dutch prison compated to the UK one, but the percentage change was still significant. There were no significant differences in any of the cognitive, personality, and behavioral testing measures used, just the actual incidents. Which is interesting. Because you can't figure out, from this data, why the incidents decreased. If you could say - oh, look, impulsivity and attentional measures improved, then you could say that's why the behavior is better. But they didn't improve. Which means maybe the cognitive measures aren't very good, or the effect was too subtle to catch. Well, I know a prison warden cares more about decreasing reported numbers of violent incidents in a prison compared than decreasing the psychologic testing measures of impulsivity.

One problem with this second study is that at the beginning, 51% of the prisoners guessed wrong as to whether they were receiving active vs. placebo pill. By the end, only 25% guessed wrong, suggesting the blind was somehow partially broken (perhaps by smell of the pills?). Violent incidents were measured by the prison staff, it is unknown whether the prisoners told the staff if they suspected active or placebo pills. So keep that in mind when interpreting the results.

Here is the Dutch researcher's conclusion, and it will serve as mine as well:

To summarize, the prospect of influencing aggression and rule-breaking behavior with nutrients in moderate doses is important enough to warrant further research. This is particularly true as adequate supplementation may also have beneficial effects on mental health and cognitive functioning [Benton, 2001; Hibbeln, 2001; Richardson, 2004]. This study, however, did not confirm this association, except for some marginal trends in this direction. Yet, as the found decrease in the outcome measure—reported incidents and rule-breaking—is in line with the earlier British prison study of Gesch et al. [2002], we feel that further research on the association between dietary status and violent behavior is warranted

* I really enjoy Paul's blog, Questioning Answers, focused on research and thoughts about autistic disorders. He is far more sober in his interpretation of the science than I am myself - which is likely a far more accurate portrayal of the validity of the results.

A Summary of Endocannabinoids and Obesity

In my last post on endocannabinoids, I was trying to do a little too much with too little time, and I don't think the science came out too clearly.  Today I thought I would use the excellent Kim et al paper again for a quick summary of what is known about the effects of the endocannabinoids on obesity, both in the central nervous system (my usual bailiwick) and peripherally.  (Also, please check out Beth's post over at Weight Maven - she has diagrams too!)

Endocannabinoid AEA will activate the cannabis receptors in the brain and in the fat tissue and skeletal muscle.  The response is to increase food intake, possibly by increasing the appetite hormone ghrelin.  AEA is found at higher levels in obese individuals than lean individuals, and seems to promote fat storage. In the muscle, it decreases glucose uptake, which is one way to increase insulin resistance.

The other major human endocannabinoid, 2-AG, also increases food intake, and is also found at higher levels in obese individuals.  The amount of 2-AG you have circulating in your body is positively correlated with how much body fat you have, and inversely related to insulin sensitivity.  It also decreases glucose uptake in the muscle.

CCK is a hormone secreted from the intestines when we eat.  Normally it sends a signal to the brain telling us that yes, indeed, we have eaten, and we can back off with the hunger signals already.  AEA and 2-AG at higher levels seem to interfere with this whole signaling process - and, once again, higher levels of AEA and 2-AG are found in obese individuals.

Leptin is a hormone that acts in the hypothalamus of the brain.  When it is working normally, leptin sends a signal that we have fed and we need to not be hungry anymore.  However, obese individuals often have high leptin levels, suggesting that the brains of obese individuals have become resistant to leptin's effects.  Leptin-resistant mice have increased levels of endocannabinoids swimming around in their plump mouse bodies.  In mice born without the ability to make leptin, treatment with leptin will very quickly lower endocannabinoid levels.  So obviously there is cross-talk and regulation that somehow becomes broken in the case of obesity.

SO - omega 6 fatty acids become endocannabinoids, which are associated with increase fat tissue, decreased insulin sensitivity, and leptin resistance.  Oops!  (But keep in mind we only have the "associated with" there, not the smoking gun.  It's just… such a pretty theory, I can't help but squee a little.)

Kim et al. are very pro-omega 3 fatty acid, suggesting that it will help reduce obesity, reduce endocannabinoid signaling, and increase insulin sensitivity.  They do use the work of William Lands to suggest that "an increase of dietary omega 3 PUFA was more efficient in decreasing eicosanoid formation from omega-6 derivatives than decreasing omega-6 PUFA in the diet."  (Eicosanoids are the bioactive molecules, such as prostaglandins, endocannabinoids, and thromboxane, that are made from omega 3 and omega 6 fatty acids.)

I just downloaded and took a gander at the Lands paper referenced, and the whole time the good Dr. Lands talks about how the current 7% of US and Denmark diets of omega 6 PUFA is too high, and increasing the total ratio of omega 3 to omega 6 PUFA is the reasonable way to go  - it seems that in systems that are deficient in omega-3, we will hungrily gobble up the omega 3, so that is perhaps what Kim et al means by "an increase of… omega 3… was more efficient… that decreasing… omega 6 PUFAs in the diet."  But who knows what they were thinking.

Very interesting quote from the Lands article about fish, however:

"A fatal hypersensitivity to environmental stimuli ("fainting shock" syndrome) is exhibited by rainbow trout that are fed diets containing n-6 fatty acids without sufficient counterbalancing amounts of n-3 fatty acids ( 10)."

Fainting shock syndrome!  Wow.  If you are a rainbow trout, do not eat corn oil.  Enough said.

Three Autism Posts at Psychology Today

Photo Credit

Diet and Autism

Diet and Autism - Newer Studies and Intriguing Links

Autism - Inflammation, Speculation, and Nutrition

An Introduction: More on Endocannabinoids *cough* With a Focus on Obesity Regulation

I'm very tempted to link a Pink Floyd song here. But, truth be told, that was a little before my time. Instead we'll do some more Metric (right click in new tab - yes, it is from the movie Eclipse, which I haven't seen. Glittery vampires aren't really my thing. But the song is rather dreamy - and I had to change the original link for one with an ad as the original was removed.  Sorry 'bout that).

I took the day off today - try to do that every four months or so, but last year was mostly unable to due to growing a new business. However, I won't be missed too much for a couple of days now, and I was finally able to clean up my room after a little too long. (Working mom, two kids, not much time - and usually I spend what moments I have reading and blogging!) In amongst the stack of papers was my last lipid profile, (yes, I am going to pull a Gary Taubes here) done back in 2009, pre-paleo, when I was on what I call a "Michael Pollan" style diet. Lots of whole grains, fruits, lean meat, fish, and vegetables, avoiding vegetable oil, not too deathly afraid of butter, but most breakfasts were oatmeal + frozen fruit + skim milk nuked in the microwave. Very different from today's breakfasts of eggs or nothing. Anyway, as I was breastfeeding at the time, the nurse did not have me fast for this test (tell a breastfeeding woman to fast on a high carb diet and she will probably take off your head and eat it). It was drawn around 1:35 pm for a disability insurance physical, so probably 60 minutes after my last meal. I had trouble losing the excess baby weight before primal/paleo and weighed 25-30 pounds more then than I do now:

glucose: 91
triglycerides: 100
total cholesterol: 183
LDL: 106
HDL: 57
Chol/HDL ratio: 3.2

It's not all that terribly interesting. I imagine total cholesterol and HDL are higher now, and who knows what my fasting glucose and triglycerides were. I should add that the only one I know of in my extended family who died of heart disease was my paternal grandfather, who succumbed to a heart attack at 89 after 30 years of poorly controlled type II diabetes. That said, I think the labs do show that a high carb diet won't necessarily throw your glucose or even triglycerides "through the roof" after a meal.

Endocannabinoids are ubiquitous in the central nervous system. Pharmaceutical companies are pretty excited about them, for if they get the formula right somehow, there is the potential to throw expensive patented medicines at "food intake disorders, chronic pain, emesis, insomnia, glaucoma, motor disorders, stroke, and severe psychiatric conditions such as depression, autism, and schizophrenia." (1)

What is an endocannabinoid, to start? Well, it is a locally acting neurotransmitter. It is made nearby to where it is used, making it unlike a hormone (or the cannabis plant active component THC), which often has effects from far away. The major endocannabinoids (eCB) in the nervous system are derivatives of arachidonic acid, itself a derivative of the omega 6 linoleic acid. eCBs are a molecular key. Don't think it escaped my attention that the omega-3 derived receptor molecules could serve as a regulation system at the endocannabinoid receptor lock, as I discussed in a previous post. That tends to be how these things work. O6 is on a see-saw with O3, and the evolutionary body and brain never saw a massive imbalance of the two known as the Western Diet coming.

Because eCBs are locally acting, one has to consider their effects locally. As a psychiatrist, one of my major interests in the prefrontal cortex (PFC). That is basically the outer rind of your brain right in front. Have a thin prefrontal cortex? You are much more likely to have impulsive behaviors and get caught doing silly things and end up in jail. A thick prefrontal cortex? You probably think too much, don't take risks at all, and would make a great living in academia. A medium prefrontal cortex? Absent a conscience, you would be master criminal, never to be caught (that might be the glass half empty view of things). Otherwise, you might end up like me, with a conservative medical practice and a renegade blog.

So, at least in mice (and I don't have reason to think human prefrontal cortexes vary much except in size and complexity), eCBs are very important in regulation of all sorts of molecular systems in the prefrontal cortex. Y'all might remember that excitatory neurotransmitter, glutamate - well, turns out that eCBs will inhibit it. And, as I discussed in the previous post, they tend to turn down the volume on excessive or repetitive stimulus in the PFC via a process known as long term depression. Though that sounds bad, long term depression is good. It's your brain's way of modulating signals. Sort of like how hopefully you can tune out the jackhammer going all day across the street while at work.

In other areas of the brain, endocannabinoids regulate key positions, such as appetite and addiction. The major endocannabinoid receptor in the central nervous system, CB1, seems to have a part in emotion processing, pain perception, and motivation for food intake (2). The CB1 receptor inverse agonist (an agonist activates a receptor, an antagonist typically merely blocks a receptor from being activated, while an inverse agonist sort of reverse-activates a receptor, just so you know), rimonabant, seemed like a hopeful drug to help with weight loss, smoking cessation, and other drug dependence. Plans for investigation of this drug included uses in cardiovascular disease, shock, liver disease, gastrointestinal disease, and arthritis.

And, as we mentioned in the last eCB post, even when rimonabant was used in psychiatrically healthy patients, the treated patients tended to struggle with mood symptoms, anxiety, and suicidal and aggressive tendencies. As my 2 year old would say, "Oopsie daisy!" On rimonabant, these anxious and suicidal symptoms occured 28% of the time, compared with 14% of those taking a placebo.

What is interesting to me is that psychiatrists traditionally viewed the opiate system as being more associated with reward and pleasure than the cannabinoid system. And yet a strong opiate blocker, naltrexone, can be used for a period of months in people with no seeming side effects. I've prescribed it a number of times, and no one developed anxiety or suicidal tendencies - quite the opposite, in fact. People noticed a decrease in cravings and overall discomfort. Not that naltrexone is an evolutionary answer - it is just interesting, compared to rimonabant (which I must admit, I've never prescribed.) And, indeed, the eCB system interacts only indirectly with the dopamine/opiate system. I find that quite remarkable.

But let's move on to something of interest to a more general audience - endocannabinoids and obesity, and we will refer to a neat paper Endocannabinoid signaling and energy metabolism: A target for dietary intervention (by Kim et al.)

I'm going to do a rare switch from alternative rock and classical at this point and recommend Dvorak's Serenade in E Major.

CB1 is found in the brain, but also in in muscle, the GI tract, and fat tissue. In obesity research, the focus is often turned on the hypothalamus, the brain's center of appetite and sleep and hormonal regulation. And, indeed, when we experience food deprivation, our eCBs go to work, making us hungry and interacting with some other rather famous hormones => orexin, leptin, and insulin. The endocannabinoid system in the muscles and gastrointestinal tract and fat tissue seems to communicate with the brain, directing overall energy intake in relation to expenditure. Loss of leptin and insulin regulation of the endocannabinoid system is suspected to be part of the cause of obesity and type II diabetes.

Omega 3 fatty acids are known to be satiating (3) (except, frankly, in sushi, which always makes me more hungry. Why is that?) Researchers have speculated (as I do now) that the increase in omega 3 PUFAs in the receptors leads to changes in the receptor affinity for the omega 6-derived eCBs. Interestingly, in the Kim paper, he notes omega 3 intake is associated with lower endocannabinoid levels (AEA and 2-AG) as less arachidonic acid (the eCB precursor) is incorporated into the cell membranes. The researchers go so far as to suggest that increasing the dietary ratio of omega 3 PUFAs would be a "practical approach for changing the fatty acid composition of cellular membrane phospholipids to alter membrane signaling to serve as a promising tactic to decrease the synthesis of endogenous ligands for cannabinoid receptors and minimize ECS activation."

In cows, dietary modulations of arachidonic acid and DHA (even studies using krill oil, which I would suggest is outside a cow's evolutionary experience) have been shown to change the levels of endocannabinoids in the central nervous system - AA increases eCBs, DHA seems to decrease them. This change occurs rapidly - within 2 weeks. The researchers move on to humans, discussing studies of omega 3 intake among obese and diabetic women and men, whose inflammatory markers, hunger, and body weight decreased within a few days of eating more omega 3s. Leptin is also thought to be increased by the omega 3 fatty acids (at least in rats).

There are a number of other hormonal systems involved with obesity, including regulation of the eCB system and ghrelin and CCK. In short, "the EC system works with the endocrine system and neural networks associated with the hypothalamus and the gastrointestinal tract to regulate the energy balance of the individual."

I could go on for a while, and I will have more posts on endocannabinoids and psychosis and neuroplasticity and neurotoxicity. But here we have a local neurotransmitter regulated system of addiction, pain, and appetite dependent (perhaps) upon dietary regulation of omega 3 and omega 6 fatty acids. You see why scientists suspect a multigenerational effect of the excess omega 6 in brain development and the earlier onset of fat gain and diabetes this last generation.

Scary, really. I avoided omega 6 (as much as I knew how) through both pregnancies, and then breastfed, eschewing formula (except for a small amount when the youngest was 11 months old) - both were weaned to whole cow's milk in addition to regular food around a year. My kids are very tall (99-110% of normal height for age) and average about 70% of normal weight for age. The charts are based on averages of singleton births in the US in the year 2000 or so, well into the reign of omega 6 PUFAs. I don't know how much of the kids' stats are due to genetics or food or what, but I'll leave it like my stats from my Michael Pollan diet - an interesting data point.

There is more to come with the endocannabinoids. I promise.

Odds and Ends and the Donate Button

I've gone on a little endocannabinoid paper feast so I should have some more entries about that up soon.  Very interesting stuff, very complicated and interrelated with everything, and a zillion papers from the last several months, so cutting edge too.  The sort of system you don't want to screw up if you can help it.

In the mean time, you might have noticed my "Donate" button added to the right there.  I held off adding one for a while but it seemed like the right time now that there are a couple of options to give people.  If you feel this website is of value to you, feel free to donate - if you don't want to donate but still want to support the site financially, click though my blog at Psychology Today.  I've already received a few donations and they are much appreciated!  The textbooks do add up - I don't anticipate these websites or endeavors to break even in the near future (if ever),  but every little bit helps it to be less of a financial drain on the family.  That said, the intellectual value to me from doing the work for the site and the participation and back and forth of ideas in the comments is really invaluable.

Thanks so much!