An Open Letter to Victorian Health Minister Bronwyn Pike

Ms Pike, get off the anti-low-carb bandwagon!

By Anthony Colpo, March 29, 2004.

Dear Ms Pike,

Recently, you announced a new campaign, to be conducted by your government at taxpayer expense, that would endeavor to alert Victorian residents to the alleged "dangers" of low-carbohydrate diets. To the best of my knowledge, this action is unprecedented in Australian political history, for no state government has ever taken it up on themselves to issue warnings against a specific diet, despite the fact that certain dietary regimens have indeed been directly linked to ill-health and death. Such potentially dangerous nutritional regimes include vegan diets, which have claimed the lives of numerous infants around the world, and resulted in legal proceedings against the misguided parents of these youngsters.(1) Along with their potentially fatal effects on infants, vegan diets have also demonstrated the ability to harm children, adolescents, and even adults. So far, while you have had much to say about low-carb nutrition, you have not uttered a word about vegan diets. Before I discuss just why you are so wrong on low-carb diets, lets take a closer look at vegan regimens.

Vegan Diets - Fast Track To Ill-Health

Among their many nutritional shortcomings, vegetarian diets supply sub-optimal amounts of vitamin B12 and essential long-chain omega-3 fatty acids such as DHA and EPA. B12 is essential for optimal cognitive function, while DHA is a major component of brain tissue. Not surprisingly, analyses of blood samples from vegetarians consistently show lower dietary and lower blood levels of long-chain omega-3 fatty acids. (2-7) These fatty acids can be formed in the body from plant-based omega-3 fats, but numerous studies show that the conversion rate is very low.(8,9) Because of their complete abstinence from animal foods, deficiencies of these and other nutrients are much more pronounced in vegans than in lacto-ovo vegetarians. Below are observations, published in peer-reviewed journals, of the harm that can befall those following these truly unbalanced diets:

• In 1986, Dutch researchers observed that vegan infants had markedly lower B12 levels and impaired psychomotor functioning when compared to control infants.(10,11) On the basis of these findings, the researchers made dietary recommendations to the families of the infants, who subsequently began switching their youngsters to lacto-vegetarian, lacto-ovovegetarian, or even omnivorous diets. On average, the children were six years old when the dietary change took place. In 2000, researchers reported on follow-up examinations of these same subjects, who were now aged between 10 to 16. Two-thirds of the formerly vegan adolescents still suffered from B12 deficiency, whereas all of the subjects in a similarly aged omnivorous control group had normal B12 levels. When given a series of cognitive tests, the ex-vegan group achieved poorer results than the lifetime-omnivore group. A significant association was found between low B12 status and poorer performance on tests measuring fluid intelligence, spatial ability, and short-term memory. Because fluid intelligence involves reasoning, the capacity to solve complex problems, abstract thinking ability, and the ability to learn, the authors pointed out that: "Any defect in this area may have far-reaching consequences for individual functioning." (12).
  
  * British researchers found that, compared to omnivores and lacto-ovovegetarians, vegans suffered a higher frequency of abnormal electroencephalogram (EEG) readings, a test designed to detect abnormalities in the electrical activity of the brain (13). In one of their studies, B12 supplementation improved EEG scores in most of those registering abnormalities, but three of the vegans failed to respond to heavy supplementation with either oral or injected B12.
  
  * In 2000, French researchers reported the case of a 33-year-old patient who lost most of his eyesight after following a strict vegan diet since the age of 20. Ironically, the man had adopted the diet for "improved health", and did not use any supplements. Blood samples showed that his levels of vitamin B1, B12, A, C, D, E, zinc, and selenium were all measurably below normal. Vitamin B12, in particular, is vitally important for maintaining the health of the optic nerve that transmits signals from the eye to the brain. Administration of intramuscular and oral multivitamins normalized blood levels of the aforementioned nutrients, but his eyesight did not recover. They concluded that the nutritional deficiencies in the patient's vegan diet - particularly the insufficient amount of vitamin B12 he had been absorbing - were the most likely cause for the optic nerve deterioration that had resulted in irreversible blindness. (14)

In a recent newspaper article, you stated that: "When we know something is bad for people, like smoking, then we let people know what the health risks are". I eagerly await to see if your department issues any warnings against vegan diets, for unlike low-carb diets, these posess a demonstrated poor safety record.

And what about low-carb diets?

In response to criticisms of your sadly misguided campaign against low-carbohydrate diets, you also stated in the aforementioned article: "Some people might come out and say, 'This is a nanny state - now they are telling us what to eat' ... But while I don't think it is the role of the politician to dictate individual preference and behaviour, it is my role to point out when something can actually harm you."

Seeing as you are taking it upon yourself to become a taxpayer-funded dietary commentator, it behooves you to learn as much as possible about the dietary regimens you intend to comment on. The statements you have made so far in regards to low-carbohydrate diets clearly show that you have not done this.

You claim that low-carbohydrate diets raise the risk of cancer, heart disease, osteoporosis, and even depression. From what peer-reviewed literature did you obtain such information?

Heart Disease

The claim that low-carbohydrate diets raise the risk of heart disease strains all boundaries of logic. Low-carbohydrate diets, via a reduction in cereal grain intake and an increase in meat and fruit and vegetable intake, increase the ingestion of many key heart-healthy nutrients. These include vitamin C, bioflavonoids, magnesium, carnitine, long-chain omega-3 fatty acids, vitamins B6, B12, and folic acid.

Bioflavonoids and vitamin C are important for the formation and maintenance of the collagen inside our arteries. Vitamins B6, B12 and folic acid lower blood levels of homocysteine and C-reactive protein (the former is believed to be directly atherogenic, the latter is an accurate measure of inflammatory activity in the body and a far superior predictor of future CHD risk than LDL cholesterol).(15-17) Long-chain omega-3 fatty acids, meanwhile, have demonstrated an ability to reduce CHD and overall mortality in randomized clinical trials, not just in the wishful-thinking minds of health bureaucrats. Magnesium and carnitine are essential for muscular contraction and energy production; both have been shown to lower mortality from CHD and heart failure in overseas trials.(18-20) When researchers compared a low-carbohydrate diet with a high-carb diet, they found that the former increased carnitine absorption, despite the equal carnitine contents of the two diets.(21)

Allegedly "healthy" cereal grains (whole or otherwise) contain no vitamin C, no B12, contain only omega-6 fatty acids but no omega-3 fats, contain phytates that impair the absorption of magnesium, and contain a substance known as pyridoxine glucoside, which has been shown to reduce the availability of vitamin B6 by 75-80%.(22) The only dietary intervention trial to compare the effects of increased whole-grain intake on CHD outcomes was the DART trial; in this study, men assigned to eat more brown bread and wheat fiber actually suffered a slight increase in CHD mortality (in the same study, men who were instructed to eat a low-saturated fat diet experienced no change, while men instructed to consume fish/fish oil reduced their CHD risk by almost a third).(23)

Sorry, but I don't see any reason why cereal grains should even be included in anyone's diet, let alone form the foundation of said diet. No-one "needs" cereal grains; in fact, those with gluten sensitivity and celiac disease should quite literally avoid them like the plague! Maybe you would care to include these facts in your future public awareness efforts...

Meat is by far the richest source of carnitine, vitamin B6, B12 and (in the case of organ meats), folic acid. Animal foods are also the only non-supplemental source of long-chain omega-3 fatty acids (brain tissue is the richest source, followed by fatty fish).

Non-cereal plant foods (fruits, vegetables, and nuts) - the kind encouraged by virtually all of the current crop of low-carb authors - contain magnesium, folic acid, bioflavonoids, and are the richest dietary sources of vitamin C.

Those who are still obsessed with "risk factors" (e.g, much of the medical establishment) should know that low-carb diets typically raise HDL cholesterol, improve the HDL:LDL ratio, and lower elevated triglyceride levels, while low-fat, high-carbohydrate diets often have the opposite effect. In clinical studies, low-carbohydrate diets have repeatedly been shown to produce significant fat loss; overweight and obesity is well-known to be associated with an increased risk of heart disease (and cancer).

Depending on one's food choices, adopting a low-carb diet will result in an increase of saturated fat intake. Despite the hysterical anti-saturated fat rantings of mainstream low-fat proponents, there exists no sound scientific evidence whatsoever to support any causative role for these fats in the pathogenesis of CHD. Consider carefully the following facts, available in the scientific literature for anyone who cares to look:

1) Four decades worth of dietary intervention trials have completely failed to produce any reduction in CHD that can be attributed to cholesterol-lowering or saturated fat restriction.(24)

2) Ironically, the only cholesterol-lowering strategy that has shown any noteworthy benefit in the reduction of CHD - the use of statin drugs - does not even work by cholesterol-lowering. These drugs operate via anti-inflammatory, artery-dilating, and antioxidant mechanisms.(25-41)

Cancer

The confident proclamations of many that meat and animal fats cause cancer are rather remarkable considering the complete lack of reliable clinical evidence to support such a notion. Even the allegedly "strong" epidemiological evidence is highly suspect. For example, if meat and saturated fat caused cancer, then vegetarians should by all rights experience lower rates of cancer. As a pooled analysis of the largest vegetarian studies shows, they don't.(42)

One of the few randomized clinical trials to examine the above topic was the Polyp Prevention Trial. In this study, over two-thousand patients who had one or more confirmed adenomatous colorectal polyps (adenomatous polyps are considered forerunners to colorectal cancer and are used as markers for colorectal cancer risk) removed within the previous 6 months were randomly assigned to follow either their usual diet, or a low fat, high fiber diet. Compared to the controls, subjects assigned to the high-fiber diet significantly increased their intake of whole-grains and legumes, and ate an average of 2.25 more servings of fruits and vegetables each day. The intervention group was also advised to reduce their consumption of red meat, which they did.

Total fat consumption in the control group averaged 34%, while those following the treatment diet reduced their fat intake to only 24%. After 4 years, colorectal cancer was diagnosed in 10 subjects from the high fiber group, and only 4 from the usual diet group eating more red meat. Even after excluding those diagnosed within the first year of the study, the results were similarly unfavorable; 4 cases in the intervention group as compared to 2 in the control group. Polyp recurrence was virtually identical between the two groups.(43)

In animal studies, the one fat that shows consistent tumor-promoting effects is the omega-6 fatty acid linoleic acid (found in so-called "heart-healthy" polyunsaturated vegetable oils).(44) While animal fat consumption in America has remained stable over the last 100 years (in terms of grams consumed per person per day), the consumption of vegetable oils and margarines has risen dramatically.(45,46) During this time, age-adjusted cancer rates have also risen in both males and females. To hold stable animal fat consumption responsible for rising cancer rates requires a complete abandonment of one's rational faculties.

Osteoporosis

Ms. Pike, the well-worn claim that high-protein diets can cause osteoporosis really is a bad joke, considering that it is a well-established fact that protein is an essential component of bones, and that epidemiological studies repeatedly show that it is low-protein intakes, not high protein intakes, that are associated with reduced bone density.(47)

It is typically claimed that high protein intakes will cause an increase in calcium excretion. Researchers recently examined this premise by performing 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". No kidding!(47)

Depression

The claim that low-carb diets cause depression has been doing the media rounds recently after Massachussetts Institute of Technology researcher Judith Wurtman and her team allegedly found an increase in depressive mood symptoms on people eating high protein diets compared to those following low-protein diets. This study has not yet been published, so there is no information on the exact diet the control and intervention groups followed, the methods used to determine mood changes, etc, etc. I contacted the MIT media department shortly after news of the study broke in the media requesting more information, and never received a reply. One should refrain from using this study as evidence until its results are peer-reviewed and published. It should be noted that Judith Wurtman has published several books promoting low-carbohydrate diets. While that in itself is no guarantee of impropriety or bias, she can hardly be considered a totally impartial voice on the subject.

And that's not all...

Ms. Pike, if you intend to be a credible and objective source of information to the Victorian public on low-carb diets, then it is incumbent upon you to point out, in addition to their alleged flaws, any health benefits they may possess. Researchers have indeed uncovered several characteristics of carbohydrate-reduced diets that could prove extremely valuable in the quest for improved public health.

• There have been over a dozen randomized dietary intervention trials published since the mid-eighties, ranging in duration from four weeks to one year, that directly compared the weight-loss efficacy of low- and high-carbohydrate diets. None of these has shown superior weight loss on the latter, apart from a highly suspect study (click here for details) conducted by Richard Fleming, the Nebraska cardiologist who obtained the late Dr. Atkins death report under highly dubious circumstances. In every study except Fleming's, low carbohydrate diets produced either markedly superior weight loss or statistically non-significant differences in weight loss.(48-65) Despite the oft-repeated claim that low-carb diets are hard to stick to, most studies reporting drop out rates have found higher rates of attrition in the low fat, high-carbohydrate diet groups.
  
  * In addition to spiraling obesity rates, we are currently experiencing an epidemic of type 2 diabetes, the prevalence of which began accelerating skywards soon after orthodoxy embraced the low-fat, high-carbohydrate paradigm. Numerous studies have compared the effects of lower- versus higher-carbohydrate diets on blood glucose control and, in virtually every instance, the carbohydrate-restricted regimens produced superior results.(66-84) Given that the United Nations has forecast over 300 million diabetics worldwide by 2025, the potentially beneficial public health implications of carbohydrate-restriction are enormous.
  
  * Low carbohydrate diets are proving themselves to be invaluable in the most surprising of circumstances. High-protein diets have been traditionally regarded as a no-go zone for individuals with kidney impairment, but in a recent issue of Diabetes, Italian researchers reported that a special low-carbohydrate, unrestricted protein diet, based on low-iron foods, produced dramatic benefits in patients with advanced kidney disease. Compared to patients following a traditional low fat, low-protein, high-carbohydrate diet, those on the low-iron, low-carbohydrate diet were 50% less likely to progress to the point where they either died or required kidney replacement.(85) Very low carbohydrate, or ketogenic, diets are also a well-established and effective treatment for childhood epilepsy.
  
  * Low-carbohydrate diets may eventually prove themselves to have life-extending properties. In animal research, the only consistent intervention that produces increases in life span is calorie-restriction. Whether the same applies to humans has not yet been established, but we do know that cutting calorie intake often produces marked improvements in important health parameters, such as blood glucose control. Unfortunately, telling people to voluntarily limit their calorie intake on a long-term basis tends to be a very poorly-received piece of advice. Low carbohydrate diets, however, may render such unpopular admonitions redundant. Dietary intervention studies have revealed a rather unique phenomenon; subjects following low carbohydrate diets, despite being told to limit only carbohydrate intake and to eat unrestricted amounts of protein and fat, often inadvertently reduce their total calorie intake to levels similar to those seen in subjects who have been explicitly instructed to lower their total calorie intake.
  
  * The possible life-extending effects of low carbohydrate diets have not escaped the attention of longevity researchers at Baltimore's National Institute of Aging. In a recent journal article they stated: "The Atkins Diet is ketogenic resulting in reduced appetite and therefore a reduced calorie intake; individuals who can comply with the diet may therefore exhibit some physiological changes observed in rodents and monkeys subjected to caloric restriction including reduced body weight, and decreased insulin and glucose levels."(86)

Do Your Homework.

Ms. Pike, it is unfortunate that you did not sit down and review the evidence before embarking on your misguided crusade to save Victorians from the supposed harm that awaits them if they adopt low-carbohydrate nutrition. Scandalous media reports arising from misleading press releases by vested interests do not constitute reasonable grounds for commencing a campaign that has the potential to affect public health, for better or worse.

Much of the recent media commotion over low-carbohydrate diets can be traced back to an American vegan organization known as the Physicians Committee for Responsible Medicine. If you are not familiar with this group, whose behavior so far has been anything but responsible, then I suggest you click here. This "Committee" in fact serves as a front-group for the People for Ethical Treatment of Animals (PETA), a radical animal rights and vegan activist group that has given documented financial aid to green terrorist groups.

Perhaps your heroic streak was triggered into action after Australia's most popular current affairs show featured footage of a Melbourne nutritionist claiming that "medically-supervised low-carbohydrate diets" had caused sixty deaths. You should know that this individual was referring to deaths that occurrred over twenty years ago among individuals following liquid protein diets, a crucial fact that was conveniently ommitted (click here to see for yourself). These deaths did not occur among people following the current crop of popular low-carbohydrate diets, people eating real food - you know, meats, eggs, dairy, fruits, nuts, and vegetables! Needless to say, several hundred calories per day derived solely from protein-based powder and water does not constitute a healthy diet, regardless of whether it accompanies a low or high carbohydrate intake.

It should also be mentioned that the individual who appeared on A Current Affair issuing these misleading claims also has authored a number of low-fat diet books. You may like to read a detailed critique of this author's work, and his subsequent reply to this critique, at the following links:

Just How Low Will the Anti-Low-Carb Crowd Go?

A Reply to Bilsborough

Ms. Pike, Your Actions Have Consequences - Bad Ones!

Several days ago, I received an e-mail from a business owner in NSW who, a little while back, started an innovative low-carb meal delivery service in response to the growing popularity of low-carb diets. The ready-made meals delivered by her business include lean meats and vegetables, and, to avert the stigma associated with saturated fats (no matter how misguided this sentiment may be), derive their fat content mainly from monounsaturated sources. Until recently, this individual was doing a roaring trade, having established a franchise chain of 15 outlets delivering delicious low-carb meals around the country. This entrepreneurial mother-of-three saw a niche and filled it, via honest and productive effort (something that more of our politicans should try to emulate), and started reaping the rewards that were rightly hers.

That is, until some misguided politician appeared on national TV and in the nation's newspapers announcing her latest novel waste of money - an anti-low-carbohydrate crusade!

"Since the negative PR has appeared in the recent news, my company is really suffering", said our understandably disheartened low-carb entrepreneur. "Here in Sydney it was as if someone has 'turned off the tap', that's how quiet our phones have been. It is a devastating blow to our businesses from which we hope to recover, but there are no guarantees."

Did customers stop ringing because they had subsequently died from heart disease and cancer, or because they were hospitalized with broken osteoporotic bones and/or depression, or because they had fallen prey to some other alleged adverse effect of low-carb diets?

Nope.

Customers stopped ringing because, not being familiar with the scientific literature, they relied on the media to deliver their diet and health information. So when a bunch of radical vegan activists from North America tried to infer that the death of the late Dr. Atkins was a result of his own dietary prescriptions, and the media lapped it up, they became worried. When some axe-grinding nutritionist from Melbourne appeared on A Current Affair and told the nation that low-carb diets had killed sixty people, they got scared. And when a Victorian politician announced that low-carbohydrate diets were such a threat to public health that her government was going to actively warn people away from them, people ran for the doors. Not being familiar with the scientific literature, which actually indicates that low-carb diets possess an array of favorable qualities and are definitely worthy of increasing research attention, these folks evidently believed what they were hearing on TV and in the newspapers.

Despite the volumes I read and hear about how people supposedly distrust politicians and how they distrust what they read in the papers and see on TV, a significant portion of the population in this country appears to have been suckered beautifully by yet another fallacious government and media beat-up!

Forgive me if I'm wrong, but I thought the notion of someone getting off their butt and "having a go" was supposed to be admired here in Australia. I don't know about others, but I think it is extremely unfair for someone who was making an honest, productive living to now be faced with the prospect of going out of business simply because of misleading, sensationalist bullshit.

I also think it is extremely unfair for some politician to take my tax money, and use it to tell me how I should abandon the very diet that has personally brought me nothing but benefits! Puhleez!

Perhaps most unfair of all is that thousands of people are being scared away from diets that have clearly been shown to benefit a number of common conditions - diabetes and obesity, for example - and hold great promise for treating many other ailments.

Conclusion

Ms. Pike, I know you have already travelled a fair way down your proposed path, and it might make you look rather silly if you abandon your sadly-misguided anti-low-carb campaign after creating such a commotion in the media. Nonetheless, I urge you to study the scientific evidence thoroughly, and then carefully reconsider your current stance. There are far better ways to spend taxpayer funds than on discouraging people from trying diets that may just benefit their health, and from sending flourishing businesses down the tube. I know such a change in stance will not impress the flour and baking industry, who are lobbying hard to try and avoid the same fate that is currently befalling their counterparts in the US, where low-carb diets have undergone phenomenal growth, but I think your primary concern should be public health, not the financial well-being of vested industries.

Sincerely,

Anthony Colpo.

To tell Bronwyn Pike that taxpayer funds should be used in a more responsible manner, e-mail: bronwyn.pike@parliament.vic.gov.au

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52. Lean ME, et al. Weight loss with high and low carbohydrate 1200 kcal diets in free living women. European Journal of Clinical Nutrition, Apr. 1997; 51 (4): 243-248.

53. Torbay N, et al. High protein vs high carbohydrate hypoenergetic diet in treatment of obese normoinsulinemic and hyperinsulinemic subjects. Nutrition Research, May 2002; 22 (5): 587-598.

54. Layman DK, et al. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. Journal of Nutrition, 2003; 133: 411-417.

55. Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factors in overweight adolescents. Journal of Pediatrics, March 2003; 142: 253-258.

56. Volek JS, et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism, July 2002; 51 (7): 864-870.

57. Fleming RM. The Effect of High-, Moderate-, and Low-Fat Diets on Weight Loss and Cardiovascular Disease Risk Factors. Preventive Cardiology, 2002; 5 (3): 110-118.

58. Brehm, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. Journal of Clinical Endocrinology and Metabolism, 2003; 88 (4): 1617-1623.

59. Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, May 22, 2003; 348: 2082-2090.

60. Samaha FF, et al. A low-carbohydrate diet as compared with a low fat diet in severe obesity. New England Journal of Medicine, May 22, 2003; 348: 2074-2081.

61. Wien MA, et al. Almonds vs complex carbohydrates in a weight reduction program. International Journal of Obesity and Related Metabolic Disorders, Nov 2003; 27 (11): 1365-1372.

62. LaRosa JC, et al. effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. Journal of the American Dietetic Association, Sept, 1980; 77: 264-270.

63. Gutierrez M, et al. Utility of a Short-Term 25% Carbohydrate Diet on Improving Glycemic Control in Type 2 Diabetes Mellitus. Journal of the American College of Nutrition, 1998; 17 (6): 595-600.

64. Coulston AM, et al. Deleterious metabolic effects of high-carbohydrate, sucrose-containing diets in patients with non-insulin-dependent diabetes mellitus. American Journal of Medicine, 1987 Feb; 82 (2): 213-20.

65. Garg A, et al. Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus. Journal of the American Medical Association, 1994; 271: 1421-1428.

66. Sestoft L, et al. High-carbohydrate, low-fat diet: effect on lipid and carbohydrate metabolism, GIP and insulin secretion in diabetics. Danish Medical Bulletin. 1985 Mar; 32 (1): 64-69.

67. Gannon MC, et al. An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes. American Journal of Clinical Nutrition, 2003; 78: 734-741.

68. Bisschop PH, et al. Dietary fat content alters insulin-mediated glucose metabolism in healthy men. American Journal of Clinical Nutrition, 2001; 73: 554-559.

69. Baba NH, et al. High Protein vs High Carbohydrate Hypoenergetic Diet for the Treatment of Obese Hyperinsulinemic Subjects. International Journal of Obesity, 1999; 11: 1202-1206.

70. Brehm BJ, et al., A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and Metabolism, 2003; 88 (4): 1617-1623.

71. Lewis SB, et al. Effect of Diet Composition on Metabolic Adaptations to Hypocaloric Nutrition: Comparison of High Carbohydrate and High Fat Isocaloric Diets. The American Journal of Clinical Nutrition, 1977; 30 (2): 160-170.

72. Volek JS, et al. Body Composition and Hormonal responses to a Carbohydrate Restricted Diet. Metabolism, 51(7), 2002, pages 864-870.

73. Layman DK, et al. Increased Dietary Protein Modifies Glucose and Insulin Homeostasis in Adult Women during Weight Loss. The Journal of Nutrition, 2003; 133 (2): 405-410.

74. Farnsworth E, et al. Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women. American Journal of Clinical Nutrition, July 2003; 78: 31-39.

75. Heilbronn LK, et al. Effect of Energy Restriction, Weight Loss, and Diet Composition on Plasma Lipids and Glucose in Patients With Type 2 Diabetes. Diabetes Care, 1999; 22 (6): 889-895.

76. Jeppesen J, et al. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. The American Journal of Clinical Nutrition, 1997; 65 : 1027-1033.

77. B Gumbiner, et al. Effects of diet composition and ketosis on glycemia during very-low- energy-diet therapy in obese patients with non-insulin-dependent diabetes mellitus. The American Journal of Clinical Nutrition, 1996; 63: 110-115.

78. Golay A, et al. Similar weight loss with low- or high-carbohydrate diets. The American Journal of Clinical Nutrition, 1996; 63: 174-178.

79. Piatti PM, et al. Hypocaloric high protein diet improves glucose oxidation and spares lean body mass. Comparison to hypocaloric high-CHO diet. Metabolism, Dec. 1994; 43 (12): 1481-1487.

80. Rabast U, et al. Dietetic treatment of obesity with low and high carbohydrate diets: Comparitive studies and clinical results. International Journal of Obesity, 3 (3), 1979, pages 201-211.

81. Fujita Y, et al. Basal and postprotein insulin and glucagon levels during a high and low carbohydrate intake and their relationships to plasma triglycerides. Diabetes, 1975; 24 (6): 552-558.

82. Facchini FS, Saylor KL. A Low-Iron-Available, Polyphenol-Enriched, Carbohydrate-Restricted Diet to Slow Progression of Diabetic Nephropathy. Diabetes, 52 (5), 2003: 1204-1209.

83. Mattson MP, et al. Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms. Journal of Neurochemistry, Feb, 2003; 84 (3): 417-431.

Anthony Colpo is an independent researcher and certified fitness consultant with 20 years' experience in the physical conditioning arena. To contact: contact@theomnivore.com

Disclaimer: This article is presented for information purposes only and is not intended as medical advice. Persons with medical conditions should institute dietary changes whilst being monitored by a competent medical practitioner.

© Anthony Colpo 2004. Copyright information:

Any articles on this website authored by Anthony Colpo may be reproduced for non-commercial purposes only, providing full credit is given to the author, and that the website name www.theomnivore.com is cited. A hyperlink would also be greatly appreciated. Those wishing to reproduce articles for commercial purposes should e-mail: contact@theomnivore.com

Cancer's Sweet Tooth

by Patrick Quillin, PHD, RD, CNS

During the last 10 years I have worked with more than 500 cancer patients as director of nutrition for Cancer Treatment Centers of America in Tulsa, Okla. It puzzles me why the simple concept "sugar feeds cancer" can be so dramatically overlooked as part of a comprehensive cancer treatment plan.

Of the 4 million cancer patients being treated in America today, hardly any are offered any scientifically guided nutrition therapy beyond being told to "just eat good foods." Most patients I work with arrive with a complete lack of nutritional advice. I believe many cancer patients would have a major improvement in their outcome if they controlled the supply of cancer's preferred fuel, glucose. By slowing the cancer's growth, patients allow their immune systems and medical debulking therapies--chemotherapy, radiation and surgery to reduce the bulk of the tumor mass--to catch up to the disease. Controlling one's blood-glucose levels through diet, supplements, exercise, meditation and prescription drugs when necessary can be one of the most crucial components to a cancer recovery program. The sound bite--sugar feeds cancer--is simple. The explanation is a little more complex.

The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first discovered that cancer cells have a fundamentally different energy metabolism compared to healthy cells. The crux of his Nobel thesis was that malignant tumors frequently exhibit an increase in anaerobic glycolysis--a process whereby glucose is used as a fuel by cancer cells with lactic acid as an anaerobic byproduct--compared to normal tissues.1 The large amount of lactic acid produced by this fermentation of glucose from cancer cells is then transported to the liver. This conversion of glucose to lactate generates a lower, more acidic pH in cancerous tissues as well as overall physical fatigue from lactic acid buildup.2,3 Thus, larger tumors tend to exhibit a more acidic pH.4

This inefficient pathway for energy metabolism yields only 2 moles of adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of ATP in the complete aerobic oxidation of glucose. By extracting only about 5 percent (2 vs. 38 moles of ATP) of the available energy in the food supply and the body's calorie stores, the cancer is "wasting" energy, and the patient becomes tired and undernourished. This vicious cycle increases body wasting.5 It is one reason why 40 percent of cancer patients die from malnutrition, or cachexia.6

Hence, cancer therapies should encompass regulating blood-glucose levels via diet, supplements, non-oral solutions for cachectic patients who lose their appetite, medication, exercise, gradual weight loss and stress reduction. Professional guidance and patient self-discipline are crucial at this point in the cancer process. The quest is not to eliminate sugars or carbohydrates from the diet but rather to control blood glucose within a narrow range to help starve the cancer and bolster immune function.

The glycemic index is a measure of how a given food affects blood-glucose levels, with each food assigned a numbered rating. The lower the rating, the slower the digestion and absorption process, which provides a healthier, more gradual infusion of sugars into the bloodstream. Conversely, a high rating means blood-glucose levels are increased quickly, which stimulates the pancreas to secrete insulin to drop blood-sugar levels. This rapid fluctuation of blood-sugar levels is unhealthy because of the stress it places on the body (see glycemic index chart, p. 166).

Sugar in the Body and Diet Sugar is a generic term used to identify simple carbohydrates, which includes monosaccharides such as fructose, glucose and galactose; and disaccharides such as maltose and sucrose (white table sugar). Think of these sugars as different-shaped bricks in a wall. When fructose is the primary monosaccharide brick in the wall, the glycemic index registers as healthier, since this simple sugar is slowly absorbed in the gut, then converted to glucose in the liver. This makes for "time-release foods," which offer a more gradual rise and fall in blood-glucose levels. If glucose is the primary monosaccharide brick in the wall, the glycemic index will be higher and less healthy for the individual. As the brick wall is torn apart in digestion, the glucose is pumped across the intestinal wall directly into the bloodstream, rapidly raising blood-glucose levels. In other words, there is a "window of efficacy" for glucose in the blood: levels too low make one feel lethargic and can create clinical hypoglycemia; levels too high start creating the rippling effect of diabetic health problems.

The 1997 American Diabetes Association blood-glucose standards consider 126 mg glucose/dL blood or greater to be diabetic; 126 mg/dL is impaired glucose tolerance and less than 110 mg/dL is considered normal. Meanwhile, the Paleolithic diet of our ancestors, which consisted of lean meats, vegetables and small amounts of whole grains, nuts, seeds and fruits, is estimated to have generated blood glucose levels between 60 and 90 mg/dL.7 Obviously, today's high-sugar diets are having unhealthy effects as far as blood-sugar is concerned. Excess blood glucose may initiate yeast overgrowth, blood vessel deterioration, heart disease and other health conditions.8

Understanding and using the glycemic index is an important aspect of diet modification for cancer patients. However, there is also evidence that sugars may feed cancer more efficiently than starches (comprised of long chains of simple sugars), making the index slightly misleading. A study of rats fed diets with equal calories from sugars and starches, for example, found the animals on the high-sugar diet developed more cases of breast cancer.9 The glycemic index is a useful tool in guiding the cancer patient toward a healthier diet, but it is not infallible. By using the glycemic index alone, one could be led to thinking a cup of white sugar is healthier than a baked potato. This is because the glycemic index rating of a sugary food may be lower than that of a starchy food. To be safe, I recommend less fruit, more vegetables, and little to no refined sugars in the diet of cancer patients.

What the Literature Says A mouse model of human breast cancer demonstrated that tumors are sensitive to blood-glucose levels. Sixty-eight mice were injected with an aggressive strain of breast cancer, then fed diets to induce either high blood-sugar (hyperglycemia), normoglycemia or low blood-sugar (hypoglycemia). There was a dose-dependent response in which the lower the blood glucose, the greater the survival rate. After 70 days, 8 of 24 hyperglycemic mice survived compared to 16 of 24 normoglycemic and 19 of 20 hypoglycemic.10 This suggests that regulating sugar intake is key to slowing breast tumor growth.

In a human study, 10 healthy people were assessed for fasting blood-glucose levels and the phagocytic index of neutrophils, which measures immune-cell ability to envelop and destroy invaders such as cancer. Eating 100 g carbohydrates from glucose, sucrose, honey and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria. Starch did not have this effect.11

A four-year study at the National Institute of Public Health and Environmental Protection in the Netherlands compared 111 biliary tract cancer patients with 480 controls. Cancer risk associated with the intake of sugars, independent of other energy sources, more than doubled for the cancer patients.12 Furthermore, an epidemiological study in 21 modern countries that keep track of morbidity and mortality (Europe, North America, Japan and others) revealed that sugar intake is a strong risk factor that contributes to higher breast cancer rates, particularly in older women.13

Limiting sugar consumption may not be the only line of defense. In fact, an interesting botanical extract from the avocado plant (Persea americana) is showing promise as a new cancer adjunct. When a purified avocado extract called mannoheptulose was added to a number of tumor cell lines tested in vitro by researchers in the Department of Biochemistry at Oxford University in Britain, they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited the growth rate of the cultured tumor cell lines. The same researchers gave lab animals a 1.7 mg/g body weight dose of mannoheptulose for five days; it reduced tumors by 65 to 79 percent.14 Based on these studies, there is good reason to believe that avocado extract could help cancer patients by limiting glucose to the tumor cells. Since cancer cells derive most of their energy from anaerobic glycolysis, Joseph Gold, M.D., director of the Syracuse (N.Y.) Cancer Research Institute and former U.S. Air Force research physician, surmised that a chemical called hydrazine sulfate, used in rocket fuel, could inhibit the excessive gluconeogenesis (making sugar from amino acids) that occurs in cachectic cancer patients. Gold's work demonstrated hydrazine sulfate's ability to slow and reverse cachexia in advanced cancer patients. A placebo-controlled trial followed 101 cancer patients taking either 6 mg hydrazine sulfate three times/day or placebo. After one month, 83 percent of hydrazine sulfate patients increased their weight, compared to 53 percent on placebo.15 A similar study by the same principal researchers, partly funded by the National Cancer Institute in Bethesda, Md., followed 65 patients. Those who took hydrazine sulfate and were in good physical condition before the study began lived an average of 17 weeks longer.16

In 1990, I called the major cancer hospitals in the country looking for some information on the crucial role of total parenteral nutrition (TPN) in cancer patients. Some 40 percent of cancer patients die from cachexia.5 Yet many starving cancer patients are offered either no nutritional support or the standard TPN solution developed for intensive care units. The solution provides 70 percent of the calories going into the bloodstream in the form of glucose. All too often, I believe, these high-glucose solutions for cachectic cancer patients do not help as much as would TPN solutions with lower levels of glucose and higher levels of amino acids and lipids. These solutions would allow the patient to build strength and would not feed the tumor.17

The medical establishment may be missing the connection between sugar and its role in tumorigenesis. Consider the million-dollar positive emission tomography device, or PET scan, regarded as one of the ultimate cancer-detection tools. PET scans use radioactively labeled glucose to detect sugar-hungry tumor cells. PET scans are used to plot the progress of cancer patients and to assess whether present protocols are effective.18 In Europe, the "sugar feeds cancer" concept is so well accepted that oncologists, or cancer doctors, use the Systemic Cancer Multistep Therapy (SCMT) protocol. Conceived by Manfred von Ardenne in Germany in 1965, SCMT entails injecting patients with glucose to increase blood-glucose concentrations. This lowers pH values in cancer tissues via lactic acid formation. In turn, this intensifies the thermal sensitivity of the malignant tumors and also induces rapid growth of the cancer. Patients are then given whole-body hyperthermia (42 C core temperature) to further stress the cancer cells, followed by chemotherapy or radiation.19 SCMT was tested on 103 patients with metastasized cancer or recurrent primary tumors in a clinical phase-I study at the Von Ardenne Institute of Applied Medical Research in Dresden, Germany. Five-year survival rates in SCMT-treated patients increased by 25 to 50 percent, and the complete rate of tumor regression increased by 30 to 50 percent.20 The protocol induces rapid growth of the cancer, then treats the tumor with toxic therapies for a dramatic improvement in outcome.

The irrefutable role of glucose in the growth and metastasis of cancer cells can enhance many therapies. Some of these include diets designed with the glycemic index in mind to regulate increases in blood glucose, hence selectively starving the cancer cells; low-glucose TPN solutions; avocado extract to inhibit glucose uptake in cancer cells; hydrazine sulfate to inhibit gluconeogenesis in cancer cells; and SCMT.

A female patient in her 50s, with lung cancer, came to our clinic, having been given a death sentence by her Florida oncologist. She was cooperative and understood the connection between nutrition and cancer. She changed her diet considerably, leaving out 90 percent of the sugar she used to eat. She found that wheat bread and oat cereal now had their own wild sweetness, even without added sugar. With appropriately restrained medical therapy--including high-dose radiation targeted to tumor sites and fractionated chemotherapy, a technique that distributes the normal one large weekly chemo dose into a 60-hour infusion lasting days--a good attitude and an optimal nutrition program, she beat her terminal lung cancer. I saw her the other day, five years later and still disease-free, probably looking better than the doctor who told her there was no hope.

Patrick Quillin, Ph.D., R.D., C.N.S., is director of nutrition for Cancer Treatment Centers of America in Tulsa, Okla., and author of Beating Cancer With Nutrition (Nutrition Times Press, 1998).

References

1. Warburg O. On the origin of cancer cells. Science 1956 Feb;123:309-14.

2. Volk T, et al. pH in human tumor xenografts: effect of intravenous administration of glucose. Br J Cancer 1993 Sep;68(3):492-500.

3.Digirolamo M. Diet and cancer: markers, prevention and treatment. New York: Plenum Press; 1994. p 203.

4. Leeper DB, et al. Effect of i.v. glucose versus combined i.v. plus oral glucose on human tumor extracellular pH for potential sensitization to thermoradiotherapy. Int J Hyperthermia 1998 May-Jun;14(3):257-69.

5. Rossi-Fanelli F, et al. Abnormal substrate metabolism and nutritional strategies in cancer management. JPEN J Parenter Enteral Nutr 1991 Nov-Dec;15(6):680-3.

6. Grant JP. Proper use and recognized role of TPN in the cancer patient. Nutrition 1990 Jul-Aug;6(4 Suppl):6S-7S, 10S.

7. Brand-Miller J, et al. The glucose revolution. Newport (RI) Marlowe and Co.; 1999.

8. Mooradian AD, et al. Glucotoxicity: potential mechanisms. Clin Geriatr Med 1999 May;15(2):255.

9. Hoehn, SK, et al. Complex versus simple carbohydrates and mammary tumors in mice. Nutr Cancer 1979;1(3):27.

10. Santisteban GA, et al. Glycemic modulation of tumor tolerance in a mouse model of breast cancer. Biochem Biophys Res Commun 1985 Nov 15;132(3):1174-9.

11. Sanchez A, et al. Role of sugars in human neutrophilic phagocytosis. Am J Clin Nutr 1973 Nov;26(11):1180-4.

12. Moerman CJ, et al. Dietary sugar intake in the aetiology of biliary tract cancer. Int J Epidemiol 1993 Apr;22(2):207-14.

13. Seeley S. Diet and breast cancer: the possible connection with sugar consumption. Med Hypotheses 1983 Jul;11(3):319-27.

14. Board M, et al. High Km glucose-phosphorylating (glucokinase) activities in a range of tumor cell lines and inhibition of rates of tumor growth by the specific enzyme inhibitor mannoheptulose. Cancer Res 1995 Aug 1;55(15):3278-85.

15. Chlebowski RT, et al. Hydrazine sulfate in cancer patients with weight loss. A placebo-controlled clinical experience. Cancer 1987 Feb 1;59(3):406-10.

16. Chlebowski RT, et al. Hydrazine sulfate influence on nutritional status and survival in non-small-cell lung cancer. J Clin Oncol 1990 Jan;8(1):9-15.

17. American College of Physicians. Parenteral nutrition in patients receiving cancer chemotherapy. Ann Intern Med 1989 May;110(9):734.

18. Gatenby RA. Potential role of FDG-PET imaging in understanding tumor-host interaction. J Nucl Med 1995 May;36(5):893-9.

19. von Ardenne M. Principles and concept 1993 of the Systemic Cancer Multistep Therapy (SCMT). Extreme whole-body hyperthermia using the infrared-A technique IRATHERM 2000--selective thermosensitisation by hyperglycemia--circulatory back-up by adapted hyperoxemia. Strahlenther Onkol 1994 Oct;170(10):581-9.

20. Steinhausen D, et al. Evaluation of systemic tolerance of 42.0 degrees C infrared-A whole-body hyperthermia in combination with hyperglycemia and hyperoxemia. A Phase-I study. Strahlenther Onkol 1994 Jun;170(6):322-34.

From The April 2000 Issue of Nutrition Science News

bantransfats.com

"BanTransFats.com, Inc. is a non-profit corporation based in California. Our goal is the reduction and elimination of trans fats from all food products. Our founder is Stephen Joseph, a lawyer based in San Francisco, who is originally from Britain. Our principal consultant is Mary Enig, Ph.D. She is widely regarded as one of the world's foremost authorities on trans fats.

There are four kinds of fats: saturated fat, trans fat, monounsaturated fat, and polyunsaturated fat. Trans fat is the most dangerous.

Many British food products contain trans fat, including Digestive biscuits. It's not just in biscuits. It's in all kinds of foods, even some "health" foods. If you see the words "hydrogenated" or "partially hydrogenated" in the ingredients, the product contains trans fat.

Recent medical research has shown that trans fat causes significant and serious lowering of HDL (good) cholesterol and a significant and serious increase in LDL (bad) cholesterol; major clogging of arteries; type 2 diabetes; and other serious health problems."

Full article, further information and links on the subject: bantransfats.com

Climb down from the bran wagon

In years to come, the past couple of decades of the twentieth century may well come to be known as 'The Bran Age'; a time when it seemed that most of the diseases of Western civilisation were being blamed on a lack of fibre in the diet, and we were all being exhorted to eat as much as possible to cure or prevent those diseases. Diseases blamed on a lack of dietary fibre include: intestinal diseases such as cancer of the colon, appendicitis, constipation and irritable bowel syndrome as well as coronary heart disease, diabetes, obesity, deep vein thrombosis, varicose veins, hiatus hernia and gallstones.

Full article: Second Opinions - Barry Groves, PhD

The Tail End of the Fiber Myth

Friday, February 02, 2001
Column by Steven Milloy

If you've been shoveling down high-fiber cereals every morning in hopes of preventing colon cancer, you can stop.

The 30-year-old notion that cereal fiber reduces colon cancer risk is turning out to be yet another government-sanctioned myth. It may be time for the Food and Drug Administration to butt out of our colons.

Full article: foxnews.com

Meat, fish and egg intake and risk of breast cancer

"Intakes of animal protein, meat, and eggs have been associated with breast cancer incidence and mortality in ecological studies, but data from long-term prospective studies are limited. We therefore examined these relationships in the Nurses' Health Study. We followed 88,647 women for 18 years, with 5 assessments of diet by food frequency questionnaire, cumulatively averaged and updated over time. We calculated the relative risks (RR) and 95% confidence intervals (95% CI) for risk of developing invasive breast cancer, over categories of nutrient and food intake. During follow-up, 4,107 women developed invasive breast cancer. Compared to the lowest quintile of intake, the RR and 95% CI for the highest quintile of intake were 1.02 (0.92-1.14) for animal protein, 0.93 (0.83-1.05) for red meat and 0.89 (0.79-1.00) for all meat. Results did not differ by menopausal status or family history of breast cancer. We found no evidence that intake of meat or fish during mid-life and later was associated with risk of breast cancer."

International Journal of Cancer
Volume 104, Issue 2, 2003. Pages: 221-227

Source: InterScience

Cohort studies of fat intake and the risk of breast cancer

"We found no evidence of a positive association between total dietary fat intake and the risk of breast cancer. There was no reduction in risk even among women whose energy intake from fat was less than 20 percent of total energy intake. In the context of the Western lifestyle, lowering the total intake of fat in midlife is unlikely to reduce the risk of breast cancer substantially."

Hunter, DJ et. al.
Cohort studies of fat intake and the risk of breast cancer - A pooled analysis. New England Journal of Medicine, 334: (6) FEB 8 1996

Intake of macronutrients and risk of breast cancer

"The largest and most comprehensive study on diet and breast cancer to date, studying over 5,000 women between 1991 and 1994, showed that women with the lowest intake of dietary fat had a significantly higher incidence of breast cancer than the women with the highest intake of dietary fat. It also found that women with the highest intake of starch had a significantly higher incidence of breast cancer than the women with the lowest intake of starch. The study found no evidence that saturated fat had any effect one way or the other on breast cancer, and that unsaturated fat had a significantly protective effect against breast cancer."

Franceschi S et. al. Intake of macronutrients and risk of breast cancer. Lancet; 347(9012):1351-6 1996

High carbohydrate diet implicated in pancreatic cancer

From the British Medical Journal

Full article: BMJ

The Skinny on Fats & Breast Cancer

by Stephen Byrnes, PhD, RNCP

"In today’s nutritional world, fat has become a dirty word. Women in particular are encouraged to eat a low-fat diet to help prevent breast cancer, as well as other ailments, including other cancers. Animal fats such as butter have taken a terrible beating in the media over the past few decades and have been blamed for horrific crimes, including obesity, heart disease and cancer. Accordingly, Western peoples have been virtually brainwashed into thinking that butter and other predominantly saturated fats like coconut oil and tallow are unhealthy. So-called safe substitutes like margarine and various vegetable oils have been heavily promoted and advertised with the result being that the public associates these things with health and well-being.

Unfortunately for us, all of these contentions and claims are false. When it comes to breast cancer prevention, and in some cases treatment, the so-called ‘bad fats’ are actually the good guys, and the ‘safe substitutes’ are increasingly being shown up for what they really are: fabricated foods that cause disease, including breast cancer."

Full article: powerhealth.net