A couple of weeks ago I wrote a post showing how the press fails to mention low-carb diets in weight loss stories, focusing instead on exercise or some other facet of an individual’s quest to lose weight and improve health. Today we’ll look at how the press, in an effort to minimize the untoward effects of carbohydrates on health, sometimes simply misrepresents the true outcome of studies.

A week or so ago a Swedish overfeeding study was released looking at the short term effects on the liver of a diet high in fast food. ABC News reported the study. Let’s first look at what the study was all about and what the data showed, then we’ll see how ABC reported it. By looking carefully at what ABC did to misrepresent the study, we can arm ourselves with the knowledge to identify this kind of press bias in future reporting.

First the study.

The goal of this study was to examine the effect of fast-food hyperalimentation (overeating) on liver enzymes and fat accumulation in liver cells. The specific liver enzyme in question was alanine aminotransferase (ALT), one of the liver enzymes routinely measured on standardize lab panels. Over the past couple of decades the prevalence of elevated ALT in routine labs has about doubled. Elevations of ALT are associated with an increased incidence of metabolic syndrome and all its attendant features, including non-alcoholic fatty liver disease. The Swedish researchers wanted to see if force feeding young, healthy subjects a diet high in fast food over a four week period would increase blood levels of ALT and increase the fatty infiltration of their livers.

Eighteen healthy subjects (12 males, 6 females) with an average age of 26 years were to try to increase their body weight by 5-15 percent in 28 days by adding two large fast-food meals daily in an effort to double their normal caloric intake. Researchers matched a similar control group for comparison.

The subjects took to their assignment with a vengeance. The average intake soared from 2273 kcal/day to 5753 kcal/day, a 153 percent increase! This caloric increase was driven primarily from an increase in fat, the consumption of which skyrocketed from 87 g/day to 261 grams per day (200% increase). Carbohydrate intake increased from about 275 g/day to 644 g/day (134% increase). And protein went up from 89 g/day to 180 g/day (102% increase). Sugar intake increased by 200%.

As a percentage of total calories fat rose from 36% to 43%. Carbs decreased from 48% to 45%. Protein also decreased from 16% to 12% of total caloric intake. So although the actual gram amounts of protein and carb went up as the subjects gorged on fast foods, their fractional percentage of the total calories went down.

What happened?

Over the four weeks subjects on the high-fast-food diet increased their weight by 9.5 percent, their serum ALT levels by 334 percent, and the content of fat in their livers by 155 percent. The control group showed no changes.

When the researchers ran the standard statistical analysis to determine which – if any – of the specific macronutrients correlated most directly with the increase in ALT, they discovered that

the average consumption of fat or proteins during the 3 days at the end of the first or third week weeks was unrelated to changes in ALT. [Blood was drawn in the non-fasting state at the end of the first and third weeks to more accurately monitor ALT levels.] However, the maximal ALT/baseline ratio correlated with carbohydrate intake during the third week.

One could, I suppose, argue with the standard statistical analysis program the researchers used to determine this correlation, but the fact remains that the researchers did report in the study as quoted above that the increase in carbohydrate intake was the driving force behind the elevation in ALT, not the increase in either protein or fat. You might imagine that those reporting the study would mention this finding.

Before we get to the biased article by ABC, let’s take a look at a more balanced piece of reporting by Yahoo! News [The Yahoo! News link was no longer active; the link above is the same article reprinted in the The Sydney Morning Herald]. Marlow Hood, the Yahoo reporter, not only read the study but took the time to track down the author and interview him as to his findings. (As most of you who are long-time readers of this blog should know, I’m always leery of study authors’ interviews with the press because the conclusions these authors often report haven’t been run through the tempering of the peer-review process and in many cases don’t jibe with what the actual study shows. In this case, however, it did.)

Said Frederik Nystrom, the lead researcher

signs of liver damage were linked to carbohydrates was another key finding…
It was not the fat in the hamburgers, it was rather the sugar in the coke…

Dr. Nystrom also pointed out another surprising finding (surprising only to those, I suppose, who don’t understand lipid biology) that wasn’t included in this study but will be published in a future paper.

We found that healthy HDL cholesterol actually increased over the four-week period — this was very counter-intuitive.
The study showed that the increase in saturated fat correlated with the increase in healthy cholesterol.

Apparently Dr. Nystrom isn’t aware that HDL-cholesterol levels are fat dependent. In other words, increasing fat in the diet, particularly saturated fat, increases HDL-C levels.

Now let’s look at how ABC News reported this study to see a masterpiece of deception.

After a gratuitous opening to the article and the briefest of descriptions of the methods of the study, Radha Chitale, the reporter, pulls out one of the most commonly-used methods of slanting a story: she interviews someone other than the author. In this case she interviewed Dr. Kieth-Thomas Ayoob, an associate professor of pediatrics at the Albert Einstein College of Medicine. Given what Dr. Ayoob says, one really wonders if he even looked at the study or if it were merely synopsized for him by the reporter during a phone call.

Here’s how the reporter led into Dr. Ayoob’s comments.

Studies have shown that a diet high in fat and calories — the magic recipe for delicious, greasy fast food — puts people at greater risk for obesity and type 2 diabetes, both of which can lead to cardiovascular diseases and heart failure.
But the Swedish study, the goal of which was to double calorie intake and increase body weight by about 15 percent, showed that the liver is also at risk when you roll up to the drive-through window.

Here is Dr. Ayoob’s take on the study in his own words.

The extra fat is the big enchilada here, the equivalent of about three sticks of butter daily. The liver is basically using its compensatory mechanism to accommodate all this extra stuff.

Say what?!?!?!

Then the reporter follows up with

The liver processes fats in the blood. Excessive calories and fats overload the organ, causing fat to build up in the liver cells and leading to liver damage.

Jesus wept.

Not no where, not no how in this report does it say anywhere that carbs were the cause of the problem, which is the point the actual authors of the study were at pains to make.

If one were to read only the ABC News report, one would come away with the notion that this study shows in dramatic fashion how an increased fat intake can ruin a liver in only four weeks. But, as we saw above, that isn’t the case at all as shown by the study and confirmed by the study’s lead author. It just one more way that the media disses low-carb diets or the idea that excess carbs may actually be harmful by misrepresenting research reports.

An interesting corroborating side note to this study is found in one of the references. I’m sure these findings were a big surprise to the researchers running the analysis of the data, so they did what all researchers do in the same situation: they looked in the medical literature to try to get a handle on the situation.

One of their references is to a  Johns Hopkins study published  in Digestive Diseases and Sciences a couple of years ago. In this study researchers found that the fatty infiltration and inflammation of the livers of morbidly obese patients who underwent bariatric surgery correlated with carbohydrate intake.

There were no significant associations between either total caloric intake or protein intake and either steatosis, fibrosis, or inflammation. However, higher CHO [carbohydrate] intake was associated with significantly higher odds of inflammation, while higher fat intake was associated with significantly lower odds of inflammation. In conclusion, present dietary recommendations may worsen NAFLD [non-alcoholic fatty diver disease] histopathology.

On another note, the Swedish fast-food study provides us with much more interesting material than the fact that excess carb intake runs up serum ALT levels. In fact this study gives us a glimpse into the subject of the existence of a metabolic advantage. It will be the subject of the next post.

Note:  Here’s another take on this Swedish study from one of the commenters on this blog.


Photo at top by Jonathan Borba on Unsplash


  1. It’s kind of sad, although not at all surprising, that the more accurate story came from the French news agency – AFP.
    And what do you know, Dr. Ayoob “is on the United Soybean Board and General Mills Bell Institute Speakers Bureaus and has presented at numerous national professional conferences.”
    How depressing that this qualifies as journalism/science.

    Hey Steve–
    Thanks for tracking this down for us.

  2. This is good news. I don’t drink soda and I don’t eat fries – but I love me a whopper!
    I don’t think the occassional bun will kill me – do you?
    Probably not.

  3. I have been reading your blog for some weeks now and am totally hooked (I had to read all the archives, too). Your method of dissecting studies is so great–it’s something most laymen could never do for themselves. I’ve become a dedicated low-carber recently–it all just finally makes sense! Thanks for doing so much to dispel ignorance.
    Thanks for the kind words; they are appreciated.

  4. Hi,
    Do you know anything about what causes metabolic syndrome and/or insulin resistance? Likewise, do you know anything about the cellular changes involved? I’ve looked for this information & found very little. This may be the promised subject of your next post, which I’m looking forward eagerly to reading.
    Thanks, Beth
    Hi Beth–
    It probably won’t be the subject of my next post, but there are posts all over this blog that address those issues. The molecular mechanisms of what precisely causes insulin resistance are still be teased out, so we don’t have a conclusive answer yet.

  5. Dr. Eades,
    Hello to you. Let me preface by saying that my question is not directly related to this post, but has nonetheless been nagging me for some time. I must confess that I’m having some trouble reconciling your replies from the two posts referenced below. You indicated that your personal protein intake hovers around 200-250 g/d. This is in keeping with the example/scenario offered by Mr. Goran Johannesson of Sweden (that is, a baseline requirement of 100 g protein per 75 kg body weight, a 60 g/d carbohydrate intake, and the 70% or so conversion rate for gluconeogenesis). However, in reply you state that 100 grams of daily protein is adequate for a 75 kg individual (presumably at the 60 g/d carbohydrate level). Additionally, you told a Mr. Freddy that one can “get by” on much less than 250 grams of protein per day, assuming no carbohydrates are ingested. Unless junk proteins (?) are providing a significant source of material for gluconeogenesis, I’m unclear on how the deficit can be dismissed. In short, I’m confused. If you could offer clarification on this issue I’d be most grateful.
    Randy F.
    P.S.- Please excuse the prolix writing style, I just wanted to make sure you knew exactly what was being asked.
    Dietary protein, serum albumin and health
    Arne Andersson, 3. July 2007, 16:19
    1 gm/kg body body weight per day isn’t a huge amount.
    My weight is 84 kg and I try to get 140 g protein per day. Keeping the carb low and calories around 2000 kcal and that works good for me. Have lost just over 20 kg (from 107 to 84) in a litte less than one year. My health has improved.
    I’m not training much. Trying to walk 10 000 steps a day on my pedometer.
    What is your opinion of the protein intake?
    Hi Arne–
    What is my opinion of what protein intake? What protein intake? Your protein intake? Your protein intake is fine. I weigh about 190 lbs (around 86 kg) and consume something on the order of 200-250 grams of protein per day.
    Glenice S, 4. July 2007, 12:15
    Mike, when you say you eat 250g protein, are you talking about weight of your protein sources or this is the actual protein amount from that. I guess being American you would have said 1bs ozs if you were talking about actual weights of meat, but sometimes it is hard to tell, for those of us who use grams not ounces?
    Thanks for such intreresting info.
    Hi Glenice–
    I’m talking about the actual grams of protein in the food I eat. Just to give you an idea of what this means in terms of food…an ounce of meat contains roughly 7 grams of protein, a whole egg, about 6 grams, a well-made protein shake, maybe 50-60 grams. So, to put the 250 grams into meat perspective, it would be about 36 ounces.
    Hope this clears it up.
    Metabolism and ketosis
    Freddy, 5. June 2007, 1:55
    Dr. Eades
    I am confused. Exactly how much protein is needed to produce glucose each day if not eating carbs. You said 130 grams of glucose were needed daily, ketones supplying the rest. That means that 185 grams of protein is needed IN ADDITION to normal protein requirements. If my calculations are correct, a zero carb diet needs about 250 grams of protein daily. Is this correct???
    Hi Freddy–
    A lot of confusion here. I’ll make a longer post on the subject soon. You can get by on much less than 250 gm protein per day.
    Goran Johannesson, 9. June 2007, 4:39
    Thank you for an very informative blogg! You write that if you keep your carbs at for example 60 grams per day, then your liver has to produce at least 60-70 grams of gloucose. To do that the liver needs about 100 grams of protein (se #17). But we also need protein for growth and regeneration. So, the conclusion is that we need about 200 grams of protein (a man weighing about 75 kg) – otherwise the liver makes glucose from muscles. Is this really correct?
    Greetings from Sweden
    Hi Goran–
    I can see from a number of comments that there is much confusion about this issue. I’ll do a post about it soon. For now, though, rest assured that 100 or so grams per day of protein is sufficient for a 75 kg person.
    I can see why you would be confused. I’m all over the place with protein recommendations.
    I, myself, consume more in the range of 200 grams per day. Occasionally I get up to 250 g, but usually I’m around 200 grams daily.
    The protein intake required is that amount that can replenish worn out protein structures and be made available for glucose production if necessary. If one is on a low-carb diet – say 60 g of carb per day – there is enough glucose coming in to meet about half the body’s needs (typically a body in ketosis requires about 130 g of carbohydrate per day). The other half comes from conversion from protein. Since a gram of protein converts to about 0.8 gms of glucose, we need around 90 g protein (70/0.8) to make the necessary glucose. But not all amino acids can be converted to glucose, so we will need more than the 90 grams. Probably about 120 or so to make the necessary glucose from dietary protein. But not all has to come from dietary protein because other proteins are being degraded and recycled. The gluconeogenic precursor amino acids can come from those sources as well. And the recycling of amino acids conserves them so that we don’t have to use a lot of dietary protein to replace degraded protein structures – they can be built from recylced amino acids.
    So, for an average sized person, I would say that we need a minimum of 100 grams of dietary protein per day if carbs are restricted to 60 g per day. If restricted to less, we need a little more. But if we consume a larger amount – say the 200 g that I consume – we have plenty to convert to carbs and to replace protein structures without having to recycle so carefully. And we have enough to build new muscle if we need it.
    Hope this clears things up some.

  6. Counter productive google ads overwhelming your headline:
    Low Cholesterol Diet
    Make Simple Changes To Benefit Your Heart Health. Learn How From Quaker
    Kashi Chewy Granola Bars
    All-Natural & Delicious. Give One A Try Today! Kashi: Food For Change
    I guess you gotta make a buck however you can.
    It’s the law of unexpected consequences writ large. The examples you cited aren’t even the worst. Some are so bad they’re actually humorous. I’m trying to get it fixed so that I at least have approval of what goes up there. And, I haven’t a clue as to how much money these things bring in. If it turns out to be pennies, then they’re all history.

  7. Too bad they didn’t have a group that opted for a burger with out the bun, iced tea or water instead of the cola and a side salad with full fat dressing sans the fries. An honest headline could have been “Fat and protein have no effect on serum ALT levels, HDL-C levels improved as did triglyceride levels”. In a related story: The heads of statinators around the world explode after reading new study.

  8. I think that it’s obvious that if any progress is made in debunking the fat-is-bad-for-you, it will not come from the USA. It’s sadly obvious to me that, that the research, food, media and health industry has been utterly corrupted by dogma and profits. A paradigm shift, if it happens at all, will probably come from Europe

  9. From http://www.bu.edu/phpbin/news-cms/news/?dept=1127&id=47674&template=228
    “Adding more hydrogen atoms to the carbon chain of a saturated fat molecule creates a trans fat molecule, ”
    I didn’t think you could add more hydrogen to a saturated fat. Is there such a thing as a “Supersaturated Fat”?

    You can’t. Saturated fat is already ‘saturated’ with hydrogen atoms. Trans fats are created from unsaturated fats by adding hydrogen atoms. Just shows how clueless this writer really is. It’s no wonder the piece on the Swedish study was so off base.

  10. What advantage does the mainstream liberal press find in mis representing this kind of report? That is unless they wish to stay in good graces with the other pinkos who are always trying to dictate what everyone else but them must do to reduce health risks.
    There must be some kind of conspiracy between the food police and big media. Now there is a conspiricy theory for Michael Moore to sink his fat teeth into.

  11. I stopped paying attention to these fast food studies long ago. They blame “saturated fat” and “animal protein”, but they are the smallest component of typical fast food meals. Think about it. A small piece of meat, two buns, a half pound or so of fries dipped in rancid vegetable oils, washed down with a huge sugar-laden soft drink or milk shake.
    I think carbs were the main reason Morgan Spurlock fattened up and got sick from his Super Size Me diet. He blamed fat, while completely ignoring the massive orders of fries and sugary drinks, and the 6+ servings of bread a day. I agree with Angeyline that the USA is the primary source of unscientific saturated fat and cholesterol bashing.
    Maybe if fast food had more protein and saturated fat, less carbs and PUFA vegetable oils, it would not have the bad health connotation that it does now.
    By Spurlock’s own admission he consumed 30 pounds of sugar and only 12 pounds of fat during his month of eating only MacDonald’s. That’s almost three times the sugar as compared to fat, but even Spurlock attributes all his problems to the fat.

  12. “Adding more hydrogen atoms to the carbon chain of a saturated fat molecule creates a trans fat molecule, ”
    The writer has a B.S. in biology and is currently doing a Masters in science journalism at B.U.
    Jesus wept.

  13. I’m sure you know this, Mike, but to be precise, trans-fats are unsaturated. They are formed in a side-reaction in the process of hydrogenating (normally cis-)unsaturated fats.
    On the other hand, your comment did make me think of my reaction to the Mediterranean diet which is to point out the existence of Soppresatta sausage, so-called because it is super-saturated (with fat).
    In my extensive research on this issue (checking spelling) I found this comment: “After years of trying soppresatta …, I can honestly say that the best I ever had is from Piazza Mercato, a recently opened Italian Gourmet market on 3rd Avenue, between 93rd and 92nd Street (next to Starbucks), in Bay Ridge, Brooklyn.”
    I will report on my experiment following up on this theory.
    I do know that trans fats are unsaturated.
    I would love to collaborate on the soppresatta study.

  14. This is slightly off topic…I saw an ad yesterday for one of the erectile dysfunction drugs and it clearly implies that there’s some sort of link between high cholesterol and erectile dysfunction. Does anyone know what their rationale might be for this? This seems really bizarre.
    There is a problem with chronically elevated blood sugar and ED, but I’m not aware of any cholesterol issues.

  15. I’ve seen the movie “Supersize Me” being used in college education to create a discussion/debate on how detrimental overconsumption of fast food is. This study sounds a lot like a controlled “supersize me”-type of experiment. I guess this study can be thrown into such debates to show that Spurlock (sp) must have done something else besides eating at McDonald’s to affect his health the way he did. Why can’t we have ‘malpraxis’ when reporters like Chitale spread their idiocy on the media? “Peer-reviewed” press… now that’s a thought! 🙂 I guess we would then be accused of hampering freedom of speech.
    I wonder what will the media comment on a recent study (http://www.nutritionandmetabolism.com/content/5/1/6) that showed that, on a low-carbohydrate diet, increased consumption of eggs, which more than double cholesterol consumption) decreased important markers of inflammation, increased HDL (and also LDL… thought they didn’t show what kind of LDL particle) and, in general, didn’t affect cholesterol levels in a detrimental way.
    Hey Gabe–
    They won’t say anything about it – they will most probably ignore it.

  16. There was a comment that the results in the study “We found that healthy HDL cholesterol actually increased over the four-week period — this was very counter-intuitive. The study showed that the increase in saturated fat correlated with the increase in healthy cholesterol.”
    What struck me about this is that it just goes to show that we can not rely on our “intuition” in some cases, especially with all the very counter-factual information coming at us from the media scrambling our subconscious minds into a state of confusion.
    Thank you for continuously bringing the true facts to us and eliminating the confusion!

  17. The MSM is owned by big pharma and the ‘food’ product manufacturers.
    ” The notion that journalism can regularly produce a product that violates the fundamental interests of media owners and advertisers … is absurd.”
    — Robert McChesney, journalist and author
    ” The corporate grip on opinion in the United States is one of the wonders of the Western world. No First World country has ever managed to eliminate so entirely from its media all objectivity – much less dissent. ”
    — Gore Vidal, novelist and critic
    ” … the media in the United States effectively represents the interests of corporate America, and … the media elite are the watchdogs of what constitutes acceptable ideological messages, the parameters of news and information content, and the general use of media resources.
    — Peter Phillips, Project Censored, 1998
    ” There’s a whole journalistic-industrial complex dedicated to keeping newsprint, TV screens and radio waves clean of destabilizing scoops damaging to corporations or the state.”
    — Alexander Cockburn, journalist

  18. Mike,
    you are misrepresenting the study. The implications of the study is not that carbohydrates damage the liver. I quote the authors in the original study:
    “We believe that a plausible explanation for the ALT elevations in this study may
    be that the sudden increased supply of metabolic substrates, to
    the liver, in particular monosaccharides, caused an enzymatic
    induction in hepatocytes and hence that the normal leakage of
    ALT through the cell membrane resulted in elevated serum
    levels. The fact that bilirubin levels decreased in the intervention
    group is in line with induction of hepatic metabolic
    capacity rather than frank liver cell damage.”
    So they are not saying that the carbohydrates did any real damage to the liver, the ALT-levels went up because of an induction of liver metabolism, according to the authors.
    Thus “normal” leakage of ALT, and no indications of frank liver damage correlated to this.
    In the introduction the authors write that incidentally discovered elevations of ALT often lead to lengthy, expensive and sometimes invasive examinations. The implications of this study is that elevated ALT encountered in the clinic might just be a benign result of a short period of high caloric diet. Thus the clinician should not only ask about recent alcohol intake, but also excessive food intake. Which could explain temporarily benign elevated ALT-levels (after the participants stopped eating the fast food their ALT-levels quickly went down to normal and no sign of liver damage was seen).
    I beg to differ. Go back and reread my post. I didn’t say that carbohydrates damaged the liver – I said that it was the carbohydrates that ran up the levels of ALT, which is precisely what the researchers wrote in their paper. The fast food hyperalimentation did result in an almost tripling of fat in the liver (which could be construed as liver damage), an event that was correlated not with any particular macronutrient, but with the increase in weight.
    We don’t know that the ALT levels were benign, we simply know that in these subjects it went back to normal after they resumed their regular diets. But what about those people chronically on such excessive diets who probably represent the increased incidence of elevated ALT levels in the general population? Are those increases benign? I wouldn’t think so.

  19. It’s one thing for the media to misrepresent the results of research. But how about when the organization that conducts or sponsors research creates an opportunity to skew the results by making vague and nebulous statements. Take for example the recent media coverage of a Salk Institute paper on insulin resistance. A summary of the paper is posted on the Salk web site under the heading ‘The Salk researchers uncover molecular connection between excessive nutrient levels and insulin resistance News and Communications’
    The thrust of the research is the discovery of an enzyme called OGT that stops insulin from pulling glucose from the bloodstream. “For the first time we have a real understanding of how the insulin signaling system is turned on
    and off,” says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute’s Gene Expression Laboratory, who led the study that appears in the Feb. 21 issue of Nature”. The article goes on to state that the researchers believe that the hexosamine pathway acts a fuel gauge in protecting the body’s cells against the toxic effects of too much glucose and other toxic high-energy molecules. But they fail to provide details of what constitutes toxic high-energy molecules. The researchers then state that excessive quantities of nutrients that result from plentiful food and optional exercise dampen the insulin response.
    Put another way, when faced with an excess of glucose in the bloodstream and other toxic high-energy molecules insulin resistance serves to protect the cells. This hypothesis supports what others have proposed for some time — that IR results from an excessive consumption of carbohydrate. But what about those toxic high-energy molecules? Could they be fat? I think this is unlikely since lipids don’t produce an insulin response. How about protein? Possibly, but nothing like carbohydrates. This brings us to the application of the research: “this could lead to a new class of insulin-sensitizing drugs that loosen the brake and let insulin work a little bit longer”.
    One one hand the researchers acknowledge that IR is caused by an excessive consumption of glucose and other high-energy molecules. On the other hand they see the solution in a new class of insulin-sensitizing drugs. And those toxic high-energy molecules? These leave the door open for the media to state as they have in the past that IR is caused by a high fat diet while conveniently ignoring glucose from carbohydrates.
    How true, how true. Sadly, I’ve gotten used to every new pathway elucidated beig looked upon as a point of drug action instead of the much more common sensical approach of looking for a nutritional solution.

  20. Dear Mr Sergel.
    I was stunned to see the recent ABC coverage of a Swedish trial of the effects of fast food on Serum ALT and fatty liver. It would seem that neither the reporter nor commentator Dr. Ayoob actually read the trial, which found: ” Sugar (mono- and disaccharides) intake during week 3 correlated with the maximal ALT/baseline ALT ratio (r = 0.62, p = 0.006)” as stated in the abstract. The article clearly states that increases in fat and protein had no effect on the the parameters measured. Yet the reporter and Dr. Ayoob stated that the fat in the protocol caused the problem. Is this incompetence or is it dishonesty? In either case, the reporting violates the minimum standards of science writing. This is the equivalent of a police reporter stating that victim was not murdered when in fact they were.
    A truly newsworthy topic for nutrition coverage would be the growing body of evidence that sugar (as sucrose or high-fructose-corn syrup) in particular, and refined carbohydrates in general, acting to promote or aggravate insulin resistance, are primary causes of contemporary chronic degenerative diseases. One need only to browse the last six months of titles in the American Journal of Clinical Nutrition to find dozens of studies demonstrating this trend.

    Paul Bergner. NASW
    Adjunct Faculty, Nutrition.
    Naropa University.
    Boulder, CO
    Let us all know if you hear back from them.

  21. There is a problem with chronically elevated blood sugar and ED, but I’m not aware of any cholesterol issues.
    Could it be the statins those people take for elevated cholesterol that causes the ED?
    Could be, I suppose, but I don’t know for sure. I haven’t really delved into the literature on this subject so anything I say is mere speculation.

  22. The revised letter as actually sent:
    Dear Mr Sergel.
    I was stunned to see the recent ABC coverage of a Swedish trial of the
    effects of fast food on serum ALT and fatty liver. It would seem that
    neither the reporter nor commentator Dr. Ayoob actually read the
    trial, which found: ” Sugar (mono- and disaccharides) intake during
    week 3 correlated with the maximal ALT/baseline ALT ratio (r = 0.62, p
    = 0.006)” as stated in the abstract. The article clearly states that
    increases in total calories, fat, or protein had no correlation to
    changes in the liver. Yet the reporter and Dr. Ayoob stated that the
    fat in the protocol caused the problem. Is this incompetence or is it
    dishonesty? This is the equivalent of a police reporter stating that
    victim was not murdered when in fact they were. In either case, the
    reporting violates the minimum standards of science writing. Were it
    in fact a murder victim, a correction and apology would be in order.
    A truly newsworthy topic for nutrition coverage would be the growing
    body of evidence that sugar (as sucrose or high-fructose-corn syrup)
    in particular, and refined carbohydrates in general, acting to promote
    or aggravate insulin resistance, are primary causes of contemporary
    chronic degenerative diseases. One need only to browse the last six
    months of titles in the American Journal of Clinical Nutrition to find
    dozens of studies demonstrating this trend.

    Paul Bergner. NASW
    Adjunct Faculty, Nutrition.
    Naropa University.
    Boulder, CO

  23. Here’s an anecdote about junk food, liver enzyme levels and the dog and pony show our medical system put me through: two years ago I got really sick for about three weeks with aches, chills, and fever. I do all the cooking for my husband and me, but I was way too sick to do it then, so my husband relied on fast food, frozen meals, and heated up canned goods to feed us. So at the same time I was sick, when I did eat, I ate a lot of junk and was too sick to care, as long as the hunger pangs subsided for a while. On my first visit to the doctor, I was told to take extra-strength Tylenol for the fever and see if I got better in another week. On my second visit, the doctor wanted to run a blood test to see why the fever wasn’t going away. The only thing the test showed was liver enzymes ten times above normal. Because of which she referred me to a gastroenterologist. He said she hadn’t checked for auto-immune hepatitis, so he tested for that. The test came back positive, but my liver enzymes were almost normal. (By this time I was well enough to cook for myself again and was back to low-carb home-cooked food.) Because of the positive, he insisted on a liver biopsy. However, the doctor who did the biopsy missed my liver!!! (it’s only the largest internal organ in the body), so I had to have a second biopsy, fortunately to be told my liver was healthy and the blood test must have been a false positive. And why are we not surprised that even though I was told the hospital would not charge for the second biopsy, of course they did, and I had to go round and round with the billing department to get that straightened out. So I found this correlation between commercially prepared food and liver enzyme levels to be very interesting and corroborative of my own experience (although I bet that 3000 mg daily of Tylenol for the fever was a culprit, too). And it goes without saying that none of the doctors I saw asked me about my diet when I was sick.
    It absolutely stuns me that anyone would do a liver biopsy at this stage of the game. Liver biopsies are not all that benign – I’ve known a couple of people who have had serious complications as a result of poorly done biopsies. I just can’t imagine not waiting a little longer in this situation to see if it didn’t resolve on its own.

  24. Slightly off topic…
    Thanks for the Health Headlines on the main page of your website. I’ve been missing them for the longest time! I really appreciate those timely links, and look for them every day.
    By the way, congrats on the new book!

  25. I first read a different horribly false article about this study on the WebMD website at http://www.webmd.com/diet/news/20080213/fatty-fast-food-idleness-may-vex-liver
    Unfortunately no comments are allowed on WebMD, so many people reading it will unfortunately take their entire twisting of the information to heart without question. They stress throughout that the high saturated fat content of the food is what caused the liver enzyme elevation, without any mention that it was really the carbohydrates.
    Did find CBS News running WebMD’s crap article and was able to comment (bottom comment). May see it at > http://www.cbsnews.com/stories/2008/02/14/health/webmd/main3831349.shtml I’m going to see if I can write the editors of that WebMD article.
    It’s hard to believe these people read the same study as the one I posted.

  26. This is way off topic so if you don’t post it I will completely understand. A couple of weeks ago I gave blood for the first time for the iron lowering benefits as prescribed in PPLP. I did the double red blood cell procedure as I assumed it would remove more iron then the usual donation. Is that a valid assumption?
    United Blood Services does a complementary cholesterol test and posts the results in your profile on there web site . It is a total C result and is therefore useless but it is just more evidence that the cholesterol is bad mantra lives on. If I was a believer in the lipid hypothesis I would be calling my doctor for script for a statin right now as my total C was 253. This is not a fasting number as they want you to eat a meal before you donate.
    The majority of the iron is in the red blood cells, so, yes, you get rid of double when you have the procedure you had.
    Are you feeling less iron overloaded?

  27. Hi Dr Mike –
    Glad to see you are back. Hope the book writing is going well.
    I have my own anecdote, sample size of one re. elevated liver enzymes.
    About a month or so ago, I posted a comment about my experience with starting VLC and it eliminating my drinking problem. And that is still the case. I have a glass or two of wine about once a week. And I’m not even trying not to drink – I really don’t want to. And I’ve dropped another 5 pounds.
    I mentioned in that post that during my 20 or so years of eating very low fat, that I had developed the drinking problem, lost my gall bladder (which I now know was due to not eating ENOUGH fat though all the medical people I encountered tried to imply it was from eating too much fat) and supposedly developed liver problems.
    I was diagnosed as having non-alcholic biliary cirrhosis a few years ago as I had very elevated liver enzymes. My first tests showed AST 206 U/L, ALT 351 U/L and GGT 648 U/L. I thought it was very funny that in spite of my drinking problem both my GP and specialist said that the drinking couldn’t have anything to do with the elevated enzymes because of the ratio of ALT to AST – and I was honest with them about it. Though my GP suggested it was probably not a good idea to drink considering my condition, my specialist said it was ok!! My intuition told me the drink was probably the reason for the elevated enzymes (at least partly) but, heh, he is the expert right? So I was put on Urso which is very expensive (and as my partner are both self-employed, no drug plan to cover it). That SEEMED to help the numbers reduce but not get close to normal. I say seemed becaused I know realize that during that time, though my drinking remained a problem, I started to reduce the carbs in my diet – no pasta, potatoes, rice – but still had some sugar.
    So I just got another round of test results after eating VLC (mainly meat, eggs, whole fat dairy and some green vegetables) AND not drinking heavily for 3 months. My numbers are now AST 18 U/L, AST 13 U/L, and GGT 14 U/L. Hmmm….seems I really do not have a liver problem. It was a problem with what I was eating and drinking! I keep getting angrier and angrier about the pig-headed mainstream nutrition advice and what it did to my health!
    I have not heard from my specialist yet. I am very curious to see what he has to say when I tell him how I have chosen to eat. I post another comment when I do speak to him.
    Thanks again for reading my long post!
    Be sure to let me know what the specialist says. I’ll be curious to find out. Glad to see you’re doing so well.

  28. I’m pretty surprised that she had a liver biopsy done, too, at that stage. Hubby’s liver enzymes were elevated for several years and a liver biopsy was only done to confirm his PSC diagnosis once his gastro had ruled out everything else. As you said, they aren’t all that benign, and hubby’s gastro didn’t like to do them unless it was absolutely necessary.
    The connection between carbs and liver inflammation is interesting. While hubby has cut way back on his carb consumption, I still think he could do better. Perhaps this will help.

  29. Here’s more bad science, or at least bad reporting on science:
    Note that the headlines claim whole grains “reduce belly fat.” But if you read into the articles, the real story is that two groups of dieters were compared, one eating whole grains, the other eating more white flour, and the dieters eating whole grains lost a bit more weight.
    All this tells us is that whole grains may be less fattening than more refined grains. They didn’t demonstrate that whole grains promote weight loss; they only demonstrated that whole grains are somewhat less likely to inhibit weight loss.
    This makes about as much sense as having one study group smoke filtered cigarettes, having another group smoke unfiltered cigarettes, and when the filtered group develops cancer at a slower rate, we claim that smoking filtered cigarettes helps prevent lung cancer.
    Lead researcher Dr. Penny Kris Etherton, by the way, is a member of the USDA — surprise!

  30. Just to follow up a little more on the liver biopsy anecdote, when the gastroenterologist said my liver enzymes were almost normal but I did test positive for auto-immune hepatitis (and I remember from PPLP you connect auto-immune disorders to high carb consumption) I asked if we could wait and maybe test a couple more times (best two out of three) and see if the positive came up each time or if the following tests came back negative. Oh no, we couldn’t do that, I was told–a liver biopsy is the only way to be sure. I wonder how much Expensive Procedure $$$$ influenced that thinking? And I didn’t mention all the mental stress of wondering whether I had this serious condition (even though I felt really good). The doctor told me it was easily treated with Prednisone, and then I read up on that and thought somebody would have to crazy to take that stuff and I had decided to refuse to take it if the biopsy showed hepatitis. I wish I had known then what I know now about nutrition and the medical system. I wouldn’t have let them jerk me around so trustingly. But I’ll be better armed for next time if, God forbid, there is one.

  31. Dr. Eades,
    It was good to see you over on Tim Ferris’s site. I was rather surprised at how positive the response was. Sure, there were a few low-fat disciples, but most people were very receptive to the ideas and many even backed you up. I don’t think we would have seen such a response a few years ago. It seems the consensus is shifting. Slowly, no doubt, but definitely shifting.
    It was an interesting experience, that’s for sure.

  32. It seems the consensus is shifting. Slowly, no doubt, but definitely shifting.
    I think it’s a combination of the Taubes’ book and how the internet (& Google+blogging) have changed public discourse. In the past, people like Kolata & Brody could control the story just by being gatekeepers at the NY Times. But now, anyone who can read Taubes is capable of discussing the “story behind the story” of Kolata’s attempting to smear Taubes book (to push her own inferior tome), or how the diet Brody’s been pushing on America for years has given her heart disease.

  33. First off Dr. Eades I am new to your site and let me say it rocks! I have been in the media (radio) for 16 years and 1 thing i can say for cetain is this: The Media will whore themselves
    out to the highest bidder. I have worked for several companies both big and small and that truth is always the same. Trust me folks, these big media outlets are bought and paid for by big pharma i have seen it first hand!

  34. Thanks for this! I’ll read more of your stuff. I wrote about the study and your outing of it here: http://wiredpen.com/2008/05/25/abc-misrepresents-swedish-study-afp-gets-it-right/
    FYI – the “yahoo” story was an AFP (agencie france-presse) story and that Yahoo link is broken. I link to the AFP site in my post.
    Any thoughts on insulin resistance and estrogen (its absence)?
    Hi Kathy–
    Thanks for the mention in your post; I appreciate it.
    Elevated insulin levels stimulate the liver to produce more sex hormone-binding globulin (SHBG). SHGB binds to the sex hormones (which include estrogen) and make them unavailable for use. The free hormones are the ones that perform the hormone functions – the bound hormones are basically just along for the ride and are not active. Anything that increases the amount of SHBG (as insulin does) decreases the amount of free hormone.
    Hope this answers the question.

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