Gluten-Free: Healthy Alternative or Fad Diet?

Hello, readers!  Those of you who have been following my blog closely (and who wouldn't?  I know you read it religiously and check every hour for an update.  We can keep it our little secret.) may have noticed that I haven't updated at all this week.  The simple answer is that, since I was on my school's band trip to Disneyland, I couldn't update.  The longer, more embarrassing reason is that I had a post planned, and then just completely forgot about it.  So, sorry about that!  I'm going to write a really long entry here to make up for that.

So, what will this super-long post be about?  Gluten-free diets.

Go into any grocery store.  Or any cookbook isle in a bookstore.  The number one diet that seems to be advertized the most (that stands out to me, anyway) is gluten-free cooking.  One of the huge selling points of a lot of foods now is that it's gluten-free.

We've got gluten-free pancakes,

gluten-free brownies,

and various other gluten-free accoutrements. 

So, obviously being gluten-free is really popular.  But what, exactly, does "gluten-free" mean?  What even is gluten anyway??

Pictured: the mythical and mysterious gluten fairy.  No one knows who she is or what she actually does.

Gluten is actually a protein made up of two different substances (called gliadin and glutenin, for those who are interested) that is bound to the starch in many plants.  For human (i.e. dietary) purposes, the main thing we associate with gluten is wheat.

Now, for some people, eating gluten is actually very dangerous.  People who have celiac disease really shouldn't eat any gluten.  Celiac disease is a genetic autoimmune disorder, which means that, in a similar way to arthritis, the body's own immune system attacks itself.  While arthritis results in painful joints, celiac disease can actually be very dangerous if you're not careful.  If you have this disease and eat any gluten, the body begins to attack the lining of the small intestine, destroying it if the process continues for too long.

In recent years, there have been studies conducted about the possible existence of "gluten sensitivity."  Basically, a theory exists that different people tolerate gluten differently and it is more harmful to some people than others, but this theory is largely speculative and there have not really been any major conclusions.

Great job, science.

If you have celiac disease or are gluten intolerant, you can ignore what I'm going to say for the rest of this post, since (spoilers) I'm going to argue that eating gluten really isn't all that bad for you, and it's healthy for a completely different reason than you think.

Let's go off on a tangent for a little while here (bear with me).  Why do you have to inject insulin subcutaneously if you're diabetic?  Why do you have to go to all the trouble of getting out a needle and injecting it when you could just swallow it or something?

Needles are scary, okay?

Like most substances produced by the body, insulin is a protein.  Proteins really can't be taken orally because the body's digestive system (saliva, stomach, and intestines) break up any proteins you eat into their component parts (amino acids) to be recycled in other bodily functions, like gluconeogenesis, which I've mentioned before, and forming new proteins.  So you really can't use insulin if you ingest it because your body breaks it up, just like it would a juicy steak.

Alas, not the cure for diabetes.

So, if you reach back around for the actual point of this tangent, you can see that gluten is a protein bound to starch.  If your body eats a protein like gluten, it breaks it down into amino acids just like it would any other protein, which means that gluten really doesn't hang around and wreak havoc in your body.  It's just treated like steak.  Again, you should ignore this when dealing with gluten intolerance or celiac disease.

But, Emily, you might say.  I know people who are eating gluten-free, and they're so much healthier!  They've told me it's so much better, and they've lost weight!  I will simply answer, remember how gluten is bound to starch in plants like wheat?  Starch,

This ugly thing.

is a more complicated form of a carbohydrate.  Aka, glucose, the bad guy.  A large component of following a gluten-free diet is avoiding eating any grain products unless they are gluten-free.  This limits your options somewhat, so the overall volume of grains (carbs) goes down.  Since you're eating less carbs, you ingest lest glucose, which means you have less citrate leak (remember that fun graph?), and gain less weight while possible even burning some off if you go into ketosis.  So it's really just a case of false correlation: you start to eat gluten-free, which means you're eating less carbs, and you get healthier--so you attribute it to eating gluten-free rather than just eating less glucose.  Technically, what I'm doing right now is gluten-free, but I'm learning it's because of the carbs and not fat or gluten.

Some people have the opposite problem, though.  A lot of people end up gaining weight when they eat gluten-free because they substitute all of their bread and grain foods with products that come from corn and potatoes, which are also really starchy, which is the problem in the first place.

Still the silent killer, but for a different reason than previously thought.

So, basically, if you want to eat healthier, gluten is pretty much fine, as long as you just avoid any huge amount of glucose.

Thanks for reading!

Rounding at the Hospital: Part Deaux

Hey, everyone!  This is going to be the continuation of my last post because I wanted to keep a lot of the hard science all together and contained.  It's probably going to be pretty short as well, since I am, not to complain, really tired at the moment.  But you probably don't care about that, so on with the post!

First things first, I'm going to embed a video that I thought was interesting:

Dr. Walker sent me the link to this video last weekend.  For those of you who can't or don't want to watch the whole thing (it's pretty long), basically a panel answers question about low-carb diets.  However, there are differences in what this guy says and Dr. Walker's Scottsdale Keto Diet, and that's their stances on unrefined carbs.  This guy says that unrefined carbs, like brown rice and root vegetables (i.e. carrots), are completely fine to eat, and that refined carbs like sugar and white rice are the bad guys.  What I'm doing is quite different, in that I'm not allowed to eat much of any type of carbohydrate, refined or otherwise.  The real debate stems from whether your body can tell the difference between the two.  The answer?  Who knows!  I'll ask Dr. Walker next time I see him.

Maybe not the silent killer?

Alright, moving on to the hospital.  The main thing I've been learning is the different types of drugs that doctors use to treat their patients.  Things get very specific, as obviously each drug has its own effect and pathway of action (if you want to sound smart in front of your friends, this is called "pharmacokinetics."  The more you know!), so it's kind of important to know what they are before you prescribe them to your patients (as long as you want live patients, that is).  Now, since I have not actually been to medical school, where you learn this kind of stuff, I'm just trying to understand what they do and how they work, and not the names yet.

Pictured: me.  That shows me for not going to medical school.

The second thing I'm learning how to do is to look at lab results (like MRIs, x-rays, and surgery dictations) and see what's wrong with the patient in the first place.  As you might imagine, this is really important if you want to diagnose your patient in the first place.  So far, I've seen a couple of MRIs:

Yay, brains!

In one of them, a few doctors (including my dad, incidentally), were looking for the presence of an infected abscess in the neck--if the patient had this, it would have been pretty bad, since those need to be treated immediately.  Turns out she didn't have one, so she was able to be discharged later that week.

I've also been learning how to read medical charts.  I would include a picture of one of Dr. Walker's, but I'm not sure if I'm allowed to, even if it's blank, so I'll check back with him and make sure it's okay, if anyone wants to see it.  Basically, after talking with a patient, there are a couple of categories you need to check: the subjective section is any changes based on the patient's own words; the objective section is any quantifiable data the doctor and lab tests compiles or sees themselves, and the diagnosis and prescriptions section, which lists problems the patient has and suggested treatment options.  At least, the few I've seen did, so I want to see how other charts differ.

That's really it for this week, folks!  I'll let you know anything new or crazy that happens next week, and I'll keep you posted on what I'm learning at the hospital.  Thanks for reading!

Rounding at the Hospital

Hey, everyone reading this!  I hope you had a great spring break, for those of you that go to my school.  I spent mine working.

It was awesome.

And by that I mean it was pretty interesting.  First of all, Dr. Walker, his medical students, and I have been working on rewriting that Wikipedia article on the Randle hypothesis that I linked to in my last post.  However, in order to do that, I've been reading a huge amount of scientific papers that deal with what Dr. Walker calls the "anti-Randle cycle," which is pretty much what I've been doing with him for the last few weeks.

Speaking of what I've been doing for the last few weeks, as I mentioned in my last post, I would talk about cheat days.  Basically, "cheat days" are occasional carb-loading days, where you can really have as many carbs as you want, after which you detox and enter into ketosis again.  I say "as many carbs as you want" because, although bread tastes really good after not having any for weeks, it's actually really difficult to overdo it.  Once you're keto-adapted, like I am right now, eating a bunch of bread or other carbs in one sitting actually makes you feel pretty gross.

I'm not gonna lie though--it still tastes delicious.

But the newest thing I really wanted to talk about, as you probably guessed from the title of this post, is the fact that I've started going on rounds in the hospital with the med students and Dr. Walker, which means that I'm actually seeing patients and learning about specific drugs and treatment options.  However, as an "observer," (seriously, it says that on my badge and everything.  Also, I have a badge!) I'm not allowed to talk to any of the patients, so I just kind of stand at the back awkwardly without saying anything.

Pictured: me

I've only been in twice so far, but it's been a really eye-opening experience.  Most of the people I've seen are those that are about to be discharged, so they've been pretty healthy-looking (despite having type 2 diabetes or "metabolic syndrome," which just means that they're insulin resistant).  It's basically pretty scary that a lot of the problems are, while not caused directly by insulin resistance, affected and made worse because of the worsened immune response caused by diabetes and metabolic syndrome.

And on that not-so-happy note, I'm going to end here.  I know this has been uncharacteristically short for this blog because I love rambling on for pages and pages, but I will continue this post in Part 2, where I will talk more about what I've been doing specifically, as well as some success stories I have seen and heard, while still sticking to HIPAA guidelines.

[Caption REDACTED by HIPAA]

The Randle Cycle: Wrong or Just Misunderstood?

Hey, guys!  Thanks for reading!  This time I'll be talking a bit about the Randle Hypothesis, which has ended up being the basis for a lot of the nutritional information out there.  It's probably the reason why you think that fat is bad for you.  Just a little warning: I'm still in the middle of reading the scientific articles that have to do with the Randle Cycle, so don't expect anything too detailed, and, as always, take what I say with a grain of salt.

Though maybe not this much.

Basically, in 1963, Philip Randle decided to study how metabolism works at a cellular level.  He took some muscle tissue (I think it was heart muscle) and dropped some fat onto it.  The muscle cells stopped metabolizing glucose and used the fat for fuel instead, so Randle theorized that the presence of fat halts metabolization of glucose and leads to the production of fat.  In shorter words, Randle said that eating fat makes you fat.

The silent killer?

The thing is, this study was done in 1963.  We now know many things that Randle had no idea even existed.  Many of the enzymes involved in energy production,

This again.

weren't discovered until the mid-90s.  As in a full thirty years later.  And then, after we found out which chemicals existed in the first place, it took a while for us to find the exact pathways.  This:

Notice the pathway from citrate to the inhibition of the glucose reaction chain.

became this:

And now notice how the glucose chain is completely unchanged by the presence of fat.

as new experiments were conducted.

Now, I grabbed both of these from the Randle Cycle's Wikipedia page, which I hesitantly include a link to.  The reason for this is, as you may remember from my last post, that I think this page is very poorly written.  Basically, the author of the article jumped back and forth between the Randle cycle and the recently-dubbed (by Dr. Walker) "Anti-Randle cycle" with little to no warning.  The article seems rather wishy-washy on the whole topic and unable to pin down what, exactly, the Randle cycle actually is.

Meh, no one's reading this anyway.

The main point of this post is to basically say that many large organizations, including the American Diabetic Association, still use Randle's study to outline treatment plans for diabetics.  Diet plans include high amounts of glucose and low amounts of fat, which is the exact opposite of what this

I'm going to keep using it.

describes.

Next time: cheat days and more personal thoughts!  See you then, and thanks for reading!

I Went to a Conference

Hey, guys!  Sorry it's been pretty quiet over here.  Truth is, I haven't been doing too much new stuff this week.  That's not to say I haven't been learning anything, but mostly I've been applying what I have learned to papers I've been reading.  Later this week I'll probably get into some of that.

A taste of what awaits.

Now, as should come as a surprise to all who don't actually read my weird post titles, I attended a conference/seminar thing yesterday about the link between diabetes and cardiovascular disease.  Since it was aimed towards doctors and medical students and was primarily about what methods physicians could use to diagnose and treat disease, I was completely lost for part of the time.

Pictured: me.

The whole spiel consisted of discussing insulin resistance (which I've been working on, yay!) and associated risks that have to do with cholesterol and liproproteins (which I need to work more on, since I haven't really gotten into biomarkers yet).

What interested me, though, was the differences in what Dr. Walker has studied and what the general consensus is on the origin of insulin resistance.  As I'll get into later in more detail, the American Diabetic Association and other groups of its ilk follow a rather outdated and misinterpreted hypothesis called the Randle Hypothesis, formulated in 1963 by a guy named Randle (weird, right?).  I would link to the Wikipedia page, but it is horribly written and I hate it.

Anyway, the gist of Randle's theory is that the presence of fat controls how a cell metabolizes fuel in the mitochondria.  However, as more recent studies show, it looks like glucose is what really controls metabolism.

The point of that whole tangent above is basically to say that many large corporations use old or outdated studies to recommend medications.  As I heard last night, the cause of insulin resistance can be traced to not ectopic fat, but visceral fat.

More pictures of blobs.

According to many doctors the presence of visceral fat, which is fat that is not stored as a layer around muscle but within the abdominal cavity, leads to insulin resistance.  The speaker gave his reasons but I kind of spaced out and didn't really understand what he was saying.

I have no idea what you're talking about.

The thing is, his sources date back to 1997.  As in almost twenty years ago.  Now, I'm not taking sides on the visceral fat vs. ectopic fat issue (okay, a little bit, but let's ignore that fact for now).  Using sources that are twenty years old (and also disputed as an added fact) doesn't make room for any new information that could emerge and change things.  Just an observation.

In other news, hearkening back to the terrible Wikipedia article I mentioned above, I'm going to be helping Dr. Walker and his students edit the page to actually make sense!  I'm contributing to Wikipedia!  But...I'll get more into that in my next post.

Thanks for reading!

So What Causes Insulin Resistance?

Hey, guys!  Today we're going to get back to the topic of ectopic fat.  For those of you who don't remember, ectopic fat is fat that's stored in abnormal places.  The ectopic fat in muscle tissue, called "intramyocellular fat" by stuffy scientist-types, is one of the main causes of insulin resistance.

There's really not that much information out there about ectopic fat.  Its Wikipedia page is completely nonexistent, and if Wikipedia doesn't know about something, it's probably not important, right?

It's such a reliable source.

Well, actually, since it leads to insulin resistance, ectopic fat is probably one of the main causes of Type II Diabetes.  In order to show this, I will, again, use my wonderful scribbles.

We will, again, look at this chart:

Get used to seeing it.

We've talked about citrate leak, how insulin up-regulates the production of ACC, and how Malonyl-CoA shuts CPT1, which allows the cell to burn fat.  Now, the question is, where does that triglyceride molecule go?

Some of it is shipped off to regular fat cells, to be saved as extra energy if the body doesn't get enough glucose.  This is an evolutionary holdout--if early humans couldn't find enough food for the day, then extra energy is stored very efficiently as fat to be used as fuel.

The rest of it actually stays in the cell.  Since most ATP production happens in muscle tissue (because those are the cells that do the most work), a lot of that excess fat stays gooped up inside of the cell.

Gloop.

From now on, triglycerides will be abbreviated as TAG, because it is easier to type.

Now, TAG itself doesn't have any real problems.  It just kind of hangs out in the muscle cell waiting to be used.  Eventually, though, it turns from this

Friendly fat just waiting to be useful!

into this

The guy who hangs out in the bad part of town.

which is called DAG.

DAG, unlike TAG, doesn't just loiter around.  DAG interferes with certain metabolic pathways.

Glucose enters the cell from the bloodstream in a series of biochemical reactions.  In the presence of insulin, glucose can pass through the first gate.

DAG interacts with one of the steps of this reaction, specifically with an enzyme called GLUT4.

This doesn't let glucose into the cell.  The body will naturally try to neutralize the glucose within the blood, because high blood sugar causes other problems.  This means that the pancreas will have to produce more and more insulin to overcome DAG's influence on GLUT4.

Simplified, ectopic fat interferes with the body's ability to metabolize glucose.  In order to reduce blood sugar after eating large amounts of glucose, the body needs to secrete more insulin.  This insulin resistance can eventually lead to Type II Diabetes unless it's treated!

So, the answer to reducing insulin resistance?  Getting rid of ectopic fat.  If it's not there, DAG can't block the GLUT4 receptor, meaning glucose can enter the cell as per usual, so the pancreas will make less insulin.

Which makes your pancreas very happy.  Also, apparently they make pancreas plushies?

One simple way of removing ectopic fat is simply eating a low-glucose diet, which I'm currently doing.  If the body has no glucose to burn, then it will take it from ectopic fat stores in the muscle.  Once those are gone, then the body can mobilize fat from fat cells.

Another way is by using the drug Invokana.

Aw yeah.

While it won't do all the work on its own, Invokana is extremely useful for helping diabetics and pre-diabetics get rid of a bunch of glucose without keeping to such a strict diet.  Invokana is a sodium glucose transport inhibitor (SGTI).  What does this mean?

Well, in order to see that, we have to look at our kidneys.  Our kidneys are in charge of removing toxins from our bloodstream and getting rid of them through urine.  Kidneys have certain transport proteins that put glucose back into the bloodstream, which means that glucose stays in the blood until it is metabolized.  Invokana blocks that transport protein, so that glucose is secreted from the body in urine.  How much sugar is gotten rid of?

Seventy to one hundred grams of sugar.  That's a lot.

In order to illustrate, here's the amount of sugar that ends up getting flushed down the toilet.  Let's be cautious and say 85 grams.

Mmm, pure sugar...

So, Invokana is really useful in reducing the amount of glucose and, by extension, ectopic fat, which is the problem in the first place.

Thanks for reading!