What with the very recent post link from PaNu, and Chris Kresser tweeting and facebooking (eesh is that a word?) my last post (thanks Chris!), it looks like I have some new readers. Hi! I can understand you not wanting to go back through 130 some-odd posts to catch up, but a lot of my posts build on previous ones, which have built on previous ones... well, I wouldn't want anyone to miss out. And one of my goals of this blog is to break down these topics so that the layperson can understand it (sometimes I am more successful at that than other times), but I don't want to keep repeating myself, either.
So here we are, an Evolutionary Psychiatry primer, if you will.
Basic Premise (includes monetary disclaimer, for giggles)
One of the key factors in studying obesity and metabolism is the idea that inflammation is the root of all evil. Well, it turns out the same is true of depression and other mental illness. Here are a couple starter posts for that: Depression 2 - Inflammation Boogaloo, and Depression Crashed Your Party. Here's one related to Autism.
Another theme of my blog is how mental illness is changing over time. As an example, back in the age of large asylums, a great many folks with schizophrenia were of the hebrephrenic type. Meaning they were disorganized and silly, and generally obstinate. In recent times the hebrephrenic type has essentially disappeared - I've seen only one in my career. No one knows why (as far as I know) - perhaps it is particularly responsive to medication, perhaps it was due to some sort of severe vitamin deficiency issue that general vitamin repletion has fixed in society at large - all total speculation. Changes like that in mental illness interest me, especially changes that have escalated with the escalation of obesity and metabolic syndrome, because that says "diet" to me. Here's a post on the history of depression: Depression 3 - Not Quite What It Used to Be. Here's one about Eating Disorders.
Here's some important stuff about the links between metabolic syndrome and depression: Chronic Stress is Chronic Illness and Stress is Metabolic Syndrome
If you want the basics on how neurons work, look at Ketogenic Diets and Bipolar Disorder 2.
Here's my most popular post (by a lot) and requires no explanation: Your Brain on Ketones.
One of my themes is that a single nutrient on its own is rarely the answer - we need an anti-inflammatory diet rich with nutrients (and do the best we can to control sleep and stressful lifestyle factors as well). Alzheimer's Pathology and the Dementia-Free Kitavans is a bit heavy, but makes the point.
Here's another self-explanatory one: Your Brain on Omega 3s.
So I think that pretty much covers the bare bones basics. However, if you have a particular interest, I encourage you to check out my post map, which (more or less) has everything broken down by condition or nutrient.
And, last but not least, a few of my favorite posts (though I'm narcissistic enough to like quite a lot of them, perhaps I'd be better off writing less and thinking/revising/consolidating more!)
Zombieland
The Evolution of Serotonin
That Tapeworm Ate Your Depression
The Case for Evolution
Genius and Madness
Sunday, January 9, 2011
Saturday, January 8, 2011
Alzheimer's, Mild Cognitive Impairment, and Ketosis
Funny thing is, not even a month ago I was commenting over at Dr. Parker's Diabetic Mediterranean Diet blog that there weren't really any studies about ketogenic diets and Alzheimer's and dementia. There were a few case reports that it was helpful, to be sure, but nothing much on Pubmed. Which is disappointing, because if you know anything about (very low carb or coconut oil heavy) ketogenic diets, you know that they should reduce inflammation, enhance energy efficiency, and decrease hyperinsulinemia, all of which are implicated in the pathogenesis of Alzheimer's.
Thank heavens I follow Dr. Eades' twitter feed. In December 2010 and January 2011 not one, but two academic papers have come out related to dementia and ketogenic diets or glucose metabolism. So here they are:
Dietary ketosis enhances memory in mild cognitive impairment
In this study, researchers did the obvious thing and put 23 older folks with mild cognitive impairment (MCI, a type of early dementia) on a very low carbohydrate diet or their normal diet for 6 weeks. Most people with MCI will progress to Alzheimer's, and MCI is important, because at this point your brain still has more than a fighting chance. Interventions at this point, if they work, might mean you don't progress to Alzheimer's.
Oh dear, here is a depressing quote from the article:
So the elders were recruited, given a battery of cognitive tests, then randomized to either a high carbohydrate diet (>50% of calories) meant to mimic an ordinary older American's diet, or a very low carbohydrate diet (10-20g of carbohydrate daily) for six weeks. Protein, fat, and calories were not restricted. "All subjects were advised to choose monounsaturated fats when possible, although this was not controlled."
At the beginning of the studies, the subjects were pretty ordinary older Americans (though anyone with frank diabetes was excluded). They tended to be overweight, had normal fasting glucose, but were at the high end of fasting insulin levels. Fasting insulin levels correlated with waist circumference.
After six weeks, the ketogenic diet group got skinnier waists, lower fasting glucose and lower fasting insulin (which shouldn't be a surprise for anyone). Ketone bodies were measurable in the urine of the very low carb subjects, and total calorie intake was also lower - fat and protein were not significantly different than the high carb group, however. Basically the low carb folks ditched the carbs and didn't replace them, resulting in lower calories overall.
And the brain effects? Memory was improved in the low-carb subjects, but not the tests of executive functioning (like trailmaking tests), suggesting a specific hippocampal and parahippocampal effect of ketones in the brain. Very interesting!
Got it! Moving on.
Second paper is Brain fuel metabolism, aging, and Alzheimer's Disease from the January 2011 edition of Nutrition. This paper is a review article rather than a study, with lots of interesting evidence for shoddy glucose metabolism in animal and human studies of Alzheimer's disease. I like this paper because it targets every piece of dietary insult on our brain that a Kitavan avoids just by being a horticulturist and not subsisting on a diet of *insert the vast majority of foods in the middle aisles of the modern Western grocery store here* - and the Kitavan happens to avoid dementia at the same time. Poor glucose metabolism, poor omega 3 (DHA status), and poor mitochondrial function are all found time and time again in folks with Alzheimer's, especially those with the ApoE4 allele or a maternal family history of Alzheimer's dementia.
This paper is 18 pages long and rather amazing, but I'll skip to the ketogenic part here:
Ketogenic supplements would mean medium chain triglycerides, such as coconut oil, which the Kitavans eat in spades.
I know, the prescription is very nearly always the same on my blog. The scientific explanation to get to the prescription in different disease states are often very different. Avoid the neolithic dietary agents of disease (I count them as many paleo types do as wheat, fructose, and vegetable oils), not to mention other novel fake foods we were never designed to eat, just to be safe. Ratchet down the carbs if you have love handles or metabolic syndrome. Dabble with ketosis by intermittent fasting, coconut oil, very low carb, or all three depending on your own personal brain status. There's plenty left to eat that is gorgeous and yummy. And you get to keep your brain.
Thank heavens I follow Dr. Eades' twitter feed. In December 2010 and January 2011 not one, but two academic papers have come out related to dementia and ketogenic diets or glucose metabolism. So here they are:
Dietary ketosis enhances memory in mild cognitive impairment
In this study, researchers did the obvious thing and put 23 older folks with mild cognitive impairment (MCI, a type of early dementia) on a very low carbohydrate diet or their normal diet for 6 weeks. Most people with MCI will progress to Alzheimer's, and MCI is important, because at this point your brain still has more than a fighting chance. Interventions at this point, if they work, might mean you don't progress to Alzheimer's.
Oh dear, here is a depressing quote from the article:
Contemporaneous with the developing dementia epidemic
is an epidemic of obesity and associated metabolic disturbance.
Currently, 64% of the USA adult population is overweight and
34% obese (Flegal et al., 2010). It is projected that by the year
2030, 86% will be overweight and 51% of adults in the USA
will be obese (Wang, 2008). Likewise, diabetes prevalence is
accelerating, particularly in the aging population (National
Institute of Diabetes and Digestive and Kidney Diseases,
2008). Hyperinsulinemia, which is a precursor to type 2 diabetes,
occurs in more than 40% of individuals aged 60 and
older (Craft, 2005; Ford et al., 2002).
So the elders were recruited, given a battery of cognitive tests, then randomized to either a high carbohydrate diet (>50% of calories) meant to mimic an ordinary older American's diet, or a very low carbohydrate diet (10-20g of carbohydrate daily) for six weeks. Protein, fat, and calories were not restricted. "All subjects were advised to choose monounsaturated fats when possible, although this was not controlled."
At the beginning of the studies, the subjects were pretty ordinary older Americans (though anyone with frank diabetes was excluded). They tended to be overweight, had normal fasting glucose, but were at the high end of fasting insulin levels. Fasting insulin levels correlated with waist circumference.
After six weeks, the ketogenic diet group got skinnier waists, lower fasting glucose and lower fasting insulin (which shouldn't be a surprise for anyone). Ketone bodies were measurable in the urine of the very low carb subjects, and total calorie intake was also lower - fat and protein were not significantly different than the high carb group, however. Basically the low carb folks ditched the carbs and didn't replace them, resulting in lower calories overall.
And the brain effects? Memory was improved in the low-carb subjects, but not the tests of executive functioning (like trailmaking tests), suggesting a specific hippocampal and parahippocampal effect of ketones in the brain. Very interesting!
On balance, these preliminary data provide evidence that
dietary ketosis by means of carbohydrate restriction can provide
neurocognitive benefit for older adults with early memory
decline and increased risk for neurodegeneration.
Got it! Moving on.
Second paper is Brain fuel metabolism, aging, and Alzheimer's Disease from the January 2011 edition of Nutrition. This paper is a review article rather than a study, with lots of interesting evidence for shoddy glucose metabolism in animal and human studies of Alzheimer's disease. I like this paper because it targets every piece of dietary insult on our brain that a Kitavan avoids just by being a horticulturist and not subsisting on a diet of *insert the vast majority of foods in the middle aisles of the modern Western grocery store here* - and the Kitavan happens to avoid dementia at the same time. Poor glucose metabolism, poor omega 3 (DHA status), and poor mitochondrial function are all found time and time again in folks with Alzheimer's, especially those with the ApoE4 allele or a maternal family history of Alzheimer's dementia.
This paper is 18 pages long and rather amazing, but I'll skip to the ketogenic part here:
Nevertheless, two observations in particular support the notion
that the neurons affected in AD are still functional: (1) in AD,
brain ketone uptake is apparently normal or at least less
impaired than is glucose, and (2) there is a functional
response to nutritional supplements that increase brain fuel
availability, particularly ketones. Hence, if brain fuel metabolism
could be optimized or even partially returned toward normal, the
risk of further cognitive decline may diminish. Raising plasma
ketones to 0.4-0.5 mM would contribute to 5-10% of the brain’s
energy requirements (Fig. 3), which is equivalent to the early
cortical glucose deficit in those genetically at risk AD. Such
a mild, safe level of ketonemia is achievable with ketogenic
supplements, so if implemented before symptoms develop, it
seems plausible that they could diminish the risk of further
metabolic deterioration and clinical onset of cognitive decline.
Ketogenic supplements would mean medium chain triglycerides, such as coconut oil, which the Kitavans eat in spades.
I know, the prescription is very nearly always the same on my blog. The scientific explanation to get to the prescription in different disease states are often very different. Avoid the neolithic dietary agents of disease (I count them as many paleo types do as wheat, fructose, and vegetable oils), not to mention other novel fake foods we were never designed to eat, just to be safe. Ratchet down the carbs if you have love handles or metabolic syndrome. Dabble with ketosis by intermittent fasting, coconut oil, very low carb, or all three depending on your own personal brain status. There's plenty left to eat that is gorgeous and yummy. And you get to keep your brain.
Friday, January 7, 2011
The Power of a Woman's Tears
First off a big thanks to Kurt Harris over at PaNu for his props for my blog (at the same time he recommended Andrew's) - glad to see you back into blogging, and Professor Gumby is certainly a fascinating fellow. A bit more housecleaning - there are a couple new studies out about Alzheimer's and Mild Cognitive Impairment and ketosis that I want to cover, and I'll probably get to that this weekend. However, this morning into my mailbox tumbled a new study that has "Evolutionary Psychiatry" written all over it (or maybe not, but it is cool nevertheless), "Human Tears Contain a Chemosignal" from pretty much the premier academic science journal in the world, Science (actually this one is in Science Express, which is the advanced online publication arm of Science.)
The paper starts out with Charles Darwin, and that's always a good sign. Basically the evolutionary question is why do we cry? It builds on nicely from yesterday's post on sex. Emotions are troublesome, after all. While some (like love) are typically sweet and enjoyable, others (like grief) are just plain painful. We really don't have much choice about feeling them - if you somehow suppress anger or grief, for example, it usually pops out in other unhealthy ways, such as anxiety, substance abuse, or irritability. Take it from a psychiatrist - the best thing to do with your powerful, driving emotions is to feel them and to act on what they are telling you in a reasonable way (that would not usually include busting a beer bottle over someone's head when you are angry). For example, I'm still pretty angry about what I consider the misappropriation of medical and nutritional "science" to peddle cheap commodity grains at the expense of our health. Each time I read Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Vintage)
, it gets thrown across the room a few times. So I write a blog, and I promote the blogs of like-minded folks to the right. Not because many of them also have me on their blogrolls, but because I like how they put their minds to the real problem of nutrition, lifestyle, and health in the 21st century, and I inevitably learn something from them.
But back to the paper. These researchers started out small. They took the tears of two women, ages 30 and 31, who watched sad movies in isolation. They also took a vial of saline that had been trickled over the skin of the women and let each of 24 young men (mean age 28) have a sniff - the men couldn't tell a difference in smell between the emotional tears and the saline. Then another 24 men (mean age 27) smelled the tears of three women (mean age 30) or saline and filled out some rating scales about the experience.
Then the young men were given a pad pasted to their upper lip with 100 microliters of tears or saline dribbled onto the pad. While thus anointed, the young men were asked to rate picture's of women's faces for sadness and how sexually attractive the faces were, and men were given a standard questionnaire to assess empathy. Each subject (in double blind fashion, and on different days) did the tests both with a saline and tear-stained pad. Tears or saline didn't change the men's empathy ratings or their ratings of sadness on the women's faces, but 17 out of 24 men smelling tears found the women's faces to be less sexually attractive (p <0.02).
The researchers at this point brought in 50 men and used a sensory paradigm to generate negative emotions, all the while measuring heart rate, sweating, respiration rate, skin temperature, and self-rating of mood and arousal. Salivary levels of testosterone were also measured before, during, and after smelling the tears or trickled saline of 5 donor women. After sniffing, the subjects watched sad movies (one of the news reports mentioned Terms of Endearment). Once again, the subjective arousal of tear-sniffing men was decreased, as was the level of arousal in general measured by sweating, respiration, etc., and, more tellingly, the levels of testosterone in saliva dropped.
Then the researchers got very cute (and this last bit is likely why the paper made it into Science). They took 16 young men with saline or tear-stained nose pads and had them watch sexually arousing movies and view sexy pictures - then stuck them into fMRIs. The sexual arousal signal apparently is visible in the hypothalamus and left fusiform gyrus of the brain, and within these regions, activity was significantly lower in men who were sniffing tears.
All in all, ladies, if you are looking to dampen the mood, take him to a tear-jerker. Otherwise, maybe stick with an action film or comedy. Also, tears may be a quick way to diffuse a man's overall emotional arousal - it may be an ancient hormonal way to tell an aggressive man to back off.
Now other animals also have tears, though it is thought humans are the only ones to shed emotional tears. In any event, the lacrimal secretions of mice contain chemosignals, as do human urine and sweat. Chemosignals in mammalian studies have uncovered pheromones that increase receptive sexual behavior or decrease arousal as in this study, while other chemosignals trigger sexual maturation or provide information (such as kinship - this may be why women will tend to be most attracted to men who have the most different major histocompatibility genes).
I'll let the researchers finish up:
My question is - what are we doing to our behaviors by masking scents with bathing, deodorant, and perfume? Would I be a more perceptive psychiatrist if my patients stopped bathing? Hmmm.
The paper starts out with Charles Darwin, and that's always a good sign. Basically the evolutionary question is why do we cry? It builds on nicely from yesterday's post on sex. Emotions are troublesome, after all. While some (like love) are typically sweet and enjoyable, others (like grief) are just plain painful. We really don't have much choice about feeling them - if you somehow suppress anger or grief, for example, it usually pops out in other unhealthy ways, such as anxiety, substance abuse, or irritability. Take it from a psychiatrist - the best thing to do with your powerful, driving emotions is to feel them and to act on what they are telling you in a reasonable way (that would not usually include busting a beer bottle over someone's head when you are angry). For example, I'm still pretty angry about what I consider the misappropriation of medical and nutritional "science" to peddle cheap commodity grains at the expense of our health. Each time I read Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Vintage)
, it gets thrown across the room a few times. So I write a blog, and I promote the blogs of like-minded folks to the right. Not because many of them also have me on their blogrolls, but because I like how they put their minds to the real problem of nutrition, lifestyle, and health in the 21st century, and I inevitably learn something from them.But back to the paper. These researchers started out small. They took the tears of two women, ages 30 and 31, who watched sad movies in isolation. They also took a vial of saline that had been trickled over the skin of the women and let each of 24 young men (mean age 28) have a sniff - the men couldn't tell a difference in smell between the emotional tears and the saline. Then another 24 men (mean age 27) smelled the tears of three women (mean age 30) or saline and filled out some rating scales about the experience.
Then the young men were given a pad pasted to their upper lip with 100 microliters of tears or saline dribbled onto the pad. While thus anointed, the young men were asked to rate picture's of women's faces for sadness and how sexually attractive the faces were, and men were given a standard questionnaire to assess empathy. Each subject (in double blind fashion, and on different days) did the tests both with a saline and tear-stained pad. Tears or saline didn't change the men's empathy ratings or their ratings of sadness on the women's faces, but 17 out of 24 men smelling tears found the women's faces to be less sexually attractive (p <0.02).
The researchers at this point brought in 50 men and used a sensory paradigm to generate negative emotions, all the while measuring heart rate, sweating, respiration rate, skin temperature, and self-rating of mood and arousal. Salivary levels of testosterone were also measured before, during, and after smelling the tears or trickled saline of 5 donor women. After sniffing, the subjects watched sad movies (one of the news reports mentioned Terms of Endearment). Once again, the subjective arousal of tear-sniffing men was decreased, as was the level of arousal in general measured by sweating, respiration, etc., and, more tellingly, the levels of testosterone in saliva dropped.
Then the researchers got very cute (and this last bit is likely why the paper made it into Science). They took 16 young men with saline or tear-stained nose pads and had them watch sexually arousing movies and view sexy pictures - then stuck them into fMRIs. The sexual arousal signal apparently is visible in the hypothalamus and left fusiform gyrus of the brain, and within these regions, activity was significantly lower in men who were sniffing tears.
All in all, ladies, if you are looking to dampen the mood, take him to a tear-jerker. Otherwise, maybe stick with an action film or comedy. Also, tears may be a quick way to diffuse a man's overall emotional arousal - it may be an ancient hormonal way to tell an aggressive man to back off.
Now other animals also have tears, though it is thought humans are the only ones to shed emotional tears. In any event, the lacrimal secretions of mice contain chemosignals, as do human urine and sweat. Chemosignals in mammalian studies have uncovered pheromones that increase receptive sexual behavior or decrease arousal as in this study, while other chemosignals trigger sexual maturation or provide information (such as kinship - this may be why women will tend to be most attracted to men who have the most different major histocompatibility genes).
I'll let the researchers finish up:
The findings pose many questions: What is the identity of the active compound/s in tears?...Moreover, could the emotional or hormonal state (menstrual phase, oral contraceptives) of the crier/experimenter influence the outcome? In turn, what if any are the signals in men's tears... children's tears, and what are the effects of all these within rather than across gender?
My question is - what are we doing to our behaviors by masking scents with bathing, deodorant, and perfume? Would I be a more perceptive psychiatrist if my patients stopped bathing? Hmmm.
Thursday, January 6, 2011
Sex, and Drugs, and Sex
Not too terribly long ago, Jamie Scott made a mockery of Mr. Kellogg, who if legend holds true peddled breakfast cereal as an armament against masturbation and excessive sexual behavior. Now why someone else would care that much what any other random person does while naked is a continuing puzzlement to me (or not really if you want to delve into the psychology, which is a whole different sort of blog post. Let's just say that there is a primitive defense called "projection" and it is typically why outspoken proponents of sexual prohibitions typically exhibit the sexual behavior they loathe the most. Also, never put anything in writing, on facebook, text message, in a blog, or in photos you desperately wouldn't mind showing up in a court of law or public eye later on. Just common sense, people. For doctors specifically - never write anything in the medical record you wouldn't want your patient and his or her lawyer to see.) In the comments on Jamie's post, I made note of the findings that the young men in Minnesota noticed considerable lack of sexual interest during their semi-starvation experiment.
And let's be frank. Evolution is all about sex, genes, and breeding. The latter two topics might not sound sexy, but sex has everything to do with why you and I are here, and why you and I behave the way we do. Sex is ultimately why I write this blog (narcissism, fame, my picture on computer screens far and wide across the world - all should increase my local fitness and enhance the fitness of my children if all goes well, or at least fools my brain into thinking so). I've been reading The Red Queen: Sex and the Evolution of Human Nature
, so genetics is a bit on the mind. I'm a psychiatrist, in America a discipline mostly inherited from the theoretical perspective of one dirty old man. Nothing in human evolution makes sense without considering sex. In my mind one of the positives of a paleolithic style diet is the anecdotal reports of (mostly) increased sexual drive. Vegetarians (in anecdote also) will often report a decreased sex drive.
In the comments for Jamie's post I quipped that decreased libido was probably a bad sign if it seemed to be caused by diet. If your body doesn't think you are fit for reproducing, it won't send you signals leading that direction, after all. And if your body doesn't think your diet is good enough to support little ones, it makes sense that your diet is not likely optimal for human health.
So that's the sex part. What about the drugs? Well, as a psychiatrist, I happen to have a lot of experience with drugs that decrease libido. And I hate being a hypocrite. Some of the data can be clouded by the fact that depression itself causes decreased libido. But the fact of the matter is that SSRIs and their cousins seem to cut down sexual desire and other phases of sexuality. With SSRI's it seems that the drugs cause a direct pharmacologic "anti-viagra" in men, and more commonly in women a decreased sexual interest caused by mucking around with certain varieties of serotonin receptors. These are different problems than the low-protein diet - which seems to affect sex hormone production (here's an explanatory bit from a book about pigs, anyway).
Ideally, we could figure out a way to get depressed and anxious people feeling better without messy pharmacologic interventions. I would start with therapy, exercise, and a primal-style diet (Mark Sisson's 100-150g carbs a day with a pass on the starchy tubers as part of the non-toxic carbs, to be crystal clear).
And why sex (and males) in the first place, when parthenogenesis is just so much neater and cleaner and doesn't require all this vast effort to blog, not to mention black eyeliner, platform black suede boots, and haircuts? The Red Queen: Sex and the Evolution of Human Nature (pg 86) has the best argument I've heard - disease.
It is not an accident that the most polymorphic genes are the immunologic histocompatibility genes. Meaning that each generational variability seeks above all to outwit the pathogens that feed on us. Sex is the best generational bet to supply different MHC genes to confuse the viruses, bacteria, parasites, and fungi. There are no long-lived species without sex. Which, using somewhat un-rigorous thinking, means I will never be a vegan.
And let's be frank. Evolution is all about sex, genes, and breeding. The latter two topics might not sound sexy, but sex has everything to do with why you and I are here, and why you and I behave the way we do. Sex is ultimately why I write this blog (narcissism, fame, my picture on computer screens far and wide across the world - all should increase my local fitness and enhance the fitness of my children if all goes well, or at least fools my brain into thinking so). I've been reading The Red Queen: Sex and the Evolution of Human Nature
, so genetics is a bit on the mind. I'm a psychiatrist, in America a discipline mostly inherited from the theoretical perspective of one dirty old man. Nothing in human evolution makes sense without considering sex. In my mind one of the positives of a paleolithic style diet is the anecdotal reports of (mostly) increased sexual drive. Vegetarians (in anecdote also) will often report a decreased sex drive. In the comments for Jamie's post I quipped that decreased libido was probably a bad sign if it seemed to be caused by diet. If your body doesn't think you are fit for reproducing, it won't send you signals leading that direction, after all. And if your body doesn't think your diet is good enough to support little ones, it makes sense that your diet is not likely optimal for human health.
So that's the sex part. What about the drugs? Well, as a psychiatrist, I happen to have a lot of experience with drugs that decrease libido. And I hate being a hypocrite. Some of the data can be clouded by the fact that depression itself causes decreased libido. But the fact of the matter is that SSRIs and their cousins seem to cut down sexual desire and other phases of sexuality. With SSRI's it seems that the drugs cause a direct pharmacologic "anti-viagra" in men, and more commonly in women a decreased sexual interest caused by mucking around with certain varieties of serotonin receptors. These are different problems than the low-protein diet - which seems to affect sex hormone production (here's an explanatory bit from a book about pigs, anyway).
Ideally, we could figure out a way to get depressed and anxious people feeling better without messy pharmacologic interventions. I would start with therapy, exercise, and a primal-style diet (Mark Sisson's 100-150g carbs a day with a pass on the starchy tubers as part of the non-toxic carbs, to be crystal clear).
And why sex (and males) in the first place, when parthenogenesis is just so much neater and cleaner and doesn't require all this vast effort to blog, not to mention black eyeliner, platform black suede boots, and haircuts? The Red Queen: Sex and the Evolution of Human Nature
(pg 86) has the best argument I've heard - disease. Sex is about disease. It is used to combat the threat from parasites. Organisms need sex to keep their genes one step ahead of their parasites. Men are not redundant after all; they are a woman's insurance policy against her children being wiped out by influenza and smallpox (if that is a consolation). Women add sperm to their eggs because if they did not, the resulting babies would be identically vulnerable to the first parasite that picked their genetic locks.
It is not an accident that the most polymorphic genes are the immunologic histocompatibility genes. Meaning that each generational variability seeks above all to outwit the pathogens that feed on us. Sex is the best generational bet to supply different MHC genes to confuse the viruses, bacteria, parasites, and fungi. There are no long-lived species without sex. Which, using somewhat un-rigorous thinking, means I will never be a vegan.
Tuesday, January 4, 2011
Bipolar Disorder and the Psychiatry War of the 20th Century
I'm going to start with a little history of psychiatry in America and the DSMIV. Up into the 60s and 70s, psychiatry in America was heavily influenced by psychoanalysis - Freudian stuff (patient is on a couch free-associating, and the therapist is a "blank screen" - theoretically, though it hardly ever worked out like that), primarily because most of the psychoanalysts fled Germany during WWII and set up shop in London and New York and Boston - these places are still hotspots of psychoanalysis today and the center of East Coast academic training in psychiatry. Psychoanalysts spend a lot of time talking about rage and repression and the unconscious and the mind, all very interesting, if you like that sort of thing. But psychoanalysis isn't exactly neuroscience, and when biological correlates to some of the major psychiatric disorders started coming out, psychiatry swung the other direction.
In some respects there is a lot to admire about psychoanalysis as a science - Freud, a Victorian, met his match in a young girl with symptoms of hysteria named Ida (he called her Dora), and he came up with all sorts of Victorian theories about repression and sexuality to explain her symptoms of not being able to speak, and some neurological hand problems. The case is often studied in academic feminism as an example as to why psychoanalytic theory is patriarchal and misogynist. And yes, it certainly was, because that was the prevailing idea of the time. However, it is often missed that the whole reason Freud published Dora was to present a failure of his therapy. He missed the boat, he knew it, as a Victorian he didn't quite understand why. In that respect, Dora is a humble case study and real medical science circa 1901. Now we would get to the brass tacks that Dora at the age of 14 was by her account repeatedly sexually propositioned by the father of the children she babysat, and the children's mother was also the lover of Dora's father. Such a situation would be difficult now - imagine when one could not speak of such things and would not have been believed in any event.
Well. Dora has a lot of dream analysis in it, and maybe that was a Victorian indirect way to get to the truth. In 2011 we prefer more direct methods - saves time. And I certainly prefer to look at much of psychiatric pathology from a neuroscience perspective, as it seems only rational. The analysts will say we have lost the art of listening and all the modern psychiatrist does is shove pills down people's throats. The biologic psychiatrist will say that psychiatric illness has more causes than just mental distress and to ignore those causes is unscientific and unconscionable. The analyst will say the biologist is "mindless," the biologic psychiatrist will say the analyst is "brainless."
The truth of the matter is that we cannot afford to lose our ability to listen to patients - that is the problem in all of medicine at this time, and psychiatrists may be the last bastion of listening. On the other hand, we can't afford to base psychiatric treatment on medical science circa 1901 (I'm being a little unfair here - hardly any analysts are Freudian drive-based anymore, most use a mix of more modern theoretical concepts derived from attachment theory, relational therapy, and even chaos theory). So into the fray between biologic sorts and analytic sorts came the DSMIII and IV. These books were written to be atheoretical. Causes (whether it be genes and inflammation or history of trauma and personality style) are left out, on purpose, I think in part due to the fight between the analysts and the biologic psychiatrists. I came into training rather at the end of this "war" but apparently it raged for decades. (One of my teachers, an analyst, said of another, a biologic psychiatrist, "I don't think he even believes in the unconscious!" Another teacher talked about how he was forced as a resident to give psychoanalysis to actively psychotic individuals in state mental hospitals, and when it didn't work, was blamed for his failure.)
The DSMIV is merely a recipe book of traits. Have the traits, match it up to the diagnosis, and there you go. Mostly it was intended for research - since we don't have lab tests to define psychiatric illness, psychiatrists in one research center needed to be studying the same disorders as in another center - thus a checklist of sorts. And then psychiatrists in the field needed to be talking about the same sort of problem that the researchers were studying treatments for. It all makes perfect sense, but the DSMIV is maddeningly boring and the atheoretical part makes it a lightning rod for critics. Then managed care and insurance and services based on diagnosis came along and the DSMIV became way more important than it should have been.
But the DSMIV is what we have, and there are certain definitions for bipolar disorder. Bipolar I is when you have a manic episode (a period of insomnia, hypersexuality, impulsivity, rapid speech, increased religiosity, irritability, racing thoughts, manic psychosis often with religious delusions or grandiose delusions, increased energy, and euphoria - you don't need all of these to be manic, just enough of them, and to be mania, it needs to be serious enough for you to be psychotic or hospitalized.) Bipolar I people usually have major depressive episodes also, but they don't have to. Some people are only manic.
Then there is Bipolar II, where people tend to be depressed most of the time but occasionally have hypomanic episodes - mostly insomnia, irritability, increased goal-directed behavior, impulsivity, euphoria - but not as serious as a full manic episode. Bipolar II is a little hard to sort from regular depression - most of the people who show up at your clinic will be depressed, and hypomanic symptoms are often forgotten about, even when you ask directly about them.
Neither of these are the same thing as "moody." Being moody and irritable does not make you bipolar, though if you are bipolar, you will likely be more moody and irritable than average during an episode. In a lot of ways, bipolar disorder overlaps (and sometimes exists at the same time with) other disorders - substance abuse, personality disorders, anxiety, depression, ADHD, which makes it all the more controversial.
Bipolar symptoms also tend to be different at different stages in life. Kids will tend to cycle very rapidly between mood states and could hit many in the same day. Adults tend to stick with one for several weeks or more. (Bipolar disorder in kids is a bit controversial - it's called bipolar disorder because the same criteria fit to describe the behaviors, and often kids with bipolar symptoms do grow up to be adults with standard adult bipolar disorder, so it seems to be the same animal. It is also highly genetic. However, every kid with a temper or a bratty streak is not bipolar. Bipolar in kids tends to be very serious - these kids are often kicked out of school (or preschool) for behavior problems.)
In a lot of ways, bipolar disorder is poorly understood.
Which brings me to the paper I'm blogging about today, "An admixture analysis of the age at index episodes in bipolar disorder." In this study, researchers interviewed 390 people with bipolar disorder in Canada about the history of illness, threw a bunch of data into a number cruncher, and came out with some interesting correlates.
First off, people with early onset bipolar disorder (average onset age 18) tended to be more likely to have a family history of bipolar disorder, and more likely to have psychosis, anxiety, suicidal thoughts and behaviors, and a chronic and rapid cycling course, and were more likely to have migraines. People with late onset (usually starting around age 33) disease were more likely to also have diabetes. Typically, bipolar disorder begins with a depressive episode, and often earlier in women than in men (which would match up with women's greater vulnerability to mood disorders in general). I can add further speculation that the later onset bipolar being more associated with diabetes would suggest that it is possibly part of metabolic syndrome in certain vulnerable people. Early onset bipolar disorder may be more it's own animal. I do think in both cases, inflammatory Western diets may be contributory, and there is some (bad epidemiologic) evidence that doesn't dispute that speculation. Also interesting is the connection between bipolar disorders and migraines - both can respond to medications for epilepsy and theoretically from a ketogenic diet.
A modern psychiatrist is hamstrung without time to get a good history and the psychological savvy to establish an excellent rapport with the patient and the understanding of basic human nature - but a modern psychiatrist is also crippled by a lack of knowledge of neuroscience, nutrition, and general medicine. We need to pursue both threads in 2011. It all comes back together for the betterment of everyone.
In some respects there is a lot to admire about psychoanalysis as a science - Freud, a Victorian, met his match in a young girl with symptoms of hysteria named Ida (he called her Dora), and he came up with all sorts of Victorian theories about repression and sexuality to explain her symptoms of not being able to speak, and some neurological hand problems. The case is often studied in academic feminism as an example as to why psychoanalytic theory is patriarchal and misogynist. And yes, it certainly was, because that was the prevailing idea of the time. However, it is often missed that the whole reason Freud published Dora was to present a failure of his therapy. He missed the boat, he knew it, as a Victorian he didn't quite understand why. In that respect, Dora is a humble case study and real medical science circa 1901. Now we would get to the brass tacks that Dora at the age of 14 was by her account repeatedly sexually propositioned by the father of the children she babysat, and the children's mother was also the lover of Dora's father. Such a situation would be difficult now - imagine when one could not speak of such things and would not have been believed in any event.
Well. Dora has a lot of dream analysis in it, and maybe that was a Victorian indirect way to get to the truth. In 2011 we prefer more direct methods - saves time. And I certainly prefer to look at much of psychiatric pathology from a neuroscience perspective, as it seems only rational. The analysts will say we have lost the art of listening and all the modern psychiatrist does is shove pills down people's throats. The biologic psychiatrist will say that psychiatric illness has more causes than just mental distress and to ignore those causes is unscientific and unconscionable. The analyst will say the biologist is "mindless," the biologic psychiatrist will say the analyst is "brainless."
The truth of the matter is that we cannot afford to lose our ability to listen to patients - that is the problem in all of medicine at this time, and psychiatrists may be the last bastion of listening. On the other hand, we can't afford to base psychiatric treatment on medical science circa 1901 (I'm being a little unfair here - hardly any analysts are Freudian drive-based anymore, most use a mix of more modern theoretical concepts derived from attachment theory, relational therapy, and even chaos theory). So into the fray between biologic sorts and analytic sorts came the DSMIII and IV. These books were written to be atheoretical. Causes (whether it be genes and inflammation or history of trauma and personality style) are left out, on purpose, I think in part due to the fight between the analysts and the biologic psychiatrists. I came into training rather at the end of this "war" but apparently it raged for decades. (One of my teachers, an analyst, said of another, a biologic psychiatrist, "I don't think he even believes in the unconscious!" Another teacher talked about how he was forced as a resident to give psychoanalysis to actively psychotic individuals in state mental hospitals, and when it didn't work, was blamed for his failure.)
The DSMIV is merely a recipe book of traits. Have the traits, match it up to the diagnosis, and there you go. Mostly it was intended for research - since we don't have lab tests to define psychiatric illness, psychiatrists in one research center needed to be studying the same disorders as in another center - thus a checklist of sorts. And then psychiatrists in the field needed to be talking about the same sort of problem that the researchers were studying treatments for. It all makes perfect sense, but the DSMIV is maddeningly boring and the atheoretical part makes it a lightning rod for critics. Then managed care and insurance and services based on diagnosis came along and the DSMIV became way more important than it should have been.
But the DSMIV is what we have, and there are certain definitions for bipolar disorder. Bipolar I is when you have a manic episode (a period of insomnia, hypersexuality, impulsivity, rapid speech, increased religiosity, irritability, racing thoughts, manic psychosis often with religious delusions or grandiose delusions, increased energy, and euphoria - you don't need all of these to be manic, just enough of them, and to be mania, it needs to be serious enough for you to be psychotic or hospitalized.) Bipolar I people usually have major depressive episodes also, but they don't have to. Some people are only manic.
Then there is Bipolar II, where people tend to be depressed most of the time but occasionally have hypomanic episodes - mostly insomnia, irritability, increased goal-directed behavior, impulsivity, euphoria - but not as serious as a full manic episode. Bipolar II is a little hard to sort from regular depression - most of the people who show up at your clinic will be depressed, and hypomanic symptoms are often forgotten about, even when you ask directly about them.
Neither of these are the same thing as "moody." Being moody and irritable does not make you bipolar, though if you are bipolar, you will likely be more moody and irritable than average during an episode. In a lot of ways, bipolar disorder overlaps (and sometimes exists at the same time with) other disorders - substance abuse, personality disorders, anxiety, depression, ADHD, which makes it all the more controversial.
Bipolar symptoms also tend to be different at different stages in life. Kids will tend to cycle very rapidly between mood states and could hit many in the same day. Adults tend to stick with one for several weeks or more. (Bipolar disorder in kids is a bit controversial - it's called bipolar disorder because the same criteria fit to describe the behaviors, and often kids with bipolar symptoms do grow up to be adults with standard adult bipolar disorder, so it seems to be the same animal. It is also highly genetic. However, every kid with a temper or a bratty streak is not bipolar. Bipolar in kids tends to be very serious - these kids are often kicked out of school (or preschool) for behavior problems.)
In a lot of ways, bipolar disorder is poorly understood.
Which brings me to the paper I'm blogging about today, "An admixture analysis of the age at index episodes in bipolar disorder." In this study, researchers interviewed 390 people with bipolar disorder in Canada about the history of illness, threw a bunch of data into a number cruncher, and came out with some interesting correlates.
First off, people with early onset bipolar disorder (average onset age 18) tended to be more likely to have a family history of bipolar disorder, and more likely to have psychosis, anxiety, suicidal thoughts and behaviors, and a chronic and rapid cycling course, and were more likely to have migraines. People with late onset (usually starting around age 33) disease were more likely to also have diabetes. Typically, bipolar disorder begins with a depressive episode, and often earlier in women than in men (which would match up with women's greater vulnerability to mood disorders in general). I can add further speculation that the later onset bipolar being more associated with diabetes would suggest that it is possibly part of metabolic syndrome in certain vulnerable people. Early onset bipolar disorder may be more it's own animal. I do think in both cases, inflammatory Western diets may be contributory, and there is some (bad epidemiologic) evidence that doesn't dispute that speculation. Also interesting is the connection between bipolar disorders and migraines - both can respond to medications for epilepsy and theoretically from a ketogenic diet.
A modern psychiatrist is hamstrung without time to get a good history and the psychological savvy to establish an excellent rapport with the patient and the understanding of basic human nature - but a modern psychiatrist is also crippled by a lack of knowledge of neuroscience, nutrition, and general medicine. We need to pursue both threads in 2011. It all comes back together for the betterment of everyone.
Sunday, January 2, 2011
Zombieland 2 - You Are What You Eat, Mommyblogger Style
First the Zombieland movie trailer, just for fun. Now take a peek at one of my more popular posts, Zombieland, which a brilliant psychiatrist friend of mine described as "food for thought." The post was about phospholipids, primarily phosphatidylserine and phosphatidylcholine, delectable and important nutrients nature has supplied most richly in the consumption of brains (though eggs are perhaps a more palatable source). (Linus Pauling Institute article about choline is here.)
(Hey, Nephropal is back! Sorry about the jump around. I spent a good part of the morning playing video games and my attention span is shot, though my reaction times are *awesome*!)
Little did I know that choline would become a very fashionable nutrient in the paleoblogosphere. Chris Masterjohn, Paul Jaminet, and Stephan Guyenet all did a post or three, and everyone who is anyone doubled down on his or her egg consumption thereafter. Much of the to-do was focused on fatty liver disease (one really must eat choline to protect one's liver from the rigors of modern life). But, as it turns out, while the liver is on the front lines, the brain is where the battle really rages.
The data in humans is... scarce (there are some small human trials of induced choline deficinecy and fatty liver, reversed by choline repletion). But let's throw out what we have, be it epidemiology or mice or rats, and do some speculation.
First off, choline is part of the folate cycle, which I discussed a bit in this post here. The folate cycle is exceptionally important for liver and brain/nerve health, and includes some key players - iron, vitamin B6, vitamin B12, folate, methionine, choline, oxidized choline (called betaine), SAM, niacin, and riboflavin. All the players need to be on the field for the full folate cycle to run efficiently. Most choline absorbed by humans is immediately made into phosphatidylcholine and incorporated into cell membranes. Choline is also made into betaine in the liver, where it serves as a methyl donor for many important chemical reactions (1). One of the phosphorylated products of these many reactions is phosphocreatine, by the way. Also important to neurons and the brain is sphingomyelin.
Problems or deficiencies in the folate cycle (including choline deficiency) are implicated in fatty liver disease, neural tube defects (like spina bifida), cardiovascular disease, and cancer. The cycle begins with methionine (an amino acid), which using various B vitamin cofactors is made into SAM. SAM is a methyl donor and is vital in nearly sixty important chemical reactions in the liver, from making neurotransmitters to cell membranes to DNA. After being used as a methyl donor, SAM becomes SAH which becomes homocysteine. Having high homocysteine is associated with dementia and cardiovascular disease - in my mind it is associated with poor nutrition in general. Without all the players, homocysteine has a hard time being recycled for use in the folate cycle again. In order to get the majority of the players, you need to eat a lot of whole grains, or vitamins, or organ meats/eggs. Whole grains have their issues, so I'll stick to the latter sources, thank you very much.
All right, so choline is necessary, but why? Fatty liver develops because you need choline to make VLDL particles. VLDL carries triglycerides from the liver into the bloodstream. If you don't have enough phospholipids like phosphatidylcholine to form the coat of the VLDL particle, you end up with triglycerides stuck in the liver ==> fatty liver. Now if you don't have enough phospholipids to even get your triglycerides out of the liver, how could you possibly have enough for use in your other cell membranes (or in the neurons of the brain, which are especially rich in phospholipids)? And how would they even get there without your cholesterol/fat carrying particles? Fatty liver is just a harbinger of even more serious problems to follow.
Neural tube defects are extremely common birth defects that result from faulty closing of the ends of the neural tube. In very early development, we humans spend some time being sort of flat, like an elongated pancake. Then we roll up in a couple of ways to become more... wormlike, before we grow limb buds and all sorts of other interesting things to become babies. Rolling up properly requires the folate cycle to be running at full efficiency. And, sure enough, epidemiologic studies have linked choline deficiency in human mothers to neural tube defects in their offspring (those in the bottom 25% of choline intake have 4 times the risk of babies with neural tube defects as those in the top 25%), and in mice, choline restriction is shown to cause neural defects.
Pregnancy and lactation are periods in a woman's life when she needs some serious choline to keep the machinery going. Placental/amniotic fluid levels of choline are nearly 10 times mother's serum levels (2) Moms seem to benefit from an enhanced choline-making machinery during pregnancy, but mom still ends up with depleted levels after childbirth (which will continue during lactation). It's best to have time to replete this vital nutrient between kiddos.
Beyond the neural tube defect issue is the memory issue. Neural tube defects usually begin within the first month of pregnancy, so by the time you realize you are expecting, it's pretty much too late to do anything about it. But studies of rats have shown that choline depleted mothers in the latter half of rat pregnancy results in offspring with lousy memories. The hippocampus is the part of the brain at the epicenter of memory (and depression). Pregnant rats who have plenty of choline seem to be able to make all the membranes, DNA, and stem cells you need to make an awesome hippocampus. Pregnant rats without choline have baby rats who just don't remember as well. In addition, choline supplementation in the second half of pregnancy seems to protect offspring rats from the detrimental brain effects of alcohol given to their mothers (3). There are no studies in humans showing this link. However, elevated human maternal homocysteine levels are linked with preeclampsia, prematurity, and low birth weight, and most studies have shown that the higher a mother's choline levels, the lower her homocysteine tends to be.
Other studies (including the Nurses Health Study and the Framingham Offspring Study) have shown that higher choline levels are associated with lower inflammatory markers of many kinds, including IL-6, TNF-alpha, and C reactive protein. Keep in mind that in the PROSPECT-EPIC study, even those women in the highest quartile of choline intake fell below the Institutes of Medicine number for Adequate Intake of 425 mg a day for women (to get that amount, you need to eat half a pound of chicken, two eggs, and a quart of 1% milk (not sure why anyone would be drinking that, but okay)! And those are relatively rich sources!) In the Nurses' Health Study, 95% of women fell below an average daily intake of 411 mg. In addition, nearly 50% of seem to have a genetic polymorphism where we have a hard time making methionine into choline, meaning choline becomes even more of an essential nutrient. This fact may be why some people have bulletproof livers, and others develop fatty liver just by looking at a bottle of wine.
The women with adequate intake in these large studies had a higher than average intake of eggs. I wonder if choline is the reason recent studies have shown that eggs in conjunction with a calorie restricted diet seem to improve diabetes, despite all that fat and cholesterol. (I like these studies and how they seem to annihilate the lipotoxicity hypothesis).
I find the information about choline to be convincing, and I eat eggs for breakfast about 4X a week (as do my kids). The perinatal period where baby rats' brain development benefits from increased choline consumption can be extrapolated to about 4 years old in humans. So eat up your eggs and offal, especially if you are a rugrat or plan to have rugrats any time soon!
*Wheat germ and soy lecithin are the richest vegetarian sources, but they won't be on my menu.
(Hey, Nephropal is back! Sorry about the jump around. I spent a good part of the morning playing video games and my attention span is shot, though my reaction times are *awesome*!)
Little did I know that choline would become a very fashionable nutrient in the paleoblogosphere. Chris Masterjohn, Paul Jaminet, and Stephan Guyenet all did a post or three, and everyone who is anyone doubled down on his or her egg consumption thereafter. Much of the to-do was focused on fatty liver disease (one really must eat choline to protect one's liver from the rigors of modern life). But, as it turns out, while the liver is on the front lines, the brain is where the battle really rages.
The data in humans is... scarce (there are some small human trials of induced choline deficinecy and fatty liver, reversed by choline repletion). But let's throw out what we have, be it epidemiology or mice or rats, and do some speculation.
First off, choline is part of the folate cycle, which I discussed a bit in this post here. The folate cycle is exceptionally important for liver and brain/nerve health, and includes some key players - iron, vitamin B6, vitamin B12, folate, methionine, choline, oxidized choline (called betaine), SAM, niacin, and riboflavin. All the players need to be on the field for the full folate cycle to run efficiently. Most choline absorbed by humans is immediately made into phosphatidylcholine and incorporated into cell membranes. Choline is also made into betaine in the liver, where it serves as a methyl donor for many important chemical reactions (1). One of the phosphorylated products of these many reactions is phosphocreatine, by the way. Also important to neurons and the brain is sphingomyelin.
Problems or deficiencies in the folate cycle (including choline deficiency) are implicated in fatty liver disease, neural tube defects (like spina bifida), cardiovascular disease, and cancer. The cycle begins with methionine (an amino acid), which using various B vitamin cofactors is made into SAM. SAM is a methyl donor and is vital in nearly sixty important chemical reactions in the liver, from making neurotransmitters to cell membranes to DNA. After being used as a methyl donor, SAM becomes SAH which becomes homocysteine. Having high homocysteine is associated with dementia and cardiovascular disease - in my mind it is associated with poor nutrition in general. Without all the players, homocysteine has a hard time being recycled for use in the folate cycle again. In order to get the majority of the players, you need to eat a lot of whole grains, or vitamins, or organ meats/eggs. Whole grains have their issues, so I'll stick to the latter sources, thank you very much.
All right, so choline is necessary, but why? Fatty liver develops because you need choline to make VLDL particles. VLDL carries triglycerides from the liver into the bloodstream. If you don't have enough phospholipids like phosphatidylcholine to form the coat of the VLDL particle, you end up with triglycerides stuck in the liver ==> fatty liver. Now if you don't have enough phospholipids to even get your triglycerides out of the liver, how could you possibly have enough for use in your other cell membranes (or in the neurons of the brain, which are especially rich in phospholipids)? And how would they even get there without your cholesterol/fat carrying particles? Fatty liver is just a harbinger of even more serious problems to follow.
Neural tube defects are extremely common birth defects that result from faulty closing of the ends of the neural tube. In very early development, we humans spend some time being sort of flat, like an elongated pancake. Then we roll up in a couple of ways to become more... wormlike, before we grow limb buds and all sorts of other interesting things to become babies. Rolling up properly requires the folate cycle to be running at full efficiency. And, sure enough, epidemiologic studies have linked choline deficiency in human mothers to neural tube defects in their offspring (those in the bottom 25% of choline intake have 4 times the risk of babies with neural tube defects as those in the top 25%), and in mice, choline restriction is shown to cause neural defects.
Pregnancy and lactation are periods in a woman's life when she needs some serious choline to keep the machinery going. Placental/amniotic fluid levels of choline are nearly 10 times mother's serum levels (2) Moms seem to benefit from an enhanced choline-making machinery during pregnancy, but mom still ends up with depleted levels after childbirth (which will continue during lactation). It's best to have time to replete this vital nutrient between kiddos.
Beyond the neural tube defect issue is the memory issue. Neural tube defects usually begin within the first month of pregnancy, so by the time you realize you are expecting, it's pretty much too late to do anything about it. But studies of rats have shown that choline depleted mothers in the latter half of rat pregnancy results in offspring with lousy memories. The hippocampus is the part of the brain at the epicenter of memory (and depression). Pregnant rats who have plenty of choline seem to be able to make all the membranes, DNA, and stem cells you need to make an awesome hippocampus. Pregnant rats without choline have baby rats who just don't remember as well. In addition, choline supplementation in the second half of pregnancy seems to protect offspring rats from the detrimental brain effects of alcohol given to their mothers (3). There are no studies in humans showing this link. However, elevated human maternal homocysteine levels are linked with preeclampsia, prematurity, and low birth weight, and most studies have shown that the higher a mother's choline levels, the lower her homocysteine tends to be.
Other studies (including the Nurses Health Study and the Framingham Offspring Study) have shown that higher choline levels are associated with lower inflammatory markers of many kinds, including IL-6, TNF-alpha, and C reactive protein. Keep in mind that in the PROSPECT-EPIC study, even those women in the highest quartile of choline intake fell below the Institutes of Medicine number for Adequate Intake of 425 mg a day for women (to get that amount, you need to eat half a pound of chicken, two eggs, and a quart of 1% milk (not sure why anyone would be drinking that, but okay)! And those are relatively rich sources!) In the Nurses' Health Study, 95% of women fell below an average daily intake of 411 mg. In addition, nearly 50% of seem to have a genetic polymorphism where we have a hard time making methionine into choline, meaning choline becomes even more of an essential nutrient. This fact may be why some people have bulletproof livers, and others develop fatty liver just by looking at a bottle of wine.
The women with adequate intake in these large studies had a higher than average intake of eggs. I wonder if choline is the reason recent studies have shown that eggs in conjunction with a calorie restricted diet seem to improve diabetes, despite all that fat and cholesterol. (I like these studies and how they seem to annihilate the lipotoxicity hypothesis).
I find the information about choline to be convincing, and I eat eggs for breakfast about 4X a week (as do my kids). The perinatal period where baby rats' brain development benefits from increased choline consumption can be extrapolated to about 4 years old in humans. So eat up your eggs and offal, especially if you are a rugrat or plan to have rugrats any time soon!
*Wheat germ and soy lecithin are the richest vegetarian sources, but they won't be on my menu.
Saturday, January 1, 2011
Happy New Year
One of my favorite Copland pieces is the second movement from Rodeo - the Corral Nocturne (right click in new tab to play). It's on most of my lullaby playlists, and is modern and sweet without being precious. It is also quite brief at a little over three and a half minutes, so lean back, close your eyes, and sit a spell, if you do that sort of thing. I find many people can't unwind, can't unfold. Corral Nocturne might help if you are in that predicament. Orchestral music may not be terribly old, but it sure does speak to something within us.
Here's a picture we took on the last evening of 2010, looking forward to 2011.
Here's a picture we took on the last evening of 2010, looking forward to 2011.
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