Wednesday, October 29, 2014

Walkabout wednesday: Jetlagged mice, Calculus and population models.

Mice with jet lag, the effect of adding Calculus to a F&W curriculum, and population models in adaptive management. Also, I think I've been bloggin in my PJs, oops

Tuesday, October 28, 2014

Evolving one's diet

I recently heard an interview of Dr. Steven Gundry over at Jimmy Moore's Livin' La Vida Low Carb site. Gundry said a few things that intrigued me, so I felt I should try and follow up by reading his book, "Dr. Gundry's Diet Evolution" [1].

Gundry's basic premise is that our diet affects which genes are turned on, and which off. That's not earth-shattering, the notion that environment shapes gene expression is pretty old hat. And most of what Gundry introduces in the first chapter is well supported stuff from the literature. But there's one thing that doesn't have any citations, and that's his notion that there is a genetic program designed to kill us off once we've served our purpose: transmitting our genes to the next generation. 

This "killer gene" program got my attention because there's a new hypothesis for the evolution of aging  in the evolutionary literature, and that is called the "programmed death" hypothesis. The basic idea is that our genes articulate a "use by" date, and once we're past it all sorts of things come unglued. In models at least, the advantage appears to be an increase in a lineage's ability to evolve [2]. There are species that do not age, and cell lineages that also don't age. 

Gundry's assertion is that once we've reproduced our genes prefer we get out of our offspring's way. He brings up a few interesting observations, like why do clots in our arteries form in the heart, brain and legs, but not say, in our noses and ears? It's almost as if they're targeting essential survival systems ... Gundry's idea is that our modern western diet, full of refined sugars and starches, is so good at getting us to reproduce quickly that our genes then quickly kill us off to reduce competition for our offspring. 

I'm willing to grant the programmed death idea as a hypothesis, but Gundry takes it to extremes. For example, he asserts that overeating until you are overweight also triggers the killer genes because "your genes percieve [this] as threatening the food supply of others." [page 16] That's just one example of how he has bought into a group selection argument for the existence of these killer genes. And convincing your genes that you're not a threat is the basis for phases 2 and 3 of his diet plan. 

Phase 1 of Gundry's plan is pretty standard -- drop the refined carbohydrates and starchy vegetables. Where he differs from a LCHF plan is by focusing on lean protein as the replacement for carbs, rather than fat. The logic is that you're trying to convince your body that "Winter's here", and animals would be lean in winter. There are a few little inconsistencies though. The key "Gundryism" here is "If it's white, out of sight", like sugar, flour and WHAT MAYONNAISE! There's no rationale for that, but in an earlier chapter he mentions that soybean oil (the main ingredient in commericial mayonnaise) should be avoided because of a high Omega-6 : Omega-3 ratio. OK, but then why is tofu listed as an acceptable protein? It's actually white too, now that I think about it. This "teardown" phase is supposed to last until your weight loss plateaus, and you're not showing signs of illness. 

In Phase 2, "Rebuilding", the main emphasis is on reducing the protein and increasing the green stuff. This is meant to imitate the diet of our pre-agricultural ancestors. He draws on the diet of a silver-back gorilla as inspiration -- lots of calorie sparse leaves*. The biological hypothesis in this section seems to be that eating protein raises metabolism, and a high metabolism is bad. So eat less protein, lower the heat, and you'll be better off for it. He also cites the China Study as support for this perspective. If you're still thinking that's a good idea, you should read the critiques by Denise Minger or Chris Masterjohn. Sorry Gundry, you're loosing me here.

In Phase 3, "Longevity", the goal is to keep those gene's from thinking you're a threat and providing a little bit of stress via plant toxins. Eat raw food, because that preserves those phytochemical toxins. Eat less, because that way you convince your genes you're not competing with your offspring. Calorie restriction is associated with longevity, at least in animal models, from the citations he provides. One thing that is slightly alarming here is that calorie restriction increases cortisol, and that's one mechanism that can increase fasting blood glucose levels. Which might be fine, if you're not insulin resistant.

To wrap up, I'm convinced that our genes matter and that our environment (including what we eat) influences which genes are on or off. But I was convinced of that before. I agree that programmed death is a valid hypothesis, but I don't see any evidence for the "competing with my offspring" as a trigger for killer genes. I agree that lots of low calorie vegies are good, but not sure about being able to get the majority of my protein from them without growing a gorilla sized colon. Eating less, check, as long as I'm not hungry. Back to the library with you, Gundry. 

[1] Steven R. Gundry. 2008. Dr. Gundry's diet evolution: turn off the genes that are killing you -- and your waistline -- and drop the weight for good. Crown Publishers, New York.

[2] Joshua Mittledorf and Andre Martins. 2014. Programmed Life Span in the Context of Evolvability. The American Naturalist, 184:289-302.

*But, but, gorillas have colons more than twice the size of a human which is why they can survive on calorie sparse food!

Monday, October 27, 2014

Blood sugar targets

or how low should I go? How high is too high? Is having targets even a good idea for Adaptive Management?

Friday, October 24, 2014

Testing hypotheses for high morning Blood Glucose

I've focused more on measurements of Hemoglobin A1c than blood sugar, as that gives a time average indication. Even so, my A1c numbers, while good for a diabetic at between 5% and 5.4%, are not great by Steve's targets. A value of 5.4% corresponds to an average BG of 108 mg/dL. Going the other way, having an average BG less than 100 mg/dL means an A1c of 5.1. The fact that my averages are much higher than my fasting levels during the day suggests that my post-meal levels, and early morning levels, are very much higher than I'd like. I've got a series of experiments underway looking at BG after eating, but what about overnight highs in Blood Glucose?

So I think this is a perfect setup for adaptive management.

There are two hypotheses for high morning blood glucose in a Type 2 diabetic. The "hormone hypothesis" posits that an increase in growth hormone production in the middle of the night triggers a cascade of events leading to the release of glucose from the liver. Presumably this is to set one up for a vigorous start to the day. In a healthy person this extra glucose triggers an insulin response, and blood glucose remains steady. In a person with insulin resistance (like me), the insulin response is not effective, and blood glucose rises. The second hypothesis is "The Somogyi effect", where low blood glucose values overnight trigger the the release of glucose from the liver to avoid too low blood sugar values. That also involves hormones, but they are activated for different reasons.

Which of these hypotheses is true does matter; under the 2nd hypothesis I should be able to avoid high morning sugar by making sure my overnight sugar levels don't drop too low. I could eat a snack before going to bed, for example. Under the hormone hypothesis there's not much I can do except to try harder to ameliorate the insulin resistance. I could start taking Metformin, which acts in two ways, first by suppressing liver production of glucose and second by reducing insulin resistance. Both of those actions should act directly on the dawn phenomenon.

I can also learn which of these hypotheses is true by monitoring my blood sugar. Ideally, I'd measure my blood sugar every hour or so all night ... hmm. That sounds like a sucky experiment. According to this article, I can get away with just measuring at bedtime, 3 a.m., and the morning.

So I tried it for 2 nights, and I think I've discovered a 3rd hypothesis, the "Drew Tyre Effect"! On the first night, 9pm 101, 3am 116, and 6am 122! OK, that's consistent with the hormone hypothesis, but maybe I missed a drop in BG between 9pm and 3am. So last night I took the middle measurement earlier, and 9:20pm 112, 12:25am 110, and 6:40am 116. My BG is high all night. 

So, a bit of reading on what stimulates Cortisol levels is warranted. As it happens, sleep deprivation stimulates cortisol production, so this could be an instance in which the observation of a process affects the process itself. I need one of those continuous glucose monitors!

Here's another hypothesis: I've been taking a fish oil supplement for the past 3 months after learning that I was low in tissue levels of EPA and DHA. However, it turns out that fish oil supplements can blunt insulin response and increase resting glucose levels. So looks like I have to wait 18 weeks and then try this experiment again.

And another hypothesis! I'm swimming in the damn things ... It turns out that taking a statin can interfere with blood glucose control. I starting taking 10 mg of Crestor every evening about the same time I started taking fish oil. Well, the results of my latest bloodwork will be very interesting. 

It's harder to be healthy when you're poor

I'm not poor. But I came across a very illustrative example of how eating real food is more expensive this week.

Wednesday, October 22, 2014

Walkabout Wednesday: peak meat, what math you should know, and Tiny Data.

The USA hit peak meat in 2004, Bryan McGill laid out a perfect math ecology curriculum, and Tiny Data should be all the rage in the near future.

Monday, October 20, 2014

Famine & the evolution of diet

One cornerstone assumption of a lot of diet theories based on emulating hunter-gatherer diets is that famine was a constant companion. Predictable seasonal famines occur in all environments, the dry season in the tropics and winter in the high latitudes. The just-so story goes like this: in a predictable feast-famine environment "thrifty genes" that take advantage of feast times to store fat in preparation for the lean times would be selected for. And when you take a population that has these thrifty genes and put them in a constant "feast" environment, they get fat and develop diabetes. Like the Pima Indians in North America*, and the Tokelau people in the south pacific. To avoid triggering these "thrifty genes", paleo diet proponents suggest avoiding the products of agriculture, both modern and historical.

Colette Berbesque and co-authors [1] decided to test the frequent famine assumption by looking at anthropological evidence of famine in a fairly sophisticated way. In particular, they controlled for the effects of habitat richness by only comparing hunter gatherers from warm climates (Effective Temperature > 13C) with agriculturalists, and by using a metric of habitat productivity (a linear combination of Net Primary Productivity and Effective Temperature) as a covariate. From their abstract, they found:
... if we control for habitat quality, hunter–gatherers actually had significantly less—
not more—famine than other subsistence modes.
Digging into the details though, we find that this is true for some measures of famine but not others. For instance, on the variables Occurrence, Severity, Persistence, Recurrence, and Contingency of famine warm climate hunter gatherers do better (that is, less famine). In terms of short term or seasonal famine however, there is no difference between warm climate hunter gatherers and agricultural peoples. And that's important, because it is seasonal famine that would lead to the evolution of thrifty genes. And there was plenty of time for such genes to arise in paleolithic people before the advent of agriculture, so the fact that agricultural peoples are no better at avoiding seasonal famine simply means the selection for these genes wouldn't go away after agriculture.

Although Berbesque et al. paint their research as a critique of the "paleo diet" approach, it seems to me that it reinforces a key tenet: paleolithic peoples had it better than their agricultural neighbors. Hunter gatherers do significantly better on  "ordinary nutritional conditions and endemic starvation", have no difference in seasonal famine, and less long term and unpredictable famine. Huh.

[1] J. Colette Berbesque, Frank W. Marlowe, Peter Shaw and Peter Thompson. 2014. Hunter−gatherers have less famine than agriculturalists. Biology Letters 10, 20130853.

*The Pima aren't necessarily a good example, as they were agricultural before becoming "modern western". It is interesting to me that the National Institute of Diabetes and Digestive and Kidney disease article I linked to focuses on the increase in fat in the Pima diet, rather than the exchange of whole grains for refined carbohydrate.

Thursday, October 16, 2014

Today is National Feral Cat Day

And I feel I should say something. After all, feral cats are an issue in our fair city, Lincoln NE, and I have some relevant expertise ...

Wednesday, October 15, 2014

Walkabout Wednesday: people vary, what should ecologists learn less of, and a Republican cries "Climate Change"!

This week I got a little pre-occupied and didn't spend alot of time following up things on the interwebs. I did meditate a lot.

My Health

It turns out that people's physiological responses to fructose vary. Unsurprising, but good that the mechanisms are getting worked out.

AND, researchers at Harvard have figured out how to get embryonic stem cells to act like pancreatic beta cells, sensing glucose levels in the environment and releasing insulin. Cures Type I diabetes in mice. Don't hold your breath waiting for the cure though. 

Your Education

Jeremy Fox ran a little poll last week asking what ecologists (graduate and undergraduate) should learn less of. The results didn't surprise me too much. Most popular "learn more" subjects are math, statistics and programming. It might surprise some to learn that I didn't say ecologists should learn more of those things. The trouble with any curriculum decision is that putting something in means you have to take something else out. At the undergraduate level I think chemistry could be reduced in programs focused on pre-medicine students. At least here at UNL they pratically get a minor in chemistry, which is fine if you're going to be a doctor, but if not they could use the space for more important things like evolution and natural history. I answered 'it depends' for what could be left out, because some graduate students will need more chemistry, some more physics, and maybe some more math, depending on the direction they want to go in. I answered 'Philosophy of Science' for what should be added. After all, its the foundation for all inference in science. No kidding. And typically ecologists take 0. Zip. Null. I recall the first day of my philosophy of science class at University of Alberta. The prof asked 'how many of you are Physics majors', and the front half of the class put up their hands. Then, 'how many of you are Philosophy majors', and the back half of the class put up their hands. Then, 'what about the rest of you'. I put up my hand. I looked around, and I was alone. 'And you're in?' Zoology ...?

Universities are increasingly run like corporations, says Noam Chomsky in some remarks transcribed from a speech to the Adjunct Faculty Association of the United Steelworkers. I learned some new words, (like neoliberal and precariat), and an interesting hypothesis that corporatization is a way to ensure students are appropriately indoctrinated. Load them up with student debt and limit their contact with faculty, and you've got a recipe for dependent and therefore controllable workers. I certainly see the focus on the bottom line at UNL as well as increased reliance on adjunct and non-tenured faculty. Or as I mentioned last week the dependence of the public R&D machine on graduate students and postdocs. Not sure about indoctrinating future workers part.

The news isn't all bleak, however. Apparently Michigan has increased funding for public higher ed, and Iowa State has hired 41% more full time faculty over the last 8 years while simultaneously reducing administration. Wow. How does UNL compare on that statistic?  Well, 2009 to 2013 we went from 1556 "general regular faculty" to 1644, an increase of 5.7%. However, "general regular faculty" includes Professors of Practice, lecturers and senior lecturers. Tenured faculty have actually decreased 3% while non-tenure faculty have increased 27%. Administrators and staff increased 3% over the same period. So, the question is, can we describe UNL as a cannibal rat infested ghost ship, as Rebecca Shuman characterizes public instutitions other than Michigan and Iowa State? Given that Fall semester student credit hour production only increased 2% between 2009 and 2013, I'd have to say yes.

Our Environment

Henry Paulson was secretary of the treasury in the years leading up to the 2008 crash. In this op-ed he highlights a few lessons for dealing with global climate change that he sees in the lead up to that recession.
The solution can be a fundamentally conservative one that will empower the marketplace to find the most efficient response. We can do this by putting a price on emissions of carbon dioxide — a carbon tax.
That sounds like it would be a good idea. I wonder why I haven't heard more about this idea in the 6 months since this was published.

Tuesday, October 14, 2014

Diabetes Management Experiment I

One of the key tenets of Adaptive Management is to "learn while doing", or using management actions to reduce uncertainties. In the management of Type 2 diabetes the real key is figuring out how your body responds to different meals. Meals are management actions, and the uncertainties are how one's body responds to each meal.

I just did one of these experiments. I've been trying to figure out why my A1c levels are representing an average blood glucose level higher than I measure before eating (pre-prandial). There are two possibilities. First, I know I have high blood glucose in the morning, which could be the "Dawn Phenomenon". The other possibility is that I experience high blood glucose levels after eating, a "post-prandial spike". The typical recommendation is to measure post-prandial blood glucose 2 hours after starting a meal. My post-prandial values then are typically pretty good, < 120 mg/dl.

So today I measured at 30, 60, and 90 minutes as well. The results are not good:

Minutes   BG
0              83
30            106
60            120
90            150
120          110

Check that out! A rise of more than 60 mg/dl! Now, if I'd eaten something loaded with carbohydrate... but no: stir fried vegies (cabbage, onions, carrots and green pepper. Not many carrots and green pepper either) along with 4 Lightlife Tofu dogs, and a couple tablespoons of Mayonnaise.

Now comes the difficulty with Adaptive Management. N=1. Even attempting to repeat the experiment I'll never replicate the conditions I had today exactly. However, the hypothesis that stirfried veg + tofu dogs isn't spiking my blood sugar just dropped in probability.

Monday, October 13, 2014

Do you know your APO E status?

I didn't, until recently. I'm a 3/3 genotype. According to Dr. Steven Gundry, people with the 4 allele are badly affected by animal fat. About 25% of the population has at least 1 or more of the 4 allele. So what is this thing anyway, and should you worry about it?

Friday, October 10, 2014

Go Gluten Free or Not?

Lots of people are going gluten free. In this post Fiona Willer argues that many people, especially young women, are doing so unnecessarily. In particular, she (and just about everyone else, like this guy) refer to a really neat study that experimentally isolated gluten and other components of grain, and determined that gluten was not responsible for intestinal symptoms. Instead, the culprits appear to be a group of short chain carbohydrates collectively known as "Fermentable, Oligo-, Di-, Mono-saccharides And Polyols.", or FODMAPs, that are poorly absorbed in the small intestine. However, it turns out that FODMAPs are found in things that also contain gluten (wheat, barley etc. as well as some fruits and vegetables). So if you avoid gluten ... In addition, restricting gluten containing foods will reduce your carbohydrate load, which helps with blood glucose control.

I found it interesting that Dr. Willer's argument for NOT avoiding gluten is that avoiding gluten might lead one to eat less wheat flour fortified with folate. Wait. You want me to eat wheat flour not for itself, but because it has something else added? I can take a multivitamin for that ... or you know, eat all sorts of real foods that naturally contain folate.

In 2012 I shifted my diet to reduce carbohydrates in response to being diagnosed as a Type 2 diabetic. Although this eliminated bread and beer, my 2 main sources of gluten containing carbohydrate, it did not eliminate gluten altogether. As a vegetarian, I was very keen on finding protein sources with relatively low carbohydrate, and many of those include wheat gluten as an ingredient. So, I reduced my consumption of lentils and chickpeas in favor of tofu and seitan, and processed foods containing soy and wheat protein. I lost ~25 pounds and brought my blood sugar back under control as a result.

Fast forward to spring 2014, and I finally got around to reading David Perlmutter's book "Grain Brain". Now that's a scary read. And although critics like Fiona Willer diss the book as "Alternative Medicine", I found the references to the scientific literature more compelling than that. As a result, I took a hard look at what I was eating, and went one step further, purging products containing wheat gluten from my diet. So, N=1 remember, and the plural of anecdote is not data! But here's my anecdote anyway. To borrow a phrase from the video linked above, my "satisfaction with stool consistency" dramatically improved, and more significantly, I felt better emotionally than I had in years. 

I had taken antidepressants for about 5 years, and I would occasionally forget to take my tablets in the morning. Typically I would start to feel withdrawal symptoms within a few hours of forgetting ("brain zaps"). A couple of months after I removed gluten from my diet I realized I was forgetting to take my antidepressant, and not experiencing any symptoms at all! With the support of my doctor, I began reducing the dosage of antidepressant, and 6 months later I've stopped altogether. And I feel great. 

So, I eliminated gluten, and coincidentally FODMAPs, and I feel good. Was there a cause and effect? I don't know. I'm not going to put gluten/FODMAPs back in my diet though. Your mileage may vary!

And here's a little (NSFW) light humor on Gluten courtesy of Southpark. It's not that bad. Really. It won't fly off. 

Wednesday, October 8, 2014

Walkabout Wednesday: doublethink, and starving cancer cells.

My Health

Dr. Malcolm McKendrick always writes great posts, and this one is no exception. He uses some great Orwell quotes to highlight some shenanigans about public data from the European Heart Study. Between 2008 and 2012 they dropped a table showing the relationship between saturated fat intake and per capita deaths due to coronary heart disease. Guess what? The data don't support the orthodoxy.

Understanding the deep evolutionary origins of cancer might help us treat it. The idea is that prior to being multi-cellular, immortality and vigorous cell proliferation were survival traits. Environmental stresses then put cells back into "survival mode", forgetting their evolved functions.
So the team predicts that treating patients with high levels of oxygen and reducing sugar in their diet, to lower acidity, will strain the cancer and cause tumors to shrink.
The fact that they implicate sugar there is interesting, as I also came across another study that found starving breast cancer cells of sugar reverses the phenotype of cancerous cells back to non-cancerous cells. And remember that all carbohydrates in your diet ultimately end up as sugar in your bloodstream.

And as long as I'm thinking about cancer cells, soy protein changes gene expression in breast cells in vivo, and those changes relate to cancer growth rates. This study isn't completely conclusive though, because they did the experiment 7 - 30 days before removing the tumors surgically. As a result we don't know if gene expression changes would in fact have changed tumor growth.

And more on cancer! A large, randomized diet intervention in post-menopausal women found no effect of a low fat diet (< 20% kcal from fat) on risk of breast or colon cancer. 

I'm a fan of breastfeeding babies, and if you need more evidence it is a good thing, here you go. Breastfed babies have lower levels of chronic inflammation as adults.

Your Education

Over the last 2 years or so enrollments in the Fisheries and Wildlife major at UNL have fallen after more than a decade of strong growth. Turns out that reflects a broader trend, and it's at least a symptom of a good thing. For someone. Not us. (ht: Dynamic Ecology)

It's pretty common for professors to share course content around with colleagues. I benefited from course notes and lectures from Helen Regan when I started at UNL. But this article raises a different spectre; taking someone else's hard work on course development and using it without asking them. Made even easier by the widespread use of online course management software. (ht: John Janovy)

A long time ago, in a country far, far away, a University President wrote an op-ed piece bemoaning the surfeit of post-graduate students his faculty were writing into grant proposals. My response, which was actually published, was that it's obvious dude, they are cheap (below the poverty line), highly motivated (willing to work 60 hours a week motivated) and well trained workers. In an environment where funding for public  R&D gets tight, permanent research tech jobs get replaced with postgraduate stipends. Never mind that there's no work for them once they get their shiny PhDs. Now it appears the same perverse incentives are starting to bite here in the USA, with this piece in the Boston Globe highlighting a "glut of postdoc researchers". This quote says it all:
The problem is that any researcher running a lab today is training far more people than there will ever be labs to run. Often these supremely well-educated trainees are simply cheap laborers, not learning skills for the careers where they are more likely to find jobs — teaching, industry, government or nonprofit jobs, or consulting.
Yup. Unfortunately throwing money at this isn't the solution either; a fundamental rethink of how we train researchers and finance public R & D is needed. I guess they could always work as adjuncts, 'cuz that's such a satisfying career. (ht: Natalie West)

Our Environment

Emily Nicholson and Ben Collen have a piece in Science on measuring progress on Biodiversity conservation. I like their point that metrics need to be projected forwards under different policies if they are going to be useful. They also use the excellent approach of virtual ecology (see excellent introduction here) to test how well a biodiversity metric can track reality.

Regular visitors might have noticed that I don't believe improved knowledge leads to changes in behavior. This is a nice little piece summarizing some social science that demonstrates just how bad it really is. One of my FB colleagues wondered what it would mean if applied to scientists. Hint: see the link at the top of this post on disappearing data tables. Scientists are human, unfortunately for science, and the incentives to parrot the paradigm are rampant. (ht: Tala Awada)

Not really about environment, but MotherJones is running a series of charts on income inequality. This one caught my eye because of the increasing variance over time in the income of the top 1%. Rising variance is a signal of an impending tipping point between dynamic regimes in complex systems, as Trevor Hefley's paper in theoretical ecology demonstrates for simple population growth models (which is about our environment!). 

Monday, October 6, 2014

The whole soy?

I've just finished reading "The Whole Soy Story" by Kaayla Daniel. It is a pretty typical offering of the "somethings wrong with our food" genre. In Daniel's case, the something wrong is soy. This book has tons of references to follow up on, but does precious little synthesizing or summarizing. There are plenty of anecdotes from people with horrible soy experiences too, if you're looking for company.

I found the history of soy section pretty fascinating. The takeaway message is that soy based foods are a relatively recent innovation in Asia. Soy was used as a cover crop and fertilizer for millenia, but only in the last few centuries did it start to play a significant role in the food supply. Fermented soy products, like miso and tempeh, have a longer history. Soy oil was a lamp fuel in China! Even now unfermented soy foods like tofu are a small component of the diet, used in conjuction with eggs, fish, poultry and meat. As a population biologist I find it pretty interesting that soy foods increased in importance with increased population size. 

Daniel is pretty clear throughout the book: traditional soy foods are not the target. The fermentation processes used to make miso, tempeh and many others greatly reduce or eliminate "antinutrients" in raw soybeans. Tofu is borderline because the relatively mild processing it receives does not reduce antinutrients to the same extent as fermentation. 

The vitriol is focused primarily on industrial uses of soy in processed foods. If you want to get completely turned off of a product, just read her chapter on first generation soy products. There's clearly a profit motive to using soy everywhere possible, and you won't find me promoting processed foods as healthy. I confess, if you look in our refrigerator you'll find soy dogs with an ingredient list that goes: "Water, Soy based protein Isolate, Soybean Oil, Evaporated cane syrup ..." ugh. Non GMO soybeans though! Nowadays I buy them because they are easy for a teenager to heat and eat, and boy, do teenagers eat. 

The steady introgression of soy products into nearly everything processed is problematic because of the many anti-nutrients associated with soy, and Daniel devotes a substantial amount of the book to detailing these. The trouble with these industrial processes is that they do not reduce antinutrients like phytates and trypsin inhibitors. What about these things in real food, like tofu*? This turns out to be a really good example of how risk tolerance influences the interpretation of data. According to the research Daniel cites, tofu retains 2.5 to 7.9% of the Trypsin inhibitors in the raw soybean. Compare that to 0.3 % retention in Miso and you can see why fermentation is a good thing. Reductions of this magnitude eliminate growth deficits in rats caused by trypsin inhibition. And most of the trypsin in our guts exists in cationic form which is resistant to these inhibitors. So I look at that and say, "well, seems like there's nothing to worry about from tofu." Daniel on the other hand says (I'm paraphrasing) "but it's not ALL gone, and there's SOME effect, and we don't know EVERYTHING." 

But, but, I hear you sputtering, soy is GOOD for us! It's true that these same trypsin inhibitors are being investigated as treatments for cancer. However, the devil is in the details. If you chemically isolate Bowman-Birk inhibitors from soy, treat them to change the relative rates of inhibition of chymotrypsin to trypsin, then feed that chemical product to rats predisposed to get cancer, the rats get less cancer. But that's a long ways from what you're getting in soy food, real or processed. Daniel comes back to the claims that soy protein or isoflavones reduce cancer risk in a later chapter, and similarly, the evidence is equivocal at best, and absolutely in the opposite direction at worst. 

The section that got my attention was the one on phytoestrogens. Soy has a lot, and if you eat a lot of tofu like I do you're getting a pretty hefty dose. The primary negative effect here seems to be on the thyroid gland. Well that's OK, because I had mine removed in 2000 because of Hashimoto's Thyroiditis. What's that? Oh, Hashimoto's has the highest incidence in Japan (hence the name ...), which also has the highest consumption of soy products. Hmmm. Well, correlation doesn't equal causation.

Overall, I call this one a draw. Processed food is bad, yep. I'm with you on that. Infant formula bad, yep, soy infant formula really bad, got it. Breastfeed as long as you can stand it, and then keep going for a few more months please! Easy for me to say, I'm not the one producing the milk. Hey, I tried to do my part by getting up and carting the little devils around after feeding in the middle of the night. 

Am I going to stop eating tofu? Not yet. 

*Yes, I know, tofu is actually processed. However, if I could make it on my kitchen counter then I'm going to call it real food. Like Beer and Wine. :) 

Thursday, October 2, 2014

Throwback Thursday: AM and the National Parks system

Way, way back I wrote a paragraph on Tony Prato's research paper on how AM could be used by the National Park System. That post is my all-time-highest visited post! AND, someone provided an intelligent comment on it. So what's Tony up to now?

Wednesday, October 1, 2014

Walkabout Wednesday: replication, wolves and student evaluations.

Replicating scientific research is important. The ability to replicate a study's results is what sets science apart from other ways of knowing. And sometimes, failure to replicate can overturn an entire paradigm. It turns out that Angus Bateman's classic study on fruit fly sex had a fatal flaw, exposed when Patricia Gowaty* and colleagues attempted to replicate the work after 64 years. And so goes the notion that women are passive objects of male-male competition. Finally. Probably not. Overturning paradigms is hard. 

And here's another example of replication leading to self-correction from physics.

It's been a banner week for replication! Here's a nice article on how Bayesian statistics is helping many disciplines, arguing that Bayesian methods allow checking conventional Frequentist conclusions and therefore improving replicability. Most interesting to me are the references to Andrew Gelman's work on detecting spurious results. However, he takes issue with way those ideas were presented in the article. While I agree there's a "crisis of replication" in science, I'm not sure Bayesian methods are the cure-all the article makes out.  (ht: Jeff Thompson)

I love wolves, and they've provided plenty of fodder for people interested in the intersection of science and policy (see here and here, for example). Now a federal judge has put management of Wyoming's wolves back on the USFWS, calling the handover to Wyoming's state agency "arbitrary and capricious". I gave Wyoming a D- on their AM strategy, so maybe that played a role?

The public regards Scientists as competent but not warm. And they can tell when we're playing "stealth issue advocate" so we should always seek to be "honest brokers". I think stealth issue advocacy is responsible for much of the crisis of replication mentioned above. 

The federal government is preparing to rate colleges and universities to improve students and families ability to make good decisions, and ultimately reduce costs. Here's one op-ed that suggests it won't work, at least at public institutions like mine. "At public colleges, then, the explanation for rising tuition prices isn’t spiraling costs. The costs are the same, but the burden of paying those costs has shifted from state taxpayers to students." (HT: Jeremy Fox @ Dynamic Ecology)

Pre and post testing of physics students at MIT indicates that students taking a MOOC do better than a traditional format.  But: "Although approximately 17,000 people signed-up for 8.MReV, most dropped out with no sign of commitment to the course; only 1500 students were “passing” or on-track to earn a certificate after the second assignment." That's the problem with MOOCs, if it is a problem. The paper is open-access, and uses alot of interesting ideas about how to measure student performance. (HT: Jeremy Fox @ Dynamic  Ecology)

And student evaluations suck. 

This is quite a good talk about Gluten; I hadn't heard of Rodney Ford before but he's a pretty good speaker. I eliminated gluten from my diet completely in early 2014. I will write a post about how I've been feeling since then soon. But here's a teaser: better.

*I was lucky to meet Patty when I was an MSc student at Simon Fraser University in the early 1990's. Really cool work then and now!