Definitely good enough to reproduce here...
Just how low will the anti-low carb crowd go?
Misleading claims and biased research reviews - all in a day's work for opponents of low carbohydrate diets!
By Anthony Colpo.
February 19, 2004.
(link above in Valewis's original post)
On Wednesday, February 18, 2004, Channel Nine Australia's A Current Affair featured a piece entitled Why we've got an insatiable appetite for diets. I don't watch a whole lot of TV, but every now and then I just happen to be in the lounge when a segment dealing with nutritional matters airs. Whenever I sit down to see what the invited commentators have to say, I almost always find myself shaking my head in disgust at some of the scientifically-unfounded nonsense being spewed forth.
Last night's ACA segment was certainly no exception.
When the narrator introduced Shane Bilsborough, a nutritional scientist, low-fat diet author, and long-time enemy of low-carb diets as "the weight-watching whistler blower who lifted the lid on the dangers of low carbohydrate diets, such as the Atkins diet, on ACA a month ago...", my B.S. meter started to quickly head north. When ACA then proceeded to play a clip from its January 7 show where Bilsborough boldly told the nation that low-carbohydrate diets had caused sixty deaths, my bullshit meter flew right off the scale!
After making this outrageous claim, the story then went on to lament the inevitable confusion among consumers arising from the current plethora of conflicting dietary advice and schemes. This coming from the same show that, less than a year ago, hailed the publication of two studies that appeared in the May 22, 2003 edition of one of the world's foremost medical journals, The New England Journal of Medicine, as convincing evidence that the late Dr. Robert Atkins, the most famous and widely-denounced low-carbohydrate guru of all time, was right after all. That show even featured footage of yours truly, and one of my personal training clients, singing the praises of low-carbohydrate nutrition. Judging by the comments in the copious volume of e-mail I received after the show, a lot of Australians decided that very night to begin low-carbohydrate dieting.
Not even ten months later, we have the bizarre spectacle of ACA doing their utmost to scare these folks off the very diet that they began as a result of the highly-positive coverage from last year's show.
The catalyst for the January 7, 2004 ACA segment, entitled Low-carbohydrate diets: why they're hard to swallow was a review of low carbohydrate research conducted by Bilsborough and Deakin University's Tim Crowe which appears in the latest issue of one of the lesser-known nutrition journals, the Asia-Pacific Journal of Clinical Nutrition.
Before I proceed to explain why Bilsborough and Crowe's review is one of the most biased, misleading, and one-sided pieces of tripe I have ever read, I first want to address the alarming claim that low-carbohydrate diets have allegedly caused sixty deaths. It goes without saying that this is a grave charge; one that, as a person who has appeared on national television endorsing the use of low-carbohydrate diets, I take very seriously. No doubt, many of the thousands of low-carbohydrate dieters around Australia who heard Bilsborough's claim are now understandably worried.
They shouldn't be.
What Bilsborough conveniently "forgot" to mention when he made his claim was that these sixty deaths had occurred over 20 years ago among people following very-low calorie, low-fat, liquid-protein diets! (Those who have been following the nutrition arena for any length of time will remember how liquid diets had their day in the sun back in the seventies and eighties, but quickly fell out of favor after their potentially-fatal shortcomings became all-too apparent). Needless to say, liquid-protein diets bear little resemblance to the meat-, egg-, dairy-, fruit-, vegetable-, and nut-based diets that most low-carbers eat. Indeed, none of the low-carbohydrate plans that Bilsborough and Crowe enthusiastically denounce endorse the use of liquid diets in any way.
Bilsborough's omission of these crucial facts, quite frankly, reeks of opportunistic scare-mongering. By airing Bilsborough's comments in January, and again last night, ACA has no doubt caused a great deal of unwarranted apprehension among thousands of low-carbohydrate dieters around the nation.
Why didn't the folks at ACA bother to verify Bilsborough's claim? Furthermore, why didn't they bother to get an opposing viewpoint to balance the story, preferably from someone who had read Bilsborough's and Crowe's paper? I guess hysteria and hype attract a lot more viewers than commonsense, logic, and balanced reporting…
Selective Quotation Rears Its Ugly Head… Again
Before we take a look at the many flaws within Bilsborough's and Crowe's APJCN article, a brief discussion of selective quotation is in order. Among the thousands upon thousands of medical journals that are published each year, one can find studies that, when quoted in isolation, can support just about any hypothesis. However, good science does not involve quoting only those studies that support one's point of view, and conveniently ignoring those that do not support or even contradict one's point of view. Objective science involves coming to a conclusion only after the evidence has been reviewed in its entirety.
As an exercise in objective research, the Bilsborough and Crowe APJCN paper fails miserably. In fact, if I were a lecturer charged with educating budding young researchers about the pitfalls of selective quotation, I would use the APJCN article as a classic textbook example of the phenomenon.
To fully address every misleading and erroneous claim contained within the APJCN paper would take many, many pages. Because I and most readers lead busy lives, I will limit the following discussion to the most serious and pertinent claims within the article.
Let's begin with their claim that: "Studies examining the efficacy of using low-carbohydrate diets for long-term weight loss are few in number…" and that these studies do not support the notion that low carbohydrate diets offer any weight loss advantage. To support their claim, the authors cite a mere three studies that directly compared the weight loss effects of low-carbohydrate versus high-carbohydrate diets, even though I have fifteen such studies sitting in my file.(Rabast, et al. 1981)(Baron JA, et al. 1986)(Wadden TA. 1993)(Foreyt et al. 1993)(Alford BB, et al. 1990)(Golay A, et al. 1996, 1996)(Lean et al. 1997)(Torbay et al. 2002)(Layman et al. 2003)Sondike et al. 2003)(Volek et al. 2002)(Fleming RM. 2002)(Brehm et al. 2003)(Foster et al. 2003)(Samaha et al. 2003)(Wien et al. 2003)
To illustrate their contention that low carb diets offer no advantage over high carb diets they cite a study that was not even a comparison trial (LaRosa 1980 studied only a low carb diet) and a single one-month study that actually utilized two low-carbohydrate diets! The latter study (Greenwood CE, 2003) compared two 600-calorie diets, one containing 10g of carbs per day, the other containing 76g of carbs. In anyone's language, seventy-six grams of carbs is a low carbohydrate intake, falling well under the 100g limit that even Bilborough and Crowe have themselves set as the upper limit for defining a low carbohydrate diet. The authors skirt around the issue by simply referring to the two diets as "ketogenic" and "non-ketogenic". Technically-speaking they are correct: ketosis is generally believed to kick in when carb intake drops below 50-60g, but the author's careful wording, and the context in which they have cited the study, gives the distinct impression to the unsuspecting reader that they are in fact referring to a low carb versus high carb diet study.
After citing these two papers that don't even support their claims, the authors state that: "These aforementioned studies confirmed many previous studies, which concluded that lower energy intakes rather than low carbohydrate intakes may be the key to successful weight loss." The citation they then give for the "many previous studies" is a single 1981 paper by Rabast (Rabast et al. 1981) and colleagues which in fact contradicts their claim. In this study, the researchers found that 28 days on a high-carbohydrate liquid diet produced a mean weight loss of 9.5kg. In contrast, subjects following a low carbohydrate diet in which the principal source of fat was corn oil lost an average 11.4kg, while those on a low carbohydrate diet where saturate-rich butterfat constituted the fat source lost 12.5kg!
Bottom line: the authors have quoted two irrelevant studies and a contradictory study to support their claim that low carb diets offer no weight loss advantage. To quote Bilsborough himself, "That's bizarre!"
Out of the fifteen studies that I have been able to track down that simultaneously compared folks following either high- or low-carbohydrate diets, the latter produced superior weight loss in nine. In seven of these, greater weight loss was seen among the entire low carbohydrate group, while in the remaining two it was observed among closely-matched sub-groups.
The only published paper to have ever found greater weight loss among high carbohydrate dieters was authored by a Nebraska cardiologist by the name of Richard Fleming, who just happens to be an outspoken critic of low carb diets. I recently explained at length in a recent article why Fleming's findings are very, very questionable.
The results of some of the non-supportive studies warrant further comment; A recent study by Foster et al. failed to detect a significant weight-loss difference after 12 months (Foster et al, 2003), but did in fact detect a significant difference at the 6-month point. Weight regain in both groups at the conclusion of the study strongly suggests that deteriorating compliance was the culprit. Needless to say, the greatest diet in the world won't produce results if not adhered to. Among the other non-supportive studies, those that measured insulin function (Alford et al, 1990, and two 1996 papers by Golay et al) recorded significantly greater glycemic improvements among the low carbohydrate dieters. As such, carbohydrate-restricted diets would still be the preferred option for the ever-growing army of diabetic and pre-diabetic overweight individuals, even in the absence of greater weight loss.
Instead of discussing these studies, Bilborough and Crowe do what all desperate anti-low carb campaigners do: that is, cite the results of the National Weight Control Registry, (Wyatt et al 2000) which was set up by Brown University researchers to record individuals who had successfully lost 30lbs or more, and successfully maintained that weight loss for one year or more. According to these researchers, low carbohydrate dieters are poorly represented on the Registry's database. Now, if the main goal of embarking on a weight loss diet was to increase one's willingness to register for national databases, then the National Weight Control Registry would indeed be highly relevant. However, as a measure of the relative fat-loss efficacy of low and high carbohydrate diets, the Registry is scientifically baseless. After all, there could be countless reasons why the names of low carbohydrate dieters appear infrequently on the Registry; to attempt to guess what these reasons might be would be just that - speculative conjecture. To cite the National Weight Control Registry, and ignore the data from randomized clinical trials that directly compare the effects of low and high carbohydrate diets reveals a shameless disregard for the scientific method.
Bilsborough and Crowe claim that: "The nature of a low-carbohydrate diet … is one that is low in fruits, vegetables (if starchy vegetables aren't adequately replaced with other types of low-carbohydrate-containing vegetables) and grains thus potentially placing an individual at an increased cancer risk if the diet is followed long term. Furthermore, the evidence strongly suggests that it is not the consumption of one or two varieties of vegetables and fruit that confer benefit, but rather the intake of a wide-variety of plant foods (the latter being a common factor in those who have a lower risk of cancer)."
The claim that low carbohydrate diets by their very nature are low in fruits and vegetables is repeated throughout their paper. Here we see Bilsborough and Crowe shamelessly employ the use of what philosopher and author Ayn Rand used to call the "false dichotomy". That is, they carefully make sure that readers are presented with only two alternative options: a high carbohydrate diet rich in fruits and vegetables, or a low-carbohydrate, high-protein diet lacking in fruits and vegetables. They neglect to mention the third option, the one that most low carbohydrate authors call for: an increase in fruit and vegetable consumption at the expense of cereal grains, which are a nutritionally inferior food (for an extensive review on the nutritional shortcomings of cereal grains, whole or refined, see Loren Cordain's outstanding paper, Cereal grains: Humanity's double-edged sword, free download available here). As a result, most people who follow low carb diets as most-commonly prescribed will see, not a decrease, but an increase in fruit and vegetable consumption. Furthermore, the fruits and vegetables most commonly advocated on low-carbohydrate plans are low-carbohydrate, low-glycemic, antioxidant-rich items such as salad greens, cruciferous vegetables, berries, cherries, and other whole fruits - as opposed to high glycemic items like potatoes and fruit juices. This is especially true of paleolithic-style low carb diets, in which minimally-processed non-cereal plant foods and fresh, free-range meats are an integral feature of daily eating. Furthermore, Bilsborough and Crowe's 100g limit that they have stipulated as the cut-off point for defining a low carb diet allows for consumption of a considerable quantity of low-carbohydrate, low-glycemic, and antioxidant-rich fruits and vegetables. As an example, 100g of carbohydrates allows for the daily consumption of 1 large salad (comprised of cos lettuce, fennel, olive oil, grated carrot, a little lemon juice, parsley, basil, etc), one pound of mixed cruciferous vegetables (broccoli, cauliflower, cabbage, etc), a cup of cherries, and two medium-sized peaches (figures based on USDA data). Rest assured, if you begin eating this amount of fruit and vegetables each day, you will propel yourself way ahead of the average Joe in terms of nutrient-rich fruit and vegetable consumption.
According to Bilsborough and Crowe: "Low-carbohydrate diets promote the restriction of dairy products, particularly milk and yoghurt, which are the main sources of calcium in the diet." Astute readers will notice how they carefully left out cheese, which is both high in calcium but low in carbohydrates, and therefore included on the "allowed" list of most popular low-carbohydrate plans. Readers should know that calcium can also be obtained from other sources, such as mineral-rich spring waters, the chewable ends of chicken bones, and small fish with bones intact. According to USDA figures, a 3oz (86g) serving of sardines (with bones) contains more calcium than a cup of milk (325mg versus 290-300mg).
Bilsborough and Crowe repeatedly allude to alleged mineral and electrolyte losses that occur from following low-carbohydrate diets. To address this concern, I will again refer to the study by Rabast and colleagues, (Rabast 1981) in which each of the three different 1340-calorie diets was ingested as a liquid formula under tightly-controlled metabolic ward conditions. Sodium excretion was greater among the low carbohydrate dieters during the first 7 days, but after 28 days was actually highest in the high carbohydrate group. Potassium excretion was also initially greater among the low carbohydrate group, but by the end of the study was similar to that seen in the high carbohydrate group. The researchers stated: "...it appears that the alterations in the water and electrolyte balance … are reversible phenomena and should thus not be regarded as causal agents of the different weight reduction". Despite the fact that these findings were published over twenty years ago, and have since been confirmed by numerous other researchers, folks like Bilsborough and Crowe still persist with the tired old claim that the marked weight loss seen on low carbohydrate diets is simply a product of greater water loss (one has to seriously wonder whether Bilsborough and Crowe have even read the paper by Rabast et al.!)
The authors cite a study by Best et al, (Best et al 2000) which investigated potential cardiac complications in 20 young patients following a ketogenic diet for management of epilepsy. Best and his colleagues reportedly found ECG-detected cardiac abnormalities in three of the patients. Now, if I walk into a Weight Watchers conference, pull twenty of the participants out and hook them up to an ECG and find evidence of cardiac abnormalities in three of them, is this an indictment of Weight Watchers' dietary recommendations, or some other confounding factor? Bilsborough and Crowe state that: "…there was a significant correlation between prolonged QT interval and low serum bicarbonate (suggesting increased blood acidity) and high beta-hydroxybutyrate (levels of which are elevated in ketosis)". As any eighth-grade science student should be able to tell you, association does not necessarily equate to causation. Is it not possible that some of the children were not eating sufficient calories, and therefore receiving insufficient amounts of vitamins, minerals, coenzymes, and nutrients such as carnitine (found in meat by the way) that are crucial for proper cardiac function? The authors themselves acknowledge that similar changes in the QT interval have also been observed in anorexia nervosa and very-low-calorie diets for obesity, "both metabolic states where ketosis is very likely to occur". Is it the excessively low calorie intake in these conditions, or ketosis, that is to blame? While we do know that excessively-low calorie intakes can indeed be deletrious to the heart, there exists no reliable evidence in humans to suggest that the same is true of ketones. Indeed, if ketogenic diets cause such cardiac abnormalities, why were they not evident in Greenland Eskimos who lived solely on ketogenic diets of fish and whale meat? This population, in fact, was renowned for its extremely low prevalence of heart disease.
It should be mentioned that meat - particularly lamb, which we in Australia are blessed to have plentiful access to - is a very rich source of l-carnitine, a substance absolutely critical for heart function. A 1987 study (Cederblad G, 1987) found that individuals following a low carbohydrate, high fat diet absorbed more carnitine from their diet than those following a low fat, high carbohydrate diet. Both diets contained a similar amount of carnitine.
No anti-low-carb review would be complete without the misleading inference that low carb diets can lead to kidney damage, and the APJCN paper is no exception. For the record, there is not a single study that supports the notion that lowered carbohydrate intakes and/or increased protein intakes can damage healthy kidneys.
Furthermore, a recent study appearing in Diabetes (Facchini FS, et al. 2003) seriously challenges the widely-held notion that protein-restriction is desirable for those with existing kidney damage. The study in question compared an iron- and carbohydrate-restricted, but ad libitum protein (derived from white meats, eggs, and dairy) diet with the low protein, high carbohydrate diet traditionally used with kidney patients. Over a period of almost 4 years, those on the carb-restricted low-iron diet were 50% less likely to either die or deteriorate to point where they required dialysis.
In addition to misleading claims about kidney damage, no low-carb-trashing endeavor would be complete without inclusion of the good ol' myth that high protein diets cause bone loss and osteoporosis. Again, Bilsborough and Crowe uphold a long tradition of anti-protein propaganda by claiming that low-carb diets, due to their increased protein content, will lead to bone loss.
The "protein-causes-bone-loss" theory originated after numerous studies demonstrated that high protein diets often increased urinary calcium excretion. The commonly accepted explanation was that this increased urinary calcium was derived from bone, where most of the body's calcium is stored. It was further believed that the release of this alkaline mineral from bone was an attempt by the body to counter increased acidity in the bloodstream. The inference, of course, was that over time this alleged 'leaching' of calcium from the skeletal system would lead to significant decreases in bone mineral density, increasing the risk of osteoporosis.
The problem with theories, of course, is that reality often refuses to acknowledge them. In the real world, it is low protein intakes that are most commonly associated with bone loss, not vice versa (Kerstetter 2003). It appears that the increased calcium excretion frequently seen on high protein diets is not due to mineral loss from bone, but rather a result of increased calcium absorption in the intestine, which ultimately makes more calcium available for excretion in the urine. In other words, when you increase protein, instead of pooping out most of your calcium, you pee it out. In terms of bone health, it's what happens to the calcium when it follows this alternative path that matters.
At the 2002 Annual Meeting of the American Society for Bone and Mineral Research, scientists from the University of Connecticut, John Hopkins Bloomberg School of Public Health, and Yale University presented the results of 8 years of laboratory research which examined the effects of high and low protein intakes on calcium metabolism. As expected, these experiments showed that high protein intakes increased urinary calcium excretion. However, it was also observed that, in both men and women, protein intakes at or below the U.S. recommended daily allowance (RDA) of 0.8g/kg for periods of up to four weeks consistently induced what is known as secondary hyerparathyroidism. The parathyroid glands, located behind the thyroid gland, secrete parathyroid hormone (PTH) in order to regulate the level of calcium in the bloodstream. Secondary hyperparathyroidism typically occurs in response to deficient calcium intakes, but in the aforementioned studies, the calcium intake of the subjects was kept constant regardless of protein intake. So while the high protein diets increased urinary calcium levels, it was actually the low protein intakes that induced clinical signs of calcium deficiency.
The researchers proposed that the level of dietary protein may have been influencing the body's absorption of calcium. They performed a series of experiments in which intestinal calcium absorption was measured (using dual stable calcium isotopes) in pre- and postmenopausal women who were fed diets of varying protein content. Unlike a number of similar previous experiments, the diets of the women were tightly controlled, and the wide variations between individuals in calcium absorption were countered by using each women as her own control. Under these well-controlled conditions, the researchers found that calcium absorption was significantly lower during periods of low protein consumption (0.8g/kg and below) than during periods of high protein consumption. The researchers concluded, in a rather understated manner, that these studies "call the traditional high protein hypothesis to question". (Kerstetter 2003). No kidding!
So yes, high-protein diets increase calcium excretion - but they increase calcium absorption to an even greater degree! This of course, is why the overwhelming majority of epidemiological studies show low bone density to be more closely associated with low protein intakes, and vice-versa for high protein intakes.
Meat and cancer
To quote Bilsborough and Crowe: "In a recent review of prospective cohort studies on meat consumption and colorectal cancer risk, it was found that daily increases of 100 g of all meat or red meat is associated with a significant 12-17% increased risk of colorectal cancer. Epidemiologic evidence on colorectal cancer risk and meat consumption from 32 case-control and 13 cohort studies supported the hypothesis that meat consumption (in particular red meat), is associated with a modest risk of increased colorectal cancer risk."
To their credit, the authors correctly point out: "Not all the evidence however is equivocal and it has been suggested that the epidemiological data are much more consistent with there being a protective role of fruit, vegetables and whole-grain cereals and no role for meat in colorectal cancer." To their shame they follow this comment up by claiming yet again that "A low-carbohydrate diet promotes increased meat consumption at the expense of fruit and vegetable intake". For the umpteenth time, low-carb diets promote an increase in meat and fruit and vegetable intake at the expense of cereal grain and processed food intake!
As for the dubious claim that meat causes colon cancer, most of the aforementioned studies have failed to account for some very important confounders. Overcooking meat, for example, dramatically increases the formation of carcinogenic compounds known as heterocyclicamines. Numerous studies have found that individuals who regularly consume their meat well done have up to five-fold higher cancer rates than those who eat their meat medium-rare.(Sugimura T. 2000) This strongly suggests that, because most studies have failed to include this potential confounder in their risk analyses, any link between meat and cancer (colon or otherwise) has likely been greatly overstated. By the way, turning meat regularly whilst cooking, marinating meat with herbs such as garlic, avoiding high temperature frying, and slicing meat thinner to reduce cooking time can all help to dramatically reduce HCA formation.
If Bilsborough and Crowe truly wish to help people avoid cancer, they should focus on factors that have been repeatedly shown to reliably promote tumor growth in animal studies, such as high consumption of linoleic acid, (Rose DP 1997) an omega-6 fat found in abundance in so-called "heart-healthy" vegetable oils, the consumption of which rose dramatically after the American Heart Association began enthusiastically endorsing their cholesterol-lowering properties in 1961. The eight-year Los Angeles Veteran Administration trial found a significantly higher incidence of cancer among those randomized to follow a polyunsaturated oil-rich diet, compared to those eating a saturated fat-rich diet. (Dayton S, et al, 1969) This was in spite of the fact that the saturated fat group was disadvantaged by a significantly greater number of heavy smokers! Suppression of melatonin, the sleep-inducing hormone (and potent antioxidant) our bodies begin to secrete as darkness falls, also promotes cancer growth in animals with stunning regularity. (Anisimov VN 2003) Leaving lights on at night, staying up late, and letting light filter into our bedrooms all act to suppress melatonin. In support of this notion, epidemiological studies have shown increased breast cancer rates in women working nightshift.
Another important point the authors neglect to mention - or maybe are not even aware of - is that meat itself is a potent source of antioxidant, anticarcinogenic nutrients, such as conjugated linoleic acid (CLA) and carnosine.
Perhaps the most dubious section of all in Bilsborough's and Crowe's paper is the section where they - in all seriousness - attempt to convince the reader that high-carbohydrate diets are superior to low-carbohydrate and/or high-protein diets in terms of blood glucose control. At this point, Bilborough's and Crowe's one-sided analysis becomes more than just irritating; if taken seriously by its readers, it is potentially dangerous. The research clearly shows that practitioners who uncritically accept Bilborough's and Crowe's assertion, and advise their diabetic clients accordingly, could be treading a very perilous path.
As I have stated before, telling diabetics to eat a low-fat, high-carbohydrate diet is about as dumb as trying to put out a fire with gasoline. When researchers from Santa Barbara, California, placed 28 Type 2 diabetics on a low carbohydrate diet (25% carbohydrate) for 8 weeks, they observed significant improvements in glycemic control, as reflected by decreases in both fasting blood glucose and hemoglobin A1c, a measurement that reflects the average blood sugar level over the previous 3 months or so. Nineteen of the patients had been taking oral diabetic drugs prior to the onset of the study; all were able to discontinue the use of these drugs during the study. However, when the patients were switched to a 55% carbohydrate diet, blood glucose control and hemoglobin A1c measurements significantly deteriorated. (Gutierrez et al. 1998)
Similar results were noted in a 1987 study which also compared higher and lower carbohydrate intakes in Type 2 diabetics. In this study, one of the diets contained 20 percent protein, 20 percent fat, and 60 percent carbohydrate. The other contained 20 percent protein, 40 percent fat, and 40 percent carbohydrate. Unfavorable glucose and insulin responses, and significantly greater 24-hour urinary glucose excretion, were observed when subjects followed the high carbohydrate diet. (Coulston et al. 1987)
A 1994 edition of the Journal of the American Medical Association reported how Type 2 diabetics consumed a 40% carbohydrate, 45% fat diet for 6-14 weeks, and a 55% carbohydrate, 30% fat diet for another 6-14 weeks in a randomized crossover fashion. The high carbohydrate diet increased daylong blood glucose and insulin values by 10%. (Garg et al. 1994)
Yet another study with Type 2 diabetics showed that raising the dietary carbohydrate content by a mere 10%, from 40% to 50%, resulted in a significant increase in both post-meal blood glucose and insulin concentrations. (Sestoft et al. 1985)
Finally, researchers from the University of Minnesota recently found that Type 2 diabetics consuming a 30 percent protein, 30 percent fat, and 40 percent carbohydrate diet, showed significantly lower blood glucose levels after meals and greater reductions in glycated hemoglobin levels than those following a 15 percent protein, 30 percent fat, and 55 percent carbohydrate diet. (Gannon et al.)
Type 2 diabetics are not the only folks who experience improvements in blood sugar metabolism when carbohydrate intake is restricted. A recent study compared the effects of three different diets in healthy volunteers; 1) zero fat, high carbohydrate, 2) moderate fat, moderate carbohydrate, and 3) high fat, low carbohydrate. Researchers observed significantly lower insulin concentrations on the high fat, low carbohydrate diet. In addition, those on the high fat, low carbohydrate diet burnt more fat and less glucose for fuel. Glucose disposal rates between the three diets was similar, indicating that those on the high fat, low carbohydrate diet were storing more glucose as glycogen, a highly positive development; after all, glucose driven from the bloodstream and stored as muscle glycogen can later be used for fuel, whereas elevated blood glucose levels do little apart from dramatically accelerating glycation and free-radical damage. (Bisschop et al. 2001)
To be fair, high carbohydrate diets can lead to improvements in blood sugar and insulin function if caloric intake is restricted to the point where fat loss occurs, but most studies comparing such regimens with similarly-restricted low carbohydrate diets show the latter to still be more effective in terms of glycemic control. (Baba et al. 199)Brehm et al. 2003)(Lewis et al. 1977)(Volek et al. 2002)(Layman et al. 2003)(Farnsworth et al. 2003)(Heilbronn et al. 1999)(Jeppesen et al. 1997)(Gumbiner et al. 1996)(Golay et al. 1996)(Piatti et al. 1994)(Rabast et al. 1979)(Fujita et al. 1975) And while calorie-restriction may help mitigate the harmful glycemic effects of high carbohydrate diets, what happens when diabetic individuals eventually return to maintenance-calorie intakes? If the studies comparing maintenance-calorie high- and low-carb diets that we discussed above are any indication, the result will be steadily deteriorating glucose tolerance.
One has to seriously wonder what sort of peer-review process - if any - the folks at the Asia Pacific Journal of Clinical Nutrition employ. For such a poorly-written, biased review to appear in a journal supposedly aimed at health professionals and to have instigated the scare-mongering ACA reports is, quite frankly, pitiful. The February 18 ACA story, and its January 7 predecessor, has likely caused great apprehension among many of the thousands around the country who have adopted low carbohydrate diets.
The sad reality is that most journalists, even those assigned by editors to focus on health and nutrition issues, have very little first-hand knowledge of nutrition and biochemistry. As such, when sensationalist health-related press-releases come floating out of their fax machines they typically have little idea of how to gauge the validity of what they are reading. That's why the media is such a prolific source of dietary confusion and misinformation; one minute they're telling us how low carbohydrate diets are the greatest thing since grass-fed meat, the next we're hearing alarmist claims about mystery deaths, kidney damage, and cardiac complications.
Despite pretending to lament this sad state of affairs, the February 18 ACA segment was actually a classic example of this phenomenon in action.
Anthony Colpo is an independent researcher and certified fitness consultant with 20 years' experience in the physical conditioning arena. To contact: contact~theomnivore.com