My comments in answer to Jonny Bowden’s Huffington Post take on the sugar tax where he suggested that despite it’s flaws, “it’s all we’ve got.” I insisted that It’s not all we’ve got. We have the science and, in one afternoon, Bloomberg could convene a panel of scientists to evaluate presentations by all the players including me who believe that sugar is a smokescreen for not facing the importance of total carbohydrate restriction which you [Jonny Bowden], among others, have explained. Everybody should be heard. What I see is another rush to judgement like the low fat fiasco which we still have with us.
That you “have to do something” comes right out of Senator McGovern’s mouth as in Fat Head. And “deadly white substance that literally creates hormonal havoc and appetite dysregulation … promoting metabolic syndrome, diabetes, obesity and heart disease” is way outside of the bounds of science. I am not the only one to point out that Lustig’s population study represented the return of Ancel Keys.
We go with science or we don’t.
One has to point to the rather remarkable disconnect between a near absolute refusal to accept the therapeutic value in reducing carbohydrate across the board and the rush to judgement on the proposed need to reduce specifically fructose. Low-carbohydrate diets have demonstrated their therapeutic value, in numerous studies. They have met every challenge from nutritionists and continue to outperform other diets for as long as comparisons are made. Nonetheless, they are generally ignored by government and private agencies. In distinction, there appears to be a rush to restrict availability of sugar — if necessary by coercive government means — without any substantial prospective study showing benefits. It is hard to think of any experimental study at all that has shown the benefits of reducing fructose alone that meets the results found for total carbohydrate reduction and replacement by fat, although there may be some.
Which study would you point to where only removing sugar has improved things? Which trial was long enough and sufficiently well controlled to rush to judgement? Which RCT met high standards?
Richard David Feinman 
Here’s the thing. Nobody wants to be accused of fiddling while Rome burns, so it seems always a better plan to do SOMETHING than to understand a situation that may require doing nothing first. And, yes, I would like to hear your opinion.
I am writing a review for the scientific literature. As soon as that’s done, I will write a summary.
Thanks again for sharing your perspective!
I hope you wrote this in the comments section of the article itself. I have posted a link to here in the comments. We’ll see if they take it. I agree with you 100%.
I did post it there but they may have rejected it.
I agree that we need more high-quality controlled studies when it comes to sugar and health. The data that does exist certainly suggests that excess sugar is problematic. I personally suspect that adding sugar to grain-based high glycemic carbohydrates and omega 6 fatty acids–typical junk food, it the source of our dietary woes.
Sugar is a carbohydrate. Occam’s Razor dictates that you have to exclude the extent to which fructose is acting as a carbohydrate or has some unique properties. Right?
McGovern’s comment – and Exceptionally Brash’s – are perfect exmples of the Politician’s Syllogism:
‘We must do something’
‘This is something’
‘Therefore we must do it’
And we all know where this has got us. Sad to see Lustig falling into the same, un-scientific trap.
I am reading Richard Johnson’s book “The Fat Switch” for the second time. He does make the case that fructose does have distinct properties by increasing uric acid levels which tip the balance towards fat storage on a cellular level. It’s an interesting theory but at this point in time it’s still just a theory. Have you read the book?
I haven’t read it and I am not sure that fructose reliably raises uric acid. And I don’t know what the connection to fat storage is but I am looking into that.
Richard:
Rick Johns has done a number of studies that show a connection between fructose intake and elevated uric acid:
Click to access Week4_DIABETES%20PARADIGM%20Excessive%20fructose%20intake%20induces%20the%20features%20of%20metabolic%20syndrome%20in%20healthy%20adult%20men.pdf
http://ajpcell.physiology.org/content/293/2/C584.full
http://ajprenal.physiology.org/content/290/3/F625.full
http://www.nature.com/nrneph/journal/v1/n2/full/ncpneph0019.html
Dr. Johnson is more or less married to fructose/uric acid so perhaps he is blind to the other factors that feed this pathology. Omega 6 fatty acids and carbohydrate load top my list of suspicious characters.
Thanks for these, I may know some of them. The first question is mechanism and I am not sure about the depletion of ATP theory but we’ll see.
Richard:
Rick will be in Boston this week to give Grand Rounds at BU. If you have any questions for him, let me know.
K.
Cola and apple juice each have 3g of sugar per oz. So, why is cola bad and apple juice good if it’s the sugar we’re trying to avoid.
Mr. Bowden appears to support the government intervening when it comes to sugar in our diet, yet says nothing about getting government out of the production of sugar/HFCS. Myopic
Cheers
You’ll have to ask Hizzona’ on that one.
I would be nice to get our government out of subsidizing all farm products. The sugar growers just got handed a big chunk of cash:
http://online.wsj.com/article/SB10001424127887324096404578356740206766164.html
Still, that’s separate from the role of sugar in metabolism, in nutrition or in public health.
Johnny Bowden in his other writing is 100% advocating for the effectiveness of carbohydrate restriction. Perhaps he sees sugar in soda as (pardon the pun) the low-hanging fruit – the concentrated, micronutrient free form of carbohydrate, with no fat or fibre to slow its absorption. On his past record I don’t think that it’s his intention to be giving starch any alibis.
This would be the smart move for Bloomberg; to say I know it’s really the carbs, and soda is the most worthless carbohydrate “food” I can think of, so it’s gonna be the first to go.
Anyway, for the defense, this interesting study “Dietary Fructose Intake and Severity of Liver Disease in Hepatitis C Virus-infected Patients”
http://www.ncbi.nlm.nih.gov/pubmed/23426443?dopt=Abstract
In this vulnerable population there was no link between fructose consumption and hepatic fibrosis.
However the variation wasn’t that great (30-80g) – I’d like to know about the extremes, including the people who avoided fructose – and of course total carbohydrate wasn’t considered.
Also, fibrosis not steatosis was the result looked for.
however this next study did pick up a correlation between PUFA consumption and steatosis in a similar population (but not SFA or MUFA) and linked higher carb and lipid intakes to fibrosis.
http://www.medscape.com/viewarticle/585010
Table 5 shows that (besides alcohol) PUFA is the strongest correlation with steatosis and carbohydrate the strongest correlation for fibrosis (staging), with calories and lipids having some input but trailing well behind.
This should be a ‘canary in the coalmine’ population for the idea that fructose specifically causes liver disease, and these (admittedly crude) studies, taken together, aren’t confirming it, but instead seem to be fingering linoleate and total carbohydrate.
Sugar gets a lot of attention these days. But excessive PUFA may be the greater health hazard because it erodes health no matter how wholesome the remainder of the diet may be. I learned that the hard way. Google – the Omega-6 hazard.
As you know, I think we need really neutral scientific panels to hear all sides. It’s not good for us to all learn the hard way.
David:
I think you are onto something. Barry Sears has been beating this drum for decades and he lives just a few miles from me. I agree that we need to look at the fatty acid content of our modern diet–it sucks!
Here’s another study of similar design (but all 3 so far are not sufficiently consistent in what they’re isolating to convincingly – as opposed to suggestively – support each other): http://www.ncbi.nlm.nih.gov/pubmed/21188525
Dietary history and physical activity and risk of advanced liver disease in veterans with chronic hepatitis C infection.
In this one, “upper normal” carbohydrate consumption is associated with steatosis, and (drum roll) higher sweet consumption is associated with a lower degree of fibrosis.
I can think of a plausible explanation – this was a hard-drinking population sample. Alcoholics in recovery often replace alcohol with sugar, so higher sweet consumption might be a marker for abstinence (alternately, it might mark the absence of diabetes that people report higher sweet intake, but I do prefer the first explanation). If so, it suggests that fructose may not be the same as alcohol after all (Duh).
As I said, this is a vulnerable group where we would expect to see hepatotoxic effects of sugar magnified. Instead we see effects of alcohol (natch), carbohydrate, and PUFA (which will tend to be omega 6).
Generally this evidence supports the recommendations William L. Wilson has given here, rather than those of Lustig. It is always possible that fructose becomes synergistic with PUFA and carbohydrate at some point, but it doesn’t look like an important driver of hepatotoxicity, which is an outcome that Lustig bases part of his argument on.
A better reason to restrict, or at least not encourage, sugar would be because of its role as a “gateway carb” if sugar use tends to increase carbohydrate intake, and its role in promoting snacking or round-the-clock feeding. If these effects can in fact be demonstrated.
The problem will remain if we go after sugar or even carbs. Before we condemn sugar and carbs, we have to liberate fat, especially saturated fat. To wit, “everybody knows fat makes you fat, saturated fat causes heart disease, etc”. Every new study – even Fine’s insulin/cancer study – shows fat has been wrongly accused and condemned. It’s time for a new McGovern committee to finally give a full pardon to fat and saturated fat. That’s where it all started. It’s the first link in the chain, and it’s as strong as it ever was. Doesn’t matter what we do if this link is still there. Cut the carbs? Sure, but what about the fat? Cut the sugar? Sure, but what about the saturated fat? We even believe that fat – even if it’s good – somehow suddenly turns bad when we add sugar.
Set the record straight about fat first, the rest will follow. I mean, we did set the record wrong about fat first, and the rest did follow.
Thou hast said it.
I agree that fat has been lost in the shuffle. There simply is no good evidence that saturated fat is bad for you when incorporated into an otherwise healthy diet. I’m a big fan of using coconut oil for cooking. Get rid of the trans fats, cut down on the omega 6 fatty acids and increase saturated fats and omega 3 fatty acids. While you’re at it, I would also eliminate sugar and most grain-based carbohydrates.
But you and I don’t get to decide. Many people do fine with sugar and grain-based carbohydrates (I’m not one of them) and it is, in fact, up to the government to provide, at least, guidance but that requires scientific analysis. Sugar should be controlled if it were a toxin but there is no way that that description fits. What’s the LD50 for fructose? Where are the emergency room admissions?
Richard:
If sugar is a toxin, it is a chronic toxin like cigarette smoking. John Wayne smoked for decades and still rode off into the sunset with his horse and a beautiful woman at his side–that is until the wheels fell off.
Chronic toxins don’t kill you today or tomorrow–it takes decades. That’s why it’s so difficult to study. Nobody funds studies for decades. I don’t know about you, but I’m not taking any chances. I don’t consume sugar. I do consume some fructose when it comes in the form of my wife’s homemade baklava (in the form of honey). To do anything else certainly would not be wise!
If.
Quote from Robert Lustig
“The play I’m making is not sugar per se, the play I’m making is insulin,” he says. Foodstuffs that raise insulin levels in the body too high are the problem. He blames insulin for 75% to 80% of all obesity. Insulin is the hormone, he says, which causes energy to be stored in fat cells. Sugar energy is the most egregious of those, but there are three other categories: trans fats (which are on the way out), alcohol (which children do not drink) and dietary amino acids.”
Ok I see this pop up now and again
That Fructose is actually good for diabetics
http://articles.timesofindia.indiatimes.com/2013-01-01/diet/32367661_1_fructose-simple-sugar-sievenpiper
My question is on a low carb diet .. less than 50 grams or in some cases 20 grams of carbs.
Could fructose not only be a non issue . But could it in fact be an esp beneficial form of carbs.
interview with the researcher here
http://evolvinghealthscience.blogspot.com.au/2012/05/fate-of-fructose-interview-with-dr-john.html
“The study you’re quoting, or the meta-analysis we did, was looking at so-called small or catalytic doses of fructose at a level that would be obtainable from fruit (so, basically, less than 10g per meal). We took that to mean 36g per day (meaning 10g per meal and two snacks with 3g each; like 30 percent of a meal). That’s how we came up with eligibility criteria for that meta-analysis. That was just a snapshot that looked at low doses of fructose.
We saw this benefit for hemoglobin A1c (HbA(1c)) — almost a 0.5 percent reduction. That’s a 0.5 percent absolute reduction (not a proportion) similar to what you would see with antidiabetic agents at the lower range of efficacy. And, we saw that without adverse effects on triglycerides, body weight, insulin, and uric acid. So, we concluded that there was an overall a net metabolic benefit from these low doses of fructose at a level really that is obtainable from fruit.
That correlated quite nicely with what we saw in a very large glycemic index trial we published in patients with type 2 diabetes. What was the most important low-glycemic index food item that best predicted reduction of HbA(1c)? It was low-glycemic index fruit. The level of fructose that you would’ve obtained with the most commonly consumed low-glycemic index fruit (apples, it turns out) would be 10g per serving. So it fit nicely with this idea of this catalytic dose of about 10g per meal. And in that study we saw an identical 0.5 percent reduction of HbA(1c) units. So, further confirming that there may be something to fruit.”
The name of the game is cognitive dissonance and self-delusion. The default diet for the treatment of type 2 diabetes and as adjunct to type 1 diabetes treatment and for metabolic syndrome is carbohydrate restriction. Removing starch is probably better than removing sugar. “Default” means that if it doesn’t work you can try something else but it’s what you do first. Neither of these guys can face it leading them to say foolish things (Lustig) and duck the issue (Sievenpiper). I don’t know what their motivation is and maybe neither do they.
When looking very carefully at the science, some will argue that it is seed oil (or PUFAs to be more precise) that drives “total carbohydrate”:
http://high-fat-nutrition.blogspot.com/2012/11/protons-physiological-insulin-resistance.html
PS: I will not get tire to point out that the consumption of seed oil (rich in linoleic acid) results in the production of series-2 prostaglandins, which some people consider “bad” (or rather “more inflammatory”, to use the precise medical term).
http://en.wikipedia.org/wiki/File:EFA_to_Eicosanoids.svg
PPS: I would argue that “total carbohydrate” looks like a smokescreen as well, and not the root cause of our problems.
And just for good measure I throw in Bill Lands. He does not know much about carbohydrates or how to write a best selling book (or even how to make a good presentation), but he knows his lipids.
I thought Bill Lands’s presentations are good but incorporating any science into nutrition seems strangely difficult.
Very interesting paper and while it is hard to see how PUFAs drive total carbohydrates, it is certainly part of the mix. Total carbohydrate is not a smokescreen in that if you remove it and replace it with fat you improve obesity, glycemic control and have a cure for many people with type 2 diabetes; how much of the effect is due to the fat that you add is not known but the experiments are clear on replacing carbohydrate with fat although less well studied, you get benefit from replacing carbohydrate with protein.
And one more thing about carbs: We don’t consume “carbohydrates”, we consume food with ingredients that contain carbohydrates. I would argue that some of those sources of carbs are more problematic than others, with wheat probably the worst.
So I doubt it is “carbs” per se (or even the amount of carbs) that is a problem. I would argue that some foods contain substances that interfere with carbohydrate metabolism, with PUFA over-consumption through seed oil being possibly the most prominent. If you never eat those foods that interfere with carbo metabolism, you eat a diet rich in carbs and stay health (cf. The Kitavans). Once your carb metabolism is broken, this looks different however.
Only shortly: Another food that is can create health problems is dairy from pasteurized milk. But for this, we’ll have to wait until the science comes in. You write:
“Many people do fine with sugar and grain-based carbohydrates (I’m not one of them)”
The same holds true for dairy.
(Plus I doubt that those how do “fine” with grains or dairy, will do fine in the long run.)
I suggested in my post on Occam’s razor that if you describe Y as the outcome of an experiment and Y “can be expressed with a rough sort of equation: Y = A + B + C +… and if A explains Y, then you don’t want to drag in B, C, etc unless you absolutely have to.” We know that if we take out carbohydrate things get better. All this may have to be modified by type of carbohydrate, type of oil, amount of dairy or whatever but right now we only have Y = A.
Dr. Feinman,
In you article you state “creates hormonal havoc ” you are aware of course that havoc can neither be
created nor destroyed. Havoc can only be wreaked, (conservation of havoc)
Gary Rees
It was a quotation from the article which I described as “way outside of the bounds of science.”
However,
Merriam Webster is Ok with ‘create havoc”
and the FreeDictionaysays that one definition of wreak is “To bring about; cause: wreak havoc.”
It’s from Middle English wreken, which was probably pronounced “frickin'”
Thank you — the emperor has no clothes. I just finished Fat Chance — you’d think with such a reputation riding ahead of him, he could have used his soapbox for something beyond pretty much confirming the status quo. I saw very little new and useful at all.
Reputation and soapbox are an iffy combination.
Dr. Feinman ~ I almost created havoc on my laptop reading Gary Rees’ issue with havoc. 😉
My mother would have agreed with you about the havoc her 5 daughters created in the house & would yell at us for “wrecking the house” (not pronounced “frickin”). Havoc – as a noun meaning “devastation” – could obviously be created, caused or wreaked by God, nature or kids – to which most mothers could testify. I simply can’t resist quoting that great creator of English prose:
“Caesar’s spirit, ranging for revenge,
With Ate by his side, come hot from hell,
Shall in these confines, with a monarch’s voice,
Cry “Havoc!” and let slip the dogs of war.”
~ Shakespeare
I know the quotation but, after much pondering, I can’t figure out what the message refers to.
“Lab Rat” Update: Awaiting confirmation of lab tests. Internist (diabetes specialist) was very surprised by 20 lb. lost in just 2 months, and impressed by documentation of Mediterranean-Low Carb Combo Meals, which will be maintained for the next 6 months. Only variable in next 3 mo. (June-Aug) is increased exercise levels. Dr. agreed to ‘NO MEDS’ as the only variable Sept-Nov. Final lab test will be in Dec. Discovered the ‘Joy of Cooking’ as an unintended consequence!
Daily carbohydrate intake went from 180+ g/day before to average daily intake in 8 weeks:
Carbs Fat
64 47
51 51
44 61
39 57
49 54 = 4 week average daily Carb & Fat grams
44 61
86 74
39 46
45 64
54 61 = 4 week average daily Carb & Fat grams
Dr. Feinman ~ I can’t thank you enough – my body thanks you, too!! Hugs ~ Moms aka Eve
PS: Carbs are total gms – not net of fiber. I don’t eat grains and very limited legumes (hummus) and fruit (limited to 5 gms carbs for 1/4 C grapefruit slices/fruit). Bulk of carbs come from low-carb vegetables with high fiber. I estimate that Net Carbs = 1/2 to 2/3 of total Carbs.
Congratulations. You are the Queen of Lab Rats (and you even keep your own lab notebook). Hang in the there.
RDF
Lab Report: Dr. wrote “WOW! Great” on Lab Report, which tells you something. In 2 months, LDL dropped from 119 to 81 & HDL went from 48 up to 52 (ratio now 1.6). Hemoglobin A1c declined from 7.1 to 6.2 (next goal = 5.6).
Triglyceride only dropped slightly (157 to 151). I need advice on how to get that down to <150.
In addition to maintaining food intake records, I'm recording daily exercise & strength training, plus weekly BMI measurements now for next 3 mo. My personal trainer is an ex-Navy SEAL (SWCC Team), who uses similar interval techniques adjusted for my age/gender/condition. There will be NO SLACKING OFF! ;~)
Sounds like you’re doing great and you have the perfect set-up. (Aversive stimulation is frequently what it takes). I don’t jog now but I used to run with my wife in Prospect Park (site of the Battle of Brooklyn in the American Revolution). She would keep telling me “The British are coming.”
“Aversive stimulation”~ LOL! Good term for avoiding daily injections or losing toes, but you probably meant my personal trainer so I’m going to call him my “Aversive Stimulator” from now on. ;~})
My own trainer is Fred Hahn and although I think highly of Slow Burn http://www.seriousstrength.com/site/ and its benefits for me, Fred has avoided stating his position on torture.