Sugar – Could it really be killing us?

Ordinary table sugar or sucrose: half glucose and half fructose

Sugar! My sweet, most-beloved! Are you really my enemy? How could that be when I love you so much?

That sugar was killing us was the accusation made by its most widely known and harshest critic, Robert Lustig, MD, back in 2009 with his now-viral, first YouTube video. He’s continued the theme with numerous other videos, journal publications, and, relatively recently, a book and very professionally produced  YouTube mini-series. To be more precise, he’s really complaining about the “bad” half of what we commonly call sugar: i.e., fructose. But, chances are good if you’re reached this page you already know all that. And, chances are also good, whether you know it or not, that some degree of the dysfunction that many are finally agreeing can be attributed to chronic, excessive fructose intake is already present in your body.

At the time of Lustig’s initial Bitter Truth video release, his views were very alternative to say the least. It was a turning point in time and the very beginning of general public awareness that fructose might be a problem. But always there is initial resistance to a paradigm shift, and  I think for most, one lone man crying wolf is almost certain to be ignored. Especially true considering the absence of warm reception in academic circles. For example, witness the 2010 dismissal from the very well-respected Alan Aragon where he summarized with:

I disagree (as does the bulk of the research) with his myopic, militant focus on fructose avoidance. He’s missing the forest while barking up a single tree.

And so, I followed suit. While I wasn’t exactly ignoring Lustig, I didn’t see his position as anything I wanted to publicly support, much less as a call to action. The mainstream-medicine position for years has been that obesity and diabetes are simply a matter of overnutrition – as Lustig says, “gluttony and sloth.” Although Lustig’s indictment did change my thinking enough to cause me to moderate my fructose intake, especially drinks, I admit to being swayed by the pejorative language and negative reactions from the entrenched medical establishment and my obesity-as-sin viewpoint prevailed.

Well, fast forward to two weeks ago when I encountered this book:

The book was nothing special from the cover. I only read it because I read everything I can get my hands on that claims to know something I don’t about Western disease. But when I was finished with the book, I read it again. And then a third time – this time writing up a Cliff Dan Notes summary of it – which can be downloaded here.

The author, Richard Johnson, MD, currently at the University of Colorado, has come to obesity and diabetes research as one of the leading experts in  kidney disease. What I find most compelling is that, with the exception of a few minor differences, Lustig and Johnson are telling essentially the same story. The major difference is one of emphasis. Lustig’s emphasis, with him coming from a background of treating pediatric, endocrine-related weight problems, is on fructose causing insulin resistance and it’s induced leptin resistance. Johnson, on the other hand, with his background in nephrology,  sees the intermediate step of high uric acid as the kingpin: ie, fructose raises uric acid levels which then can be associated with a whole lot more than just obesity/diabetes. Lustig does observe that the high uric acid induced by the fructokinase enzyme causes hypertension, but he does this almost in passing, I suppose because high blood pressure is so easily treated by BP meds. For Johnson, the uric acid produced and its devastating effect on kidney function was the tip-off that something a whole lot more sinister and far-reaching was at play here besides simply diabetes.

I’ve immersed myself in the internet fructose discussion deeply over the last two weeks, reviewing what’s been said over the last five or so years. What I’ve found is that now instead of a single, lone voice, many, many others have joined the fray and are echoing the same warning. And here with this book, a second well-respected doctor, with over 300 journal articles to his name, with everything to lose and little to gain, has staked his reputation on the claim that fructose is a killer.

My growing impression is that Johnson’s work provides those crucial pieces that make the whole puzzle come together. What if the main reason paleo, Ornish, McDougall, Pritikin, pre-industrial, etc diets all work is that they eliminate sugar? The fact that fructose metabolism and alcohol metabolism share the same disastrous overwhelm of the mitochondrial TCA cycle capacity predicts that they will produce similar disease in the body and, guess what, they do. Insults to the liver, be it from alcohol, tylenol, or fructose are additive, so more of one means you have less tolerance for some of the other.

Here’s what I really find striking. If you’ve read my previous blog posts, you’ve likely noticed that although I adhere somewhat to the paleo philosophy of avoiding evolutionarily-new additions to the food supply, what I really adhere to is avoiding carbohydrate foods that raise my blood glucose. These turn out to be those with high glycemic load, either in their natural state or thanks to the industrial processing that has destroyed their cellular integrity. And what I found was that contrary to the paleo proscription on legumes, the more I added to my diet, the better my lab numbers got, so that now, I’m seeing the best lab numbers since I started getting tested 30 years ago. Yes, at age 70, instead of everything falling apart, I’m still apparently moving towards greater health. And with what I’ve learned from Lustig/Johnson these past two weeks, I feel like the veil over my insides has been lifted and I can see into my digestive tract and understand why it all works as it does. It’s all very satisfying!

At this point, I’m completely ready to grant that fructose is most likely a poison. Before anyone goes crazy with that thought, please remember that in toxicology it is understood that “the dose makes the poison.” So the dose concept grants us that for a chronic toxin like fructose, there is some a tolerable upper limit below which for most people, it is safe. In the case of fructose when found naturally in fresh fruit, the value of the antioxidants and fiber completely mitigates any potential toxicity of the fructose. But fruitarians, be warned – the website, 30 Bananas a Day comes to mind – a 30-banana a day diet might just well challenge the toxic limits for many people. Especially if you like to eat very ripe fruit, since as fruit ripens, according to Johnson, fructose content increases and antioxidant content decreases.

The fructose as poison argument is an easy one to make, and Lustig does so in,  Fructose: It’s “Alcohol Without the Buzz”. No question, an ethyl alcohol buzz is fun, but it’s generally recognized as a chronic liver poison. Fructose engages the same hepatic metabolic pathways. So at toxic levels, it would be expected to carry much the same disease burden stemming from liver toxicity, and, in the CNS, stimulation of the same reward pathway similarly promoting problematic continuous consumption. And it does. But fructose ups the ante by also producing uric acid which then inhibits the action of nitric oxide so as to cause high blood pressure. Solid research. Undisputed.

But is it generally acknowledged that fructose is a poison? No. Lustig thinks that the food industry is influential in blocking this perception. Has the gold-standard for medical research, a really good double-blind randomized clinical trial been performed so as to establish beyond question that fructose is killing people? No. But, as Lustig has pointed out, there are huge obstacles to doing this study and the research situation is analogous to that of climate change and tobacco smoking. The RCT hasn’t been done, but we have enough solid evidence to establish causal inference. Indeed, we have to ask ourselves: is the evidence compelling enough to warrant reducing fructose intake to levels commensurate with our evolutionary past?

My answer is yes. Of course for me, even small amounts of fructose induce sugar cravings that are enough to drive me crazy, so it’s a no-brainer. And on top of that, I’m diabetic with blood sugar controlled by diet and exercise.  I’m super-sensitive. When I cut back on the little fructose I was eating, my fasting blood glucose dropped by 10 mg/dl. But for the general population, there’s the type I vs type II error to consider. If Lustig and Johnson are wrong, but you unnecessarily avoid fructose, in the grand scheme of things, you haven’t lost much. If they are right but you continue consuming them, you invite: de novo lipogenesis, dyslipidemia, elevated free fatty acids (FFA), high uric acid, insulin resistance, high blood sugar and inflammation; leading to: high blood pressure, stroke, kidney failure, obesity, heart disease, type 2 diabetes, Alzheimer’s Disease, cancer, autoimmune problems and polycystic ovarian syndrome (PCOS). For an intro to how all this disease comes about, its consequences and what to do about it, I invite you to watch a very well done series geared to the general public: Here‘s the first in the series.

Before I leave this toxicity question, if you remain unwilling to think of our sweet, darling fructose and poison in the same mental breath, here‘s an excellent discussion of toxicology as it relates to sugar. Especially relevant from that article is the finding from toxicology that we vary in our capacity at tolerate poisons, as depicted in this skewed bell-shaped response curve for tylenol LD50 toxicity:

What this means of course, is that even it were true that a little fructose is harmless to most people most of the time, that wouldn’t stop it from being most correctly classified as a toxin.

More interesting and potentially more useful than the question of whether it can be correctly labeled as a toxin, is comparing the two viewpoints – Lustig’s and Johnson’s – to see  which has the most utility, and, where they differ, could they both be right or is there a conflict?

To be continued in part 2 …