Why is Blood Sugar Sometimes Higher Than Expected on Keto?

We have a numbers problem in the keto community. 

We place too much stock in numbers without a good understanding of what they mean. 

We measure the level of every little molecule without an appreciation for the myriad feedback mechanisms and overlapping biochemical pathways that govern the systemic regulation that determines those levels. We assign way too much meaning to single measurements taken at single points in time rather than looking at longer term trends and patterns. It’s like seeing one frame of a movie—one isolated, frozen frame—and making wild guesses as to what the movie is about. It’s ridiculous. 

Allow me to tell you a story. Sometime in the early 1980s, when I was a little girl, my family took a trip to Disney World in Florida one winter. We lived in New York, so Florida was a way for me and my sister to see Disney World and for us to spend a few days away from the freezing cold and bask in the warmth of the Sunshine State. Well, a freak cold front happened while we were there. Yes, a freak, unexpected cold snap in Florida. Sea World was closed because some of the water was frozen. We had to buy winter coats down there, because who packs winter coats to go on vacation in Florida? 

Imagine if we knew nothing about Florida and based our assessment of Florida’s climate on the short-term weather of those few days. We would have assumed Florida was a bitterly cold place, rather than the hot, steamy swamp it usually is. The lesson here is, don’t mistake an acute occurrence for a general pattern, trend, or tendency. 

What does this have to do with blood glucose? 

(If you’re pressed for time and you want an abbreviated version of my take on this topic, watch this video. If you have a minute or two to read, the first part of this post will give you a brief synopsis of the most salient points. But if you have some extra time to spare and you want the juicy details, cozy up, settle in, and happy reading.) 

Watch Me PRESENT LIVE ONLINE on TUESDAY!

Good news, everyone!

If you haven’t been able to make it to any of the low carb or keto events where I’ve presented in the past, you’re in luck …

You can watch me speak LIVE at the Durham, North Carolina low carb support group meeting on Tuesday, March 5 at 6:30pm. Tune in by going to the Facebook page for HEAL Clinics – they will broadcast it live right there on the page. Dr. Eric Westman, Durham and Duke University’s king of keto, will kick things off, but then I’ll be giving a presentation on keto for mental & emotional health issues.

If you and/or someone you love deal with anxiety, depression, bipolar disorder, mood swings, panic attacks, or any other mental, emotional, or psychological issue, you’ll want to watch if you can. (But no worries if you’re not available at that time – you’ll be able to catch it anytime afterward on the HEAL Clinic page.) I’ll be talking about mechanisms behind why and how ketogenic diets can be beneficial for these conditions. I mean, weight loss? Sure. Diabetes? Old news. Tell me something I don’t know, right? How about physiological and biochemical reasons why keto is a stunningly logical and rational thing to try for anyone dealing with these difficult-to-treat issues?  

It will be very similar to the video I did on this topic for my YouTube channel, but this will be the live version, so hopefully there’ll be some fun interaction with the audience, and I’ll know some of you out there will be watching, too, which will keep me even more energetic and enthusiastic.

More on the support group:

If you happen to live in the Raleigh-Durham area, or within a reasonable driving distance, the support group meets on the first Tuesday of every month at the Durham Hilton near Duke University (3800 Hillsborough Road, Durham, NC 27705). I’m not always there, but I’m there fairly often, and will probably be there more now that I’ve relocated to Durham. There’s a low carb buffet dinner for a reasonable price, but you don’t have to eat; you can just come grab a seat and spend an evening with other people on low carb/keto diets, for free! There’s always a bit of education, some Q&A with Dr. Westman, and often some very inspiring success stories of people who are experiencing the wonderful yet darn near predictable benefits of low carb: fat loss, reducing or stopping their meds for T2 diabetes, total resolution of acid reflux/GERD, reductions in chronic pain and fatigue, improved GI function, restoration of menstruation and fertility after PCOS…y’know, just the regular run-of-the mill stuff that happens to people daily on keto. ;-)

Come in person to the support group on March 5 if you can!

More on HEAL Clinics:

Did you have to learn about low carb/keto on your own? Did you have to fight with a doctor, dietitian, or health coach who told you keto was dangerous, and that you should not eat that way? Did you spend years—decades, maybe—overweight or obese, paying astronomical sums for multiple medications, exhausted, in pain, and generally debilitated with physical and emotional malaise because you simply felt BLAH?

Are you tired of inexperienced people spouting all kinds of nonsense about keto on the interwebs—misinformation that, at best, makes it harder for people to lose weight, but at worst, is actively harmful for people on various medications who need proper medical supervision to implement keto safely? (I am! It’s why I started making my own videos, in fact.)

HEAL Clinics wants to help people to not have to overcome the multiple barriers so many of us might have faced on our journey to finding and successfully implementing keto/LCHF. Dr. Westman is the Chief Medical Officer, and his right-hand woman, the Director of Clinical Protocol, is Jackie Eberstein, RN—Jackie was the head nurse at Dr. Atkins’ clinic in NYC for almost 30 years and she was actually one of Dr. Westman’s teachers! (What, you thought he learned keto all on his own?) Lemme tell ya, dear readers, she is low carb royalty. If you want help losing weight, reversing your T2 diabetes, reducing your insulin needs for type 1, reversing fatty liver, improving PCOS, or anything else keto is a slam-dunk for, there’s pretty much no one with more experience to help you than these two long-time keto professionals.  

HEAL Clinics has two options:

1. If you’re taking certain medications for diabetes, you will need to be seen by one of their medical providers in person to get started. (After the initial in-person visit, follow-ups can be done remotely, I think.) Right now, they have clinics in North Carolina and Virginia, but will be expanding into more states over time. (Note: this doesn't mean you have to live in NC or VA to be a HEAL patient, but you would have to travel there for your first visit.)

2. If you have a relatively “uncomplicated” case and are not on certain meds, you can be seen entirely remotely and don’t have to go to one of the clinics in person.

Learn more about the program here: How It Works

Don’t need help with keto? HELP SOMEONE ELSE! You can actually invest in HEAL Clinics. If you want to make trustworthy, safe, reliable, and effective keto-oriented healthcare and coaching available to as many people as possible—so they don’t have to face the criticism, naysaying, and other negativity you might have experienced when you started out—consider investing so that HEAL can keep expanding. The investment is just that: an investment. It’s not a donation, like it is with a Kickstarter or some other form of fundraising. You will actually own stock in the company. And the sad truth is, with 88% of Americans being metabolically unhealthy, reversing illnesses that are entirely or to a great extent driven by diet is a damn wise thing to invest in. We are awash in a tsunami of type 2 diabetes, cardiovascular disease, PCOS, Alzheimer’s disease, fatty liver, and other conditions caused or exacerbated by chronic hyperinsulinemia. Keto can go a long way to completely reversing these, or at least having some degree of beneficial impact.

Many of us can do LCHF/keto on our own, but some people need a bit more moral support, and some need professional medical supervision. For those people—and so that Dr. Westman and Jackie can train more doctors, nurse practitioners, physician assistants, and other medical professionals so that this kind of care can be available to as many people as possible, consider investing if you have the means. And if you’re not in a position to invest, please let your friends and family know about HEAL Clinics, if you think they would benefit from keto, and you want them to do it correctly and safely.

(Full disclosure: I am a HEAL investor, so yes, I’ve put my own money where my mouth is! And no, there's no affiliate link or anything, so I receive no financial compensation whatsoever if any of you happen to invest. I'm just spreading the word about what I hope we can all agree is a good cause.)

See you on March 5!

Disclaimer: Amy Berger, MS, CNS, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician. Links in this post and all others may direct you to amazon.com, where I will receive a small amount of the purchase price of any items you buy through my affiliate links.

The Personal Fat Threshold Concept

Hey Kids!

It’s been ages since I’ve posted what I would call a “real” blog post. Something meaty and educational. Something you can really sink your teeth into. The last one was way back in August, when I wrote about whether protein is bad for the kidneys. (Hint: it’s not.) I’ve posted a few things since then, but nothing all that substantial. I’m glad to say today’s post makes up for lost time, because it is LONG. So grab yourself a cup of coffee or tea (or...*gag*...broth, if you must), put your phone on silent, and dig in.

I’m excited to share this with you. So excited, in fact, that I’ve been procrastinating on writing this for no less than 6 months. In looking at the folder of blog post drafts on my computer, I started jotting down notes for this in July 2018. The reason I kept putting it off is that I knew this was going to be a LONG post—massively long, even for me. But then I gave a talk on this topic at a keto event in Canada in December, so I finally had to organize my thoughts and put them together coherently. Once that was done, I figured it would be easier to get this written, since I could just flesh out the details of what was on the slides. Don’t kid yourselves, though. This still took four days to write and edit. (It’s much faster to talk and show images on slides than it is to type everything out in detail in a blog post!) Nevertheless, I’ve wanted to write this for a long time, so here we finally are. And the benefits a blog post has over a talk is that you can read this at your leisure, click on whatever links you’d like to explore further, and go as deeply down any of those rabbit holes as your heart desires. And to any of you who are happy at such a long post and who prefer reading to watching videos, I’m with you. I started my YouTube channel to bring my message of Keto Without the Crazy™ to a wider audience, but I, myself, prefer reading.    

One of the things I love most about writing my blog is sharing with you, my beloved readers, the fascinating and important things I learn as I deepen my understanding of human metabolism and physiology. The reason they call it “commencement” when you graduate with a degree in something is that it’s the start of your education, rather than the end of it. This has certainly proven true for me since getting my M.S. in nutrition.

One of the most intriguing things I’ve come across recently is the concept of the personal fat threshold. I don’t know who first coined this term, but it appears to have been Roy Taylor and Rury Holman, in their 2015 paper, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Other researchers wrote about the concept long before this paper, but I think Taylor & Holman were the first to use the phrase personal fat threshold. (Their paper is the first place I ever saw it in print, anyway. A researcher named Keith Frayn wrote some outstanding papers on the same topic years before without using the term. I cite his work liberally throughout this post. If you’d like to read the full text of any of the key papers I cite here, feel free to email me and I’ll send you a copy.)

Book Review: The Case Against Sugar

Gary Taubes wrote another book.

Gary Taubes! (*Fangirl squee!*)

Do I really need to say more?

I don’t, but since this is my blog, I will.

TL;DR: I loved this book and you will too. READ IT.

If you don’t read a lot of blogs and websites outside the low carb bubble, then allow me to tell you that there’s a large contingent of people who loathe Taubes. He takes a boatload of criticism, as does anyone who writes something that condemns or exonerates something other people love or hate (e.g., red meat and saturated fats, refined carbohydrates, and raw milk). But put me squarely in the camp that loves his work and is grateful for his meticulous research. (The endnotes and bibliography of Good Calories, Bad Calories are almost as large as my entire book.) I’m not saying he’s right about everything, nor that I agree with him on everything. I’m only saying I’m a big fan and have been for several years.

I had the pleasure of meeting Gary in spring 2017, first at a reading and book signing in Washington, DC, and then a few weeks later at a literary event in Charlottesville, VA. I actually drove him from Charlottesville back up to Dulles airport in my neck of the woods, so we had some time to chat and shoot the low carb breeze. Let me tell you, folks: I read GCBC during my deployment in Iraq, circa 2008. Having always been a sucker for salt & pepper hair, intellect, and a wry and somewhat dark sense of humor, I developed an immediate nerd crush on Gary. Never in my wildest imagination—and mine is pretty wild—did I think nine years later, I’d have him all to myself on the road for two hours.

Get your minds out of the gutter. Nothing happened except good conversation and Gary being an exceptionally good sport about the fact that my decade-old car has seen better days. (He assured me that his car is older and in even worse disrepair. We writers don’t exactly break the bank; not even ones like Gary, who garner big advances and have multiple bestsellers to their names.) Without revealing too much, I’ll say that it was really nice to talk with a writer of Gary’s caliber, and to find out that many of the emotional demons that plague me are not unique to me. Gary deals with his by throwing himself into work; I deal with mine by avoiding work. Neither strategy is all that healthy, long term. But I can look to Gary as someone with a lot of dark thoughts and inner turmoil who still manages to get shit done produce great work. It helps that he has a wife and two sons depending on him, so he sort of has to bring home the proverbial (and literal) bacon. 

As an aside, Gary has spent time in France, and he longs for it. As he talked about it, his desire to be there—and, maybe, to be the person he was when he was there—was palpable. He has also written and spoken a lot about his history as a smoker. I could totally see him as the quintessential ex-pat, sitting at a roadside café in Paris, sipping coffee and reading poetry, complete with a black turtleneck and a cigarette.  

But enough about Gary. On to the book!

Ketogenesis, Measuring Ketones, and Burning Fat vs Being in Ketosis

This post is long overdue.

I cannot tell you how many emails I get from people fretting over their ketone levels. It’s time to set the record straight on this issue. I wish there was someplace I could refer people for reliable information on this subject, but I haven’t come across a blog post or podcast interview that explains things satisfactorily. At least, not to my satisfaction. And that is and always has been my goal in writing my blog: I explain things the way I would want someone to explain them to me, if I were new to all this. And since no one—as far as I know, anyway—has tackled this subject the way I would, I finally had to just sit down and write this. If you feel it’s educational, please share it in the low carb and/or ketogenic circles you frequent, because I know this issue comes up all the time in ketogenic forums and Facebook groups. (And if you know of other good resources on this topic, feel free to provide a link in the comments, and I’ll update this post to include it.)

Okay, here goes.

There are few issues more controversial regarding ketogenic diets than whether you should measure your ketones. There are valid reasons to measure, but there are also a lot—a lot—of misconceptions about measuring ketones and how to interpret the data. So let’s get into when and why it’s a good idea to measure, who doesn’t need to measure, and most important, what the numbers mean. (I said who “doesn’t need to” measure rather than who shouldn’t measure because if you want to measure, then go ahead. There’s really no should or shouldn’t here. But if you choose to measure, you need to understand how to interpret and understand the numbers so you don’t jump to illogical and false conclusions.)     

I will also be covering the difference between being fat adapted versus in ketosis. I tried to do it in a few posts awhile back, but I think I the way I explain it here is much better because I will show you the biochemical pathways involved so you will be able to see how it actually works. My hope is that this will go from a vague concept in your mind to, “Oh! NOW I get it!” And you will understand very clearly how you can absolutely, positively have a fat-based metabolism and lose body fat even if you’re not in ketosis. 

More Than You Ever Wanted to Know About Protein & Gluconeogenesis

My dear readers, the website/blog update has run into some snags. Rather than continuing to keep you waiting, though, I’m going to publish new posts and I’ll worry about transitioning them over later on. And since it’s been a few months since I last posted anything of substance, I’ve decided to drop this enormous, enormous post on you to make up for that lost time—and it might take you equally long to read it. Sorry about that, but hey, I haven’t written anything meaningful since May, so, depending on your point of view, this post is either a gift or a punishment. As I’ve said in the past, if you’re an insomniac or a cubicle dweller with lots of time to kill, you’re welcome. (The rest of you, go get yourself a cup of coffee or tea, come back, and get comfy.)

I’ve been meaning to write this post for over a year, but it’s such a big topic and so much can go wrong that the thought of tackling it all was enough to make me not write it. But it’s gotten to the point that I’m tired enough of seeing the same questions asked and the same myths propagated over and over on various keto and low carb forums that I’ve decided this needs to be done, no matter how painful I might find it. Because seeing nonsense and fearmongering regarding the role of protein in low carb or ketogenic diets is even more painful. So if finally managing to organize my thoughts into some kind of coherent prose means I never have to read the phrase, “too much protein turns into sugar” ever again, it will be worth it.

So that’s what’s on tap today, kids: Gluconeogenesis.

That’s right, friends, it’s time to do some myth-busting surrounding the whacked-out notion that protein—lean protein, in particular (like a skinless chicken breast, or tuna canned in water)—is the metabolic equivalent of chocolate cake. (Or cotton candy, or gummy bears, or any other insanely sugary thing that might raise your blood glucose and insulin far more than protein does.) 

Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.5A)

Graphic adapted from Seyfried et al., 2015

OH. EM. GEE!!!!!

It’s baaa-aaaaack!

Today is June 1, 2016. Looking back through the blog archives, I saw that the previous post in this series on the metabolic theory of cancer was published on June 1, 2015. Yes, kids, it’s been a year. A full year! An entire year to the day. If you have been waiting and waiting (and waiting!) for me to get back to this and address some key concepts we haven’t gotten to yet, believe me, nobody wanted me to get back to this more than I did. I absolutely did not plan on it taking a year. But alas. Hopefully, in that time, you’ve learned a thing or two about insulin, stubborn fat loss, and the use of ketogenic diets for Alzheimer’s disease and other neurological conditions. In fact, I am in the process of adding a new installment to the “ITIS/It’s the Insulin, Stupid” series, but when I saw that I was coming up on the one-year anniversary of neglecting the cancer series, I knew I had to get my rear in gear and just DO IT. I really wanted to do the insulin post first, but considering the date, I thought it would be apropos for me to do this one instead.

Also, just to let you know, since the writing of that last post, I have had the honor of meeting Drs. Seyfried, D’Agostino, and Poff in person. {Squee!!}  I also got to meet Dr. Cunnane, Dr. Newport, Dr. Rho, and Dr. Maffetone. Holy moly…it was a nonstop conference of metabolism rock stars.

I am most definitely going to get to the mamma-jamma, granddaddy of all topics we’ve been waiting for in this cancer series—the ketogenic diet—but please be patient. I’ve very recently had more work stuff come up (in a good way), and I am feeling a bit overwhelmed. I will write about ketosis. I can’t promise when, exactly, that will happen, but I promise it won’t take a year. (Maybe just a couple weeks, considering I’m already working on it.)  ;-)

If you’re new to my blog and have no idea what’s going on right now, the series I’ve written on the metabolic theory of cancer is a “fan favorite” – at least, among the people who like to geek out on the science with me. The cancer series is representative of when my blog becomes a free course in (very basic) biochemistry and physiology, and is peppered with links and quotes from the scientific literature. If you prefer my rants, shakedowns of food labels, and other casual-type posts, no prob! Whatever floats your boat. But for those of you who need to kill lots of time at your desk job, or who perhaps need help falling asleep, you might want to start way back at the beginning and work your way toward today’s post. (Actually, that’s sarcasm. The truth is, I think this stuff is fascinating, and perhaps some of my best work. I swear, that hexokinase 2 stuff STILL blows my mind.)

Since it has been a year (!!) since the last installment, I’ll make it easy for you and list all the posts in order, from first to most recent: 

1. Introduction
2. Cells Behaving Badly
3. Cellular Energy Generation 1 - Glycolysis
4. Cellular Energy Generation 2 - Mighty Mitochondria (Krebs Cycle, Electron Transport Chain)
5. Mitochondrial Dysfunction 1
6. Mitochondrial Dysfunction 2 - They ARE Broken
7. Glycolysis Run Amok & Mutant Hexokinase
8. Aerobic Fermentation (a.k.a. "The Warburg Effect")
9. Cancer Cells are Sugar Junkies
10. Mutations vs. Mitochondria
11. Cancer as a Protective Mechanism
12. Speculation on the Causes of Cancer (Pt.1)
13. Video Lesson! (Thomas Seyfried, PhD)
14. Speculation on the Causes of Cancer -- and How to Mitigate Risk (Pt.2)
15. Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.3 - Viruses)
16. Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.4 - Carcinogens)

Buckle up and hang on tight, everyone. HERE WE GO!

ITIS -- It's the Insulin, Stupid (pt 6/8)

LOOKS CAN BE DECEIVING!

We’re in the home stretch with all this insulin stuff, folks, I promise. Just two more posts after this, and we’ll be done. (I also promise to get back to the cancer series soon. I know I’ve got some readers who’ve been waiting a long time for that to be resurrected.)

Okay, I left off last time asking why chronically elevated insulin causes some people to gain body fat, but not others. I also hinted that the accumulation of adipose tissue might actually be a protective mechanism. We’ll start with the first issue, since it’s quicker to address. I also want to start with it because it is probably the zillion-dollar question in all of human metabolism in our current dietary  & cultural zeitgeist. Upon consuming the same diet—the same number of calories, possibly the same macronutrient ratios—and maybe even having the same degree of hyperinsulinemia/insulin resistance, why do only some people get fat?

And here, my friends, is my zillion-dollar answer:

I don’t know.

I don’t know if anyone knows. Most likely, there are genetic factors involved. After all, some people are tall; some are short. Some have blue eyes; some have brown eyes. In the face of chronically elevated insulin, some of us accumulate lots of adipose tissue, some don’t. (Lucky bastards…) How come some people’s bodies are so good at not accumulating excess adipose? Put more bluntly—and in terms most of us have probably said to ourselves a hundred times about friends and relatives who have never had weight problems—despite eating junk and being sedentary—Dammit, why don’t they ever get fat?!

ITIS -- It's the Insulin, Stupid (pt 5/8)

In part 3 of this series, we covered the role of insulin as a counter-regulatory force that keeps catabolic glucagon in check. (Reminder: in the absence of insulin, glucagon run amok will cause the body to waste away by catabolizing its own muscle and fat tissue for fuel). And in part 4, I mentioned that lowering blood glucose (BG) is probably not insulin’s primary function, but rather, one of the ways by which insulin helps keep BG in check gives us a clue as to one of its more important functions: it is anti-catabolic. While several other hormones break tissue down in order to provide glucose and fatty acids to fuel the body, insulin builds tissue up.

That’s right. Insulin is an anabolic hormone. It stimulates tissue growth, be it of muscle or adipose. (If the phrase “stimulates tissue growth” reminds you of cancer, hang onto that thought. I’ll be addressing insulin eventually in the cancer series.) If a lack or insufficiency of insulin causes type 1 diabetics to waste away due to catabolizing muscle and fat, then that tells us that insulin helps build up muscle and fat. (Or, at the very least, insulin hinders its breakdown.) Veteran bodybuilders can tell you that insulin spikes (properly timed) can help build muscle mass, and veteran low-carbers can tell you that insulin spikes can help build fat mass. Remember: insulin isn’t “toxic.” It’s all about context. Since we’re focusing on obesity here, we’ll leave muscle out of the discussion and focus on fat.

ITIS -- It's the Insulin, Stupid (pt 4/8)

“Insulin is vital for lipogenesis. Its role as a lipogenic hormone is underplayed, but we know that without insulin, you can’t get fat.”
                                        --Dr. Roger Unger

Having raved about Dr. Unger’s lecture in the previous insulin post, obviously, I think he’s pretty brilliant. That being said, chronically elevated insulin isn’t the only mechanism by which people accumulate excess adipose tissue. (For the newbies out there, “accumulating excess adipose tissue” is the fancy way to say “get fat.”) I prefer to use the word adipose instead of fat, because I am trying to make a distinction between dietary fat that we consume in food, and the body fat that we all love to hate so much on our bellies, hips, thighs, and elsewhere. Even if they both occur in the form of triglycerides, I still want to keep them separate, since eating dietary fat does not automatically result in said fat depositing itself on our rear ends or forming second and third chins.

Apart from insulin, there are several other things that contribute to the regulation of body weight, and, perhaps more important, the composition of that weight. And I’m not ignoring those. Sometime in the next few weeks, I’ll be writing a post about the myriad other reasons someone might not be losing weight on a low-carb diet (unrelated to this insulin series). For our purposes right now, though, we’ll stick with insulin. Because even if there are other factors playing a role in excess adiposity, when we look at changes that have occurred to the food supply and the general dietary guidelines from various government and professional medical/health organizations during the last several decades, systemic hyperinsulinemia is probably one of the largest influences, if not the single largest.

In tackling the role of insulin on the accumulation of adipose tissue, first we need to explore just a few more things about insulin’s biochemical & physiological roles. After that, we’ll see how it all plays out in the real world—that is, in the body.

ITIS -- It's the Insulin, Stupid (Pt 3/8)

If you made it through the encyclopedic posts that were part 1 and part 2 of this series on insulin, and you’ve come back for more, thank you! It is one of my biggest flaws as a writer: brevity is not my strong suit. (But at least I admit I have a problem. That’s the first step, right?) This post is no exception. In fact, it's probably longer than the first 2. So go grab a cuppa joe, or tea, or whatever you like, and hunker down for a nice, long read.

Okay. So I left off last time pointing out that, in covering the effects of elevated insulin and glucose on the cardiovascular system, reproductive function, the brain, kidneys, eyes, and inner ear & balance mechanisms, I had not said one word about obesity. I hope we’re all on the same page and can agree that insulin resistance is not something limited to people who are carrying around a few—or a couple hundred—extra pounds. Obviously, there are millions of non-overweight people who are infertile, have heart disease, kidney disease, vision problems, dementia, and more. (I have written about this before. One of my personal favorite posts on this entire blog is the one where I explained that obesity is simply one more effect of metabolic derangement, rather than its cause. I also wrote about this topic for Designs for Health.)

Nevertheless, we’d be missing a substantial piece of the insulin puzzle if we didn’t talk about the role of insulin in regulating body weight. Before we get to that, however, we first need to look at the actual functions of insulin, as well as the pancreas. It is an unfortunate byproduct of our epidemic of “diabesity” that we automatically think of blood glucose when we hear the word insulin. And there’s no doubt insulin does have an important role in regulating—or, more specifically, lowering—blood glucose (BG). But that’s not insulin’s only function. In fact, I would argue it’s not even the primary function. We will get to weight, I promise. But just like we did in the cancer series, we’ve got to trudge through a lot of biochemical weeds before we get to the good stuff. So here goes.

Time for a brief extremely verbose endocrinology lesson.

Food for Thought Friday: Yes, You *Are* Hungry

One of the frequently repeated claims about low carb and ketogenic diets goes something like, “I don’t get hungry anymore.” Many people find that being in ketosis suppresses the appetite. In some cases, the higher the ketones and/or the free fatty acids, the less desire there is to eat. But is this really true? If you follow a low carb diet, will your appetite go away completely? Will you never be hungry? I find this hard to believe, so let’s dissect this claim, shall we?

If you’ve been reading my blog for a while (and if so, I thank you!), then you know I’ve reserved these Food for Thought Friday posts as my place to do a little ranting, albeit in a humorous way. I hope I’m not becoming too negative, though. It’s just that I get pretty hung up on language, and I don't like us playing fast and loose with how we say things. It’s probably the writer in me. So I got a little annoyed the other day when I was catching up on Robb Wolf’s podcast, and I heard Perfect Health Diet author Paul Jaminet say something about this phenomenon of magically disappearing hunger.

ITIS -- It's the Insulin, Stupid (pt 2/8)

Warning: This is a ridiculously long post. I was going to break it up into two, but I figured, what’s the difference between one really long post, and two semi-long ones? You can always read a couple paragraphs and then come back later if you don’t have time to read it all at once.

Also: My blog has a very eclectic audience. I have physicians, PhDs, and others well-educated in biochem and A&P reading this, but I think the bulk of my readers are interested laypeople. I try to tailor my posts to the laypeople, keeping in mind that they are of above-average intelligence, and certainly above-average knowledge about all this low-carb, high-fat, Paleo, and ancestral health "stuff." Just wanted to remind everyone of the diverse audience here, because this post, in particular, contains simplified explanations of complex processes, and I apologize if any of the pros find themselves bored. :-/ 

OKAY! Now we come to the next part of why all of this insulin stuff is so important. (Missed the first part? Click here. And you’ll notice I’ve changed the title of this post to say it’s part 2 of I-don’t-know-how-many. In starting to write part 3, I realized this is going to be more like 5 or 6. I am learning new things about this every day that I feel are important enough to write about, and the number of posts it will take to include them keeps rising.) 

Here we go...

Statins: Sugar-Coating the Truth

A priest, a rabbi, and a cardiologist walk into a bar.

No, that’s not it…

Why did the cholesterol cross the road?

Nope, that’s not it either…

Did you hear the one about statins and increased risk for type 2 diabetes?

YES! That’s the one I meant. Only, this isn’t a joke.

Statin drug use is now associated with an increased risk for developing type 2 diabetes. Is this just fearmongering headlines, or is there really something to it?

  

ANNOUNCEMENT!!

It’s a boy!

It’s a girl!

It’s a book!

I did it! The e-book I’ve been dropping hints about is finally finished and available for sale! Go check it out:

The Alzheimer’s Antidote: A Comprehensive Nutrition and Lifestyle Strategy to Fight Alzheimer’s Disease, Memory Loss, and Cognitive Decline.

I apologize for hawking my wares here, but I’ve got to get the word out, right? Just be thankful I am completely clueless about web design, otherwise you’d have annoying things popping up right in your face the minute my site loads, as you might be familiar with from other sites you frequent.

And since I am the least tech-savvy person alive, before I even tell you anything about the book, I would like to express my deepest and sincerest thanks to Ms. Ellen Davis, for her untiring support and encouragement on this project … and, oh, yeah, by the way, she did all the design and layout. I am not kidding when I say this book wouldn’t exist without her. I sent her all my writing in MS Word, sent all the images I either created or purchased (from iStock Photo, in case anyone’s curious), and she magically transformed them into the e-book that is going to change the way people think about Alzheimer’s and cognitive impairment. Ellen is not just a great designer, however. She is the mastermind behind the Ketogenic Diet Resource, the single best blow-your-mind, one-stop-shop I know of for information on low-carbohydrate and ketogenic diets. (She also happens to have a master’s in nutrition, and is the author of the fantastic, amazing book, Fight Cancer with a Ketogenic Diet. Her most recent project was a collaboration with Keith Runyan, MD, on Conquer Type 2 Diabetes with a Ketogenic Diet.)

Okay. Now that we’re done with the preliminaries, let’s get down to business!

Metabolic Theory of Cancer: Cancer as a Protective Mechanism

“Cancer cells were producing energy in a way that evolution had set aside as an auxiliary pathway, a highly inefficient generator that kicked in when the power went out.” (Christofferson, p.20) 

“Tumors bypass many of the biochemical constraints that regulate metabolism, in order to maximize their survival at great expense to the host.” (Mathupala, Ko, Pedersen, 2010)

The amplified rates of glycolysis “indicate a strategy used by highly malignant tumors to survive as well as thrive within the host using a remarkable set of coordinated molecular mechanisms. These mechanisms, which are very similar to those utilized by some highly successful parasites, indicate a sophisticated strategy devised by tumors to survive even the most inhospitable microenvironments within the host.” (Mathupala, Rempel, Pedersen, 1997)

Throughout this series on the metabolic origins of cancer, I have been hinting that cancer—destructive, devastating, scary cancer—might be an evolutionarily conserved protective mechanism. I realize this is politically incorrect. But when we understand some of the biochemistry and physiology involved, this is actually a fairly logical conclusion to arrive at.   

I have gone to great lengths to explain some of the relevant biochemical pathways involved in how and why cancer cells accomplish all the seemingly horrible things they do. In looking at glycolysis, the shift to hexokinase 2, aerobic fermentation, the upregulation of glucose transporters, and more, we have explored a lot about the how of cancer. And we’ve certainly talked a bit about the why. Today, let’s go a little farther down the rabbit hole of the why, because, as I left off saying last time, if we can figure out why cells become malignant, we might have better odds at preventing cancer. We can certainly develop more effective treatment protocols if we understand the how of cancer, but understanding the why will give us even more of an advantage in devising treatments, as well as creating (potentially) better prevention strategies and strategies to prevent recurrence.    

Metabolic Theory of Cancer: Mutations vs Mitochondria

“Let’s get ready to RUUUUMBLLLLLE!”

“Maybe we’ve mischaracterized the origin of cancer. Maybe cancer is not a genetic disease after all. Maybe we are losing the war against cancer because scientists are chasing a flawed scientific paradigm, and cancer is not a disease of damaged DNA but rather one of defective metabolism.” (Christofferson, xiii)

“If scientists have mischaracterized the origin of cancer, then we have lost three decades trying to target mutations that are a side effect rather than the motor driving the disease. (Christofferson, p.223)

“It is interesting to note that none of the current approaches to brain cancer management discussed at a recent symposium involved strategies to target tumor cell energy metabolism. Several presentations at this symposium discussed the failures associated with current approaches to management. As long as [brain] cancer is viewed as something other than a disease of energy metabolism, the failures will likely continue in our opinion.” (Seyfried et al., 2012)

Metabolic Theory of Cancer: Cancer Cells are Sugar Junkies

“One of the most common and profound phenotypes of cancer cells is their propensity to utilize and catabolize glucose at high rates.” (Mathupala et al, 1997)

“The higher the glucose levels, the faster the tumors grew. As glucose levels fall, tumor size and growth rate falls.” (Seyfried et al., 2012)

“Hyperglycemia was also directly linked to poor prognosis in humans with malignant brain cancer.” (Seyfried et al., 2012)

Cancer cells are sugar junkies.

If those five words, strung together in that order, are a surprise to you, then you haven’t been paying much attention so far. If you’ve been keeping up with the previous posts in this series on the metabolic origins of cancer, you will have seen this coming a mile away. (Or, rather, four or five blog posts away.)

Cancer cells love glucose. They need glucose. And they do everything in their power to suck up as much of it as they possibly can, even at the expense of healthy tissue elsewhere in the body. Short of actually taking control of the motor functions of your arms and hands in order to pour you a giant bowl of sugar-frosted breakfast cereal and cram it down your throat, cancer cells do everything they can to ensure they have access to a never-ending supply of glucose. 

In the past few posts, we’ve looked in detail at the main reason why cancer cells do this, and a few mechanisms for how they do it. I have been saying all along that cancer cells are wily little things, and they perform some stunningly impressive feats of metabolic Twister in order to accomplish the nefarious task of keeping themselves alive by gorging on glucose.

Since it’s been a while since the last post, let’s take a quick look back at what we’ve covered so far, regarding cancer cells’ dependence on glucose as their primary fuel.

Alzheimer's Follow-up: Q&A (a.k.a. World's Longest Blog Post)

WARNING: THIS POST CONTAINS MAJOR RANTS AND HARSH LANGUAGE. Read at your own risk.

Anyone out there watch Ancient Aliens? If so, you are probably cracking up right now. If not, you’re scratching your head, because you have no idea why this is funny. (Trust me, though, it’s hilarious.)

Seriously, though, the answer is not aliens. I might not know for sure what the answers are, but I’ll provide my best guesses/hunches.

What are the questions? Here goes:

It’s no secret that I am trying to get the word out about Alzheimer’s disease as a “disease of civilization” – that is, a condition that results from the mismatch between our physiology and the modern Western diet (refined carbohydrate-heavy, vegetable oil-heavy, low in micronutrients), and the modern Western lifestyle (inadequate sleep, inadequate physical movement, too much psychological stress, loss of human emotional connections). As of 1/18/2015, the post I wrote pointing folks toward the article I wrote for the Weston A. Price Foundation, has 1470 views. Not all that many, considering the one on Vitamin J has 13,512. (If I could get Mark Sisson to include the Alzheimer’s post in one of his Sunday Weekend Link Loves, maybe it would have more, since, thanks to a reader and friend who alerted the MDA people to it, that is where the vast majority of hits came from on Vitamin J.)

But word is spreading, if slowly. (In fact, someone is launching a Kickstarter campaign to fund a documentary about preventing Alzheimer’s, called Bread Head.) More people here and there are stumbling onto my blog, and finding the Alzheimer’s article, which is nice. One such newcomer left some very good questions in the comments section. They were good enough—and my answers complex enough—that I thought it would benefit more people if I answered in the form of a blog post, where everyone would see it, versus responding in the comments section, where almost no one would.