January 10, 2012

Nutritional Biochemistry

Sugar 101 – How harmful is sugar?

Read Time 6 minutes

Any discussion on the culpability of poor nutrition as the cause of our health woes begins with a discussion on sugar.

One of the world’s experts on this topic is Dr. Robert Lustig, a pediatric endocrinologist at UCSF.  Dr. Lustig has great experience treating children with obesity and is really on the front lines of what is becoming an epidemic of childhood obesity.  About two-and-a-half years ago, he gave a lecture on the perils of fructose (fruit sugar, which also makes up half of table sugar and high fructose corn syrup). It’s about 90 minutes in length, but the time goes by pretty quickly as Dr. Lustig is an engaging speaker. In addition, Gary Taubes wrote a great piece on sugar toxicity in the NY Times Magazine last year, which references the work of Dr. Lustig.  You can find it here.  Gary’s article on this topic was the fourth most read feature of 2011 on NYTimes.com (and the most read of all health-related topics).   Here’s the video of Dr. Lustig’s lecture:

I’ve highlighted the key points (with corresponding time in video), for those who may not want to watch the video in its entirety:

  • 0:09:40 – Helpful summary showing the reduction in fat consumption in the U.S. from 1960 to 2000 (about 45% to 30%) and the concomitant rise in obesity (about 12% to 31%) [Which, of course, doesn’t “prove” anything, it’s just another correlation.]
  • 0:23:00 – Change in fructose consumption over time: Prior to WWII (16-24 gm/day); 1977-78 USDA survey (37 gm/day); 1994 NHANES III (54.7 gm/day); Adolescents today (73 gm/day).
  • 0:24:00– Perfect political storm of 3 events:
    • Nixon and USDA secretary (1973) – insistence to stabilize/reduce food prices.
    • Invention of High Fructose Corn Syrup (HFCS), which was half the price of cane sugar and enabled cheap substitution.
    • USDA, ADA, AHA, AMA – all call for reduction in fat intake.  Why? (For a quick primer on “cholesterol,” you may want to check my previous post on, What is cholesterol?)
      • Early 1970’s – LDL-C (The so-called “bad” cholesterol) is discovered (more specifically, a test to measure LDL-C is discovered)
      • Mid 1970’s – Observation that dietary fat is correlated with rising LDL-C (“A implies B”) in a subset of people.
      • Late 1970’s – Observation that elevated LDL-C is correlated with heart disease and cerebrovascular disease (“B implies C”) [Note: It’s not actually clear this correlation has causation attached to it, in fact most evidence today would tell us that elevated LDL-C does not lead to heart disease and stroke.]
      • Early 1980’s – The following connection is (erroneously) made: A implies B, and B implies C, hence A implies C, so no-A means no-C.  [I guess it’s easy to see how an untrained person could make this mistake, but anyone who has taken even an intro course in logic knows that if A implies C, it is not the case no-A implies no-C, it is only the case that no-C implies no-A. It’s hard to believe such poor logic was, and is, used to drive health policy. Last editorial point on this – any card-carrying lipidologist today will tell you that the so-called “bad” LDL-C is as relevant to your getting heart disease as your eye color.  Heart disease is caused by lipoprotein particles carrying oxysterols into your artery walls.  This is not measured or reasonably predicted by LDL-C.]
  • 0:33:00 – Overview of Ancel Keys’ flawed “Seven countries study:” Showed the correlation of fat intake and coronary mortality, but failed to explain the cross correlation of sucrose with the fat (that is, sugar consumption rose too, but this was ignored in the analysis).
  • 0:58:00 – Fructose metabolism overview (technical, but interesting – feel free to skip if you don’t like biochemistry): Fructose requires more ATP for the first step in its metabolism (fructose to fructose-1-P) than glucose.  This requires an AMP scavenger to recycle the ADP and AMP.  AMP goes to IMP, which goes to uric acid.  This creates the link between fructose consumption and gout and hypertension (uric acid blocks nitric oxide synthase).  In addition, the byproducts of fructose-1-P to pyruvate, such as xylose-5-P, upregulate the enzymes that favor the reaction of citrate being turned into acetyl CoA being turned into fatty acids (staying in liver, causing fatty liver) and VLDL (exported out of liver) [i.e., de novo lipogenesis].  In other words, on a per unit basis, much more fructose is hepatically converted into fat than glucose.
  • 1:09:00 – Comparison of chronic ethanol exposure and fructose exposure; very high overlap (not surprising, given that ethanol is fermented fructose).  As Lustig correctly puts it, fructose is ethanol, but without the buzz…

You could leave Lustig’s lecture thinking that fructose alone is the cause of obesity.  There is little doubt that a massive reduction in fructose (e.g., elimination of dietary sucrose and HFCS, and only modest consumption of fruit) does a lot to reduce obesity.  But does this mean the rest of carbs get off the hook?

The problem with the “fructose-alone-is-the-root-of-all-evil” argument

Much of what Dr. Lustig says may be correct, but I believe he overstates the importance of exercise in controlling weight (though he acknowledges that most “experts” fail to realize the calorie burning component of exercise is meaningless), the role/importance of fiber, and the lack of harm associated with glucose.  I am going to write extensively about these topics at a later date.  The “fiber story” is another sad example of observational epidemiology causing more harm than good.

Back to fructose…the main flaw in Dr. Lustig’s argument, in my humble opinion, is that he claims glucose is benign and that fructose (alone) is the culprit of obesity and metabolic syndrome.  In this sense, he is partially correct.  Fructose, in excess, may be “evil,” to be sure.  However, Lustig claims that glucose is “good” in any amount.  He does this based on the assumption that the metabolic priority for glucose metabolism is, first, direct oxidation (i.e., real-time use by organs that need it), and second, glycogen formation and storage by the liver and skeletal muscles.   He overlooks a few problems, though.

  • Direct oxidation of glucose at rest (the state we are in >90% of the time) is quite low.  At rest, most adults oxidize less than 20-25 grams of glucose (about 60-90 kcal/hour of glucose).  In fact, even during exercise, it is difficult for the mitochondria to oxidize more than 1 gram of glucose per minute.  In other words, while this “sink” for glucose is a high priority, it is very limited in size and rate.  Most of the time we consume carbohydrates (i.e., glucose precursor) we are supplying much more than we can oxidize at that moment in time.
  • Conversion of glucose into glycogen is limited to how much “room” is left in the glycogen tank.  Even the most highly trained athlete can only store a finite amount of glucose in the form of liver and muscle glycogen: approximately 400 kcal (120 gm of glucose) in the liver and approximately 1200 kcal (~400 gm of glucose) in the sum of all skeletal muscles, assuming one is starting from a completely depleted reservoir (a profoundly rare physiologic state).  The body does not have the potential to store excess glucose, beyond this amount, in a form that is recoverable as glucose.  Any excess glucose that is not immediately metabolized, or converted to glycogen, is turned (irreversibly) into fatty acid for storage.  At about 47:00 min into the video, Dr. Lustig talks about the fact that glycogen is non-toxic (true) and that regardless of how much the liver stores, it doesn’t cause hepatocellular damage, unlike fructose (true).  The problem is, he fails to mention the storage capacity issue.  When the liver stops storing glycogen, which it does at about 120 grams, it does convert the excess to fat.
  • While the most highly-trained, insulin sensitive individual might be able to replace glycogen (assuming liver and/or muscle have capacity) when they ingest carbohydrate, rather than store fat, an insulin resistant individual is less able to import glucose into muscle to form glycogen.  Furthermore, when insulin levels are elevated, fat lipolysis is inhibited, and obviously this problem is confounded in the insulin resistant individual.

Even in the absence of fructose, a diet high in glucose, beyond everything I’ve stated above, still stimulates insulin release from the pancreas.  Elevated levels of insulin “turn off” our ability to burn fat and increase our capacity to store fat (see figure below – you’re probably getting used to seeing this figure by now).

 

Insulin levels versus fat breakdown

Clearly fructose is a significant culprit in obesity and metabolic syndrome.  I’ve personally seen many patients with fatty liver (usually a tell-tale sign of alcoholic liver disease), who rarely consumed alcohol, but consumed high amounts of sugar.  At the time (i.e., when I was operating on them), I couldn’t make sense of this observation.  Now I can.

The impact of chronic sugar exposure is probably more significant than that of tobacco.  I’m actually not being hyperbolic. However, eliminating fructose alone will not cure metabolic syndrome and its associated pathology.  It will go a long way, but not all the way, at least not in all people.  We simply eat too much glucose in our current carbivore lifestyle.

Scientists have done studies showing that if one removes all fructose (e.g., all sucrose, high-fructose corn syrup, and fruit) from subjects’ diets, they tolerate glucose better, PROVIDED glucose intake is limited, in keeping with the constraints I outlined above.  If, however, in the presence of fructose restriction, we consume massive amounts of glucose, we will still convert glucose into fat and, as importantly, through elevated insulin levels, switch off our ability to oxidize our fat stores.

To quote Dr. Lustig from this talk, “it’s a numbers game.”  We consume far too much glucose to simply fill our glycogen tanks.  Invariably, we keep them topped off, and continue to pour the extra glucose into fat, all the while we force our bodies to survive in a high insulin environment.

 

Photo by Sylvanus Urban on Unsplash

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141 Comments

  1. Is there anyway to make a printer friendly version & button? This ends up being 30 pages with all of the side text and images 🙂
    thanks (student)

  2. Hey, Peter. I was doing some digging lately, and I discovered an article stating that when ketosis leads to increased production of acetone, some of this acetone is converted into methylglyoxal by the CYP2E1 enzyme. I’ve read scattered reports that methylglyoxal is only increased about 1.5 times by ketosis. I have also read it is upwards 40,000 times more potent an than sugar in produce AGE’s. I’m still intending to experiment with ketosis, but what are your thoughts on this matter?

  3. Hi Peter, I was just wondering if there are any known mechanisms by which people like your wife, who don’t seem to be affected by excess glucose or carbs in general, deal with (or use, excrete, convert, etc.) what would be dangerous levels of sugar for many if not most people?

    Thanks for the blog and keep up the good work!

  4. Hey Peter,

    At the 44 minute mark Dr. Lustig says that fructose doesn’t cause a spike in insulin and therefore, leptin doesn’t go up and your brain doesn’t see that you ate something so you eat more.

    How does this work on a keto diet? Since we don’t get an insulin spike on keto and therefore, leptin doesn’t go up wouldn’t the same above logic apply to a keto diet and you would want to keep eating more due to low leptin hormone?

    Thanks… I love your blog! This is coming from a fellow Mechanical Engineer with a keen nutritional interest.

    • this was essentially my question too, but much more concise

      would like to add, just over a year ago, I completed a certificate 3 in engineering studies as part of year 12…………yesterday I couldn’t even spell engineer, now I is one!

  5. Hi Peter, I’m loving this site – some great information. Five days ago I embarked on a nutritional ketosis experiment. I did so because I have some cortisol/hpa axis issues that I think are exacerbated by blood sugar swings.

    Since going low carb (<60/day) I have been tracking my blood glucose and have been quite shocked. After eating a very high fat meal with low protein and low carb my blood glucose has been getting up to 140. Might these blood glucose fluctuations lessen over time or are they an indication that low carb dieting is causing unwanted stress on my body? If my blood sugars are indeed this high is there any chance my body will ever go into ketosis?

    Much appreciated and keep up the useful posts!
    Josh

  6. Peter, thanks so much for your amazing work. I have been trying to adopt the principles you set forth while following a vegan (plus plain full-fat greek yoghurt for bfast) diet. However, dinner has been exceptionally hard. It would seem for a vegan Lustig would advise whole fruit, no sugar added, and only whole grains, and all is fine. However, per above your advice appears to restrict sugar/carbohydrate beyond that. What would your advice be for a vegan who is also trying to follow your advice as closely as possible? (I have been eating essentially tofu and/or hummus every night and this seems too restrictive). Thanks!

    • Brian, in my clinical experience a well put together vegan diet can work for someone who is not terribly carb sensitive. I did it for 3 months with no success before adopting CHO-restriction. I suspect, due to my hyperinsulinemia, it was not right. That’s not to say it can’t work for someone who is a bit more insulin sensitive.

  7. Hi Dr Attai,

    I watched your video about that women you treated who was diabetic with the bad foot. Very humbling indead!
    There are so much do’s and dont’s regarding what a Diabetic should or shold not eat… I was diagnosed with Type 2 Diabetes Sept 2014. In hospital I lay beside a women whoh had Type 2 Diabetes for many many years. Long story short she was massivley obese and advised me to NEVER take insulin because it had made her so overweight! They tried Glucophage and other metmorfin meds on me but it made me very ill and my liver was in constent pain. Eventually they put me on Humalin Insulin But only after a week I was had this hunger like never before .. even wheny tummy was full I wanted more food! I coulnt satisfy my hunger! I stopped the insulin immedately and was put on Victoza! This only brought my conunt down by 3 and not much more. I am cold turkey at the moment, have been for almost a year. No meds. My count ranges between 15 and 24 … Medication for Diabetes is extremley expensive in South Africa and I refuse to go to our Government Hospitals, they are just terrible places. If you dont have private med aid in this country? You’re in trouble… I have yet to discover the miracle cure for Diabetes. Hopefully your studies that you spoke of will bring us the cure or the prevention … Diabetes is an awful illness and I can tell you from personal experience that those that do not have it could not possibly understand how awful you feel most ofthe time, weak, tired and in pain (liver). I have lost 24 kgs in the last year mostly due to the thirst I constantly have, I go through litres of water everyday. I refuse to use anything Metformin because it hurts my liver crazy, insulin is like taking poison. So I wait B-) and hope that something of a cure and affordable will become available to all diabetic people out there.

  8. Hi Peter!

    First off I wanted to say I love your site but what I love most about it is your refusal to frame things in an overly reductionistic manner. I take a similar approach to epistemology in general so I really appreciate it.

    A few questions though. If this is true:

    “Any excess glucose that is not immediately metabolized, or converted to glycogen, is turned (irreversibly) into fatty acid for storage”

    Why does everybody keep insisting that DNL is such a rare metabolic pathway? Do the “extra” carbs actually convert to FFA and then store themselves so it isn’t really direct DNL?

    Also, the literature seems to suggest to me, that due to their place on the oxidative hierarchy, carbs seem to desperately try to metabolize themselves as you increase your rate of ingestion. What’s happening there? Increase in BMR, increased thermic effect (which I understand to be lower for carbs – which doesn’t explain why I’m running so hot now that I’m low carb!), a mixture of both, or something else entirely?

    Thanks!

    • Depends who you ask and in which state. In a hypocaloric state, very little CHO is converted via DNL. It also depends on the metabolic state of the patient. Super complicated topic, to be sure.
      Lastly, there is still confusion in the literature about the differences between hepatic DNL and peripheral (i.e., in the adipose tissue) DNL.

  9. Also wanted to add I’ve never had anything but sugar cravings in my adult life (surely caused by wildly fluctuating blood sugar) until recently adopting high fat/low carb principles.

    Suddenly I’ve started having vegetable cravings and – most strangely because I’ve always hated it – fish cravings. I remember reading that lots of vegans experience these intensely (and I’m no vegan!). I just read that too much omega six might cause omega 3 deficit. Do you think it’s possible that the starting high fat and eating so much nuts now has throw off my ratio like a vegan eating lots of nuts? That my body is trying to ingest more omega 3?

    Cheers!

  10. Hi Peter,
    Sincere thanks for everything you are doing! – including this site, and NUSI.org.
    On the 2 items below, I haven’t used these methods but have been in
    related conversations and haven’t had enough information to respond.
    I would appreciate hearing your thoughts on these.
    1) Net Carbs. The common practice of subtracting Dietary Fiber &
    Sugar alcohol from Total Carbohydrates .
    2) Using a fiber supplement like Metamucil in an effort to make a
    food more acceptable (from a Net Carbs standpoint).

    And a couple questions:
    Do you consider MCT Oil a good supplement for general use, or is that
    more related to athletic recovery ?
    Any preferred time for taking supplements (morning/night, with/without food) ?

    thanks a bunch,
    Allen

  11. Peter,

    I greatly appreciate the time you dedicate to sharing your knowledge, and look forward to reading more here, and of NUSI outcomes.

    When I exercise rigorously (day 0) I wake up 4 hours into my sleep during the following 1-3 nights and cannot get back to sleep. I recently read that waking up like this may be attributed to glycogen depletion, for which the suggested solution was to consume 1 teaspoon of honey before bed. Because honey has much more fructose than glucose at this quantity, I experimented with 1 teaspoon of maple syrup. This appears to have mitigated the “insomnia” symptoms.

    A) Can glycogen depletion result in “insomnia”?
    B) If so, and if this were you, how would you approach keeping your glycogen stores “topped off”?

    I’ve been eating LCHF for the last year, and paleo the prior 3 years. I currently eat breakfast and dinner Monday through Friday, and eat a “social” light lunch on weekends.

    Thank you,
    Nick

    Dosage: 1 teaspoon (source: nutritiondata.self.com)
    Honey: Sucrose: 62 mg / Fructose: 2865 mg / Glucose: 2502 mg / Maltose: 100 mg / Galactose: 217 mg
    Maple Syrup: Sucrose: 3752 mg / Fructose: 58 mg / Glucose: 158 mg / Maltose: 0 mg / Galactose: 0 mg
    Agave Nectar: Sucrose: 82 mg / Fructose: 196 mg / Glucose: 238 mg / Maltose: 0 mg / Galactose: 0 mg

    • Nick, I’m not sure about glycogen depletion causing insomnia. Also, need to be clear what you mean by “depletion.” Even someone in strict NK probably maintains 50% of their glycogen.

  12. Hey Peter,

    Great post, as usual, and I have seen Rob Lustig’s lecture on fructose. I decided to revisit it today, and one of the bad things he points out is there’s no insulin response from fructose, therefore no leptin response, therefore, no satiety.
    This kind of makes me think insulin secretion is involved, or even required, for leptin secretion.
    I recall from your appearance on Ben Greenfield’s podcast (so awesome to find that and hear it!!!! my 2 biggest idols, in 1 episode!!!!!!!!), that there’s very little scientific evidence of leptin resistance occurring in chronic low carb diets.
    I realise there may be some silliness in that comment, as there’s not much evidence on anything for anyone doing a low carb diet in the long term (as far as I know), but I’d like to know, given your answer to Ben’s question on leptin resistance, which people seem to imply that a low carb diet (lack of insulin) leads to, how would you explain or even counter what Rob has said?

  13. Hi Peter,

    Like most people I really appreciate your rigor, and your willingness to take the time to explain in common sense terms your ideas for those of us who aren’t as well educated in science and medicine.

    This is probably a dumb question, but I’m from Maine and I was wondering if you had come across any evidence that some sugars, in my case maple syrup, are easier to process and digest than refined sugars? Kind of an equivalent of brown rice vs. white? I don’t actually crave sugar much at all but once in a while I do like to eat a pancake or glaze a pork chop etc.

    Thanks for your time!

  14. Thank you for your comments Peter. I love your passion on the subject and your logical explanation.
    Though I loved dr Lustig lecturers ( a great speaker), but I too worried why he just looked at the bigger ” stick” from carbohydrides only. Even purely yasic chemistry has it: sugars are group of chemicals caled carbohydrides with more or less complex molecules that undergo the same common reactions when broken down to a single unit. Biolgy doesn’t stray from that as much too – it follows the chemistry.
    Unfortunatelly, that what often is the problem in mass informing people. Something along the line is missing and thus people jump to a wrong conclusion.
    Reading your articles there is hope that there are people who know how to seperate the kernel from the husk.
    Good luck to you
    Viesh

  15. Thank you for your comments, Peter. I love your passion on the subject and your logical explanation.
    Though I loved dr Lustig lecturers ( a great speaker), which I watched much before I found your site. I remember thinking, why he just only looked at the bigger ” stick” from all carbohydrides. Even pure basic chemistry has it: sugars are the group of chemicals called carbohydrides with more or less complex molecules that undergo the same common reactions when broken down to a single unit.
    Unfortunately, that is often the problem in mass informing people and particularly when is highly specialised. Rather than looking at the whole picture, we end up with half truth, as something along the line missing. So, there is no surprise that people jump to a wrong conclusion.
    Reading your articles there is a hope that there are people who know how to separate the kernel from the husk.

    Just for curiosity, I wonder, Peter, if you would like to comment on the information I read from a non-English literature. The doctor, Jan Kwasniewski who advocates and treats people with high fat, low carbs, normal level proteins for 30 years with positive results. Of course, he has many oponents too. partly to a way he expresses himself and it’s hard for some people to get their heads around all the confusing advice that is available, including the medical.
    He said, in his for a lay person explanation, that: ” Using low carbs, but high-fat diet (an optimal diet as he calls it) is possible to treat people of the type I diabetes if its duration is still short in 5 to 21 days, to 100 percent treatable. So, I guess ( but only) because there may be still some small amount of insulin produced? Then he goes on saying that diabetics with type I and II, lasting longer, can be improved up to 90 percent and is treatable in 21 to 90 days.. I assume it would a lot of variables here depending on individual cases and with careful monitoring the situation at the beginning.
    Good luck to you
    Viesh

  16. Ah! What a timely post. I’ve been reading about sugar in the last few weeks. Thanks for sharing this great info. Page bookmarked.

  17. To make sure no one misses it, I would suggest moving the “Last editorial point on this” to appear immediately following “most evidence today would tell us that elevated LDL-C does not lead to heart disease and stroke.”

  18. “This [LDL-P, or as the post has it oxidized LDL-P] is not measured or reasonably predicted by LDL-C.” I believe you (Peter) would recognize today that this is an overstatement: LDL-C is a quite adequate proxy for LDL-P in 75% of the population, and it’s still modestly correlated even in discordant people. Additionally, it’s not hard to predict those who will be discordant in a way that is most important: people with metabolic syndrome or type-2 diabetes, whose LDL-C may be close to normal despite having high levels of LDL-P, thus putting them at elevated risk (beyond what other aspects of metabolic syndrome will already show).

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