As you know, the UN WHO International Agency for Research on Cancer has listed Red Meat as Group 2A (probably carcinogenic to humans) and processed meat at Group 1 (causes cancer).

And everyone is upset. The most common reaction to these listings is to criticize WHO. The least common reaction to these listings is to learn what the listings are, what they mean, what they mean to you, to the meat industry, to cancer research, and all that. Here, I will try to provide some perspective on some of this.

WHO is probably more likely to list something as cancer causing

It is probably true that the WHO IARC is somewhat biased, in that they are more likely to attribute possible carcinogenic effects to things than other similar groups. There are many substances and behaviors listed by WHO as possibly or probably cancer causing that are not similarly identified by, for example, the US EPA. This does not mean that WHO IARC is more likely to be wrong. It just means that your reaction to a possible agent being listed by WHO should be to understand this bias, but not to assume you know what the bias means. If every single cancer-watching agencies was biased in one direction, we’d have a problem. If all cancer-watching agencies always drew the same exact conclusions form the disparate research, we’d have a conspiracy. If the range of cancer-watching agencies produces a reasonable range of decisions, we’d have real life.

Here is something you should keep in mind when comparing across agencies. Many US federal agencies are led and staffed by industry experts. Where do you get industry experts? From the industries these agencies regulate. Where did the industries get them? They got them from PhD schools, where they quite possibly paid for their higher education with grants from the industry and worked in labs paid for in part by those industries, while working on grants from the industry. This is likely more a thing in the US than in other countries that contribute expertise and do research. It is also true that US regulatory agencies are notably biased in the opposite direction of WHO.

US regulatory agencies will be staffed by well meaning well trained people who know a lot about how the industry works. That is a good thing. US regulatory agencies will be staffed by people who owe their careers to the industry, and are likely to have warm fuzzy feelings about the industry. That is likely to lead to some bias.

On the other hand, in other parts of the world, wooish thinking seems to permeate science and governmental agencies more easily. If you look at the research and regulations, related to EMF risks (like power lines and cell phones and such) you’ll see a gradient where some areas of Europe have both evidence (from research) suggesting EMF-health risks and regulations related to this, and other areas of Europe where the evidence shows now risk, to the US where we by and large don’t regulate EMF using these risks as factors. A sensible view of the research tells us that EMF does not have the alleged health risks.

The reason this is important is that WHO is an international body, so we are going to see a range of industry-fuzzy vs. woo-fuzzy fringes surrounding a hopefully larger and sensible scientifically oriented core. This is also important because of this: if every regulatory or research agency or institution in the world really were funded by the industries they study, and no other research was done by anybody, problems will arise. So go ahead and be annoyed at WHO, but also appreciate this relationship.

It is not about how bad the cancer risk is

As a substance or behavior moves from Group 3, through Group 2B and 2A, to Group 1, this does not mean that it is thought to be increasingly cancer-causing. What it means is that the certainty that the substance or behavior cases cancer, no matter how small the effect, has increased. A given agent may increase the risk of a certain kind of cancer by 50%, which sounds bad, but the original probability of cancer being caused by that agent may be tiny. So, in effect, a tiny risk has been increased to a tiny risk. According to WHO, “The classifications reflect the strength of the scientific evidence as to whether an agent causes cancer in humans but do not reflect how strong the effect is on the risk of developing cancer.”

This is not about your bacon

I find it amusing that the Internet Reaction to these listings is so widespread and negative, even angry, and at the same time so poorly informed. This is amusing because we are just coming off a way over the top Bacon Worship phase.

I stopped eating bacon about four months ago. Do you want to know why? Because of all the pictures of bacon, excessive bacon, things made out of bacon, bacon being fetishized and revered like it was a god or something, on Facebook and elsewhere. I got tired of bacon. I was reminded of a friend’s comment. He was raised in a Kosher household. He told me, “I don’t have any food taboos, I don’t keep kosher. But if I walk into a house where someone is cooking ham, I want to throw up.”

(OK, I did have a BLT the other day. But it was hard.)

The point is, do think about the nature and cause of your reaction, if you are having a hissy fit about WHO and meats. Are you objecting to the WHO IARC criteria, which you’ve carefully studied and understand, or are you simply being sensitive about your stupid bacon fetish? Think about it.

Some food research is probably inherently wrong

I just want to throw this in. If you feed human food, especially cooked food, especially food not made of raw grains, to rats and mice, they might get sick, while a human being fed the same things won’t. Why? Because humans invented cooking possibly as long as two million years ago, and have adapted to cooked foods which seem to cause nasty problems for some lab animals. And humans and their ancestors have always eaten at least some meat. And we are not rodent granivores. So, I don’t know how much animal evidence is being used to change the groups for meat and processed meat, but I personally prefer to disregard rodent data on human diet. It seems to be almost always misleading. Just sayin’

IARC Groups

Just so you know, here are the IARD Groups

Group 1: The agent is carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. In other words, there is convincing evidence that the agent causes cancer. The evaluation is usually based on epidemiological studies showing development of cancer in exposed humans. Agents can also be classified in Group 1 based on sufficient evidence of carcinogenicity in experimental animals supported by strong evidence in exposed humans that the agent has effects that are important for cancer development.

Group 2 This category includes agents with a range of evidence of carcinogenicity in humans and in experimental animals. At one extreme are agents with positive but not conclusive evidence in humans. At the other extreme are agents for which evidence in humans is not available but for which there is sufficient evidence of carcinogenicity in experimental animals. There are two subcategories, indicating different levels of evidence.

Group 2A: The agent is probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. Limited evidence means that a positive association has been observed between exposure to the agent and cancer but that other explanations for the observations (technically termed chance, bias, or confounding) could not be ruled out.

Group 2B: The agent is possibly carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when the evidence of carcinogenicity in humans does not permit a conclusion to be drawn (referred to as “inadequate” evidence) but there is sufficient evidence of carcinogenicity in experimental animals.

Group 3: The agent is not classifiable as to its carcinogenicity to humans. This category is used most commonly when the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Limited evidence in experimental animals means that the available information suggests a carcinogenic effect but is not conclusive.

Group 4: The agent is probably not carcinogenic to humans. This category is used when there is evidence suggesting lack of carcinogenicity in humans and in experimental animals.

2redWinery, makers of the award-winning Ziniphany© Zinfandel and #2red is 38% towards goal on Indiegogo with all proceeds supporting prostate cancer research through the Robert and Susan Hollander Foundation, an IRS approved 501c3 organization. Campaign supporters, in exchange for their tax-deductible support, can secure wine from the 2015 vintage or from the award-winning wine library of 2redWinery.

Robert Hollander, the winemaker and principle of 2redWinery, started small-volume winemaking in 2007 to indulge a long-standing passion. Passion changed to purpose in 2010 after he was diagnosed with prostate cancer at an incurable stage. Dr. Hollander, a highly-regarded clinician/teacher at the Gainesville VA Medical Center, affiliated with the University of Florida, then created the Robert and Susan Hollander Foundation to fund prostate cancer research. “After that, it just made sense to fund the Foundation with my winemaking. It gave my wine a dual purpose, not just to make a great wine I was proud of, but a wine that served a special purpose,” Hollander observed. In the two years the Foundation has been operational, unrestricted grants have been provided to researchers at MD Anderson Center and the Cleveland Clinic.

Dr. Hollander’s campaign goal is $35000 with all proceeds above production costs supporting prostate cancer research through the Foundation. Contributions to the campaign are processed by FirstGiving and are tax deductible. Rewards for campaign supporters include wine from the upcoming 2015 vintage or wines from the award-winning library of 2redWinery. “It’s a win-win-win-wine,” according to Hollander.

See Campaign: http://www.igg.me/at/2redwinery.com

Robert Hollander Winemaker, 2redWinery
President, Robert and Susan Hollander Foundation
doctorbobster@gmail.com
http://www.igg.me/at/2redwinery.com
https://youtu.be/zu7Bf5RubpI
https://www.facebook.com/doctorbobster

Before looking at the Mother Jones piece, here’s the bottom line: There is no known mechanism by which cell phone use can lead to cancer (usually, brain cancer is of concern). There have been many studies on this and related issues. They vary in quality and in what they look at. The studies that seem to indicate an increase in some kind of cancer with cell phone use would indicate a shift from a very very very unlikely chance of cancer to a very very unlikely chance of cancer. So if there is an effect reflected in this research, it is very small. The studies that seem to show a link are generally done by a limited group of researchers, use methodology that is not reliable and can not be used to attribute cause, and are situated within a literature that includes many studies that show no link. Different studies that may show a link between cell phone use and cancer often indicate a link to a different cancer. And, tellingly, brain cancer rates over recent decades are basically flat, cell phone use explosive. If cell phones increase the risk of brain cancer, it is a phenomenon that a lot of research has failed to clearly demonstrate, and if the effect is there, it is very small and entirely unexplained by physics or physiology.

Josh Harkinson discusses an important topic but does so that in a way is uncomfortably click-baity. (I assume this is in part the effect of the editors who chose the title and possibly the accompanying graphic). The title implies that science raises a concern (an alarm) and the article is accompanied by a doctored photograph of a woman using a cell phone; She is wincing as though suffering a health effect and red cell phone cancer-kooties are seeping into her head right there in the picture. The subtitle invokes the children: “Children in particular may be vulnerable.” And, the article begins with an appeal to the latant distrust, “Are government officials doing enough to protect us.”

The article stems from a letter signed by “195 scientists from 39 countries” who “have collectively published more than 2,000 peer-reviewed papers on the subject.” How many scientist deal with the topic of non-ionizing radiation (the kind of kootie stuff that emanates from your cell phone) interacting with tissue (what your head is made out of)? I’m not sure, but a Google Scholar search on the term “biological health effects non-ionizing radiation” yields over 14,000 results. There are probably tens of thousands of scientists who work in the general area of radiation-cell interaction. This is a huge and important area of research. Various kinds of radiation have health consequences. Radiation interacting with tissues is a widespread form of therapy and imaging (everything from x-rays to MRI). The properties of various kinds of radiation and the activity of molecules in cells is part of a lot of basic research in a lot of fields. Here in Minnesota, there are probably way over 200 scientists who routinely engage in research either about or relying on the basic physics and physiology of radiation-cell interaction. It is a big area, only some of which directly addresses health effects of non-ionizing radiation, but even that small percentage involves a lot of work, many research labs, a large number of scientists, and a lot of publications.

The letter and information about it can be found here. Watch the video. Note that the “scientists” are actually “scientist and engineers,” an unintended dog-whistle indicating the padding of consensus claim. The letter is not about people holding cell phones to their heads. It is about EMF in general (with a focus on cell phones), and suggests that the ambient EMF including power lines are the problem. This borders on Chemtrail like ideation. I strongly recommend you watch the video. Critically.

A letter with under 200 signers (across 39 countries) who claim to have published a couple of thousand papers on a topic is numerically weak. The reality and importance of anthropogenic global warming is a scientific consensus. Even so, climate science denialists have come up with lists and letters like this with much more impressive numbers, but thay amount to nothing. There are a lot of scientists out there. There are about seven million scientists. It is not hard to find a couple hundred who strongly believe something that many many more don’t accept as likely. Josh’s article does not address this context, and probably should.

That cell phones may cause cancer has been officially designated by the World Health Organization as “possible.” That sounds bad. But people need to understand, and Josh did not point this out, that the “possible” category includes anything where there is virtually any research indicating a possible link, even crappy research, and even if the research exists among a huge body of research that fails to indicate a link. There are many different categorizations of cancer risk, and different organizations maintain these definitions and lists. The International Agency for Research on Cancer, part of WHO, has these categories:

Group 1: Carcinogenic to humans
Group 2A: Probably carcinogenic to humans
Group 2B: Possibly carcinogenic to humans
Group 3: Unclassifiable as to carcinogenicity in humans
Group 4: Probably not carcinogenic to humans

Items in group one are really problems. They cause cancer and include such things as silica dust, Radon, Soot, Tobacco, and Thorium. Group 2A (Probable) is pretty long and includes a lot of nasty stuff with multi-syllabic names, as well as ultraviolet radiation. Being a hairdresser is a probable cause of cancer because of exposure to chemicals, as is working in a petroleum refinery, or being a shift worker involving changing time of work on a regular basis. These are things that we may want to worry about, but that people still argue about, but, as they say, probably are linked to cancer.

Group 2B, “possible,” the list cell phones are in, is very long, over 900 items, of which about a third are specifically considered possibly linked to human cancers (the others not linked to humans). This list also includes a lot of scary looking stuff, but for which there is insufficient research to actually make the link. Vinyl acetate is an example. It is a liquid precursor for a polymer used to make a lot of stuff. Wikipedia tells us, “On January 31, 2009, the Government of Canada’s final assessment concluded that exposure to vinyl acetate is not considered to be harmful to human health. This decision under the Canadian Environmental Protection Act (CEPA) was based on new information received during the public comment period, as well as more recent information from the risk assessment conducted by the European Union.” So that is an example of a scary sounding thing for which some research may have shown a cancer link but that was ultimately determined by at least one major agency to not be cancer causing. Potassium bromate. Used for a lot of things, it is in some of your food (baked goods mainly). It is banned in many countries, not in the US. In theory, it is broken down during baking. Coffee. Coffee has been some research indicating a link between coffee consumption and bladder cancer, but other studies show a reduced risk of intestinal cancer. Overall, the evidence for any of this is weak.

Group 2B listing is used when there is limited evidence of a cancer link and usually insufficient evidence for a cancer link in lab animals. Let’s put a finer point on it by looking at what the UN says about the 2A and 2B categories (emphasis added):

Group 2A: The agent is probably carcinogenic to humans.

This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans. An agent may be assigned to this category if it clearly belongs, based on mechanistic considerations, to a class of agents for which one or more members have been classified in Group 1 or Group 2A.

So, if you want to be careful, avoid Group 2A items. They may cause cancer, and you should worry about them.

Group 2B: The agent is possibly carcinogenic to humans.

This category is used for agents for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent for which there is inadequate evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals together with supporting evidence from mechanistic and other relevant data may be placed in this group. An agent may be classified in this category solely on the basis of strong evidence from mechanistic and other relevant data.

If you focus on the word “cancer” Group 2B may be scary to you, but many items on this long list are those for which we simply can not say there is no research project ever done that showed a possible link.

Josh notes that “For decades, some scientists have questioned the safety of EMF, but their concerns take on a heightened significance in the age of ubiquitous wifi routers, the Internet of Things, and the advent of wearable technologies like the Apple Watch and Fitbit devices, which remain in close contact with the body for extended periods.”

This points to a possibly unintended side effect of unnecessary concern over non-ionizing radiation. Non ionizing radiation is radiation that does not alter matter at the sub cellular level in a way that can lead to cancer or other negative effects. See this writeup for more detail on this important difference. All radiation reduces in its strength dramatically with distance. As your smart phone and your wi-fi router exchange information (when it is using that pathway to interact with the internet) the energy that comes out of the box across the room and the energy that comes out of the smart phone in your hand, at the point of, say, your nose (a proxy for your brain that allows us to discount the effects of your skin, skull, and dura matter reducing the signal) are many orders of magnitude different. Conflating concern over a cell phone pressed to your head with concern for wi-fi routers is like conflating concern over drowning in a pool with concern over drowning in the vapor that evaporated from the pool that give you that dank feeling as you sit nearby drinking your iced coffee drink form a polyvinyl acetate cup.

Except there really is a demonstrable risk of drowning in a pool.

This is a problem because there is a movement to remove wi-fi from all public spaces over health concerns. That is crazy talk. I wish Josh had noted that in his piece. The people who signed this letter are those same people … who want to remove wi-fi from your coffee shop.

A very very small number of researchers want to move cell phones from Group 2B to Group 2A, but even as they are asking for this, continued research on the cancer risk of cell phones a) fails to produce a mechanism by which this can happen despite a great deal of knowledge about radiation-tissue interaction and b) continues to show a possible link only in studies that are inherently flawed in their methodology. Such studies, mainly case-control studies, rely on people recalling their use of cell phones. People with brain cancer are asked to recall their cell phone use, and matched randomly chosen people without brain cancer are asked to do the same thing. (Not all studies are done just that way but key studies of relevance here were.) That is a great way to get a preliminary look at a possible health issue, but it is simply not how the actual connection between a substance, a technology or a behavior and a health effect is made.

We understand a lot about energy-tissue interaction. If non-ionizing radiation from cell phones caused cancer, we would have an inkling of the mechanism. We don’t. Cell phone use has exploded in recent decades, brain cancer has not. If cell phones caused brain cancer, it would be a visible epidemiological phenomenon. It is not.

I’ve been told (and some checking on the internet has indicated this is maybe important) that some of the material used to make cell phones comes naturally along with some radioactive isotopes. It is possible that these isotopes are not always removed properly. I do not know this is the case, but it is an interesting idea. A while back a shipment of cell phone cases that happened to be radioactive was located (and refused). Holding a radioactive cell phone case to your head several hours a day may be a health risk, though again, I don’t know this to be a fact, it probably depends on all sorts of things. The cell phone-cancer link is so weak that it may be a result of research bias, random effects, recall bias, or some effect related to the use of the cell phone but not to the non-ionizing radiation.

Smart phones are becoming so ubiquitous that they could almost be considered a key trait of our species. It is smart to be smart about smart phones. Worrying about the cancer link is probably not exactly stupid, but it isn’t particularly smart either.

This video addresses many of the topics I touch on here, and more:

Humans eat a wide variety of foods; as a species, the diversity of species we eat is greater than any other animal by a very large margin, with the only quirky exception being the animals that we take along with us, the commensals such as rats and cockroaches. Most primates eat a high diversity of foods, but about two million years ago or a bit less, according to the “Cooking Hypothesis” (which a lot of people think is correct) we took an already diverse primate diet and added to it anything we might encounter in the environment that could be made edible with heat and added that to our diet. More recently, beginning about 10,000 years ago, we applied additional technology and the new practice of plant husbandry to convert other foods, some edible some not, into more useful items for our diet. Humans around the world did this independently over several thousand years, in parallel.

Then we got boats that were capable of doing magical things like sailing up wind, and navigation technologies that allowed humans to be less lost when doing so over great distances. Some humans had done this much earlier at a smaller scale, but by the 15th century there were big wooden boats criss crossing the seas, bringing people to places they had never been before, and along with them the foods people ate all over the world.

Have you looked at photographs of traditional people living in traditional, seemingly timeless, ways in places like Africa, the Amazon, or New Guinea? Look again, and focus on the things that form the backdrop for the scenes shown in those photographs. One of the things you’ll see in many pictures is the plantain, or the banana. You might notice the huge elephant ear leaves of taro plants. If you look closely you might notice cassava growing in the fields, or maize.

Maize was domesticated in Mexico, taro, plantains, and bananas in various different locations across south and southeast Asia. Cassava comes from the lowlands of South America, and potatoes come from the Andes. Some Yams come from Africa, some from South America (I oversimplify a bit). You can’t find a modern traditional diet, as it were, that does not include ingredients from continents other than where the traditional diet lives today, except perhaps in Ethiopia. Everybody eats everybody else’s food all the time. The main determinant of where food is grown is not where it was first domesticated, but rather, the limitations of seasons, rainfall, heat and cold. And even there, the limitations are relaxed. Maize only grows in the colder regions because varieties have been developed to do so, and many plants are grown in regions normally too arid for them, by virtue of irrigation.

Adding all this up – the diverse primate diet, the addition of cooked foods otherwise not edible, the artificially selected crops, and the global exchange of horticultural goods and practices – and you get a huge variety of food, the largest variety of food any species has ever managed to include in its diet. (Other than the rats and cockroaches, of course.)

Despite all this diversity, something has remained more or less the same all along. The “traditional” diet for humans, though much altered with cooking, is relatively low quality. I use the term “low quality” in the way an ecologist uses it. How many usable calories do you get out of a kilo of the food item under consideration? Or, related, how much work do you, using food preparation, chewing, and digestion (including the work done by the friendly microbes living in your gut) to convert that kilo of food into energy?

It is easy to see how our traditional diets are low quality by comparing them to the diets of a handful of primates that live almost entirely off of insects, or tree sap, or nectar. If we look at birds, we see the same thing; many species of birds eat pure sugar of one form or another. A few other animals have very high quality diets. Generally, carnivores have higher quality diets than herbivores. There are no carnivores that use multiple stomachs or habitually regurgitates and re-consume their animal prey in order to digest it. Herbivores that eat grass or leaves spend a lot of time feeding, have massive digestive systems designed by natural selection to digest the hell out of the food, and sometimes they have to “eat” the same food multiple times to get enough energy out of it to survive. Humans are somewhere in between. Some of our digestion is done pre-consumption by cooking and processing, but for the most part our natural, traditional diet takes a fair amount of work to process. We don’t live off of sugar water like hummingbirds and many insects do.

And this is why the leading cause of death in the United States and some other countries has shifted from the usual panoply of causes – infectious disease, accident, homicide, etc. – to our diets. Our diet is the most likely thing to kill us, and lately, the primary mediating factor in this particular cause of death is obesity and/or diabetes.

The “traditional” diet of any group of people, as I’ve already outlined, is relatively recent historically, being the result of 10,000 years of developing plants and a few hundred years of transferring crops and growing methods across the world. That traditional diet was prominent globally through the 19th century and well into the 20th century. The food came from farms, and although many amazing novel technologies were being applied on those farms, such as better plows and various other things that could be drawn behind oxen, a team of ponies or horses, or a small tractor, those technologies did not change the diets too much.

But as technologies developed, farms began to scale up. This is the reason that the New England countryside is graced with young forests criss-crossed with quaint stone walls. Those stone walls were field boundaries in the old days. But as farming scaled up, it became economically inviable to have small fields on small farms. A few other things went wrong on some of these New England farms as well, including some climate glitches and some other economic effects that drove farmers off the land and in some cases into cities where there were jobs working in mills. But some of those farmers took part in the great Westward Migrations, as the country grew, and established a new kind of agriculture in the vast regions of the midwest and plaines.

Add a growing urban market for foods, government help in the form of extension and agricultural colleges, more technology such as combines, railroads to move produce to market, mills to process the produce, add some water (irrigation) as needed and salt to taste. It took decades, but we went from an agrarian economy where the same traditional diet we had been eating was produced on a somewhat larger scale, to an agricultural economy that produces mostly one single thing. This product:

OK, I’m exaggerating there. It isn’t really true that the entire US agricultural system has been converted over to the production of sugary drinks. But sometimes it seems that way. Vast expanses of corn are grown in the midwest and plains, and that corn is used to produce vast amounts of ethanol (as fuel), alcoholic beverages, sugary substances including cola, feed for animals, and some of it even makes it to the table as … well, corn. But lets step back to the original comparison of “traditional diet” and the diet many Americans eat today.

When you eat a traditional meal, a good amount of that food is low quality, relatively hard to digest, carbohydrates with a mix of proteins. There will be a little simple sugar here and there and a bit of fat here and there.

The simple sugars go right away to the liver, where they supplement the body’s immediate energy stores. The complex sugars, the carbohydrates that consist of much larger and more involved molecules, take time to digest and break down to eventually use as fuel. So the sugar gives you a small amount of immediate energy and the complex carbohydrates give you energy over the coming hours.

The fats are simply stored up. If you eat fat, the fat molecules are minimally processed, moved to your hips or wherever, and are pasted there for later use. Or, forever, depending.

When you eat a modern diet, it will have two major difference from the traditional diet. The foods at the two ends of that spectrum of availability will be in greater proportion. Instead of having a bunch of low quality food in the middle, with a little fat (for later) on one end of the spectrum, and a little simple sugar (for immediate use) on the other end of the spectrum, the modern diet will have piles of fat and piles of simple sugar and not much in between.

So, what happens? The fat goes where fat goes, as stated already, but there is more of it. The sugar overloads the liver, which detecting an overabundance of energy, converts the sugar to some form of storage, and some of that is fat that joins up with the other fat. There is also a kind of molecule the liver converts some of that sugar into, stored in your liver, for in case you get hungry between meals. That molecule reduces the chance your body will use any of that stored up fat as energy.

Two thousand traditional calories provides you with energy for now, energy for the next several hours, and a bit of energy for much later. Two thousand modern calories provides you with way more energy than you need for now, and a huge amount of fat that you’ll never use because you are never going to let much time go between meals. Because there is a fast food joint just down the street. And your refrigerator and cabinets are full of junk food.

And that’s not all. Our system of agriculture has all sorts of other negatives as well. The following is from the Food and Agriculture page of the Union of Concerned Scientists:

Food and Agriculture: Toward Healthy Food and Farms
Our agricultural system has lost its way.

Millions of acres of corn, soybeans, and other commodity crops, grown with the help of heavy government subsidies, dominate our rural landscapes.

To grow these crops, industrial farms use massive amounts of synthetic fertilizers, herbicides and pesticides, which deplete our soil and pollute our air and water.

Much of this harvest will end up as biofuels and other industrial products—and most of the rest will be used in CAFOs (confined animal feeding operations) or in heavily processed junk foods, which seem cheap only because their hidden costs don’t show up at the cash register.

Industrial agriculture is unhealthy — for our environment, our climate, our bodies, and our rural economies.

A Better Way: Sustainable Agriculture

There’s a better way to grow our food. Working with nature instead of against it, sustainable agriculture uses 21st-century techniques and technologies to implement time-tested ideas such as crop rotation, integrated plant/animal systems, and organic soil amendments.

Sustainable agriculture is less damaging to the environment than industrial agriculture, and produces a richer, more diverse mix of foods. It’s productive enough to feed the world, and efficient enough to succeed in the marketplace—but current U.S. agricultural policy stacks the deck in favor of industrial food production.

… and there is much much more than that, visit the page.

Yesterday, I went to a symposium hosted at the Humphrey Institute at the University of Minnesota and organized by the Center for Science and Democracy at the Union of Concerned Scientists. A description of the symposium is here and the entire thing was “taped” and will be available. I’m not going to tell you anything major about the symposium now; I’ll wait until the video is available, then I’ll provide you with my thoughts on it. For now I’ll just say it was quite good, eye-opening, and that you’ll definitely want to watch it. In fact, you should feel a little bad that you weren’t there.

Stay Tuned.

From the publisher: “In The Cure for Everything, health-policy expert and fitness enthusiast Timothy Caulfield debunks the mythologies of the one-step health crazes, reveals the truths behind misleading data, and discredits the charlatans in a quest to sort out real, reliable health advice. He takes us along as he navigates the maze of facts, findings, and fears associated with emerging health technologies, drugs, and disease-prevention strategies, and he presents an impressively researched, accessible take on the production and spread of information in the health sciences.”

Skeptical? No problem! Super Skeptic Desiree Schell will be interviewing Caulfield this Sunday on Skeptically Speaking. Also, Scicurious will be talking about Coffee. I won’t want to miss that.

Details for the show:

#166 The Cure for Everything

This week, we’re looking at what the evidence has to say about common claims about diet, exercise, weight loss and other hot health topics. We’re joined by health law professor Timothy Caulfield, to talk about his book The Cure for Everything! Untangling the Twisted Messages About Health, Fitness and Happiness. And on the podcast, researcher and science blogger Scicurious looks at a new study of coffee consumption, and the effect it may – or may not – have on life expectancy.

We record live with Timothy Caulfield on Sunday, May 27 at 6 pm MT. The podcast will be available to download at 9 pm MT on Friday, June 1.

But first, let’s look at the method used in this study, because that may be almost as important as a development. And for this, we will use a sports analogy.

Let’s say there’s an allele (an allele is a variant of a gene) that can boost your ability to play baseball. It really works. It causes an eye-hand coordination thing that improves batting, catching, and also affects your perception of movement in 3D space so you never miscalculate whether to throw or hold the ball or run vs. stay on base.

If you checked for this allele in professional baseball players, you might find that many have it, and even that there looks like there may be more copies of this allele in the overall genome of Major League Baseball, but perhaps at a statistically non-significant level. Yet, you are pretty sure this allele exists and has this effect.

Well, you really didn’t want to test the hypothesis that this allele causes a person to be a professional baseball player. Rather, the allele causes this special hand-eye thing, which is a trait … a phenotype … that then would make a person a great baseball player. But there may be other ways to be a great baseball player, and there may be lots of things a person with this allele may end up doing.

So, you could re-do your statistical analysis by looking not for whether someone is an accomplished baseball player, but rather whether or not they have this hand-eye coordination trait. Then, you figure out a test for the trait, and a test for the gene, develop a sampling strategy that ignores one’s involvement in baseball, and bingo, you’ve got a statistically significant result!

That is an increasing trend in genetic studies of traits (especially disease-related traits). The term that has emerged (but is not the only term used) is “endophenotype.” The endophenotype in the fictional but plausible example I gave above is a super excellent genetically determined hand-eye coordination. In the study just released as you were reading the above paragraphs, it is something physical that seems to be related to the progression of Alzheimer’s disease.

The endophenotype is a version of a protein found in cerebral spinal fluid, called CSF ptau₁₈₁. If a cell was a house, microtubules would be the 2X4s and other pieces of wood. The house would be made of them, and some of them would be used for other purposes as well. Microtubules make up the cytoskelton of a cell and are involved in a lot of day to day cellular processes. Microtubules are therefore very important, and they are made up of tiny protein globs called tubulin. So, the exact structure of tubulin, which is mostly determined by the genetic code that specifies it, has important cascading effects. The tau genes code for “tau proteins” which interact with tubulin as it is being assembled into microtubules, in particular, in the Central Nervous System. Small variations in Tau DNA can cause variations in Tau proteins that could then affect microtubule formation or stability. Thus, the potential connection between certain Tau alleles and, in this case, Alzheimer’s disease.

The current study looked at DNA variants in 846 patients and found a link between rapid progression of Alzheimer’s and the suspect pTau protein.

“We have looked at data from three separate, international studies, and in all three, we found the same association. So we are confident that it is real and that this gene variant is associated with progression in Alzheimer’s disease,” said first author Carlos Cruchaga, PhD.

In particular, the researchers report the link between this slightly variant DNA (called rs1868402) and higher levels of the CSF ptau181 protein, and a faster rate of progression of the disease. This does not seem to be linked to the risk of having Alzheimer’s or to the age of onset, which makes sense because increased levels of the protein levels is not associated with onset, nor does it occur prior to the clinical visibility of the disease.

Can this knowledge help? Probably. The researchers suggest that rs1868402 or some other variant ultimately causes a change in metabolic processes that lead to a pathological form of tau proteins, which would cause neurodegeneration. A similar metabolic glitch, if induced in mouse brains, affects neural function, supporting this idea. So there are two potential benefits: 1) Identifying those who are likely to have rapid degeneration among clinically new Alzheimer’s patients; and 2) Developing a pharmaceutical intervention to fix the degeneration process now that it is (probably) better understood.

Cruchaga, Carlos, Kauwe, John, Mayo, Kevin, Spiegel, Noah, Bertelsen, Sarah, & Et.Al. (2010). SNPs Associated with Cerebrospinal Fluid Phospho-Tau Levels Influence Rate of Decline in Alzheimer’s Disease
PLoS Genetics, 6 (9)

This is all obvious, and you already knew all this. And, finally, science is catching up to you!!!

A team of researchers at Harvard University are exploring the “Friendship Paradox” … a social phenomenon structurally similar to those I just described … as a tool for use in epidemiology.

Here is the paradox. For almost everyone reading this, the friends you identify are more popular than you are. Sorry, but it is true. Ask a bunch of people to name two or three friends, and on average, an objective measure of popularity or connectivity (similar things) will be higher for those named than those asked. Those asked, in a random sample, represent the average person plus or minus whatever variation there happens to be. But people are more likely to name those with higher popularity rankings, because those friends are more on the radar screen. The reported friends are a skewed, biased sample, as opposed to the randomly chosen set of individuals.

There is some evidence to suggest that disease works this way as well. The more popular individuals will actually catch the emerging diseases first. In the example I gave above, personal smarts lead to my friend (hypothetically) picking an excellent sample of potential disease informers, but she didn’t have to do that. All she had to do was to be one of a random sample of people who are asked not how they are doing (health-wise) but rather, how their friends are doing health-wise. If there is a still-rare emerging disease, it will be discovered using this method, harnessing the awesome power of the Friendship Paradox, more quickly than by taking a random sample.

(And yes, this is a little like the Placebo Effect across events rather than outcomes! Brilliant of you to notice that!)

From the study:

Current methods for the detection of contagious outbreaks ideally give contemporaneous information about the course of an epidemic, though, more typically, the indicators lag behind the epidemic … However, the situation could be improved, possibly significantly, if detection methods took advantage of a potentially informative property of social networks: during a contagious outbreak, individuals at the center of a network are likely to be infected sooner than random members of the population. Hence, the careful collection of information from a sample of central individuals within human social networks could be used to detect contagious outbreaks before they happen in the population-at-large.

So, the bad news is that your friends are more popular than you are. But this is offset by the fact that they are going to get sick and die first!!!!

Here’s a picture of a social network where you are B and your popular friend is A:

Figure 1. Network Illustrating Structural Parameters.

This real network of 105 students shows variation in structural attributes and topological position. Each circle represents a person and each line represents a friendship tie. Nodes A and B have different “degree,” a measure that indicates the number of ties. Nodes with higher degree also tend to exhibit higher “centrality” (node A with six friends is more central than B and C who both only have four friends). If contagions infect people at random at the beginning of an epidemic, central individuals are likely to be infected sooner because they lie a shorter number of steps (on average) from all other individuals in the network. Finally, although nodes B and C have the same degree, they differ in “transitivity” (the probability that any two of one’s friends are friends with each other). Node B exhibits high transitivity with many friends that know one another. In contrast, node C’s friends are not connected to one another and therefore they offer more independent possibilities for becoming infected earlier in the epidemic.

As an infection spreads, there is an exponential increase in number of infected individuals followed by a leveling and trialing off. Because of the dynamics of this process, those in more central locations in a network (your friends, the ones that are more popular than you are) will experience different timing of exposure than, say, you and the other losers (the “B’s”). Like this:

Figure 2. Theoretical expectations of differences in contagion between central individuals and the population as a whole.

This all makes sense once you understand the Friendship Paradox, and is especially interesting because it is so counter-intuitive: A good synchronous well-designed random sample sucks compared to this strange quirky approach which relies heavily on human psychology.

Christakis, N., & Fowler, J. (2010). Social Network Sensors for Early Detection of Contagious Outbreaks PLoS ONE, 5 (9) DOI: 10.1371/journal.pone.0012948

In neurodegenerative diseases specific proteins escape the cell’s quality-control system and associate together, forming insoluble aggregates. … we discovered that the aging process itself, in the absence of disease, leads to the insolubilization and increased aggregation propensity of several hundred proteins in the roundworm Caenorhabditis
elegans. These aggregation-prone proteins have distinct structural and functional proprieties. We asked if this inherent age-dependent protein aggregation impacts neurodegenerative diseases. We found that proteins similar to those aggregating in old worms have also been identified as minor components of human disease aggregates. In addition, we showed that higher levels of inherent protein aggregation aggravated toxicity in a C.
elegans Huntington’s disease model. Inherent protein aggregation is a new biomarker of aging. Understanding how to modulate it will lead to important insights into the mechanisms that underlie aging and protein aggregation diseases.

According to one of the study’s authors, Cynthia Kenyan, “If you take people with Alzheimer’s and look at their aggregates, there are many other proteins in the clump that no one has ever paid much attention to. It turns out that about half of these proteins are aggregating proteins that become insoluble as a normal part of aging.”

There are several hundred proteins involved in this system, many associated with cell growth.

The paper, published in the Open Access journal PLoS Biology, is downloadable here.

David, D., Ollikainen, N., Trinidad, J., Cary, M., Burlingame, A., & Kenyon, C. (2010). Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans PLoS Biology, 8 (8) DOI: 10.1371/journal.pbio.1000450