I am still in my hotel in California - planning to meet the New Zealand contingent later today for some hiking (for some reason they aren't interested in the Walk of Fame) and then fly back tonight. Since my arrival on Thursday afternoon, this little space of an hour or so on Monday morning has been my first moment, while rested and contemplative, to do a real post. I believe I will split up the posts into my thoughts on the talks, then a reflection on the people, then one on MovNat (which I attended yesterday). It's been busy, and a blast.
First, the conference. The speakers (including myself!) were an eclectic mix of academic bigwigs and paleo luminaries with fewer credentials. It should be no surprise that the talks by the less-credentialed luminaries were, in general, more enjoyable. After all, the paleo bloggers and book writers in general made their mark with a bit of flair, some have extensive public speaking experience and and they are not as conditioned to the expectation of the classic powerpoint talk in a dark room at an academic conference.
The first talks were by the true "paleo grandfathers," Boyd Eaton and Loren Cordain, and of course the amazing "Kitava" and paleo diet researcher, Staffan Lindeberg. I agree with many that Dr. Eaton appeared to have a rosier view of paleolithic life than I would expect, but the talks were full of interesting information, and it was delightful to see these professors in person. Dr. Lindeberg's talk was my favorite of those three, though that may be because I am still in awe of his amazing textbook, Food and Western Disease. And Dr. Lindeberg has an MD and real live patients - there is definitely a difference in perspective among those of us seeing patients and those of us who spend all our time studying science. (Eaton is an MD too, but his talk didn't reflect the patient experience as much).
The morning wrapped up with Robb Wolf, who gave an engaging and charismatic presentation as expected. The afternoon I popped over to the alternate room for my presentation with Jamie - which was well-received. I'm laughing a bit at my description of speakers as I am neither a "paleo luminary" or an "academic bigwig" - and I think my presentation was somewhere between a basic powerpoint slide-reading and some entertaining and interesting facts. The gist of it (and the slides should be uploaded for all to see fairly soon, if they aren't already…) is that: there is compelling evidence that many mental health disorders (including eating disorders, depression, anxiety, psychosis, bipolar disorder, ADHD, etc.) are, in fact, diseases of civilization. There are many, many lines of evidence showing plausible physiologic mechanisms for how the differences between our diet and lifestyles of today compared to the diet and lifestyle for which we are evolved could result in mental illness. I hope people found the presentation (a little less dry than those last two sentences) enjoyable and thought-provoking.
Dr. BG and Dr. Gerstmar did a great talk on the intestinal biome and clinical implications right after our presentation. (More will follow in my "people" post, but it was gratifying to realize that most folks in person are very, very much like their online personas.)
Later in the afternoon I caught the last part of Dr. Eades's talk, then went back to the alternate room for Dr. Feinman and Chris Masterjohn. Dr. Eades makes a great speaker (unsurprisingly) but I have to admit I don't remember much about the facts of the talk - same is true for Dr. BG's - must have to do with the post-presentation adrenaline meltdown. My facilities came back online about halfway through Feinman's, which was an expose of crappy interpretation of dietary studies and even crappier media coverage (the best example was a media article about how fat causes something horrible in humans and we should NEVER EVER eat it except to choke down our tiny requirements with no enjoyment and great repentance (I may be exaggerating that just a little) - based on the findings of a study not in humans, but of mice… but oh wait, it wasn't even mice, it was mouse cells in a test tube!)
Dr. Lustig attended Feinman's talk and harangued him a bit about how actual amounts of fat have not decreased in the modern diet, but that carbohydrate/sugar have increased along with total calories so the percentage of fat has decreased… it was not particularly relevant to Dr. Feinman's point in this presentation, as he was merely making the case that the literature vilifying fat is ridiculous, not that high fat is necessarily good or bad. But it was fun to watch. (My thought during this exchange was - but how much of those absolute fat grams today are omega 6 compared to 100 years ago? How much was trans fat during some of the initial studies. Mark Sisson said "fat is not a monolith" in one of his recent posts, and the whole low-carb/high-carb paleo issue frustrates me, because macronutrients alone are not the entire picture by any stretch of the imagination. If they were, obesity, inflammation, and type II diabetes would be cured and we could all go home.)
Chris Masterjohn gave a fantastic talk on cholesterol - very similar to his recent podcast with Chris Kresser. Lustig was taking notes, and Dr. K asked some interesting questions at the end with respect to leptin, thyroid, etc.
Now on to day 2: In the morning I really enjoyed Lustig's talk, which was not very similar at all to "Sugar, The Bitter Truth" as he focused more on leptin. I happened to be sitting behind Dr. Feinman (who is not the world's biggest Lustig fan) at the lecture, and someone asked him what he thought of the talk - he maintained that Lustig is "half-right, half wrong" about biochemistry, similar to the blog post I linked above on the subject. I have to admit I liked Lustig's leptin talk much better than his fructose one. The funny thing is (well, I think it is funny, but that's because I'm particularly amused by brain biochemistry) is that at the poster presentation 10 feet from the lecture hall on Day 2, Dr. David Pendergrass from the University of Kansas had a fabulous diagram he's painstakingly cobbled together from the literature outlining the brain feedback mechanisms and neuroregulation of appetite and fat storage and how it becomes derailed to promote obesity. Frankly, it renders the entire fructose/glucose argument somewhat irrelevant. But more on that later.
Mat Lalonde PhD "The Kracken" had the next talk - excellent, hard-hitting, and I agree with him in fact if not always in spirit. His talk was mostly a warning about thinking you are an expert on much of anything without being very careful about your knowledge and qualifications - especially if your audience is a hard science crowd - or you will be dismissed as an ignorant idiot. I definitely agree with that part… he also said that combing through the literature to find studies that support the evolutionary medicine hypothesis is biased and therefore unscientific. As a factual matter I do agree. As a practical matter, the literature is so vast and the confounders and physiology as yet not fully understood, that our comprehension and understanding of the vastness is only possible by using context. We have to interpret the facts, and we must interpret them within a framework. Again, as a practical matter - we have two methods for determining context for further study - epidemiologic studies showing that people who do this or eat that or take this pill are healthier than those who don't. As we know, epidemiologic studies have major weaknesses that can make even the best of them unreliable for establishing context. The other method is to use common sense (which includes using evolutionary theory as a basis). The main danger of bias must be taken on by accepting and analyzing negative as well as positive studies with regards to evolutionary medicine theory, but I do not think we should throw out the context altogether. I'm fairly certain he has the same thoughts with respect to taking care and bias, but I just wanted to put up my thoughts on the subject, as it is important to the accuracy and meaning of my blog.
After Lalonde I saw Denise Minger - who was delightful (more about her in the "people" post). Then I went to Melissa McEwan and John Durant, who between had some of the most factually interesting and provocative talks of the entire conference. Andreas Eenfeldt, the Diet Doctor from Sweden, did a great job at his talk about Low Carb High Fat diet success in that country. He included the amazing fact that if the obesity trend in America continues, we will all be obese or overweight by 2048. My tweet of this fact prompted Dave from ThriveNaturally to respond thusly in what I considered to be the best tweet of the event :-) I was sitting behind the Drs. Eades at that talk and it was gratifying to see the solidarity.
By this point in the afternoon, I wasn't as focused, and the exercise talks aren't as interesting to me as the biochem, anthropology, and science… but I did truly enjoy Erwan Le Corre's MovNat talk, and I will have a lot more to say about it in my third post of this series.
I missed the last hour of talks as I was milling around the poster presentation and chatting with people, but I'm sure my blood would have boiled in either one - the last one apparently had a random slash at SSRIs while promoting statins (both have serious problems and both have some modest usefulness in the right setting, frankly). The other talk was about the modern healthcare system, and no matter what the context, I find such talks infuriating :)
SO… if you have made it this far, I would have to say my very favorite talks/speakers were:
Day 1: Lindeberg, Wolf, Dr. BG, Masterjohn
Day 2: Lustig, Lalonde, McEwan, Durant, Eenfeldt, LeCorre
Talks I'm sorry I missed and am looking forward to watching online:
Day 1: Stephan Guyenet, Bastos, Stanford
Day 2: Seth Roberts and Tucker Max (would have liked to have seen Nikoley and Naughton but I am told Naughton's talk was similar to his "Low Carb Cruise" presentation, which I saw and enjoyed very much online. Nikoley's talk on self-experimentation I imagined would be similar to his blog, which I have read most of the posts from the last year or so, and I was very anxious to see Eenfeldt. So will catch online! Also would have enjoyed Sisson, of course - and apparently people were playing with beach balls in the audience for that one!)
All right. Now I'm ready for the people post - which will probably be written during the interminable airport/airplane gauntlet tonight. Today - hiking in Malibu!
Monday, August 8, 2011
Friday, August 5, 2011
AHS is here!
My presentation with Jamie is this afternoon at 1:55 pm at Rolfe Hall. Bigger post with pictures later… yesterday I was thrilled to meet (or meet again) seemingly most of the Paleoblogosphere, including Jamie Scott, Melissa McEwen, Chris Masterjohn, John Durant, Stephan Guyenet, Mark Sisson, Paul and Shou-Ching Jaminet, Dave Csonska, Andrew from Evolvify, Denise Minger, Richard Nikoley, Mike and Mary Dan Eades, Robb Wolf, Brent Pottenger, Jimmy Moore, and a bunch of other amazing people. From the looks of them, they practice what they preach (everyone really looked terrific.)
I'll see many of you (perhaps) around UCLA today.
I'll see many of you (perhaps) around UCLA today.
Tuesday, August 2, 2011
Sunday, July 31, 2011
Reflections on the Whole30
Good morning! It is the last day of July, and thus Day "31" of the Whole30, a strict 30 day plan designed by (the gorgeous) Melissa and Dallas Hartwig with no processed food, no alcohol, no legumes, no grains whatsoever, no white potatoes, no dairy (including butter), no sugar or sugar substitutes (even honey and whatnot).
I don't do diets, by the way. They don't work. And they make you crazy. And yet, in many ways, the Whole30 is unsustainable perfection unless there is a darn good reason.
So why did I do the Whole30? An experiment. And there is scientific validation for elimination diets - it is the gold standard way to determine certain food intolerances. What I admire about Dallas and Melissa is they make that clear - the Whole30 is about health and seeing if you find some positives with a strict month, it is not the rest of your life, it is not about losing weight. It is not a "diet" in that sense.
It was interesting to go forward with the Whole30 when my regular eating pattern was already fairly similar. That way, if there were issues, it would be easy to figure out the exact problems. And there are exactly seven differences between the Whole30 and the way I ate for most the year before the Whole30 (there is a Whole30 meal template that I did try to stick to also, which constitutes another difference, but just in terms of types of food consumed):
1) Rare added sugar (usually honey). By rare I mean rare. A teaspoon of honey in tea every couple of weeks. Honey in a flourless chocolate cake twice in six months. Except chocolate, which was usually a piece of a 85% dark chocolate bar every other day. A bar would usually last a week.
2) Artificial sweeteners (gum and Diet Coke)
3) Cheating (usually gluten in homemade pizza, sometimes Mexican food - but not that often - once a month)
4) High fat dairy - after 3 months of NO dairy at all last year, I added back butter regularly, sometimes yogurt, sometimes cream with berries, sometimes cheese. All told I probably ate high fat dairy not counting butter 3X a week.
5) White rice and white potatoes - these and other starchy carbs (winter squash, sweet potatoes, turnips) once daily - you are supposed to eat starchy carbs like winter squash and sweet potatoes on the Whole30, but not rice and potatoes.
6) Alcohol - 5 glasses of wine a week (I did try to keep it away from 2 hours before bedtime, as even one glass of wine will disturb my sleep if I drink it too close to bedtime)
7) IF ing - prior to Whole30, 24 hours usually on Monday, 16 hours a couple of other times during the week
Things I deliberately didn't change - amount of exercise and amount of starchy carb. I did try to eat Whole30 approved starchy carb in about the same amounts in my meals as I did before Whole30. In all likelihood I did consume more fruit on the Whole30 than before.
As I wrote about a week ago, I did go on vacation to a city with very fine restaurants, which means my Whole30 was not pristine. In addition, ever since having rather extreme morning sickness during my pregnancies, sometimes I still get very nauseated in the mornings, and a half a teaspoon of honey in tea cures it instantly. It's psychosomatic plus my typical lowish blood sugar, I believe. Anyway, I did have honey once, and several cheat meals involving a touch of dairy on the trip - fish with a very sparse crust of parmesan and (literally) a drizzle of buttermilk dressing on some romaine, for example. Which is fine, because it means that my Whole30 was more like my real life and the number of "differences" up there drops to 5 - forget 1) and 3).
So, what were the results and what was it like? I've lost 7 pounds - five of that happened in the first 10 days (I think - that is when the dress size loss happened). I feel energetic. I'm sleeping through the night better, but it is much harder to get to sleep - I used to collapse around 9 or 9:30 and wake up at 2-3am for a few hours. Now I can't generally get to sleep before 11, but I don't tend to wake up until 5am.
So fairly dramatic. I started out with a BMI of 23.2 and now it is 21.8. I'm wearing size 4-6 currently, which is typically a small. My clothes from 10 years ago (which was usually 6 or 8 or 10 or medium but sizes have ballooned in the intervening years) fit or are a little loose.
And I'm pretty convinced the major causative factor is the high fat dairy - because I had done little experiments in the past year removing artificial sweeteners or alcohol for a couple of weeks, and my weight was rock steady. And I don't see a qualitative difference between a similar amount of sweet potato and a regular potato or rice with respect to sudden weight loss that happens in a week. Also, there is a family history (two first degree relatives) with dairy intolerance so I should just buck up and cut it out (both family members can tolerate butter). But it could also be the chocolate or the insidious cheat creep that can happen.
What do I plan from here? I'm going to experiment with adding back in rice and white potatoes - they are cheap, convenient, and the kids love them. I will not add back artificial sweeteners. Honestly my strongest motivation for the Whole30 was not weight loss so much as kicking the Diet Coke habit that had crept back in over the last 6 months. I will drink wine, but will tend keep it more to special occasions, parties, meals out, etc. instead of "Woo it's friday night!" Heh. And life is too short not to have chocolate - maybe it won't be a bar a week. Chocolate keeps well. Chocolate is pretty much awesome in every way.
Oh, and IFing. I like the health data behind the intermittent fast, and I did like the "buzz" I got in the afternoon (probably cortisol, however), and I like the convenience. I didn't IF on the Whole30 because I was hungry, and I believe in eating when one is hungry. I'm guessing I will add it back in but not as aggressively as before. I hadn't realized how IF added stress in some ways until I stopped doing it.
So life after the Whole30 will be mostly similar to life on the Whole30, with more chocolate and alcohol. I'll do a more careful experiment with rice and potatoes. I'm very glad I decided to do the Whole30, even though I wasn't perfect and I already knew a lot about myself and diet from the "paleo" experiment of the previous year - I still learned a great deal. Elimination diets can be very useful for a variety of reasons.
Once again I am traveling this week - flurry of work to do then leaving Thursday morning for the Ancestral Health Symposium. This will likely be the last blog post (save, perhaps, some quick uploads to Psychology Today) until then.
I don't do diets, by the way. They don't work. And they make you crazy. And yet, in many ways, the Whole30 is unsustainable perfection unless there is a darn good reason.
So why did I do the Whole30? An experiment. And there is scientific validation for elimination diets - it is the gold standard way to determine certain food intolerances. What I admire about Dallas and Melissa is they make that clear - the Whole30 is about health and seeing if you find some positives with a strict month, it is not the rest of your life, it is not about losing weight. It is not a "diet" in that sense.
It was interesting to go forward with the Whole30 when my regular eating pattern was already fairly similar. That way, if there were issues, it would be easy to figure out the exact problems. And there are exactly seven differences between the Whole30 and the way I ate for most the year before the Whole30 (there is a Whole30 meal template that I did try to stick to also, which constitutes another difference, but just in terms of types of food consumed):
1) Rare added sugar (usually honey). By rare I mean rare. A teaspoon of honey in tea every couple of weeks. Honey in a flourless chocolate cake twice in six months. Except chocolate, which was usually a piece of a 85% dark chocolate bar every other day. A bar would usually last a week.
2) Artificial sweeteners (gum and Diet Coke)
3) Cheating (usually gluten in homemade pizza, sometimes Mexican food - but not that often - once a month)
4) High fat dairy - after 3 months of NO dairy at all last year, I added back butter regularly, sometimes yogurt, sometimes cream with berries, sometimes cheese. All told I probably ate high fat dairy not counting butter 3X a week.
5) White rice and white potatoes - these and other starchy carbs (winter squash, sweet potatoes, turnips) once daily - you are supposed to eat starchy carbs like winter squash and sweet potatoes on the Whole30, but not rice and potatoes.
6) Alcohol - 5 glasses of wine a week (I did try to keep it away from 2 hours before bedtime, as even one glass of wine will disturb my sleep if I drink it too close to bedtime)
7) IF ing - prior to Whole30, 24 hours usually on Monday, 16 hours a couple of other times during the week
Things I deliberately didn't change - amount of exercise and amount of starchy carb. I did try to eat Whole30 approved starchy carb in about the same amounts in my meals as I did before Whole30. In all likelihood I did consume more fruit on the Whole30 than before.
As I wrote about a week ago, I did go on vacation to a city with very fine restaurants, which means my Whole30 was not pristine. In addition, ever since having rather extreme morning sickness during my pregnancies, sometimes I still get very nauseated in the mornings, and a half a teaspoon of honey in tea cures it instantly. It's psychosomatic plus my typical lowish blood sugar, I believe. Anyway, I did have honey once, and several cheat meals involving a touch of dairy on the trip - fish with a very sparse crust of parmesan and (literally) a drizzle of buttermilk dressing on some romaine, for example. Which is fine, because it means that my Whole30 was more like my real life and the number of "differences" up there drops to 5 - forget 1) and 3).
So, what were the results and what was it like? I've lost 7 pounds - five of that happened in the first 10 days (I think - that is when the dress size loss happened). I feel energetic. I'm sleeping through the night better, but it is much harder to get to sleep - I used to collapse around 9 or 9:30 and wake up at 2-3am for a few hours. Now I can't generally get to sleep before 11, but I don't tend to wake up until 5am.
So fairly dramatic. I started out with a BMI of 23.2 and now it is 21.8. I'm wearing size 4-6 currently, which is typically a small. My clothes from 10 years ago (which was usually 6 or 8 or 10 or medium but sizes have ballooned in the intervening years) fit or are a little loose.
And I'm pretty convinced the major causative factor is the high fat dairy - because I had done little experiments in the past year removing artificial sweeteners or alcohol for a couple of weeks, and my weight was rock steady. And I don't see a qualitative difference between a similar amount of sweet potato and a regular potato or rice with respect to sudden weight loss that happens in a week. Also, there is a family history (two first degree relatives) with dairy intolerance so I should just buck up and cut it out (both family members can tolerate butter). But it could also be the chocolate or the insidious cheat creep that can happen.
What do I plan from here? I'm going to experiment with adding back in rice and white potatoes - they are cheap, convenient, and the kids love them. I will not add back artificial sweeteners. Honestly my strongest motivation for the Whole30 was not weight loss so much as kicking the Diet Coke habit that had crept back in over the last 6 months. I will drink wine, but will tend keep it more to special occasions, parties, meals out, etc. instead of "Woo it's friday night!" Heh. And life is too short not to have chocolate - maybe it won't be a bar a week. Chocolate keeps well. Chocolate is pretty much awesome in every way.
Oh, and IFing. I like the health data behind the intermittent fast, and I did like the "buzz" I got in the afternoon (probably cortisol, however), and I like the convenience. I didn't IF on the Whole30 because I was hungry, and I believe in eating when one is hungry. I'm guessing I will add it back in but not as aggressively as before. I hadn't realized how IF added stress in some ways until I stopped doing it.
So life after the Whole30 will be mostly similar to life on the Whole30, with more chocolate and alcohol. I'll do a more careful experiment with rice and potatoes. I'm very glad I decided to do the Whole30, even though I wasn't perfect and I already knew a lot about myself and diet from the "paleo" experiment of the previous year - I still learned a great deal. Elimination diets can be very useful for a variety of reasons.
Once again I am traveling this week - flurry of work to do then leaving Thursday morning for the Ancestral Health Symposium. This will likely be the last blog post (save, perhaps, some quick uploads to Psychology Today) until then.
Thursday, July 28, 2011
The Incredible Shrinking Human Brain
Thanks to Tim who sent me the link to this Wall Street Journal article:
Brain Shrinkage: It's Only Human
Yup. Many parts wither as we age, our brains among them. Octogenarians are liable to have brains 15% smaller than Justin Bieber's brain. Imagine that! Humans it seems are unique among primates in that we are longest-lived with the largest brains, and are also susceptible to neuropathology in the late stages of life, such as dementia.
There are several types of dementia, but even normal human aging is characterized by neural deterioration and cognitive impairment to some extent. Various pathologies are common - amyloid beta deposits, neuron trees dying off, reduced synapse numbers, loss of specific receptors… these seem to occur specifically in areas that are part of learning, memory, and executive function. Some of these same changes occur in other primate species whose members (rarely) get, well, senile. There have been case reports of elderly gorillas or chimps with Alzheimer's like plaques and tangles. So for a long time, scientists apparently assumed that as a large extended family, our big primate brains kinda sputter out at the end, especially humans, with the biggest and longest-lived brain.
The (free for now) WSJ article reports on a new study done by Sherwood et al in PNAS, called Aging of the cerebral cortex differs between humans and chimpanzees.
Sherwood and his compatriots had the bright idea to get brain MRIs of a bunch of humans (87) and a bunch of chimps (69) spanning a wide age range - in chimps, ages 10-51, in humans, ages 22-88. And, sure enough, among the humans, there was significant shrinkage in every area of the brain measured. But, surprisingly, no significant shrinkage among the chimps. Boom. Humans are very vulnerable to dementia (except, of course, the famous Kitavans - and I will get back to that later). Chimps don't seem to be.
Now there are a few wrinkles to understand here. The age ranges of both humans and chimps were chosen for the study by how long humans and chimps are expected to live (if they don't get killed in an accident or illness) in the wild - about 45 for chimps, and into the 80s for humans. But, when the human data for this study were parsed out by age, it seems that all the major shrinkage occurred in the 7th and 8th decades of life, not before, and other human studies show there is minimal shrinking between ages 25 and 50, with accelerated shrinking thereafter. This age is well above the age of any known chimpanzee in the wild. One post-mortem study of captive chimps had a very minimal decline of brain size with age - the oldest captive chimp was 59. Another study involving macaque monkeys (some 30 million years removed in lineage from humans, I believe) also showed no brain degeneration with age.
So… it would appear that humans are relatively unique in that our brains self destruct into a smokey inflammatory puddle of shrunken senility. And we can't just say the chimps didn't get as old as we do - relatively speaking - they do. Chimps start to slow down and become more physically frail with worn teeth in the 30s, though the females are fertile until nearly the end of the normal chimp lifespan. Humans have a longer childhood and are generally still quite robust through the 30s and 40s, and women obviously hit menopause around age 50, followed by (generally) 2-3 more decades in a normal lifespan. It is clear, then, that humans age more slowly than chimps.
Now, evolutionarily speaking, the authors of this paper throw out the grandmother hypothesis - humans clearly live long because there was a survival advantage among the grandchildren who had grandmothers around collecting food and passing on cultural knowledge. But does that longevity have a cost unknown to other, grandmother-less primates?
As we well know, dementing brains have a build-up of protein aggregates and rely on the shoddy energy production of poorly functioning, reactive oxygen species-producing damaged mitochondria. As we get older, our oxidative stress protection gene expression is upregulated - until I suppose it can be upregulated no more, and the cost of being a human with our big, energy hogging brains for so long is too high, and everything goes to hell in a hand basket.
The sticking point I have with this study? Well, none of the subjects were "wild-type." All the chimps were captives from the Yerkes National Primate Research Center in Atlanta. The humans were volunteers, all right-handed, about equal numbers men and women, and all were healthy, with no psychiatric disorders, heart disease, hypertension, or diabetes. I'm fairly convinced that Staffan Lindeberg did not take an MRI machine with him to Papua New Guinea. So I don't know if the dementia-free Kitavans in the last century had shrinking brains.
So is dementia a human thing, the direct cost of being the brightest and longest-lived of all primates, design specs maxed out at a biochemical level? Or is it a modern, industrial human thing, wrought from micronutrient deficiencies, infection, chronic hyperglycemia, and mucking around with our capability to produce cholesterol? What do they feed those chimps in the Yerkes center, anyway?
I know what I think - what makes sense is that we aren't meant to become senile and a long-term survival burden as we age. Okay, so maybe our big glorious brains are derived in part from sexual selection - thus an expensive ornament like a peacock's tail, meant to woo women, with a survival cost and not just survival benefit. And yet… why evolve grandmothers just to have them get senile? The grandmother hypothesis would be completely backwards if our brains are just designed to slowly sputter out. I don't have the proof - but my speculation is that true wild-type humans, even the very old, have robust brains too, like old chimps or gorillas.
A couple of other things before we go - today my podcast with Jimmy Moore came out - you can listen to it here (I remember saying I eat 18 eggs a week, which isn't true - my family eats about 18 eggs a week. I eat about 12 of those :-) ) In any case it was a lot of fun talking to Jimmy. He has an infectious enthusiasm.
And I have a couple new articles up at Psychology Today. Please give them a click!
Sleep, Hyperactivity, and Behavior in Children
A Case of Scratchy Mice
Brain Shrinkage: It's Only Human
Yup. Many parts wither as we age, our brains among them. Octogenarians are liable to have brains 15% smaller than Justin Bieber's brain. Imagine that! Humans it seems are unique among primates in that we are longest-lived with the largest brains, and are also susceptible to neuropathology in the late stages of life, such as dementia.
There are several types of dementia, but even normal human aging is characterized by neural deterioration and cognitive impairment to some extent. Various pathologies are common - amyloid beta deposits, neuron trees dying off, reduced synapse numbers, loss of specific receptors… these seem to occur specifically in areas that are part of learning, memory, and executive function. Some of these same changes occur in other primate species whose members (rarely) get, well, senile. There have been case reports of elderly gorillas or chimps with Alzheimer's like plaques and tangles. So for a long time, scientists apparently assumed that as a large extended family, our big primate brains kinda sputter out at the end, especially humans, with the biggest and longest-lived brain.
The (free for now) WSJ article reports on a new study done by Sherwood et al in PNAS, called Aging of the cerebral cortex differs between humans and chimpanzees.
 |
| Flickr Creative Commons |
Now there are a few wrinkles to understand here. The age ranges of both humans and chimps were chosen for the study by how long humans and chimps are expected to live (if they don't get killed in an accident or illness) in the wild - about 45 for chimps, and into the 80s for humans. But, when the human data for this study were parsed out by age, it seems that all the major shrinkage occurred in the 7th and 8th decades of life, not before, and other human studies show there is minimal shrinking between ages 25 and 50, with accelerated shrinking thereafter. This age is well above the age of any known chimpanzee in the wild. One post-mortem study of captive chimps had a very minimal decline of brain size with age - the oldest captive chimp was 59. Another study involving macaque monkeys (some 30 million years removed in lineage from humans, I believe) also showed no brain degeneration with age.
So… it would appear that humans are relatively unique in that our brains self destruct into a smokey inflammatory puddle of shrunken senility. And we can't just say the chimps didn't get as old as we do - relatively speaking - they do. Chimps start to slow down and become more physically frail with worn teeth in the 30s, though the females are fertile until nearly the end of the normal chimp lifespan. Humans have a longer childhood and are generally still quite robust through the 30s and 40s, and women obviously hit menopause around age 50, followed by (generally) 2-3 more decades in a normal lifespan. It is clear, then, that humans age more slowly than chimps.
Now, evolutionarily speaking, the authors of this paper throw out the grandmother hypothesis - humans clearly live long because there was a survival advantage among the grandchildren who had grandmothers around collecting food and passing on cultural knowledge. But does that longevity have a cost unknown to other, grandmother-less primates?
As we well know, dementing brains have a build-up of protein aggregates and rely on the shoddy energy production of poorly functioning, reactive oxygen species-producing damaged mitochondria. As we get older, our oxidative stress protection gene expression is upregulated - until I suppose it can be upregulated no more, and the cost of being a human with our big, energy hogging brains for so long is too high, and everything goes to hell in a hand basket.
The sticking point I have with this study? Well, none of the subjects were "wild-type." All the chimps were captives from the Yerkes National Primate Research Center in Atlanta. The humans were volunteers, all right-handed, about equal numbers men and women, and all were healthy, with no psychiatric disorders, heart disease, hypertension, or diabetes. I'm fairly convinced that Staffan Lindeberg did not take an MRI machine with him to Papua New Guinea. So I don't know if the dementia-free Kitavans in the last century had shrinking brains.
So is dementia a human thing, the direct cost of being the brightest and longest-lived of all primates, design specs maxed out at a biochemical level? Or is it a modern, industrial human thing, wrought from micronutrient deficiencies, infection, chronic hyperglycemia, and mucking around with our capability to produce cholesterol? What do they feed those chimps in the Yerkes center, anyway?
I know what I think - what makes sense is that we aren't meant to become senile and a long-term survival burden as we age. Okay, so maybe our big glorious brains are derived in part from sexual selection - thus an expensive ornament like a peacock's tail, meant to woo women, with a survival cost and not just survival benefit. And yet… why evolve grandmothers just to have them get senile? The grandmother hypothesis would be completely backwards if our brains are just designed to slowly sputter out. I don't have the proof - but my speculation is that true wild-type humans, even the very old, have robust brains too, like old chimps or gorillas.
A couple of other things before we go - today my podcast with Jimmy Moore came out - you can listen to it here (I remember saying I eat 18 eggs a week, which isn't true - my family eats about 18 eggs a week. I eat about 12 of those :-) ) In any case it was a lot of fun talking to Jimmy. He has an infectious enthusiasm.
And I have a couple new articles up at Psychology Today. Please give them a click!
Sleep, Hyperactivity, and Behavior in Children
A Case of Scratchy Mice
Tuesday, July 26, 2011
Fat and Happy
Yesterday, Julianne and Stabby were tweeting about this new paper, which Jamie was kind enough to send along to me later - Fatty acid-induced gut brain signaling attenuates neural and behavioral effects of sad emotions in humans.
Now that title has three words I like rather a lot - "gut," "brain," and "humans." It begins to feel a little lonely sifting through the rodent literature, wondering what could be applicable to you and me. I wonder if you feed a rat a hot dog, would it be just as bad as getting a mouse to smoke a cigarette?
But back to the humans - 12 non-obese subjects agreed for some reason to have nasogastric tubes slithered down into their gullets before the subjects crawled into a very small but expensive tube to have functional MRIs done. The subjects were given either a saline infusion or an infusion of dodecanoic acid (que? Also known as lauric acid, or the main component of coconut oil. Interestinger and interestinger!) During this procedure, the subjects also had "sad" or "neutral" classical music piped into the tube, and were shown sad faces or neutral facial expressions matching the music. They were also asked to fill out scales rating fullness, nausea, and hunger, as well as indicating mood on a scale of 1 (sad) to 5 (neutral) to 9 (happy). All of the subjects went through all variations - saline + sad music, fat + sad music, saline + neutral music, and fat + neutral music in 4 different scans on 4 different days, but in randomized order, and always after a 12 hour fast.
The results? Well, hunger increased significantly with the sad music and sad faces. The lauric acid decreased both hunger and the sad feelings significantly more than saline. Hunger did not increase with neutral music and faces, and the difference in hunger between the fat and saline groups listening to the neutral music was non-significant, suggesting that fat sluiced down into the stomach was indeed the factor that attenuated the sad/hunger connection. In addition, the "sad" subjects experienced less sensation of fullness after the fat or saline infusion than the "neutral" subjects.
The mechanism thought to explain the emotion/hunger connection is in the reward system of the brain. This is thought to be the case both in healthy volunteers, and in people with eating disorders or obesity.
The fMRI data showed that certain areas of the brain associated with mood and the reward system* were activated differently based on the different stimuli. Under neutral emotional conditions, fatty acid infusion activated the metabolism in these regions more than the saline infusion. Sad emotion also activated the metabolism in these regions, and the activation decreased upon fatty acid infusion compared to saline. It appears, then, that fat activated the emotional centers of the brain, as did sadness, but that fat seemed to cool off the sadness (which was reflected in the mood scores of the participants). The effect of fat on sadness was two-fold decrease compared to saline. This effect is about the same as the change in mood scores in those treated with antidepressants.
The authors note that previous studies (which are hard to compare, as they involved eating food and all the associated smells, textures, and pleasures associated with that) typically rated mood and carbohydrate response, and these studies were also done over the course of a few weeks (the fat or saline was infused over the course of 2 minutes in this experiment).
So - what do we learn? Does fat make us happy? Well, what do you want to eat when you are feeling blue - an apple or a chocolate bar? The editorial for the study we're discussing is quite interesting (but not free without academic access). Another independent study done in mice showed that increasing stress resulted in increased ghrelin secretion, increased corticosteroid secretion, and increased fat-seeking behavior (for the typical rat high fat diet pellets.) The authors note that young people in a longitudinal study from New Zealand who have a major depressive episode during youth have a 2.3 fold increase in the incidence of obesity in adulthood. So there is a presumed mechanism - stress causes us to want to eat, and eating alleviates stress. However, 40% of people report increased appetite during stress, and 40% report decreased appetite. And certainly other adipose mass control mechanisms should eventually compensate - is it our stressful modern lives, or a combination of our stressful lives plus our poisonous modern foods?
There are many more questions raised than answered by the human study - what is the actual mechanism? The editorial discusses the possible action of the gastric hormones ghrelin or CCK**, which are both known to have emotional and brain effects. And what would happen with infusions of protein or carbohydrate, or in other emotional states, such as aggression, happiness, or arousal? Would there be any difference in subjects who are obese or have eating disorders? Women vs. men, women in different stages of the menstrual cycle? If I had an fMRI, a few hundred nasogastric tubes, and a bunch of willing subjects, I would crank out papers as fast as I crank out blog posts with this experimental design. Hopefully this article is not the last we hear from these researchers!
* specifically the medulla/pons, midbrain, hypothalamus, thalamus, caudate head, putamen, cerebellum, right hippocampus, left pACC (pre- genual anterior cingulate cortex), MCC, and PCC.
** From the editorial: "Since the fatty acid solution was administered directly to the stomach, likely mechanisms include the peptide hormone ghrelin, which is produced predominantly by distinct ghrelin-producing cells in the stomach and other parts of the gastrointestinal tract, as well as stimulation of parasympathetic terminals located in the stomach. The latter would implicate a function for the gut peptide cholecystokinin (CCK), which has previously been shown to have a crucial role in mediating the effects of intragastric fatty acid solutions on brain activity. Additional support for a role for CCK is provided by the fact that phylogenetically, receptors for CCK are known not only for their role in digestion, but also for roles in memory function and learning and in modulation of panic and anxiety."
Now that title has three words I like rather a lot - "gut," "brain," and "humans." It begins to feel a little lonely sifting through the rodent literature, wondering what could be applicable to you and me. I wonder if you feed a rat a hot dog, would it be just as bad as getting a mouse to smoke a cigarette?
But back to the humans - 12 non-obese subjects agreed for some reason to have nasogastric tubes slithered down into their gullets before the subjects crawled into a very small but expensive tube to have functional MRIs done. The subjects were given either a saline infusion or an infusion of dodecanoic acid (que? Also known as lauric acid, or the main component of coconut oil. Interestinger and interestinger!) During this procedure, the subjects also had "sad" or "neutral" classical music piped into the tube, and were shown sad faces or neutral facial expressions matching the music. They were also asked to fill out scales rating fullness, nausea, and hunger, as well as indicating mood on a scale of 1 (sad) to 5 (neutral) to 9 (happy). All of the subjects went through all variations - saline + sad music, fat + sad music, saline + neutral music, and fat + neutral music in 4 different scans on 4 different days, but in randomized order, and always after a 12 hour fast.
The results? Well, hunger increased significantly with the sad music and sad faces. The lauric acid decreased both hunger and the sad feelings significantly more than saline. Hunger did not increase with neutral music and faces, and the difference in hunger between the fat and saline groups listening to the neutral music was non-significant, suggesting that fat sluiced down into the stomach was indeed the factor that attenuated the sad/hunger connection. In addition, the "sad" subjects experienced less sensation of fullness after the fat or saline infusion than the "neutral" subjects.
The mechanism thought to explain the emotion/hunger connection is in the reward system of the brain. This is thought to be the case both in healthy volunteers, and in people with eating disorders or obesity.
The fMRI data showed that certain areas of the brain associated with mood and the reward system* were activated differently based on the different stimuli. Under neutral emotional conditions, fatty acid infusion activated the metabolism in these regions more than the saline infusion. Sad emotion also activated the metabolism in these regions, and the activation decreased upon fatty acid infusion compared to saline. It appears, then, that fat activated the emotional centers of the brain, as did sadness, but that fat seemed to cool off the sadness (which was reflected in the mood scores of the participants). The effect of fat on sadness was two-fold decrease compared to saline. This effect is about the same as the change in mood scores in those treated with antidepressants.
The authors note that previous studies (which are hard to compare, as they involved eating food and all the associated smells, textures, and pleasures associated with that) typically rated mood and carbohydrate response, and these studies were also done over the course of a few weeks (the fat or saline was infused over the course of 2 minutes in this experiment).
So - what do we learn? Does fat make us happy? Well, what do you want to eat when you are feeling blue - an apple or a chocolate bar? The editorial for the study we're discussing is quite interesting (but not free without academic access). Another independent study done in mice showed that increasing stress resulted in increased ghrelin secretion, increased corticosteroid secretion, and increased fat-seeking behavior (for the typical rat high fat diet pellets.) The authors note that young people in a longitudinal study from New Zealand who have a major depressive episode during youth have a 2.3 fold increase in the incidence of obesity in adulthood. So there is a presumed mechanism - stress causes us to want to eat, and eating alleviates stress. However, 40% of people report increased appetite during stress, and 40% report decreased appetite. And certainly other adipose mass control mechanisms should eventually compensate - is it our stressful modern lives, or a combination of our stressful lives plus our poisonous modern foods?
There are many more questions raised than answered by the human study - what is the actual mechanism? The editorial discusses the possible action of the gastric hormones ghrelin or CCK**, which are both known to have emotional and brain effects. And what would happen with infusions of protein or carbohydrate, or in other emotional states, such as aggression, happiness, or arousal? Would there be any difference in subjects who are obese or have eating disorders? Women vs. men, women in different stages of the menstrual cycle? If I had an fMRI, a few hundred nasogastric tubes, and a bunch of willing subjects, I would crank out papers as fast as I crank out blog posts with this experimental design. Hopefully this article is not the last we hear from these researchers!
* specifically the medulla/pons, midbrain, hypothalamus, thalamus, caudate head, putamen, cerebellum, right hippocampus, left pACC (pre- genual anterior cingulate cortex), MCC, and PCC.
** From the editorial: "Since the fatty acid solution was administered directly to the stomach, likely mechanisms include the peptide hormone ghrelin, which is produced predominantly by distinct ghrelin-producing cells in the stomach and other parts of the gastrointestinal tract, as well as stimulation of parasympathetic terminals located in the stomach. The latter would implicate a function for the gut peptide cholecystokinin (CCK), which has previously been shown to have a crucial role in mediating the effects of intragastric fatty acid solutions on brain activity. Additional support for a role for CCK is provided by the fact that phylogenetically, receptors for CCK are known not only for their role in digestion, but also for roles in memory function and learning and in modulation of panic and anxiety."
Sunday, July 24, 2011
Bipolar Case Study on the Web and Whole30 on Vacation
Greetings! I'm back in town. The tomatoes, flowers, cats, and fish survived thanks to our very able house sitter, and we're all in good spirits despite air travel with small children (and no, we were not fondled or irradiated extra times in security).
Here's a new song I rather like - Whirring by The Joy Formidable (right click in new tab).
We went to Santa Fe, a lovely New Mexico mountain town and as far as I know, at 7200 feet or thereabouts, the highest state capital in the United States. Though it is not Disney World or anything, we were able to keep the kids well occupied with the Santa Fe Children's Museum, Grandparents, daily walks through old town to the plaza (they have live music there every day), and a couple of cool parks around town. These parks had lots of spiced up natural spaces to make it fun for the kids - large sandboxes housed next to tree trunk amphitheaters, stacks of rocks for climbing, slides built into a hillside, tunnels, etc.
The Whole30 did not survive intact, however, I was mostly very compliant with the rules. But the Whole30 is not about mostly, it is about a strict 30 days of no cheating for a couple of good reasons - 1) it's meant to be an elimination diet to help establish any issues with dairy or gluten or whatnot, and it is important to be quite strict on an elimination diet 2) it's about establishing your supremacy as a human with a will over cravings and food issues.
So what happened? Well, it turns out that in my normal environment is is relatively easy for me to say no to temptation Who cares if I sip mineral water instead of wine at this backyard gathering or that one, or skip ice cream at the kid's birthday party? There will be another backyard gathering next month, and it's not as if the ice cream and cake and pizza at birthday parties are particularly good anyway. Even when I'm not doing a Whole30, I tend to skip that stuff.
But in Santa Fe, a couple of circumstances came up - food I'm not able to get well made where I live or within a 1000 miles of where I live, and eating at very good restaurants with the chef sort of standing over me. So a couple of banned foods slipped through - a Whole20 + a Whole10 do not make a Whole30, but I think I'll try to put together 30 days in September instead, when no vacations are planned. For the most part I stuck to the rules, however (2 meals in 24 over vacation had small infractions, not counting the vegetable oil the fajitas were probably cooked in) - though it was difficult finding safe starches when eating out so much (around here most restaurants have sweet potato as an option - not so popular in the Mexican food arena, I'm seeing). I ended up eating quite a few bananas over the week. And when I was out of my normal environment for such a long period of time, it became more clear just how different strict paleo is from what most people eat all the time.
Now onto something perhaps more interesting - an article online by Michael Ellsberg - How I Overcame Bipolar II and Saved My Own Life. This article was emailed to me and pointed out to me on twitter, and it is a detailed, heartfelt, and well-written account of how some dietary changes (mostly eliminating sugar, refined carbohydrates, coffee, and alcohol, and originally by adding a complete multivitamin/multimineral) dramatically reduced symptoms of bipolar disorder (you'll notice that when he added together bunches of serotonin-boosting supplements he ended up with similar side effects to being on an SSRI). It is a case study, of course, but I find case studies very intriguing and useful when they involve simple interventions that are unlikely to cause harm (such as eliminating sugar). Even I don't think even very strict dietary and lifestyle interventions will cure everyone of everything. I've always felt the major possibilities of nutritional interventions for something as complex as mental illness would be to possibly ameliorate some symptoms and in prevention of a lot of chronic Western disease in general. And when they are dietary and lifestyle interventions that would lead to better health overall, it seems to fit that "do no harm" bill very nicely indeed.
A huge pile of research papers and common sense tell us that maximizing "real food," minimizing food toxins, and eliminating micronutrient deficiencies are vital for the body to work well, including the brain. It does not surprise me that some people will have huge mental health benefits from following that sort of plan - and it shouldn't surprise doctors or neuroscientists either. To me the most striking thing about the article are the number of critical comments (despite his disclaimer) telling Mr. Ellsberg he is being irresponsible for telling his own story.
There are some things, it is fair to say, that we don't want to believe.
Here's a new song I rather like - Whirring by The Joy Formidable (right click in new tab).
We went to Santa Fe, a lovely New Mexico mountain town and as far as I know, at 7200 feet or thereabouts, the highest state capital in the United States. Though it is not Disney World or anything, we were able to keep the kids well occupied with the Santa Fe Children's Museum, Grandparents, daily walks through old town to the plaza (they have live music there every day), and a couple of cool parks around town. These parks had lots of spiced up natural spaces to make it fun for the kids - large sandboxes housed next to tree trunk amphitheaters, stacks of rocks for climbing, slides built into a hillside, tunnels, etc.
So what happened? Well, it turns out that in my normal environment is is relatively easy for me to say no to temptation Who cares if I sip mineral water instead of wine at this backyard gathering or that one, or skip ice cream at the kid's birthday party? There will be another backyard gathering next month, and it's not as if the ice cream and cake and pizza at birthday parties are particularly good anyway. Even when I'm not doing a Whole30, I tend to skip that stuff.
But in Santa Fe, a couple of circumstances came up - food I'm not able to get well made where I live or within a 1000 miles of where I live, and eating at very good restaurants with the chef sort of standing over me. So a couple of banned foods slipped through - a Whole20 + a Whole10 do not make a Whole30, but I think I'll try to put together 30 days in September instead, when no vacations are planned. For the most part I stuck to the rules, however (2 meals in 24 over vacation had small infractions, not counting the vegetable oil the fajitas were probably cooked in) - though it was difficult finding safe starches when eating out so much (around here most restaurants have sweet potato as an option - not so popular in the Mexican food arena, I'm seeing). I ended up eating quite a few bananas over the week. And when I was out of my normal environment for such a long period of time, it became more clear just how different strict paleo is from what most people eat all the time.
Now onto something perhaps more interesting - an article online by Michael Ellsberg - How I Overcame Bipolar II and Saved My Own Life. This article was emailed to me and pointed out to me on twitter, and it is a detailed, heartfelt, and well-written account of how some dietary changes (mostly eliminating sugar, refined carbohydrates, coffee, and alcohol, and originally by adding a complete multivitamin/multimineral) dramatically reduced symptoms of bipolar disorder (you'll notice that when he added together bunches of serotonin-boosting supplements he ended up with similar side effects to being on an SSRI). It is a case study, of course, but I find case studies very intriguing and useful when they involve simple interventions that are unlikely to cause harm (such as eliminating sugar). Even I don't think even very strict dietary and lifestyle interventions will cure everyone of everything. I've always felt the major possibilities of nutritional interventions for something as complex as mental illness would be to possibly ameliorate some symptoms and in prevention of a lot of chronic Western disease in general. And when they are dietary and lifestyle interventions that would lead to better health overall, it seems to fit that "do no harm" bill very nicely indeed.
A huge pile of research papers and common sense tell us that maximizing "real food," minimizing food toxins, and eliminating micronutrient deficiencies are vital for the body to work well, including the brain. It does not surprise me that some people will have huge mental health benefits from following that sort of plan - and it shouldn't surprise doctors or neuroscientists either. To me the most striking thing about the article are the number of critical comments (despite his disclaimer) telling Mr. Ellsberg he is being irresponsible for telling his own story.
There are some things, it is fair to say, that we don't want to believe.
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