Tag Archives: Basic Science

Oh, noes, GMOs!

Oh, noes, GMOs!


Everyone calling vociferously for labeling GMOs on the internet seems to go silent when they are asked specific questions about why, and how much labeling they’re actually asking for. Turns out, they usually don’t know how genetic modification is done, how many different kinds of modifications there are, how much actual potential harm there is or isn’t, or, quite frankly, how digestion works. (If it worked the way some alarmists believe it does, I’m afraid we might have to turn to cannibalism!)

Labeling something “Contains GMOs” is not only uninformative and misleading, but will add an average of $500 to each American’s food bill if it were to be instituted. Also, in order for a label to be useful and valid, it would need to be much more detailed. So I would like to break it down a little more realistically.


Bacillus thuringiensis is applied liberally on organic crops to control pests. Catalogs that sell Bt to home gardeners describe it as “Bacillus thuringiensis (Bt) is a natural occurring, soil-borne bacteria that has been used since the 1950s for natural insect control.” (Planet Natural) and “Bt is a naturally occurring bacteria with many powerful insect-specific strains. Like other biologicals, Bts biodegrade in sunlight and may require reapplication. Bt for Caterpillars & Worms: Safe for the user and the environment, Bacillus thuringiensis v. kurstaki is a pest control mainstay for organic vegetable growers.” (Grow Organic) You would not find any food in the supermarket that would be labeled “Genetically modified with Bt,” because those crops are not used to feed people, but for animal feed and other industrial uses. You would, however, find lots of foods labeled “Sprayed with Bt,” at least if labeling were honest.

So why is it that Bt is safe and organic when sprayed in large quantities (where it drifts and affects insects that are not feeding on the crops, including some beneficial species) but suddenly becomes “Bt toxin” when it is engineered into the crop and affects only the pests that feed on the crops? The EPA has done thorough testing on Bt (http://www.epa.gov/pesticides/biopesticides/pips/regofbtcrops.htm) and assured that GM crops with the gene that produces the Bt protein are not in foods meant for human consumption, even though humans do not have the body chemistry that allows Bt to be absorbed.

Big Organic wants to have its cake and eat it, too. In order to continue using Bt itself for pest control, but demonize it as a toxin when it’s made by the plant itself, the very sites that make these statements do some unscientific speculation as to how this is so and present it as factual. Were they to admit that Bacillus thuringiensis is Bacillus thuringiensis and is harmful only to specific species (not human) that are directly exposed to it, they would not be able to continue their hypocritical campaign to use and sell it while simultaneously representing it as a life-threatening dangerous substance.


You would see “Roundup Ready,” but that would be pretty uninformative, also, because many crops that are not “Roundup Ready” are treated with Roundup, because it is an effective dessicant. For example, a wheat farmer would use it to kill and dry his entire field so that all the wheat would be usable, and would not need careful (and expensive) sorting to ensure that a few green grains wouldn’t rot an entire silo of harvested wheat. So, GMO or not, a label saying “glyphosate exposed” would be much more useful. That, however, would be a decision one should make based on environmental concerns rather than personal ones, because glyphosate is toxic to humans in such large doses that you would need to drink about three gallons of it straight to get sick.


There would also have to be a label for trans-species modification. Scientists take a gene for a trait from one species (usually another species of something that we also eat, so we’re eating that gene already, just in some other food) and insert it into another. You would need to do some serious mental gymnastics to see how this would be harmful. You would also have to start giving up a lot of foods, organic or otherwise, because this is also used to protect crops against diseases that would wipe them out. Bananas and papayas and oranges would no longer exist, or might go extinct in the future, without the modifications that allow them to resist the fungi that kill them. You might also want to check out foods that contain other foods, and perhaps stop using recipes. Your Manhattan Clam Chowder has fish genes and tomato genes. . .


The last label would be a cross-species modification. This is when a gene for a particular trait is taken from one species and transferred to a related species – like the gene from one type of salmon that triggers larger size to a smaller sized salmon. Again, if you were to avoid foods with this label, you would need to deny yourself foods that have been cross-bred and hybridized by man for thousands of years, which would be everything we eat. It’s the same process, but accelerated and without the negative characteristics of traditional manipulation by sexual selection.

Look at what we’ve done to purebred animals – hip dysplasia in German Shepherds, seizures in Boxers and Spaniels. . .When we tried to breed a rot-resistant potato by hybridization, we ended up with a potato that was kinda poisonous. Genetic modification is working on a rot-resistant potato that won’t make you sick.


Golden rice was created by moving a gene that produces Vitamin A from the leaves and stem of the plant to the grain. This is a technology that may be applied to other species later on. People destroying entire crops of golden rice because it’s GMO is an example of uninformed hysteria. So we’d need a label for this at some point.

If all you want is a nice, simple label that says “Contains GMOs” so you can make buying decisions without thinking, then stick with buying things that say “GMO-Free.” The GMO labeling being proposed by the Organic Foods Industry is not designed to inform or help people make healthy decisions, but to direct buyers to their own products. If you want labels that actually give you useful information, they’re going to be on almost every item in the store, and it’s going to cost all of us. And if you really want to know what’s in your GM food, check the EPA, the ISAAA’s GM Approval Database, and consumer information from the FDA.

If you want to see why the studies being cited as proof that GMOs are dangerous are not valid evidence, here are a few links. Academics Review looks at a large selection of studies and explains what they actually found and whether those findings are accurate. The Seralini rat tumor study was so deeply flawed that even a low-impact journal retracted it out of embarassment – lots of scientific explanation and criticism is collected at David Tribe’s blog. Skeptical Raptor breaks down the information in a recent meta-analysis of 1,783 studies, including at least 600 independently funded, which found no tangible dangers and many benefits of GM crops.

(Image source Also a good article!)

Where I Go For Science

Where I Go For Science

A friend of mine asked me for a few links to science sites so she could learn a little more, so I set to copying and pasting my bookmarks for her. Now I know why I lose so much time sitting at the computer. Most of these sites are life sciences, so sorry about the lack of Chemistry and Physics and such. Here’s the list. . .

Sites in my WordPress Reader, loosely arranged by subject:

Skepticism/Critical Thinking
Science or Not?
I fucking hate pseudoscience
Edzard Ernst
Why Evolution is True
Violent Metaphors

Brain Stuff
Left Brain Right Brain
Mind Hacks
Neurologica Blog
Wiring the Brain
Science Over a Cuppa
Gabriela Tavares
BPS Research Digest

Science Based Medicine
Science-Based Pharmacy
Science-Based Life
Drug Monkey

Bits of DNA
Code for Life

Skeptical Raptor’s blog
Shot of Prevention
The Poxes Blog

Other. . .
Inspiring Science
Double X Science
Bishop Blog

Not on wordpress:

Not Exactly Rocket Science Not only a lot of interesting articles on Biology, but a weekly roundup of interesting links. (You can also visit The Loom and Only Human from here, plus some others, but these three are my favorites.)
In The Pipeline Chemistry, but a lot of it related to Pharmaceuticals.
Skeptical Medicine A critical look at both conventional medicine and pseudoscience.
Scitable Nature Publishing Group’s educational site.


Research Blogging
Science News (limited access for free, but still a lot of good science.)
Science Seeker (you can filter what you see by checking the subject boxes to the right.)

I’m always checking for new places, especially those that would be good for people who are not scientists, but want to understand. I’ll take suggestions for anything that’s not behind a paywall or too difficult for non-academics!

Learning From Research – The Discussion

Learning From Research – The Discussion

It’s been a while, and I’ve had a lot of stuff going on both in my life and in my mind, but I’m determined to finish this thing. Previous posts:

Part 1
Part 2

This is the section in which everything that was talked about before is kind of recapped and explained and, well, justified. I approached this in a much simpler format, because that’s really all it needs. My comments are bolded.


It was first demonstrated here that the fidelity of replicating methylation patterns of CGIs in the promoter regions is significantly higher than that of CGIs outside the promoter regions. (CGIs in promoter regions replicate themselves more accurately than the ones outside of promoter regions.) It was also demonstrated here that methylated genomic regions show much higher fidelity than unmethylated genomic regions. (If the genes are methylated, they tend to stay methylated, if they’re unmethylated, they can become methylated.) These showed that maintenance methylation of hemimethylated CpG sites into fully methylated CpG sites at DNA replication was highly reliable, while unmethylated CpG sites tended to be methylated by de novo methylation. (Methylation sticks.) It is well-known that exogenous DNA is exposed to a de novo methylation pressure (Doerfler et al. 2001; Bird 2002), and a similar methylation pressure seems to be working on the endogenous DNA. (Unmethylated sites are vulnerable to methylation from outside sources.) To maintain the unmethylated status of CGIs, protection mechanisms from the de novo methylation pressure seem to be necessary. (Unmethylated CGIs need something that protects them from methlyation or they’re vulnerable to it.) Since the MPERs were significantly lower in CGIs in the promoter regions than in CGIs outside the promoter regions, the presence of a protection mechanism(s) specific to the promoter regions, in addition to a mechanism(s) common to all CGIs, was indicated. (Promoter region CGIs probably have stronger protection against methylation of unmethylated regions, because they resist methylation better than non-promoter-region CGIs do.) Although the details of the mechanisms are still unknown, binding of transcriptional factors, such as Sp1, has been indicated as a promoter-specific mechanism (Han et al. 2001). (Hint, hint – this is something someone might want to look into, guys, ‘cuz our grant has been spent! Heh.)

The differential fidelities in replicating methylation patterns of CGIs in the promoter regions and those outside indicated that aberrant methylation of CGIs would occur at different rates depending upon their locations. This will be important when tumors are analyzed for the CGI methylator phenotype (CIMP), which are considered to be caused by molecular defects that allow accumulation of aberrant CGI methylations (Toyota et al. 1999). The differential fidelities shown here suggest that there are two types of CIMP, one due to a defect(s) in the protection mechanisms common to all CGIs and the other due to a defect(s) in the protection mechanisms specific to CGIs in the promoter regions. Actually, a correlation between the CIMP and the diffuse-type histology was clearly observed in gastric cancers when CGIs in the promoter regions were used for CIMP analysis (Kaneda et al. 2002b), while it was unclear when CGIs outside the promoter regions were used. (This will help us do more research that will help with cancer prediction/prevention/treatment, in case you don’t think that these findings have a worthwhile purpose of their own. When in doubt, reference cancer. For people with maybe a little less vision or curiosity. Just sayin’.)

In order for an impaired fidelity in maintaining a methylation pattern to exert any biological effect, methylation statuses of multiple CpG sites in a CGI must be altered. (One change at a single location isn’t going to make a big difference.) A significant increase of MPERs would be necessary for this, and quantitative analysis of MPERs in cells with suspected increase of MPERs is necessary. (We don’t know how many besides “more than one,” so another study would be required.) DMR of the H19 gene had a polymorphism at nt. 391 (nt. 8217; GenBank accession no.AF125183), and this served to distinguish the two alleles clearly. (This location was where we could best see what happened.) The G-allele was methylated in all of the six cultures, and the T-allele was unmethylated. The methylation patterns of the T-alleles were similar in HMEC11 and HMEC15, but were essentially variable among the six cultures. This indicated that, although the original cells in HMEC11 and HMEC15 might have had a common ancestral cell, methylation patterns in a tissue alter significantly during a human life span. (Methylation may change because of time, not necessarily because something came in and methylated stuff. No pointing at a specific environmental influence like a chemical or somesuch. Just demonstrating that it happened, and where and why it would be more or less likely to happen.)

Future clarification of what protection mechanisms are involved and how they are impaired in various diseases will contribute to understanding of aging (Ahuja et al. 1998; Issa et al. 2001) and various pathological conditions. (This is a single step in a huge process, but it puts us on a track to learning more than what we know now.)

Science Education – How I Would Do It.

Science Education – How I Would Do It.

Of course, this is assuming that the world was a sensible place and I was in charge of all the important decision-making. Heh.

Over time, I’ve come to realize that a lot of the things I was taught in school didn’t stick because they weren’t interesting. They weren’t interesting because they were unrelated to my life, and I couldn’t see how they could possibly be important to me. I memorized things for tests, and I did a darn good job of it, good grades, good standardized test scores, but only because I had to, not because I wanted to.

As I got older some of it came back – and it stuck better because I had context to put it in. Before kids and before antidepressants, I read a lot of romance novels for escape (I know. . .I’m not proud, but I had an excuse.) Soon I discovered that there was a sub-genre of Historical Fiction – and some of these authors were real history buffs who included a lot of factual information. In the context of a story, with characters and plots that engaged me, I was finally learning something about history, which had bored me to tears in High School.

Later, I started reading some of the books and papers that had been assigned back then. . .suddenly they were interesting and made sense – because I now had a context for them. The context continued to expand, and more information became part of what I knew.


For me, possibly moreso than for many people, context is essential. My ADHD mental filing system demands context and associations not only for learning, but for retrieving that learning. So when I teach people what I know, I teach it in context. I learn a lot by making mistakes, so I teach “do it this way because this other way doesn’t work,” and “we do it this way because otherwise we break this piece and the whole thing is ruined.” I teach “This part seems boring, but here are all the cool things we can do with it later.”

I also learned a lot from raising my own kids and volunteering in their schools, helping all kinds of other kids learn. You need to be able to express a single piece of information many different ways in order to get different kids to understand it. As a volunteer, I was able to sit with individual children and small groups. The kids who didn’t understand things when they were taught the same way to all 30-something students would get it if I spent some time with them and figured out what their individual contexts were.


Fast forward to the mid 90s – I started antidepressants, and then I discovered that my ADHD had not actually gone away as the experts had told my parents it would, and as my parents told me it had. Now I had a reason to learn about the brain, starting with disorders and injuries, and what they taught us about the functions of various structures. That gave me a context to learn about brain development and genetics. This led to investigating epigenetics. Along the way, it also tied in to reading medical and science blogs and books, and any time a piece of knowledge stuck to something that was relevant to something I already knew, it also became relevant.

So why do you want to listen to someone who doesn’t have a degree in science or medicine when it comes to science or medicine? Because of the way I’m learning it. That whole “Translating Science into English” thing I mentioned a few posts back. Scientists have their own language, and it’s important that they do so they speak with clarity and precision. But if you don’t have the context that they do, it’s hard to understand – and easy to misinterpret. I didn’t learn this in the linear fashion that they did.

If you were to teach me vocabulary and facts and mechanisms, I’d remember it just as well as I did in high school. But give me a study of something that relates to something that interests me, and I will look up all those words and facts and mechanisms, and they’ll make sense because they’re part of something else. They have more meaning when they’re in context.

The other thing I learned came from watching scientists argue with one another. While they’re not always polite, they always present evidence. Most of them are critical thinkers, when someone says something that is questionable, they will (sometimes very methodically and in great detail) explain the flaws in the reasoning. Following along with this taught me the scientific method and why it’s important, how to evaluate how robust the data is by looking at the size of the study, the quality of the blinding, the strength of the variables and controls, how well it integrates existing evidence (and how strong that evidence is) and, most importantly, no matter how good a study may be, it’s never PROOF. It also doesn’t prove other things that weren’t part of the study. It’s also probably not a major breakthrough.

I learned about p-values, journal impact factors, the good and bad of peer review, the pros and cons of open access. I learned that not all “evidence” is actually evidence.


The problem that many, many scientists have, though, is that they forget what it’s like to not know this. Sometimes they present what they know in a way that is off-putting to laypeople. Sometimes they present a press-release version of their findings, breathless with excitement and full of hyperbole, and that’s even worse. (That’s what we have The Daily Mail and Huffington Post for. Let them do their job.)

So if I were a science teacher, or I were designing a science education program, I’d throw out teaching the basics as freestanding facts. Get rid of the rote learning. Give the students just enough information to dive into a challenge and figure out the rest. Give the kindergarteners a bowl of cream and some food coloring and dish soap – let them play and then tell them how it works. Let the older kids listen to each others’ heartbeats, check each others’ blood pressure, draw pictures of hearts and veins and arteries, and use that to introduce the circulatory system. Make everything part of an experiment that related directly to them so that it was important. Let them figure out what’s correct and what’s incorrect as much as you can on their own by giving them questions as much as answers. Make the science interesting and integrate critical thinking into the lessons, and get them excited. This will be good for them, and good for society, because they’ll question everything – and come up with their answers based on what evidence is best supported.

Epigenetics Made Easy, Part 2

Epigenetics Made Easy, Part 2

Let’s reiterate from the previous post, just in case you need a recap:

All cells are made from other cells; we start with a few that are the same, and as the number of cells increases, they begin to differentiate and become cells for specific body parts.

DNA is the blueprint for the final product (a sexually mature adult human being, for illustration purposes.) RNA is a segment of DNA that begins the process of cell differentiation, but the mechanism that actually creates the proteins that build cells is the epigenetic process, which depends upon histones interpreting the genetic instructions.

Once we are full grown, our bodies are almost always replacing cells rather than making new ones, and the new cells may not be exact duplicates of the cells that created them.


histone modification

Yes, there is such a thing as histone modification. Yes, gene expression (in the form of cells that follow specific genetic instructions) can be changed during the epigenetic process. Yes, it’s possible for some of these changes to become heritable (passed on from parent to offspring.) But let me explain what’s reasonable and rational about these possibilities.

Histone Modification

You’ve heard of this, but usually in the form of “you can change your DNA by doing this thing or eating that thing” which is, essentially, not true. Histone modification takes place on a cellular level, and changes in different ways depending on what the chemicals that can modify histones are doing. I’ll save the technical terms and illustrations for another time. Baby steps.

What happens is that while a cell is preparing to replicate itself, a chemical can make the histones do something differently from the way they were instructed, and that makes the resulting copied cell different from the cell that created it. Right now, we have some very specific examples of changes that depend on specific chemical exposures (some from external environment, some from internal environment.) DNA is huge. We have a hundred trillion or so cells in our bodies. The genome is almost infinitely diverse. There are very few examples right now of direct cause and effect, and each one we discover in the future will be just as limited.

The number of possibilities alone makes it pure speculation to assume that a food given to a pregnant mouse that changes her babies’ fur color and body shape is going to do the same thing for a fully-grown adult, or even something similar!

Now the add another layer of complexity, these are the things that can happen when you modify the histones in a cell:

*a beneficial gene is suppressed
*a detrimental gene is suppressed
*a beneficial gene is activated
*a detrimental gene is activated

So if someone claims that a food or something “methylates” your genes (besides being wrong) it could easily be a bad thing!

Changing Gene Expression

I mentioned the prenatal modification above, and that’s because it’s an important thing to study. Why? Because in order for histone modification to have any observable and verifiable effect, it needs to happen early. Think about it. If you modify the histones of a four or eight celled creature, then a lot more cells are going to be made not according to plans. In an adult, modifying a single cell, or even a few cells, out of all the cells in our bodies, is going to have minimal impact. In order to change gene expression in an adult, exposure needs to be intense enough or prolonged enough to influence a large number of cells.

I like to use the example of skin, partly because it’s a cell type that’s replaced frequently, and partly because we can see a lot of the possible changes to it. It’s a good way to illustrate that an environmental factor can produce a change that does not alter gene expression, and how the level of exposure can make a difference in whether an epigenetic change is even possible.

If you go out into the sun, your skin changes color. It could get burned, it could get tanned. But when those darker skin cells make their replacements and die, the replacements are your original skin color. You have exposed yourself to an environmental factor that has an obvious effect on your body, but it doesn’t change your gene expression. Why? Because the exposure was not prolonged enough that the visible change was messing around with histones while the replacement cell was being created.

On the other hand, if you’re out in the sun all the time so that your skin is constantly in a damaged state, then those cells are more likely to be in that damaged state when they’re replicating themselves. This could still even be temporary, but it could change gene expression so that the replacement cells are cancerous, for example. (Cancer is epigenetic – but it could be caused by environment *or* part of the plan all along.) So you need to expose the same group of cells to the same environmental factor for long enough that most of the cells begin reproducing with the alteration in gene expression. . .and that is not guaranteed to be a good thing, so don’t buy into the hype.

Heritability of Epigenetic Changes

Yep, this has been studied, too, and it does sometimes happen. The most repeatable changes happen when the fathers’ bodies have changed. I credit that to the fact that sperm are constantly being made, and things like stress hormones or chemical exposures, or starvation, can change what genes go into what chromosomes in the sperm cells at that time. Give the dads some time to recover, you get a completely different result.

Keep in mind that the normal set of instructions is the default. If you look at plants or other animals who’ve been genetically altered, a lot of times you’ll find that their offspring regress to the original, dominant form. In both human and animal studies, most of the epigenetic changes that were brought about by environmental exposure get passed down to the next generation, maybe the generation after that, and in a few cases, the third generation. Then things go back to normal.

I probably missed a few things, but I hope this is clear. Ask me stuff, tell me stuff. Thanks!

Epigenetics Made Easy.

Epigenetics Made Easy.

Tightly wrapped histones

No, not really. That’s a misleading title, but my hope here is that I can explain this in terms that are simple enough for people who aren’t scientists to understand. I’m hoping that because I’m not a professional scientist but am really, really into this stuff, the language and illustrations I use serve as a bridge for the gap in understanding.

So let’s start with the cell, and let’s use humans as an example. Even though epigenetics happens in every living thing, even plants, I want you to be able to identify personally with this so the information takes hold a little better. What do we know about genetics and conception and fetal development? Well, we start off with an assortment of genes and 46 chromosomes. We got all of them from our parents and grandparents and so on down the line, but it’s a mix between Mom’s side and Dad’s side, because her eggs start off with a random selection of 23 chromosomes (see my previous post about what random means) and his sperm also start off with a random selection of matching chromosomes.

Sperm meets egg, and there you go, 46 chromosomes in a single cell, and a complete, unique strand of DNA that has all the information needed to build a human body.

If you’ve watched videos of human development, you’ve seen how that one cell splits into two, two into four, four into eight, and then things really start to happen. In the beginning, each of those cells is exactly the same. Each time they split, they’re making another cell that’s just like they are. Remember this, because I’m going to mention it again later. . . Here’s how it looks, in case you haven’t actually seen it, in a video on in-vitro fertilization:

After this point, the cells begin to differentiate. Instead of simply reproducing copies of themselves, they start to become more specialized. They still contain all the DNA, but some of the instructions will be used, and some will be silenced. This starts with the transcription from DNA to RNA. What we used to believe (or at least what I was taught in school days in ancient times) was that the RNA was the sole messenger, containing only the information needed to make cells. That’s only kind of sort of true, and doesn’t explain a lot of confusing things that happen to human bodies. You see, it is part of the picture in cell differentiation, which is, to put it in simple terms, the process that makes one cell be a bone cell and another be a heart cell and another be a brain cell and so on. The RNA puts this in process by taking the pieces of the DNA that are needed to make a specific call and creating the proteins that manufacture that cell. With these instructions, cells continue to divide, but they’re not just making carbon copies of themselves.

We see this in fetal development because parts of the body from the brain, the eyes, the internal organs, to the fingers and toes, go from being kind of blobby and alien-looking, to functional and human-like. The manufacturing of differentiated cells continues throughout fetal development, and the differentiation is pretty much complete by the time a baby is born.

But there’s a piece missing – we know that RNA has instructions for making the proteins that manufacture differentiated cells, but it doesn’t make those proteins all by itself. This is where epigenetics comes in. The actual work of taking the orders from the RNA and making the proteins is done by histones. The DNA has the construction diagrams, the RNA is barking orders, the histones are doing the work.

This is still happening inside a cell. The cells are still dividing. It’s just that this epigenetic process is making two different cells out of one cell instead of two identical cells. The new cells aren’t coming out of nowhere, they’re coming from existing cells that are multiplying.

As we get older, we tend to go back to more of a model of cell replication. A cell duplicates itself, then dies after the new cell has been made. The epigenetic process takes place then, as well. Sometimes the cells won’t necessarily die, because we’re growing and need more cells. That’s done epigenetically, too, because the blueprint from the DNA says what the final adult product is supposed to be like, not just the infant version. As we get really older, the cells are trying to replace themselves, but they don’t do quite as good a job, and that’s an epigenetic process as well, because the instructions are getting messed up *after* the RNA. The histones just aren’t doing such a great job after a while.

The point here is that epigenetics is part of the process of cell development that is already written out in the DNA. The way it works without interference is genetic and heritable, and every single one of the many trillions of cells in your body was created the same way. The DNA has the plans, the RNA is the subcontractor, the histones are giving the orders to the proteins based on the instructions from the higher-ups.

Keep this in mind when you hear things about the amazing effects of environment on epigenetics. Yes, this is the part where things can get screwed up, because, yes, histones can be modified. But I’m going to save that for later, because this is a lot to absorb. I hope this makes sense, and if anyone has questions or corrections, please comment – I want to hear from you.

Epigenetics – I do not think that word means what you think it does.

Epigenetics – I do not think that word means what you think it does.

And I kind of have a bone to pick with Scientists who are actually contributing to the problem. Epigenetics is an essential biological process that takes place at the molecular level. Each one of the hundred trillion or so cells in the human body was created via the epigenetic process. Nothing has to magically happen. All you need is cells, food for the cells (usually glucose, yum!) and DNA.

Unfortunately, the amazing and fascinating research into epigenetics has led to a description of epigenetics as “genes plus environment.” If you are a scientist, or even understand science, you recognize that this does not mean that some sort of environmental factor from outside the body is necessary for the epigenetic process to take place. But if you’re a layperson, that’s exactly what you might think when you hear that. In fact, for quite some time I’ve been debating with a couple of people who believe in this magical concept of epigenetics, and you scientists (whom I otherwise love dearly) are just not helping!

The agouti mouse study that showed a change in coat color (linked along with other references in this previous post) was really exciting, and the public glommed onto it because there was the evidence, right in front of their eyes. In no time at all, alt-med proponents and the general public were certain that this was the answer to everything that was wrong with us. It was a great boon for supplement manufacturers, diet book writers, food conspiracy theorists, and anyone who was looking for something to blame for what was wrong with them (or society, but usually themselves.) I mean, clearly if what a mother mouse ate changed the color of her babies’ fur, then what horrible things are all these toxins doing to our genes?!?!

The thought seems to be that epigenetics is a highly unstable process that actually depends upon the correct “environment” in order to occur, and that even an unpleasant event in childhood can somehow upset it and result in a dramatic condition that can be passed down to one’s offspring. Once a person has gotten this idea into his head, it is darn nigh impossible to get it out. Homeopathic amounts of a “toxin” can have traumatic results, even worse than actual poisoning from that substance, because epigenetics. Psychiatric and neurological conditions are inflicted upon perfectly healthy infants by insufficient parental attachment or attunement. Everything is caused by environmental disruption of the epigenetic process, and everything in the environment messes up epigenetics.

Look, the reality is that what epigenetics does is take the information that’s been put into the RNA from the DNA, turn on the genes that are needed and turns off the ones that aren’t, then sends proteins off with the instructions to make new cells. At conception, when there are only a few cells, there’s not a lot of differentiation, but as fetal development continues, these instructions become more specific. “Make fingers.” “Make retinas.” “Make heart valves.” Stuff like that. During growth, the instructions are more like “make more of these cells.” During adolescence, it’s “make these a little different.” As we age, it’s “make another one just like this,” and “eh, what was that, sonny?”

The environment comes in because it is the epigenetic process during which an environmental factor can possibly alter the process, turning a genetic instruction on that should have been off or vice versa. It’s quite likely that this is what triggers many cancers that are strongly associated with exposure to a particular substance. But the possibility that exposure can impact gene expression is not the same as the inevitability of exposure altering gene expression. And this, people, is a big problem. Scientists, please think about this when you talk about epigenetics. Non-scientists, I’m going to put an explanation of how this works in the simplest terms I can come up with in another post.

Boost Your Immune System in One Easy Step!

Boost Your Immune System in One Easy Step!

Get sick.

No, seriously. That’s it. Get sick. It will get your immune system working like nothing else can, guaranteed.

People have this idea that the immune system is like a neighborhood watch, cruising around your body looking for suspicious characters and picking them off before they can do any damage. That’s. . .not even wrong.

Skeptical Raptor has an excellent article called Boosting the immune system–sorting science from myth, and you should go read it, but I’m going to take the part that explains how it works and share it here. First, the Innate Immune System. . .

This is the immune system’s ability to prevent or detect foreign material, then eliminate it without a specific physiological response of the body. It is the body’s quick and initial response to disease causing organisms (pathogens) which invade our body. The innate response either directly prevents an infection or slows it sufficiently for the slower but more effective and selective adaptive Immune system to activate. But it isn’t a simple system, the innate immune system is extremely complex, consisting of:

Anatomical barriers–These consist of physical barriers. The skin itself is impermeable to pathogens providing defenses like a solid wall. Our nasal passage is lined with mucous that is constantly moved into the stomach catching pathogens and killing them. Our eyes are covered in caustic tears and our mouths in saliva which contains a variety of enzymes. all these ensure that the vast majority of pathogens are killed before they can even enter an area where they can cause harm.

Inflammation–This response include the symptoms we associate with inflammation, fever, swelling, increased blood flow, and other activities, is due to the localized response of the body to the presence of a foreign body or pathogen. It’s main purpose is to provide a physical barrier to control the spread of infection and to heal damaged tissue in the region. Damaged cells release an array of chemical factors which cause pain and blood vessels to become more permeable. This response then attracts phagocytes, cells which recognize and consume foreign or dead tissue. Inflammation is normally a healthy response to injury or pathogen invasion, but in some autoimmune diseases, such as rheumatoid arthritis, it can be painful and debilitating.

Complement System–This system is group of biochemicals, produced by the liver, that helps or “complements” the ability of antibodies and phagocytic cells to clear pathogens from an organism. It is part of the immune system that is not adaptable and does not change over the course of an individual’s lifetime. However, it can be recruited and brought into action by the adaptive immune system.

Cells–Mostly white blood cells (WBC) are involved in the innate immune system:
Mast Cells – A group of cells that mediate the inflammatory response. Although they are often associated with allergies, they are a critical part of the immune response.
Phagocytes – Large cells that move like amoeba. They “eat” other cells by surrounding them with their plasma membranes producing “bubbles” in which they can release enzymes safely without damaging other cells. They also have a “clean-up” role to remove the body’s dead and dying cells.
Macrophages – Large phagocytic cells that efficiently consume multiple pathogens. Heavily motile and actively cross from the blood stream into tissue to hunt down pathogens. They kill by manufacturing and releasing free-radical oxygen in a local area.
Neutrophils/Eosinophils/Basophils – A group of similar cells that are the “first responders” to migrate to an inflammation site. They appear at the site of a wound within a few minutes of trauma.
Natural Killer Cells – These cells recognize the body’s own cells that are infected by viruses or are cancerous. They then induce controlled cell death to halt the spread of the infected or cancerous cells. Recent research shows that Natural Killer Cells also play a role in the adaptive immune response.
Dendritic Cells and Gamma/Delta T Cells – These are the bridge between the innate and adaptive systems and their main role is antigen presentation. They harvest antigenic proteins from damaged pathogens and present them to T-Cells, which allows them to find and attack the pathogens.

Then there’s the Adaptive Immune System.

The dendritic cells, from the innate immune system, activate the body’s adaptive (or acquired) immune system. The adaptive immune system is composed of highly specialized, systemic cells and processes that eliminate or prevent pathogen growth. In acquired immunity, pathogen-specific receptors are “acquired” during the lifetime of the organism (whereas in innate immunity pathogen-specific receptors are already encoded in the germline). The acquired response is said to be “adaptive” because it prepares the body’s immune system for future pathogenic challenges. In some cases, the acquired immune response can be maladaptive when it results in autoimmunity. Antibodies, produced by B-lymphocyte cells, are the main weapon of the body’s immune system to battle pathogens. It is a larger response than innate immunity and once sensitized to an antigen, the adaptive immune system often fights of diseases even before we can exhibit symptoms of disease. Immunizations introduce the pathogen’s antigen to the adaptive immune system so that it can form those pathogen-specific receptors and, thereby, are able to quickly and efficiently respond to an attack by a pathogen.

Cells involved –There are three types of cells involved with the adaptive immune response:

T – Lymphocytes (also known as T-cell) – The main role of the cell is to recognise cells infected by viruses and trigger the apoptotic pathway that destroys the cell and its viral contamination. Since viruses only replicate inside cells by hijacking the cell’s manufacturing process, this apoptosis kills the virus (and the host cell) and phagocytes swoop in to consume the destroyed cell debris and digest the contents. The antigen of the viral cell is recognised by surface antibodies on the T-Lymphocyte, which activate it. There are also helper T-Cells whose role is control and organisation of the apoptosis response to the infected cells.

B – Lymphocytes – The main role of these cells is to produce humoral (free floating) antibodies that recognise pathogens and mark them for destruction by other cells. This process occurs by activating the complement system and by causing the pathogen to become “sticky” but only with other pathogens. This causes them to clump together and make them easier to kill by T-cells.

Memory Cells – After an infection has passed (and most of the T-cells and B-cells have died), a few do remain in circulation to remember the antigens of the pathogens who attacked. In future infections these are rapidly activated to produce a humoral response which quickly destroys any new infections even before they produce any symptoms. There are two types of these cells: Memory B cells, which, produce the antibodies that recognize the pathogens, and Memory T cells, which remember the viral antigens that infect cells.

The article continues with more specific information about how the system works, but essentially, most of the immune system’s action consists of responding to a pathogen. Ergo, if you want to “boost” it, then you need to introduce a pathogen into your system to make it work. So get sick.

If you want to boost it a little, you can cut yourself and get it infected. Some food poisoning or a common communicable disease can boost it some more. A chronic condition is the gift that keeps on giving – your immune system will constantly be boosted.

But if you really want to boost your immune system to the max, then you need to go for an autoimmune disorder. This will boost your immune system so much that it won’t attack just harmful invaders, but your own cells. Even though they’re cells you’d kind of like to keep. I’d suggest Diabetes, that’s one that’s a little easier to self-induce. But there’s always Lupus, or Multiple Sclerosis, maybe Rheumatoid Arthritis. Get yourself one of those, and you will have one of the most boosted immune systems it’s possible to have.

Unfortunately, no amount of boosting your immune system is going to make you healthier. And that’s why, even if those ads for stuff that “boosts your immune system” sold stuff that worked, you really wouldn’t want it.

Chemotherapy is Poison, That’s Why It Works.

Chemotherapy is Poison, That’s Why It Works.

Unfortunately, I’ve known a few people who have had cancer over the years. Heck, I’ve had it – still do, but it’s not an aggressive, worrisome one. I’ve seen cancers cured with surgery alone. I’ve seen cancers cured with radiation alone. I’ve seen cancers cured with chemotherapy alone. I’ve seen cancers cured with a combination of two, or all three. I’ve seen cancers that have gone into periods of remission because of these treatments, allowing people many good years. And, of course, I’ve seen cancers that simply couldn’t be cured by anything. But what I haven’t seen is doctors pushing inappropriate chemotherapy on patients because they’re sadistic monsters who want to poison people.

“Cancer” is not a single disease, but over a hundred different diseases that form from a similar mechanism. Normally, cells in our body die off, and those cells are replaced. The cell death is called apoptosis, and different cells in your body apoptose at different rates (forget what you heard about that “every seven years” thing. . .) Because of a large number of factors, occasionally those replacement cells will be faulty. Your genetics cause a misreading of your DNA, or a mixup in the instructions from the RNA, or an epigenetic flaw causes a cancer cell to be expressed or a cancer suppressor to be repressed. Exposure to a known carcinogen can trigger the production of cancer cells in a similar manner – sometimes on its own and sometimes because you have a genetic susceptibility to the carcinogen. Age is actually the biggest culprit, because cell reproduction can degenerate in accuracy over time. For the same reason all the other cells in our body change as we age, and not for the better, a cancerous cell can be created instead of an identical replacement cell when the aging process interferes.
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What Does Random Mean?

What Does Random Mean?

I’ve been reading a lot of articles about scientific journalism, and what Scientists and Journalists need to change in how they release new findings to combat public misunderstanding. There are some great ideas there, and a lot of people committed to making this happen. The problem, though, is that science has a lot of concepts and vocabulary that are either exclusive to science (and impossible for non-scientists to understand) or are used differently in a colloquial context. So I’m going to start small and pick one. RANDOM.

If you’re having a conversation with someone and the word “random” comes up, you’re likely to think “something completely unexpected,” or “something without precedent,” or “something that just makes no sense.” “Random” started off meaning one thing to scientists and mathematicians and another to everyone else, and now it’s becoming a catchword for many other things that are even further removed from the strictest definition of “random.” Pseudoscientists and peddlers of dubious ideas and products take advantage of this by using the new popular understanding of the word to misrepresent or even mock science that uses it, so I want to set you straight.

Let’s start off with a straightforward explanation. “Random,” in science or mathematics, refers to a set or subset of existing things that is separated, combined, or put in order without any plan or pattern.

Take a look at A Million Random Digits with 100,000 Normal Deviates. This book has been around for a long time, and it’s an important tool for checking probabilities and mathematical formulae to make sure that they work with numbers that have no patterns. It’s not a very exciting read, obviously, but what you will find if you look at it is pages and pages of numbers. In other words, you will not find symbols, color dots, letters, or little drawings of cats. The numbers are random because they cannot be placed in any kind of sequence – as a simple example, you wouldn’t be able to add three to the first digit, six to the next, nine to the next pair, etc.

If you were talking to your friend about this book of numbers that was, like, totally random, your friend might reasonably expect to find those symbols, color dots, letters, or little drawings of cats. But your friend would be wrong; that wouldn’t truly be random since none of those things exist in the set called “numbers.”

So let’s look at this from the point where I see most of the misinterpretation of “random”. . .genetics. I want you to imagine two bags of marbles. I’m not going to specify how many, because we’re not going to get started on the difference between chromosomes and genes or anything like that. We’re just going to be very general and say that each marble represents a piece of genetic information.


One sack is filled with marbles that represent Dad’s genetic information, the other is filled with marbles that represent Mom’s genetic information. Now let’s say that Dad’s marbles are almost all primary colors, but there are a couple of purples, a few greens, one black, and one white. Mom’s marbles are mostly secondary colors, but she does have a smattering of reds, blues, and yellows, and one black and one white. So you reach into the bags blindfolded and grab a handful of each, and this is what you come up with:


That’s random (although it’s unlikely that you’re going to get the single black marble and single white marble from each bag. I just wanted to use them.) Do you see any peach pits, or rocks, or silver marbles? Of course not. They weren’t part of the set from which you were randomly selecting. They’re not going to appear out of nowhere – and if they do, it’s not scientifically random.

Now let’s say that we’re going to pair them up. The only rule is going to be that the marble from Dad’s set can’t be paired up with the same color from Mom’s set. In real life, this happens fast, and the number of pairs is significantly bigger, but this is a decent symbolic representation. So across the top are the marbles we got from Dad, and below that are the marbles we got from Mom.


Randomly we ended up with a unique combination – but still, there is nothing there that wasn’t present in the original set. Randomly we ended up with an extra blue marble from Mom. It could have been an extra orange, purple, green, red, yellow, black, or white marble – but it could never be a peach pit, or a rock, or a silver marble.

You could take all these marbles and put them in different sequences, but nothing is going to change the number of marbles, the colors, or which marbles came from which bag. You might get different pairs of colors, or all the same pairs but in different order.

Randomness, in science or mathematics, means that we have certain things that are givens. A set of numbers will contain nothing but numbers. A set of genes will contain nothing that isn’t already in the genome. Any random thing we look at will be comprised of something very specific that already exists. What makes it random is how it ends up being put together.

I hope that makes sense. Feel free to ask questions or add to the discussion.