Wednesday, January 30, 2008

Marion Nestle Vs. The Center For Consumer Freedom

Update: January 31, 2007 - Marion responds.
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Marion Nestle is taking some heat on one of her blog posts from a group that calls itself the Center for Consumer Freedom (CCF).1 It centers around a story reported in the NYTs last week that stated, "Recent laboratory tests found so much mercury in tuna sushi from 20 Manhattan stores and restaurants that at most of them, a regular diet of six pieces a week would exceed the levels considered acceptable by the EPA."

The CCF claims that the tuna sushi tested is "nothing but safe, wholesome fish."

Marion said, "the tuna industry is fighting back through its public relations agency, the Center for Consumer Freedom." And that, "every word CCF says is paid for."

The CCF then phoned her and stated, "We intend to take legal action," claiming that her statements above are false.

So, is tuna safe? Does the Center for Consumer Freedom work without compensation? See what you think:
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Below is Marion's blog post that the CCF intends to take legal action against:
"So yesterday’s New York Times report on methylmercury in sushi tuna–a shocker because the most expensive tuna has the most of this toxin (of course it does; it’s bigger and accumulates more)–is now experiencing the expected backlash. Sushi eaters don’t seem to care much, and the tuna industry is fighting back through its public relations agency, the Center for Consumer Freedom (CCF). What is a tuna lover to do? If you aren’t pregnant, about to become pregnant, or a very young child (if you are, you should avoid big predatory fish like king mackeral, swordfish, tilefish, shark, and albacore tuna) the FDA and EPA say up to 6 ounces a week is OK. That leaves plenty of room for spending a fortune on sushi.

Here’s what Newsweek has to say about the CCF complaints. It’s great to see a news magazine blow the whistle on that group. Every word CCF says is paid for, and some tuna association pays it to say that methylmercury is not a problem."
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Below is the letter the CCF sent in response to that blog post:
"Dear Dr. Nestle,

In a blog posting on January 24, you wrote that “the tuna industry is fighting back through its public relations agency, the Center for Consumer Freedom.” You also wrote that “Every word CCF says is paid for, and some tuna association pays it to say that methylmercury is not a problem.” (source: http://whattoeatbook.com/2008/01/24/methylmercury-in-big-expensive-tuna/ )

These statements are false, and they seem calculated to do harm to our reputation.

You are free to speculate about the sources of support that our public-education efforts receive. You are not free, however, to assert things that are not true in an attempt to discredit our work. The above examples have clearly crossed the line into libel territory, and could lead to legal action.

If you have documentation that you believe substantiates your claim, I would be very interested to see it. But I am quite certain that you do not. I advise you to either post a correction or withdraw your January 24 piece entirely.

Sincerely,

David Martosko
Director of Research
Center for Consumer Freedom
cc: Richard Berman, Executive Director"
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1 Wikipedia has a brief rundown of the Center for Consumer Freedom.

Naturally Low Cholesterol? Take Note

Many of my ancestors came to this country less than a generation ago. One thing I have in common with them is low cholesterol.

That's why this study caught my eye:

An Association Between Hypocholesterolaemia And Colorectal Carcinoma In An Irish Population

I've always known that low cholesterol was associated with certain cancers but I wasn't aware of the mechanism. This study postulated one, at least as it applies to colon cancer:
"If the hypocholesterolaemia among colorectal cancer patients is not caused by a metabolic effect of the tumours, how can such a phenomenon be explained? Upon consideration of the hypothesis that bile constituents and their intracolonic degradation products influence colon carcinogenesis, it has been proposed that subjects with a metabolic predisposition towards lowered serum cholesterol may also have an increased secretion of bile and hence an increased risk of developing colorectal carcinoma. Thus, the carcinogenic effects of a high consumption of dietary fat may be more readily produced in subjects who maintain lowered cholesterol concentrations by showing an inherently greater conversion rate to bile acids than the rest of the population. Such a hypothesis could explain the paradoxical inverse relation between serum cholesterol concentrations and colorectal carcinomas detected in certain western, or at least 'westernised' populations."
In this case, it isn't the act of reducing the manufacture of cholesterol (via statins) that raises the risk for colon cancer ... it's a genetic predisposition to lose cholesterol by secreting more in bile.

Bile acids are secreted into the intestine in proportion to how much dietary fat is consumed. Bile acids are good in that they help emulsify fats, improving their digestion and absorption. But bile acids can be damaging to the cells that line the colon. This mechanism holds for everyone, but may be more ominous in people with higher levels of bile acid secretion or ineffective reabsorption.

For those who find it ridiculously easy to maintain a low cholesterol, moderating their fat intake may be helpful.
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Photo: A little bit of Irish fog, by pygment.

Tuesday, January 29, 2008

Environmental Pollutants May Up Risk For Diabetes

The buzz at work this week is that pesticides could increase the risk for diabetes, and insulin resistance - big time. This week's Lancet came out with a commentary highlighting the work of Dr. Duk-Hee Lee, et al. Dr. Lee's group found the odds of having diabetes were 38 times higher! for people with high blood levels of toxic persistent organic pollutants (POPs, such as dioxin and PCBs) than for people with low levels. And the association was dose dependant - the higher your levels, the higher your risk.

And this - He found no link with obesity. If you were overweight or obese but had low levels of POPS, you had a lower risk of diabetes than if you were lean but had high levels.

And this - "Chronic lifetime exposure to low doses of POPs could be stronger than in those with short-term exposure to high doses of POPs."

And this - "Reverse causality [that having diabetes leads to higher POP levels] is unlikely because the metabolism of POPs in mammalian systems is intractable; the half-life of the compounds ranges from 7 to 10 years in humans."

And this - POPs are detectable in the blood of greater than 80% of those tested.

And this - (I hate to say this so I'll just use a quote from one of his studies.) "Greater than 90% of POPs comes from animal foods in the general population without occupational or accidental exposures."

And this - As you can see from the US Geological Survey's diagram, pesticides are widely distributed in the environment. There's no such thing as an unaffected pasture.

The thing that's causing the buzz is the strength of this association. Not much work has been done is this area, but that which was has shown a strong and consistent pattern.
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A couple of Dr. Lee's studies:
A Strong Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants and Diabetes, Diabetes Care, 2006.
Association Between Serum Concentrations of Persistent Organic Pollutants and Insulin Resistance Among Nondiabetic Adults, Diabetes Care, 2007.

Monday, January 28, 2008

Got Vegetables?

Mark Bittman, author of the popular How To Cook Everything, New York Times' food writer, and host of the YouTube video that accompanied my post New York Times' No Knead Bread (probably the most-visited post in my entire blog archive) has a new NYTs article out. From yesterday's paper:

Rethinking the Meat-Guzzler

I can see this story driving another wedge between two groups that on the outside appear dissimilar - those who espouse a plant-based diet and those who espouse a meat-based diet - yet, as one of our commenters, Bryan, said, probably have more in common than not.

In this piece, Bittman argues that growing demand for meat in developed countries harms the environment:
"Assembly-line meat factories consume enormous amounts of energy, pollute water supplies, generate significant greenhouse gases and require ever-increasing amounts of corn, soy and other grains, a dependency that has led to the destruction of vast swaths of the world’s tropical rain forests."

"Livestock production generates nearly a fifth of the world’s greenhouse gases — more than transportation."

"[An estimated] 2.2 pounds of beef is responsible for the equivalent amount of carbon dioxide emitted by the average European car every 155 miles, and burns enough energy to light a 100-watt bulb for nearly 20 days."

"Agriculture in the United States — much of which now serves the demand for meat — contributes to nearly three-quarters of all water-quality problems in the nation’s rivers and streams."
Worsens the situation of the world's poor:
"Though some 800 million people on the planet now suffer from hunger or malnutrition, the majority of corn and soy grown in the world feeds cattle, pigs and chickens. This despite the inherent inefficiencies: about two to five times more grain is required to produce the same amount of calories through livestock as through direct grain consumption ... as much as 10 times more in the case of grain-fed beef in the United States."
And is not nutritionally necessary:
"It’s likely that most of us would do just fine on around 30 grams of protein a day, virtually all of it from plant sources."
The rats in my previous study (Now You See It, Now You Don't: Liver Cancer), the ones whose cancerous lesions regressed, were eating a human equivalent of about 22 grams of protein a day. Another benchmark is the Institute of Medicine's Daily Reference Intake: 38g/day for women, 46g/day for men. (Americans consume, on average, between 80 and 100 g/day.) These are total protein intakes for all foods, animal and plant sources combined.

Other points he raised were possible health effects of a meat-heavy diet, and animal cruelty. I found the article disturbing.
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Photo of feedlot outside of Dodge City, Kansas from Cathy Dowd's Flickr stream.

Thursday, January 24, 2008

Casein and Protein Amounts in Some Dairy Foods

Just for the fun of it, and because I've been reading studies like my previous post, I looked to see how much casein is in typical dairy foods.

Modification of Bovine β-Casein to Improve the Characteristics and Manufacturing Properties of Cow's Milk

The site above says that there are about 27.3 grams of casein in 1 liter of whole cow's milk. (The substance of that article is a little disturbing, but I was just browsing for casein content.) From that ...

Approximate! Casein Amounts:
6.5 g casein in 1 cup whole milk
5.7 g casein in 1 oz. cheddar cheese
11.3 g casein in 1 cup plain fat-free yogurt

Skim milk, low-fat cheese, and dryer cheese would provide more casein.

Approximate Protein Amounts:
3 oz. beef tenderloin - 24 g protein
3 oz. of cheese - 21 g protein
1 cup plain non-fat yogurt - 14 g protein
A half-cup cubed chicken breast - 22 g protein
3 oz white tuna - 20 g protein

Protein In Diet:
Low protein* (4.35%) of a 2000 calorie diet = 22 grams protein
High protein* (17.4 %) of a 2000 calorie diet = 87 grams protein
(Average US protein intake (15.4%) of a 2000 calorie diet = 77 grams protein)

The study in my previous post, taken in isolation, cannot inform on which component in casein affected liver tumor growth.

If it was the protein, and for whatever reason you're of a mind to apply the finding, you'd be limiting your total protein to ~22 g/day (assuming a 2000 calorie diet). (Plant-sourced protein may behave differently. This study did not elucidate.)

If it was the casein, you'd be limiting total casein intake to ~25 g/day (assuming a 2000 calorie diet).

* As defined by the previous study.

Now You See It, Now You Don't: Liver Cancer

Would it were that cancer in the real world could be so readily switched off.

Here's another study. On rats. After administering a carcinogen (aflatoxin), researchers fed rats a high-protein diet. The rats' cancer grew. Researchers switched to a low-protein diet, the rat's cancer regressed. Researchers switched back to the high-protein diet. The rats' cancer came back, with a vengeance.

High Protein Intake Promotes the Growth of Hepatic Preneoplastic Foci in Fischer #344 Rats: Evidence that Early Remodeled Foci Retain the Potential for Future Growth, The Journal of Nutrition, 1991
"Switching from the high protein diet (20% casein) to a low protein diet (5% casein) resulted in marked remodeling (regression) of the growing lesions to a response level similar to that in animals that did not receive the initial promotional stimulus of high protein feeding. However, refeeding the high protein diet caused significant reappearance of these lesions."
The protein used was casein, milk protein. Interestingly, when the rats were switched to a low-protein diet, to keep their caloric intake the same, they were given more sugar and corn starch. The addition of proportionately more carbohydrate in the form of sugar and corn starch (more than what the high-protein-fed rats were eating) did not lessen the positive effect of the low-protein diet.

Casein is about 87% protein. So, a 5% casein diet provides about 4.35% protein. A 20% casein diet provides about 17.4% protein. Americans consume on average about 15.4% protein.

Update: Out of curiosity, I checked to see how much casein is in some typical dairy foods. You can see what I found out here.
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Wednesday, January 23, 2008

Lucy Liked Nuts

Ohhhhh, I could live on a diet of fruit and nuts!!

Early Humans On The Menu

An excerpt:
You wouldn't know it by current world events, but humans actually evolved to be peaceful, cooperative and social animals, not the predators modern mythology would have us believe, says an anthropologist at Washington University in St. Louis.

In his latest book, "Man the Hunted: Primates, Predators and Human Evolution," Sussman goes against the prevailing view and argues that primates, including early humans, evolved not as hunters but as prey of many predators, including wild dogs and cats, hyenas, eagles and crocodiles.

"Our intelligence, cooperation and many other features we have as modern humans developed from our attempts to out-smart the predator," says Sussman.

"Australopithecus afarensis1 was probably quite strong, like a small ape," Sussman says. Adults ranged from around 3 to 5 feet and they weighed 60-100 pounds. They were basically smallish bipedal primates. Their teeth were relatively small, very much like modern humans, and they were fruit and nut eaters.

But what Sussman and Hart discovered is that Australopithecus afarensis was not dentally pre-adapted to eat meat. "It didn't have the sharp shearing blades necessary to retain and cut such foods," Sussman says. "These early humans simply couldn't eat meat. If they couldn't eat meat, why would they hunt?"
Well, this sure recharacterized early man for me ... climbing trees to assure a safe haven from hyenas as big as bears and giant saber-toothed cats.

Sussman said that meat-eating didn't take hold until after fire was controlled. I'll bet those first few dabbles in uncontrolled fire-making was spectacular.
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1 "Lucy" is an Australopithecus afarensis who lived ~3.2 million years ago. About 40% of her skeleton was found in Ethiopia in 1974. The photo is of a model of Lucy from BBC's site: Science and Nature, Prehistoric Life, Walking With Cavemen.

That site indicates Lucy's diet as consisting of soft fruit, nuts, seeds, tubers and bird eggs.

Tuesday, January 22, 2008

Discussion About Campbell's The China Study

Melinda raised some points in her comment that I'm motivated to counter-comment on. It's lengthy, so I decided to post them here. The original post that she commented on was T. Colin Campbell Speaking On The Effect Of Animal Protein And Casein where I provided a link to Campbell's speech summarizing his book, The China Study.
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Melinda:

I just watched both videos (all the way thru) and found them quite fascinating. As a public speaker, Campbell's folksy manner may make him a *bit* of an imperfect messenger, as it leads him to speak in generalities that probably are easier to refute than hard numbers. But he obviously has hard numbers.

I probably should read the book, but the charts he shows are rather convincing, especially as they take into account the fact that some of the rural Chinese studied were in fact office workers rather than field workers. So the exercise factor is mooted to some extent.

And the issue of immigrants taking on the diseases of their adopted country (and diet) is compelling, especially in its relationship to genetic issues (which don't change when one moves).

The issue of soy & wheat protein vs. animal protein came across clearly as well, though w/ soy I personally think some forms of soy are not healthy.

The only part where I feel like I want some clarification (which I probably would get if I read the book) is the issue of total fat intake--if one, say, eats a diet w/ 20% fat comprised of olive oil, versus 20% from non-plant sources, for example, does one still avoid the Western diseases he speaks of? Or does he mean it needs to be less than 10% fat of any kind?

As a vegetarian getting a bit closer to veganism, I'm of course interested in these issues and am not going to take up meat-eating regardless. And I agree w/ him on the problem of toxins in fish (not to mention meat). But I would like to know more about fat as he explains it--I believe he said in the 40-min video that plant fats did not cause these diseases unless they were polyunsaturated fats. And he also said that cutting fat intake leads people, often, to increase their animal foods intake. Any clarification, Bix, would be welcome!

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You watched them! I didn't think anyone would have the inclination or patience. You have my respect.

I agree with you that Campbell's generalizations make him vulnerable. But for the body of evidence he was trying to communicate, I accepted his generalizations and continued to hear him out.

In the book he supports more of his statements. You can go to the studies he cites (which he does often) and investigate further (which I've done). But always, always, at some point, when you dissect something down to a little piece, out of context, you become vulnerable again.

That path towards understanding ... moving away from generalizations and towards hard data ... is something I learned in school, and had reinforced in industry. I used to believe it absolutely, "Show me the numbers!" In engineering, someone would shake a piece of paper at you and if the number was analyzed to three decimal points, well gosh, who could argue with that! (Unfortunately, the inputs were so gross, that is, so broad and arbitrary, "Oh... about 10 pounds", that it made a result to 3 decimal points absurd.)

I've changed. I now see that the path, not forsaking that it requires you to move away from a generalization and towards data, continues to move out again. You have to put all your pieces of data together and look at the whole picture. And never let go of your doubt, always question.

Campbell said it this way:
"It is quite easy to find a weakness or an aberrant observation in every single experiment. If executed and interpreted within the context of a larger worldview/hypothesis, each experiment gives direction as to what to do next, perhaps even suggesting a sharp turn in a new direction. If a larger truth is emerging, it seldom if ever depends on one experiment. Rather, it is a matter of accumulating evidence for a series of experiments, especially to see if the evidence is logically connected and consistent."
I think Campbell, in his book and in this speech, was trying to parse decades of work (both his own and others), to look at the whole picture. In my mind, he has something to offer in that. He's worth listening to.
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Regarding some points you raised:
  • I agree, that he looked at office workers does attenuate the exercise confounder to some extent.

  • Yes, that people who move develop the diseases of the place they move to ... does make you think that environment (including diet, but not limited to it) is influential ... very influential.

  • As to animal vs. plant proteins. Wasn't that interesting? Why do animal proteins appear to react differently in the body than plant proteins? I've experienced this with clients who had arthritis. I recommended that they try to replace some animal protein with plant protein, since antigens in animal sources were thought to aggravate joint inflammation. There was some benefit.

  • The fat issue. I loved that panel where he finally showed, near the end, that the correlation between fat intake and cancer may have been confounded. That high fat intake was strongly correlated to high animal protein intake. That it may not have been the fat after all, but the protein. Who knows if there may be an even stronger confounder. (Campbell wonders this too.)

    From what I've put together over the years, I'm coming to think that fat has gotten a bad rap. That's a risky statement, because some people will run away thinking they can eat fat ad libitum, without effect. There is less of an effect for macronutrients when calories are low. But as calorie intake increases, the contribution of macronutrients plays a larger role. Another way of looking at that ... if you feed someone 500 calories a day as bread, they probably won't gain weight, or develop the chronic diseases related to weight ... diabetes, heart disease, joint inflammation, etc. But if you feed someone 2000 calories a day, 3000 calories a day as bread, then the macronutrient breakdown (how much fat, carbohydrate, protein) has a greater effect. The optimum amounts? Who knows? But it has to be said, also, that people respond differently to different diets. So no one way of eating will be the absolute best for everyone.

    Also, as calorie intake goes up, the type of fat comes into play, as does the type of carbohydrate. These things are fluid and relative.

    Personally, I don't think that a diet that provides 10% fat is a realistic goal, putting aside any possible health benefits. Even Ornish concedes this ... his 10% fat was for heart disease reversal, not for everyone. And pushing fat down that much, by default, has us eating proportionately more protein and carbohydrate. With what effect?

    A diet that provides some of all types of fat, saturated (coconut oil, palm oil, as well as from animal sources), monounsaturated fat (olive oil), and polyunsaturated fat (omega-3s are polyunsaturated), in their cleanest, least-processed forms (minimal heating, minimal chemical extraction) is probably the best.
I came away from Campbell's talk, and writing, thinking that there may be a justified positive correlation between animal protein (at high levels of intake, as I noted above) and chronic disease. No one has proven this. But there does appear to be, in my eyes, a foundation for this thinking.

One last thing, a caveat of sorts. And this goes back to my fifth paragraph up there. You have to look at the whole picture, the whole diet, how these macronutrients (and micronutrients) are coming packaged.
  • This was where the fat correlation broke down. We weren't looking to see that fat was coming packaged, oft-times, with animal protein (and maybe something else).
  • This was where the carbohydrate recommendation broke down. We weren't looking to see that carbs were being consumed, oft-times, as over-processed, nutrient-poor derivatives.
  • This may be where the casein correlation breaks down. Maybe we aren't looking to see how the casein comes packaged (denatured? a processed derivative? with calcium? etc.)
Now that I've talked too much and lost everyone, I'll stop. My next post will be pictures.
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Photo of an aluminum plate, fork, and spoon. Made from scrap metal. Used by a family who fled Estonia after WWII and settled into a Displaced Persons camp in Germany. Source: The Migration Heritage Centre of New South Wales.
Now we just have to figure out what to put on it.

Sunday, January 20, 2008

T. Colin Campbell Speaking On The Effect Of Animal Protein And Casein

You may not know about, or you may know and may not agree with, the conclusions drawn by the data presented in the recently released book, The China Study: The Most Comprehensive Study of Nutrition Ever Conducted and the Startling Implications for Diet, Weight Loss and Long-term Health. On the other hand, maybe you've already embraced them.

If you don't know about the book, below is a link to a 40-minute video by the book's author, T. Colin Campbell. He presents what I think is a clear and concise summary. If you don't have the time or inclination to buy and read The China Study, you can get the gist by clicking Mr. Campbell's photo or the link to the right:

Dr. Campbell's address summarizing his book, "The China Study":

Small format, Windows Media or Quicktime.
Large format, Windows Media.
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Some who stumble upon this post, and who spend the 40 minutes it will take to hear Dr. Campbell's argument, will walk away with a new perspective. Some will have their previous views, pro or con, reinforced. Either way, I think the information presented here is worth elevating to public discourse.

The Weston A. Price Foundation (WAPF) and its supporters, particularly Mr. Chris Masterjohn (www.cholesterol-and-health.com), have criticized the conclusions drawn in The China Study. You can read one of Mr. Masterjohn's comments at Amazon.com's listing for The China Study ... on July 5, 2005.1

Below I've linked an 11-minute question-and-answer segment where Dr. Campbell responds to criticisms by the WAPF. He also talks a little about supplements, and how protein from fish fits into his broadview.


In the above segment, Dr. Campbell referred to a written response he crafted addressing the WAPF's concerns in detail. Here it is:

T. Colin Campbell's Response to Questions Raised About "The China Study", October 2006

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1 I had seen criticisms of the book by WAPF's spokesperson, Mr. Masterjohn, on other sites. I was not aware though that he cited raw, unadjusted, correlation data in his argument. Ouch!

Tuesday, January 15, 2008

Dairy Food And Prostate Cancer

Here's another study I stumbled across while investigating the milk and cancer link that keeps cropping up.

Dairy Products, Calcium, and Vitamin D and Risk of Prostate Cancer

It's a 2001 Harvard review of the body of evidence at that time on dairy intake and prostate cancer.
"Seven of 14 case-control and five of nine cohort studies have reported statistically significant positive associations between some aspect of dairy intake and prostate cancer risk. Overall, 12 of the 14 case-control studies and seven of the nine cohort studies observed a positive association for some measure of dairy products and prostate cancer; this is one of the most consistent dietary predictors for prostate cancer in the published literature."
Now, I realize Michael Pollan and others find reductionist nutritional science misleading and useless when it comes to choosing a diet. I think he has a point. You have to look at nutrients within context. However, if we were to accept the above excerpt without trying to understand what's going on, it might lead us to toss the milk out altogether.

What's Going On?

We don't know:
"It remains unknown which compounds in dairy products might be responsible for this association."
But we do have evidence that active vitamin D (1, 25 D produced in the kidneys from D precursors) is protective against prostate cancer:
"1, 25 D has consistently been shown to inhibit prostate cancer growth."
So why are dairy foods which are a good source of active vit D precursors increasingly linked to prostate cancer? A new line of thinking has emerged fingering calcium:
"When serum levels of calcium are low, 1, 25 D acts on the bones, kidneys, and intestines to increase retention and absorption of calcium until serum levels return to a normal range. Similarly, if serum levels of calcium are high, production of 1, 25 D is suppressed by reduced parathyroid hormone production."
Here's some evidence of that mechanism:
"The strongest evidence for an association between calcium intake and risk of prostate cancer comes from the Health Professionals Follow-up Study. ... In this study, men who consumed more than 2000 mg of calcium daily [from all sources, including supplements] had a multivariate relative risk of 4.6 for metastatic and fatal prostate cancer compared with men consuming less than 500 mg calcium daily."
That means there was a 4-and-a-half times greater probability that a high calcium consumer would experience metastatic and fatal prostate cancer than a low calcium consumer.

That's a pretty strong association. It could be the calcium ... there's both epidemiological evidence and a biologically plausible mechanism. Other components being discussed are IGF-1 and phosphorous. But we really don't know. Maybe Michael Pollen is right. Maybe we should just toss out the milk altogether. Or, well, keep it if our grandmothers drank it.
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Monday, January 14, 2008

Diet Update

I can't get over how low my blood sugars have been!

Here's my story in a nut shell...

Last summer, on a fluke, I tested my postprandial (after-eating) blood glucose (BG). It was around 140 mg/dl. I had only had some melon about 2 hours previously. I thought the reading was high. I tested it subsequently, and found both my fasting BG in the morning, and a number of after-meal tests were high ... in the range of Impaired Fasting Glucose (IFG) and Impaired Glucose Tolerance (IGT).

I immediately embraced an Atkins' low-carb diet. I was eating maybe 60 grams of carbohydrate a day. My blood sugars came down. I had some good side effects and some bad side effects. But as long as my sugars were under control I was happy.

Next came two severe diagnoses of cancer in people close to me. I researched dietary risk factors and found that animal protein was often implicated. I decided to stop eating animal protein. This made eating a low-carb diet challenging especially since I don't eat processed wheat and soy proteins.

I slowly introduced carbohydrates back into my diet. What I didn't reintroduce was any product made from flour, and any product with added sugar. My diet consisted of whole grains (whole oat groats, whole hulled barley, whole quinoa, whole brown rice, whole wild rice), beans and legumes, nuts, seeds, vegetables, fruits (even my weakness - dried fruits!), and some oils (olive, peanut, coconut).

With that diet I have been experiencing the lowest blood sugars (and blood pressures) I've seen to date, lower than what I achieved with a low-carb diet.1 I'm now eating a high-carbohydrate diet. But, curiously, I'm not getting blood sugar peaks or valleys. I'm not experiencing hunger after I eat and I have more energy than when I was eating a low-carbohydrate diet.

I certainly did not expect this after reading the low-carb literature. Maybe I'm an exception to the rule. And maybe tomorrow I'll wake up with a 150 fasting. Who knows? But for now, a whole-foods, plant-based diet is working great for me!
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1 One reason for this may be the effect of fermentable carbohydrates which I talked about here.

The photo is not of me. I'm the other gender. It's a photo of Edward Batha, who also experimented with an animal-protein-free diet, although not for the reasons I did. I don't pass as a vegan because I'm still very fond of honey. My sheepskin slippers are another giveaway.

Saturday, January 12, 2008

A Question About Prehistoric Humans

I have a question ... for anyone ... because it looks like many of you know more about prehistoric man than I do.

I looked up the average lifespan for some older humans (I don't know prehistoric designations, but this chart said Neanderthal, Upper Paleolithic, Neolithic):
Wikipedia: Life Expectancy

It looks like they died young, in their 20s. So, my question is ... Is the diet that sustained a human up to their 20s tens of thousands of years ago the same diet that can sustain a human into their 80s today?
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The photo is from a story in the Daily Mail. It's a reconstruction of a person called Thea. Her remains were found in 1937, in Sicily. She was thought to have lived 14,000 years ago.

Thursday, January 10, 2008

How America Eats

In my thinking-out-loud comment under RS and Colon Cancer, I spoke of the social pressure to eat a certain way.

Below is an example. It's a photo of the entrance foyer of a large food store where I shop. A mountainous display of some food item always occupies this space. This week a mountain of soft drinks was being erected. The last display was a mountain of chips, crackers, and dip. At the top of the display (they weren't done piling yet) is often a wide screen television showing people consuming the food in the display, interspersed with "fun" activities ... sports, parties. I can't imagine these are just props, that they don't include them in their inventory without the intention of selling them.

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Photo: Homegrown

Tuesday, January 08, 2008

Nabisco Wants You To Feel Good

I saw this ad while flipping through the Sunday paper. I was going to say something about it, but I think I'll just put it up here and let you say something about it. Maybe I'll say the thing I wanted to say if no one says it. But I think someone might say it.
Click for larger.
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Photo: Homegrown. Scanned from January 6 newspaper insert.

Monday, January 07, 2008

Resistant Starch May Reduce Risk Of Colon Cancer

Given the heated interest in resistant starch (RS) these days, lab rats' diets have been getting pretty darn starchy. And by the looks of it, their colons are healthier for it.

I've read a number of studies about the benefits of RS for the colon. Below are three recent ones. It's interesting to note that the substance used to initiate and promote cancer in the rats' colons, so researchers can study the effects of a hypothesized protective substance, in this case RS, is often animal protein, in the form of meat and especially casein. Casein is the main protein found in milk and dairy products.
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High Red Meat Diets Induce Greater Numbers Of Colonic DNA Double-Strand Breaks Than White Meat In Rats: Attenuation By High-Amylose Maize Starch (Carcinogenesis, 2007)

Rats were fed combinations of red meat (beef) and white meat (chicken), with and without RS.
"Both red and white meat increased colonocyte SSB and DSB dose dependently but damage was substantially greater with red meat." (SSB and DSB are harmful breaks in DNA strands.)

"Red meat induced greater colonic mucus layer thinning than white meat but [RS] was protective in both cases." (A nice thick mucus layer is a good thing.)

"[RS] induced increases in large bowel SCFA, including butyrate, and significantly lowered concentrations of phenols and cresols." (SCFA is an acronym for short chain fatty acid.)

"Dietary RS protects against [colonic] damage and also against loss of the mucus barrier, probably through increased butyrate production."
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Resistant Starch Prevents Colonic DNA Damage Induced By High Dietary Cooked Red Meat Or Casein In Rats (Cancer Biology & Therapy, 2006)

Rats were fed varying amounts of casein (milk protein) or red meat, with and without RS.
"As expected, high dietary casein caused a 2-fold increase in colonic DNA damage compared with a low casein diet and reduced the thickness of the colonic mucus layer by 41%."

"High levels of cooked meat caused 26% greater DNA damage than the high casein diet but reduced mucus thickness to a similar degree to casein."

"Addition of RS to the diet abolished the increase in DNA damage and the loss of colonic mucus thickness induced by either high protein diet."

"Because DNA damage is an early step in the initiation of cancer, these findings suggest that increased DNA damage due to high dietary protein as cooked red meat or casein could increase colorectal cancer risk but inclusion of resistant starch in the diet could significantly reduce that risk."
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A Synbiotic Combination Of Resistant Starch And Bifidobacterium Lactis Facilitates Apoptotic Deletion Of Carcinogen-Damaged Cells In Rat Colon (The Journal of Nutrition, 2005)

Here, researchers were investigating whether some probiotics (live bacteria ingested with the goal of changing the type and size of bacterial colonies in the colon) are more cancer protective in the presence of a prebiotic (in this case resistant starch).

Rats were given Lactobacillus acidophilus and/or Bifidobacterium lactis, with and without RS.
"The synbiotic combination of RS and B. lactis significantly facilitated the apoptotic response to a genotoxic carcinogen in the distal colon of rats. It appears likely that ingested RS acts as a metabolic substrate, thus creating the right conditions for B. lactis to exert its proapoptotic action. Because the synbiotic combination of these agents facilitates the apoptotic response to DNA damage by a cancer initiator in the colon of rats, it warrants further study for its capacity to protect against colorectal cancer."
Interestingly, the beneficial effect (apoptosis) was not see with either bacterium or RS alone. You had to have the combination of RS plus the bacterium B. lactis. (The bacterium L. acidophilus was not beneficial under any circumstances ... RS or no RS.)
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Mechanism: How RS Is Thought To Be Protective

For some background on RS, you can see this post.

RS is simply a carbohydrate that passes through the stomach and small intestine, arriving in the colon where it is fed upon by resident bacteria.

One group of compounds produced by that bacterial fermentation is short chain fatty acids (SCFAs). They include acetic acid (2-carbon), propionic acid (3-carbon), butyric acid (4-carbon), lactic acid (3-carbon) among others ... usually with a length of up to 8 carbons.

The specific fatty acids produced are dependant upon the form of raw material (carbohydrate) and the strain of bacteria. Resistant starch produces higher amounts of the SCFA butyrate than other fermentable carbohydrates (such as oligosaccharides). This is a key difference since butyrate is the preferred energy source for the cells of the colon.

Eating SCFAs directly has not been shown to provide the benefits seen here since SCFAs are absorbed in the small intestine ... before they reach the colon.

It appears that RS protects the colon by:
  • Encouraging the growth of beneficial bacteria
  • Encouraging production of short-chain fatty acids, especially butyrate
  • Lowering colon pH
  • Lowering concentrations of ammonia, phenolics, and other irritants
  • Decreasing bile acids
  • Increasing the protective mucus layer
  • ... And this one from Greg: "Butyrate, by the way, is a weak inhibitor for an enzyme called Histone Deacetylase (HDAC). This is one of the enzymes involved in gene regulation. Cancer cells overexpress HDACs which turns off the cancer's tumor supressor genes. Inhibiting HDAC turns these back on and cancer cells die. This could one of the benefits of RS."
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Michael Pollan Defends Food In His New Book

A "Thank you." to RB who sent along this NPR interview with Michael Pollan.

Author Comes To Natural Food's 'Defense'

Pollan, author of the recent (2006) New York Times' best seller, "The Omnivore's Dilemma: A Natural History of Four Meals", has a new book (2008), "In Defense of Food: An Eater's Manifesto".

His manifesto, in 7 words:
"Eat food. Not too much. Mostly plants."
I liked this part:
"You're going to have to spend either more time or more money, and perhaps a little bit of both," Pollan says. "And I think that's just the reality. It's really a question of priorities, and we have, in effect, devalued food. And what I'm arguing is to move it a little closer to the center of our lives, and that we are going to have to put more into it, but that it will be very rewarding if we do."


Ok, I don't like so much the part about spending more time. Ack. But I think he's right. And I love the way he said it ... moving food "a little closer to the center of our lives." I've found that the further back I purchase my food on the food processing continuum, the more time I spend, well, processing food.

Pollan also says:
"Don't eat anything that your great-great grandmother would not recognize as food."
I think I'll pioneer a little beyond that advice. If it wasn't a potato or salt cod, my great-great grandmother might not have recognized it.
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Saturday, January 05, 2008

Types of Resistant Starch

Prior to the 1980s it was thought that most starch we ate was digested and absorbed, and that those processes occurred in the small intestine. Subsequent experiments showed that portions of some starches were resistant to hydrolysis (breakdown) by our digestive enzymes. The term resistant starch (RS) was coined to describe these starches.

Up to 75% of the starch in red kidney beans may be resistant to digestion.

RS is merely starch that resists digestion - digestion, that is, by human enzymes. Dietary fiber resists digestion too, but RS is not a fiber in the traditional soluble and insoluble sense; you likely won't see it listed as dietary fiber on the Nutrition Facts label. You will see it lumped into the Total Carbohydrate amount - although that may change.

How Much RS Is In Food?

The amount of RS in a food is found by subtracting its rapidly digested starch (RDS: starch which is reduced to glucose units within 20 minutes - bread has a lot of RDS) and slowly digested starch (SDS: starch which is reduced to glucose units within 120 minutes - some cereals) from total starch (TS):

RS = TS - (RDS + SDS)

In an earlier post (Bacteria and Blood Sugar) I listed some foods known to contain RS: legumes, raw potato, green banana, cooled cooked potatoes/grains/pasta, and some types of corn and rice that contain higher amounts of amylose. (See the bottom of this post for a picture and description of amylose starch.)

But not all RS is resistant to the same degree.

Below is the current classification used for RS. There are 4 groups, varying among other qualities by degree of digestibility:

RS1 - Starch that is resistant to digestion because it exists in a physically dense, or physically protected form. Examples are whole- or partly-milled grains, seeds, and legumes. Milling, grinding (including chewing), and homogenization free this starch for digestion.

RS2 - Starch that is resistant to digestion because it exists in a physically dense and relatively dehydrated form. This lack of water is internal to the structure of the starch granule. It's not evident by looking at it. Examples are raw potatoes and unripe banana. Boiling and homogenization free this starch for digestion.

RS3 - The most resistant kind. Starch, mostly amylose, that becomes resistant to digestion when heated then cooled. Also known as retrograded starch. Examples are cooled cooked potatoes and beans. Amounts in pasta vary and are dependant upon the structure of the pasta, and heating and cooling times.

Boiling RS3 will not easily free it for digestion, as it will RS2. In fact, moist heating will encourage the starch molecules to swell then rearrange themselves as they cool, making this starch almost entirely resistant to digestion by pancreatic amylases. Another unique feature of RS3 ... repeated heating and cooling cycles will further increase the RS content.

RS4 - Starch that is resistant to digestion because it has been chemically modified. Bonds other than naturally occurring α-(1-4) and α-(1-6) are formed. Examples are commercially made breads, cakes, crackers, etc. that contain "modified food starch".

I expect to see, as the benefits of RS accrue, more processed foods containing higher amounts of RS4 and advertising this fact prominently. Since RS4 does not occur in nature, I'm wary of it. It reminds me of the early excitement over partially hydrogenated oils ... whose trans-configurated bonds were later found to be unhealthful.
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The starch in a food can consist of all forms - rapidly digested starch, slowly digested starch, and various types of resistant starch.

Here's an excerpt of a table from Sajilata et al's, Resistant Starch - A Review:


Click for larger.

Look at that red kidney bean. Up to 75% of its starch may be undigestible. Not only will the presence of RS decrease stated caloric content, but it also decreases expected post-meal blood glucose levels. And, as I noted previously, consumption of RS can lead to decreased post-meal blood glucose for up to a day or two afterwards.

Note: Just because we (human enzymes) don't digest it doesn't mean that RS exits our body completely undigested. The bacteria in our colon have enzymes which break down RS, freeing bits of glucose (which we absorb), and producing bits of fat (which we absorb). So RS is not calorie-free. When compared to digestible starch, RS provides about 50% fewer calories. (DS: 4 cal/gram, RS: 2 cal/gram)

Snapshot Of A Moving Target

The numbers in the above table are only a snapshot of a moving target. It's difficult to pinpoint the exact amount of RS in a food because so many factors affect it:
  • Chewing decreases RS.
  • Adding oil as the starch cools decreases RS.
  • Adding spices as the starch cools decreases RS.
  • Reheating cooled starch decreases or increases RS depending on the type.
  • Germination and fermentation decrease RS.
  • Lower-temperature, longer-time baking increases RS.
  • Storage, especially low-temperature storage, increases RS.

Wikipedia lists a regular (not green) banana as having 4.7 grams RS. That accounts for almost 50% of its starch content (excluding sugars and traditional fibers). But the less ripe the banana, the more RS it would contain. I can see the difficulty in creating tables. Maybe that's why I can't find many. Please email me if you see some. None of this makes it easy to predict how much insulin a person with diabetes might need when they add up all the carbohydrate in a meal. But it does put to rest the idea that all non-fiber carbohydrate in a meal gets converted to glucose and enters the bloodstream. Now that this background info is out of the way, I hope to visit some more exciting facts about resistant starch. I'm easily entertained.
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Friday, January 04, 2008

Stuff a Duck

I hope everyone had a nice Holiday!

Mine was made that much nicer by the presence of a roasted duck on Christmas Day. (I have to thank Migrainer for her advice to prick the skin thoroughly and often as it roasts.) This duck rendered like nothing I've ever seen. It had enough fat pad to fly across the Arctic (Oops! New Years' Resolution #3: No more hyperbole.) ... enough fat pad to fly across a few pretty, snow-covered, Pennsylvania pastures.

I wasn't going to stuff it. FRE requested that it be stuffed. I didn't want to use a bread stuffing. I was considering a brown-and-wild-rice mix. FRE requested barley. Barley. FRE is not on board with whole, hulled barley yet. What was that he called it? "Like pebbles in water"? Something like that. (He's not far off, but this is a good place to mention that my fasting BG was 78 mg/dl a few days ago. I owe it to pebbles in water.) I compromised by using a quick-cooking, pearled (and it looks like rolled) barley. It was delish.

Ingredients

1/2 cup uncooked barley (quick-cooking, pearled)
1/2 of a large yellow onion, diced (or a whole small)
1 or 2 cloves garlic, thinly sliced
1 stalk celery, diced
2 or 3 tablespoon diced, dried apricots
2 or 3 tablespoons raisins
2 or 3 tablespoons vermouth, maybe 4, and some to sip
1 or 2 tablespoons olive oil
Spices (Your choice. See below for my choice.)
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1   Cook the barley according to package directions. Let cool.

Note: Bring 1 cup of water to a boil. Add a dash of salt. Add 1/2 cup barley. Turn heat to lowest setting. Cover (leave lid open a crack) and simmer for 15 minutes. Cover completely and let rest for 10 additional minutes. (I used Mother's Barley because that's all I could find. Not an endorsement, but not a bad quick-cooking barley.)

2   Sauté onion in olive oil for about 5 minutes until translucent but not browned. Add garlic and celery and sauté for an additional 5 minutes. Turn off heat. Add spices and allow them to bloom in the warm oil for a few minutes.

I used the following spices, and probably some others that I can't recall. I went a little spice-wild.
  • 1/4 teaspoon salt
  • Few grinds black pepper
  • 1/4 teaspoon dried thyme
  • 1/4 teaspoon dried crushed rosemary
  • 1/4 teaspoon dried parsley
  • 1/8 teaspoon dried sage
  • 1/8 teaspoon red pepper flakes
  • 1/8 teaspoon ground onion
  • 1/8 teaspoon smoked paprika
3   Combine barley, sautéed vegetables, apricots, raisins and vermouth in a large bowl.

Note: Hold back a little vermouth to deglaze the pan (not a reduction, just a few swirls) and pour pan drippings into stuffing. Sip vermouth as pan deglazes.

4   Stuff your duck.

Note: The spirit of Christmas Day must have been shining on my stuffing construction because this recipe perfectly filled the cavity of my 5.5 pound Peking duckling. That never happens. I always have either not enough or some left over.

Enjoy!
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Photos: Homegrown. The photo at the top is of my stuffing before it went into the bird. With a few tweaks, this could be enjoyed as a cold barley salad in its own right. Maybe. The photo at the bottom is of my stuffing after it steamed inside a duck cavity for 4.5 hours at 300 degrees F. The barley stayed nicely intact, the raisins and apricots plumped up, and the whole dish gave off an aroma of spicy, roasted poultry. Mmmmmm.