Low fat diets poitless?

One more turning point in the demise of low fat diets came this week. The Annals of Internal Medicine released the results of a two-year study examining the comparative effectiveness of a low carbohydrate diet in direct comparison to a low fat diet. Unlike many other studies, this one was comparatively long-term (two years) and explicitly factored ‘in’ education and lifestyle changes (counseling and exercise).

My buddy Jimmy Moore on the Livin’ la Vida Low Carb blog has a great breakdown of the study (he really dug deep and included lots of references), so I won’t do an exhaustive recap here, but will include a few of the highlights:

  • The low carb diet included no calorie restriction.
  • The low fat diet prescribed a limit of 1,800 calories per day
  • Both diets resulted in comparable weight loss
  • The low carb group wound up with more favorable cardiac risk factors (higher HDL, lower triglycerides, lower VLDL). The study concludes

For my part, it’s another in what I expect to be many more data points on the path to the demise of the entire low fat premise. I’ve read a number of articles about this study and remain surprised to find that the non-calorie-restricted element of the low carb diet is not emphasized more (even among those who would be inclined to point this out). Maybe it’s so well understood that many don’t think it bears repeating, but I do. This study compared one ‘diet’ that essentially asks you to be HUNGRY basically ALL THE TIME to a diet that says ‘each as much as you want until you’re sated – then stop.’ It just boggles my mind that this distinction continues to receive so little emphasis. Which one of of those two options are you likely to continue doing over a lifetime? For my part, I don’t like being hungry if I have a choice. This is the main reason why I’m convinced low fat diets will begin to wane as we come out of this phase of dietary orthodoxy. Why starve if you can accomplish the same ends via other means.

One more thing, while I’m at it. It’s not so much about this particular study, but about the metrics used for diet studies all together. As I write this, my body fat is down to about 12%, I have a 32-inch waist. Solely based on BMI calculations, I’m bordering on obese. What’s the point? The point is weight, while relevant, is not the most relevant factor to be measured. The very most important factor is abdominal (omental) fat. Failing the ability to directly measure abdominal fat, tracking overall body fat has to be a better factor to track than weight. Why are there no studies that track *fat loss* between competing diet regimens. Is it really that hard?! Would you care if you cut you body fat percentage by a 1/4 but remained at the same weight? Seems so simple, I must be missing something.

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[Pissing+child.jpg]One of the most disgusting ideas I’ve come across in following medical issues is this idea that children might be prescribed stating drugs. This unwelcome thought was triggered anew with today’s article and featured video.

"All kids need cholesterol tests" the headline blares. 

"Tens of thousands of children could benefit from medication" thus spake the oracle.

The very idea of widespread screening of children for the purpose of getting them on a lifelong regimen of statin drugs is absolutely revolting.

The underpinnings of the lipid hypothesis *in adults* has all but completely crumbled (http://thehealthyskeptic.org/images/statintrialsummary.pdf) and now we get the pharmaceutical companies floating this idea of extending the flawed hypothesis to children where there is *NO* clinical evidence proving benefit.

Recently read The Truth About the Drug Companies by Marcia Angell, here’s my recent post on it. One of the little anecdotes Dr. Angell recounts leaps to mind immediately. She published an article in the New England Journal of Medicine some years ago posing the rhetorical question "Is Medical Education for Sale?" The most telling answer came from a reader who I paraphrase: "No, of course it is not for sale. The present owner is quite happy with it!"

When you see articles like this one, remember who’s truly in the ownership position here.

Upon starting this blog, there were a number of concerns that came to mind. Would I run out of things to talk about? Would anybody listen/care? Would my opinions just come off as silly? (‘not yet,’ ‘enough, it seems,’ and ‘too early to tell’ are the answers as far as I can tell to date). But it really didn’t occur to me that I’d come off as the crotchety, perpetually peeved, quixotic nutcase (ok, it did occur to me but I didn’t want to let it in). My fear is that this ‘just below the surface’ tendency might come into sharp relief when I take on the subject of statins.

Quick primer on statins to the 5% my readers not old enough to have had this modern medical miracle come into their consciousness. Put simply, statins are a class of pharmaceutical drugs that focus on limiting the synthesis of cholesterol in the blood based on the premise that it is the presence of high concentrations of cholesterol (low-density lipoprotein, to be more precise) that is the primary causative risk factor for atherosclerosis (or ischemic heart disease) which leads to heart attacks and brain attacks (strokes).

More recently, the clever folks who brought you endless lifestyle drug commercials (with their sometimes howlingly funny litany of side effects) have come up with the bright idea that these miracle statins should be prescribed to an enormous swatch of human population. I find the very idea of this more than a little disturbing. First off, the entire premise upon which the ‘lower cholesterol to reduce heart attacks’ premise is highly questionable (see The International Network of Cholesterol Skeptics for more). Secondly, the proof for the effectiveness of statins is limited to a relatively small set of patients (primarily men under 65 who have already had heart attacks). Thirdly, the just-recently observed side-effect of statin use that reduces inflammation (as measured by C-Reactive Protein) has never been studied as an independent factor.

More recently, though, a spate of clinical trials has called the whole game into question. Thanks to a fantastic synopsis at the Healthy Skeptic blog, there’s a one-page summary that tears down the presumptions that statins are clinically useful. It’s an extremely important reference when having that all-important discussion with your doctor about statins. To say nothing of the many side-effects common with statins and that we don’t have any conclusive data about long-term use of statins (which seems important given they are being prescribed *for life*).

Now comes the all-out pressure to allow for prescribing statins as ‘preventative’ measures in a wide swath of the population.

Please be extra vigilant if your doctor proposes putting you on a statin. Educate yourself and ask really probing questions before just taking what you’re being told at face value.

Better to use diet and exercise the obviate the need for these hazardous drugs all together.

I’ve been getting lots of encouraging comments from friends and acquaintances recently now that I’ve committed to posting more often. One of the comments I’ve been getting though is to have a simple, one-pager that lists the ‘foods to seek out’ and ‘foods to avoid’ and includes a few general meal selections as well.

Seems like a simple thing, huh? Well, I do think it’s pretty simple to avoid food that quickly raises your blood glucose or otherwise results in the creation of fat (recent post on fructose is highlights that heretofore not-well-understood phenomenon). But every time I tell someone that I get quizzical stares and incredulous furrows in the brow. “There’s got to be more to it than that!” is the general thinking.

Then I go to a few of my favorite sites and find they don’t really have a simple one-pager suitable for posting on the ‘fridge either.

Seems like some white space I can fill in.

Well, not exactly me … it’s not like I’m creating this material out of whole cloth, it’s a compilation of lots of points of view, with my own little twist in there for good measure.

So, here’s my first stab at such a list – suitable for framing (or lining the bird cage as the case may be). Once I get it refined, I’ll post it as a .pdf in a more visually pleasing form.

While you already know these are my personal views and I’m not credentialed in any way. You should also know that if you’re allergic or have any other negative reaction to any of these foods, you should use your better judgment and avoid them.

Foods to seek out:

Food item Why? Notes
Beef, pork, lamb, chicken, fish, shellfish Best source of protein containing a full spectrum of amino acids. Fat in animal proteins (saturated and mono-unsaturated,typically) are your metabolic friends. Don’t cut out the fat. Enjoy the nutritious and satiating food you were meant to eat.
Dairy products Other good sources of calories and good fats. While they do contain sugars (lactose), they only moderately raise blood glucose. Milk, cheese, butter, mayonnaise etc. Do not choose low fat products or sugar-added products.
Ham, sausage and other processed meats Protein is good. While there are some concerns with some processed meats, if you choose them carefully, they can be enjoyed in good health. Avoid processed meats with carbohydrate content exceeding 5g per 100g.
Eggs The perfect protein. Better to choose organically grown eggs. Typical practices result in eggs that are too high in pro-inflammatory Omega-6 fats.
The ‘dangers’ of dietary cholesterol are wildly exaggerated.
Seasonings Enjoy your foods. Herbs, spices, stock, salt and pepper according to taste.
The ‘dangers’ of salt are also exaggerated. Not wildly so (like cholesterol) but moderate salt intake when it’s conscious is not a danger. The bigger danger is when you take in all the salt unconsciously by eating lots of processed foods.
Sauces Enjoy your foods. Be sure these sauces have low carbohydrate content. Avoid sweet sauces (sugars) and heavy gravies (flour).
Vegetables Loads of vitamins, minerals. Beneficial dietary fiber. Be sure to gravitate to the deeply pigmented (dark, bright), fibrous vegetables and you can’t go wrong.
Dressings More food enjoyment. Oil and vinegar or mayonnaise.
Oils Beneficial fats. Make sure they’re cold pressed oils (olive, linseed and coconut oil).
Supplements Vitamin D and Omega-3.

Unless your diet contains a good supply of fish with a high fat content you may need a supplement of the essential polyunsaturated fatty acid omega-3, e.g. in fish oil.

Practically all people living typical modern lives (no matter your latitude) need to supplement with vitamin D. Seek to get your circulating vitamin D (25(OH) Vit D) up to 50 ng/ml.

 Foods to avoid:

Food item Why? Notes
Potato based products High glycemic load (raises blood glucose). This includes mashed, roasted and baked potato. Also includes any kinds of potato-based chips.
Corn High glycemic load (raises blood glucose). Most people have no idea how ubiquitous corn is in the Standard American Diet (SAD).
Rice High glycemic load (raises blood glucose). Includes ‘milk.’ And, no, brown rice is not appreciably better.
Annual Grasses High glycemic load (raises blood glucose). Many are adversely affected by gluten and other proteins in grasses. Wheat, barley, etc. Which means avoiding breads, pasta, bread, crackers, breakfast cereals, etc.
My experience is this is the hardest thing for most people to give up.
What do we call it when people just keep doing things they know are bad for them because of some uncontrollable compulsion?
Addiction.
Sugar High glycemic load (raises blood glucose). Stimulates liver to produce fat. Sweets, cakes, pastries, soft drinks, juice.
See the ‘addiction’ reference above.
Chemically- processed vegetable and nut oils They contribute to an increased risk for heart and artery problems, diabetes, overweight, cancer, allergies etc. Include margarine, poly-unsaturated fatty acids (corn oil, sunflower oil, etc.). When chemically processed (as opposed to cold-pressed), these oils rich in omega-6 fatty acids which are inflammatory and detrimental to your health.
Soy Enhances estrogen dominance, impairs thyroid function, blocks mineral absorption. Take a moment to read an eye-opening post on the dangers of soy.

This seems like a hefty-enough post for now. Will follow up soon with some some of the specific choices I make on a day to day bases and begin to address some of the biggest stumbling blocks for most people (sugars, breads, grains).

Much of this list of recommendations was sources from:

Dr. Annika Dahlqvist: Low-Carb/High-Fat physician advocate in Sweden
Mark’s Daily Apple: The Primal Blueprint
New Atkins for a New You

CaloricBalanceFEH A little over a month ago I began an exchange with a blogger (James Krieger) who saw fit to award Gary Taubes with a mocking BullS*#tter of the day award. You see, James is an unwaveringly committed to the principle of caloric balance: the principal cause of fat storage is that we simply consume more calories than we burn. To refute the carbohydrate hypothesis (the principal reason we get fat is because of the consumption of easily-digestible carbohydrates) put forth in Gary Taubes’ Good Calories, Bad Calories, James creates his own ‘predictions’ he inferred from the hypothesis and, as one might expect, successfully dismantled each of the straw men he constructed. Touche.

As you may have seen in previous posts, I’m not convinced the simple caloric balance rubric works in cases where the calories that are consumed are in the form of easily-digestible carbohydrates (sugars, white bread, etc.). While he does acknowledge that different macronutrients work differently in the body, his point is that as long as there is a caloric deficit, we won’t have enough calories to make fat.

My bottom line on this line of reasoning is that there may well be some merit to the idea that as long as you live in a caloric deficit, you are not likely to retain fat. For the sake of this discussion, let’s accept this premise. For practical purposes, in an environment where there is relatively abundant, cheap sources of refined carbohydrates, it is TBU: True, but useless. The overwhelming majority of people are not going to voluntarily stay in caloric deficit their entire lives, so why orient your recommendations around an unsustainable approach? Especially since there is convincing and ever growing evidence that if one pursues long-term carbohydrate restriction it is possible to avoid getting fat without having to consciously restrict calories.

Since the original post is no longer up and the blog on which is was originally posted has been retired in favor of a new one (good move on his part, I’d say), I include the full exchange (very long, warts and all) here for posterity.

=====

Keith said…
Having read Good Calories back in 2008, and having read your blog, I’m puzzled by the ‘conclusions’ you extrapolate from the carbohydrate hypothesis. Since I was sure I hadn’t seen these conclusions stated, I re-read the portion of GCBC that laid out the hypothesis (pages 355 to 447, for those of you following at home) and was unable to find these ‘conclusions’ you state.

Now, it is fair to say that the carbohydrate hypothesis stated in the book was short on specific conclusions. For me, that was a good thing and apparently by design. The intent appeared to be to provide as much objectively verifiable information as possible and have that lead the way to re-thinking the conventional wisdom about caloric balance (among other things) so that the hypothesis may be tested clinically.

That said, it seems the burden would be first on you to provide the references for these ‘conclusions’ you offer. They may well be reasonable conclusions – as many other conclusions may be. But they are *your* conclusions, not the author’s because he didn’t state them. I submit if you are not able to find these conclusions stated by the author, then perhaps you did erect straw men to further your own rhetorical ends.

The other observation I have to share is a bit broader in scope. I find the notion of a self-appointed ‘bullshit detective’ (one wonders if this office comes with a sash … and huge epaulets) – especially on issues as complex and multi-faceted as human nutrition to be rather tedious. While I realize some find it good sport to leap to ad hominem attacks, I personally find it rather pointless.

You obviously have a lot of passion and a strong background in these issues. I am sure many people are helped in your practice. I’m at a loss, though, as to how personal attacks help us learn what we need to learn to help people get better or avoid falling into a state of disease in the first place.

Can’t we just argue the facts and leave the middle school stuff somewhere else.
April 26, 2010 1:02 AM

James Krieger said…
Keith,
They aren’t conclusions. They are predictions that naturally follow if the carbohydrate hypothesis were true. Then it’s a matter of whether those predictions hold under experimental conditions.

Regarding my style of blog, people have varying opinions on it. I will eventually be scrapping this blog and starting a couple other ones which won’t have the same style.
April 26, 2010 6:42 PM

Keith said…
I stand corrected. Predictions, not conclusions. Thank you.
The original question remains, however. Where does the author state the predictions you cite.

I still can’t find them.
April 27, 2010 3:54 PM

James Krieger said…
Keith,
That’s the whole point of my post…that Taubes doesn’t approach the carbohydrate hypothesis like a scientist and actually test the hypothesis by making testable predictions and seeing if they hold under experimental conditions. I came up with the predictions because they are predictions that must hold true if the carbohydrate hypothesis were true.

Basically my whole point is that Taubes never attempts to falsify the carbohydrate hypothesis, which is exactly what he should be doing. Instead he only looks for confirmatory data (and even some of his confirmatory data is flawed, like the data that uses self-report of food intake).
April 27, 2010 7:05 PM

Keith said…
Predictions out of whole cloth
Thank you, James. That does clarify. So you did not obtain these predictions from the author.

You take nearly 100 pages of carefully crafted and researched prose and condense it down to an elevator pitch. You construct predictions out of whole cloth predicated on an incomplete understanding of the hypothesis. You take care to construct these predictions to be imminently falsifiable and you dash your hastily-constructed straw men almost as quickly as to stand them up. By way of just one example, you assert a prediction about fructose that is in opposition to what the author clearly states in his hypothesis … and he does so only four pages in to the 90+ pages describing the hypothesis (you can look it up yourself – page 359). To say nothing of the more recent work by Dr. Robert Lustig on the lipogenic effects of fructose (hepatic synthesis of triglycerides, etc.). Hardly inspires confidence that you’ve really done your homework here.

It could be taken a bit more seriously if you had at least made some specific references to the text as you constructed your straw men, but you chose not to. What is most dismaying is that you clearly have the requisite cognitive ability to make a real go at challenging the hypothesis, but it doesn’t really matter if you don’t use what you have.

I don’t know if the whole of Taubes’ hypothesis is right – it has not been tested in any completely verifiable and conclusive way. The hypothesis he puts forth, however, is as complete, coherent and cogent a one on the causes of obesity that I’ve seen – and there is a large body of clinical research over many decades that comports well with the hypothesis. Moreover, the choices I have made in light of what I learned from "Good Calories, Bad Calories" have been more beneficial than I could have imagined – as has been the case for many others with whom I have shared this information.

I also know there are clinical results that support his hypothesis and some that do not. But your attempt at disproving the hypothesis fell short right out of the gate as you demonstrated an utter lack of understanding of the source material and a lack of seriousness in grappling with the issues in any depth.
April 28, 2010 11:56 PM

James Krieger said…
Keith,
*************
You take nearly 100 pages of carefully crafted and researched prose and condense it down to an elevator pitch.
****************
Carefully crafted?
Yes, maybe carefully crafted to tell a story. But a carefully crafted story that leaves out large amounts of conflicting information isn’t correct.
Keith, it takes me just a few minutes of reading his book to find glaring ommissions and errors in it. Maybe it’s because I’ve done over 75 lectures on obesity and obesity related research so that I’m intimately familiar with the work in the area.
For example, let’s take the very beginning of Chapter 14, where, down the page, Taubes states:
"Lean people will often insist that the secret to their success is eating in moderation, but many people insist that they at no more than the lean….surprising at it seems, the evidence backs this up."
But the EVIDENCE DOESN’T BACK THIS UP. There are dozens and dozens of studies that show that overweight people don’t accurately report their food intake and consume much more than they report. But Taubes says nothing about this. He took the self report data and assumed it was accurate, when it’s clearly not.
It took me a few minutes to find this major error in such a "carefully crafted" book.
Or how about page 273 where Taubes talks about the differing tendencies of people to gain weight, and then goes onto claim on page 274 that "something more is going on than mere immoderation in lifestyle – metabolic or hormonal factors in particular. Yet the accepted definitions of the cause of obesity do not allow for such a possibility."
Yet Taubes is wrong here as well. There are dozens of studies on the phenomena of Non-Exercise Activity Thermogenesis (NEAT) and how it plays a large role in people’s differing tendencies to gain weight, and it also fits in with the concept of energy balance. Yet Taubes says nothing about this work despite the large body of data out there.
Again, it only took me a few minutes to find this.
GCBC is nothing but a story….a story that leaves out information that doesn’t fit with the story.
*************
You construct predictions out of whole cloth predicated on an incomplete understanding of the hypothesis.
**************
If my understanding is incomplete, then please explain where and how. Please explain why each prediction wouldn’t follow from the carbohydrate hypothesis.
*****************
By way of just one example, you assert a prediction about fructose that is in opposition to what the author clearly states in his hypothesis … and he does so only four pages in to the 90+ pages describing the hypothesis (you can look it up yourself – page 359).
*******************
I discuss the issue of fructose here:
http://www.thebsdetective.com/2010/02/partial-bullsht-of-day-fructose-makes.html  
****************
To say nothing of the more recent work by Dr. Robert Lustig on the lipogenic effects of fructose (hepatic synthesis of triglycerides, etc.)
********************
Dr. Lustig unfortunately leaves out important information when discussing the effects of fructose. This is thoroughly discussed here:
http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/
**************
The hypothesis he puts forth, however, is as complete, coherent and cogent a one on the causes of obesity that I’ve seen
*****************
But it’s not complete. It’s horribly incomplete. When it takes me a few minutes to find major errors in the book, that’s a problem.
April 29, 2010 5:58 AM

Keith said…
I get it, now …
At least I think I do. It appears you have decided that every hypothesis that does not confirm the energy balance hypothesis is wrong. OK. I am not convinced of its correctness and, as I said in a previous comment, nor am I convinced that 100% of Taubes’ carbohydrate hypothesis is correct either. I’m still learning and despite my disagreement with you, I have gained from this exchange.

Your 100% surety produces its own blind spots in entertaining another points of view. The core reason why I decided to comment on your blog was the flippant nature of it – as if you are the only one in possession of the truth. Yes, I know you’ve said ‘it’s just a tone thing, get over it,’ but it does matter. Even in your own very long treatise on how fructose is processed by the liver, you admit that some lipogenesis takes place in the absence of an insulin response, and use a single 6-day study (http://www.ncbi.nlm.nih.gov/pubmed/11068955?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1)  to assert categorically that it is energy balance that is the key to whether fructose leads to lipogenesis. Isn’t that just another example of confirmation bias?

At the risk of conflating two issues here, my reading of Lustig is that he is very mindful of ‘dose and context’ in the context of fructose consumption, which is where he differs with Taubes’ hypothesis, instead emphasizing fructose in the presence of dietary fiber is a key element to whether the fructose becomes lipogenic (as well as the dose, of course).

Where I believe your own blinders have not allowed you to completely understand the carbohydrate hypothesis is that you (at least in this exchange) do not seem to take into account the key premise of the carbohydrate hypothesis which is that obesity is a disorder of fat metabolism which is engendered by metabolic and hormone imbalance (principally triggered by consumption of refined carbohydrates). Perhaps you have taken that on in other posts. Since I have not searched your blog exhaustively, I may have missed it. As long as you believe you have all the answers already and dismiss others points of view immediately when they disagree with yours, then decide to attack the person; it diminishes your argument for people like me. Maybe I’m just an outlier. I don’t watch ‘reality’ TV either.

Thank you for your time and I wish you – and those with whom you work to get and remain healthy – well.
April 30, 2010 9:55 PM

James Krieger said…
Keith,
*************
Even in your own very long treatise on how fructose is processed by the liver, you admit that some lipogenesis takes place in the absence of an insulin response, and use a single 6-day study (http://www.ncbi.nlm.nih.gov/pubmed/11068955?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1) to assert categorically that it is energy balance that is the key to whether fructose leads to lipogenesis. Isn’t that just another example of confirmation bias?
******************
I would contend that you are creating a strawman out of the argument I’ve made, and that’s probably partly my fault as I may have not been totally clear in my presentation.
First, of course lipogenesis can occur in the absence of an insulin response. In fact, that was one of the points of my original post on Taubes. Taubes likes to demonize insulin, and one of the points of my post was that you can get fat without it.
Second, lipogenesis is not a light switch. It’s not like fructose is non-lipogenic in an energy deficit and then suddenly switches to lipogenic in an energy surplus. These states exist on a continuum, with the degree of lipogenesis changing with shifts in the degree of energy status.
You also can’t just look at lipogenesis. You also have to consider fat oxidation rates at the same time. Again, it’s a matter of balance. Sure, fructose can be lipogenic, but if the rate of fat oxidation matches the rate of lipogenesis, then there will be no fat accumulation.
The body is constantly undergoing anabolic and catabolic reactions. Tissue mass only increases if the anabolic reactions, all summed up, exceeds that of the catabolic reactions, all summed up. In this case of fat, lipogenesis must exceed the rate of fat oxidation. And this is again a matter of energy balance.
**************
take into account the key premise of the carbohydrate hypothesis which is that obesity is a disorder of fat metabolism which is engendered by metabolic and hormone imbalance (principally triggered by consumption of refined carbohydrates)
****************
No, I certainly do take that into account. But there are two major problems with that tenet. First, all the hormones in the world can’t make you fat if they don’t have the substrate to work with. Hormones can’t trump energy balance. They are just signaling molecules. But they can’t cause the synthesis of new tissue if there is no substrate to build that tissue with. You can bark all the orders you want to construction men, but they can’t build a skyscraper unless they’ve got the materials to do it with.
The second problem with that tenet is the implication that obesity has a single primary cause. However, the scientific literature is quite clear that there are numerous factors all contributing to obesity. Even simple things like portion sizes have been found to be contributors. You could eliminate refined carbohydrates from the diet, and you will still have an obesity problem.
May 1, 2010 7:35 AM

SACover2010-05One more bit of evidence that we may yet see the worm turn as it regards the complex of misconceptions and falsehoods surrounding diet. None other than Scientific American has published in its May issue an article entitled:  Carbs against Cardio: More Evidence that Refined Carbohydrates, not Fats, Threaten the Heart.

The central study cited was originally published in the American Journal of Clinical Nutrition. It was a meta-analysis (combining data from a number of studies) that found “no association between the amount of saturated fat consumed and the risk of heart disease.”

No association.

Here’s another salient quote:

The finding joins other conclusions of the past few years that run counter to the conventional wisdom that saturated fat is bad for the heart because it increases total cholesterol levels. That idea is “based in large measure on extrapolations, which are not supported by the data,” Krauss says.

Check out the article. One more nail in the coffin of the lipid hypothesis.

Sugar: The Bitter Truth

December 28, 2009

Another bombshell. It’s 89 minutes of metabolic truth-telling by Dr. Robert Lustig who is a Professor of Pediatrics (Endocrinology division) of the University of California at San Francisco. His primary focus is on explaining the crucial difference between the way fructose and glucose are metabolized. His central premise could be stated as ‘It’s the fructose, stupid.’ In brief:

[Dr. Lustig] explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin

I’m always keen to get complete agreement from another perspective. The major item that makes this talk unique is that he explains the biochemistry in, perhaps to some, excruciating detail, but it’s necessary to make the point.

To watch the original in its entirety, go to the University of California Television site: Sugar: The Bitter Truth. is also available on YouTube in full form, and is available in nine YouTube-sized bites courtesy of our decidedly eccentric (and I say that in the fondest way possible) Dr. Joseph Mercola.