Category: Cancer

Diet Benefits Prostate Cancer

John McDougall, MDDr John McDougall

Diet Benefits Prostate Cancer (Another Ornish Contribution)

Clinical events in prostate cancer lifestyle trial: results from two years of follow-up by Joanne Frattaroli published in the December 2008 issue of the journalUrology found, “Patients with early-stage prostate cancer choosing active surveillance might be able to avoid or delay conventional treatment for at least 2 years by making changes in their diet and lifestyle.” By 2 years of follow-up, 13 of 49 (27%) control patients and 2 of 43 (5%) experimental patients—those encouraged to adopt a low-fat, plant-based diet, to exercise and practice stress management, and to attend group support sessions—had undergone conventional prostate cancer treatment (radical prostatectomy, radiotherapy, or androgen deprivation).

Comment: This is the second report of the Prostate Cancer Lifestyle Intervention Trial started by Dean Ornish, MD.  Given the honest facts about standard prostate cancer treatments, most patients would elect diet, and delay or avoid surgery, radiation, hormone deprivation (pills or cutting off their testicles), and chemotherapy. These damaging treatments fail to produce consistent survival benefits—and every doctor and patient should know the results of a century of research.  Doing nothing would be a better option for most patients.  Research also shows that the high-fat, meat- and dairy- rich Western diet causes this disease. Common sense says “Don’t throw gasoline on a fire.” 

Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23. Epub 2008 Jul 7.

Breast Cancers Spontaneously Disappear

John McDougall, MD


Dr John McDougall

 

Breast Cancers Spontaneously Disappear

The natural history of invasive breast cancers detected by screening mammography by Per-Henrik Zahl published in the November 24, 2008 issue of the Archives of Internal Medicine found, “…that the natural course of some screen-detected invasive breast cancers is to spontaneously regress.”1 The investigators found invasive breast cancer 22% more often in women who had a mammography every other year for 6 years than those who did not (1909 vs. 1564 per 100 000 women). If all cancer were to naturally progress and none disappear then the same number of cancers would be expected to be found in the women who received regular screening every other year and those who only had one exam after 6 years. Their conclusion was, “it appears that some breast cancers detected by repeated mammographic screening would not persist to be detectable by a single mammogram at the end of 6 years.”  The final remarks of the investigators were, “Our findings are equally consistent with the possibility that mammography either leads to a reduction in breast cancer mortality or has no effect at all. Instead, our findings simply provide new insight on what is arguably the major harm associated with mammographic screening, namely, the detection and treatment of cancers that would otherwise regress.”

Comment: Spontaneous regression of advanced breast cancer has been reported.  One recent reported identified 32 such cases, but there are certainly many more unreported cases.2 Advanced melanoma, brain cancer (neuroblastoma), and kidney cancer are also known to disappear without treatment.  Precancerous changes in the female uterine cervix and colon polyps also regress. 

Most of my readers know that I am against doing “early detection” screening tests for most cancers, including those of the breast, prostate, and lung cancer. This study provides one more reason to avoid mammography and even breast-self examination—benefits of which have been seriously questioned.3,4 The harms from these detection campaigns are, however, unquestioned.*

I often see women with breast cancer, men with prostate cancer, and both genders with many other forms of cancer in late stages.  Their doctors have given them no hope—in fact, in most cases their well-intentioned treatments add to their misery.  Hopelessness compounds the suffering.  Patients need to be told that even with advanced cancer, sometimes there is recovery, called spontaneous remission.  I believe this miracle is more likely to happen for someone in good health, rather than in poor health. The only way I know to consistently improve health is by replacing destructive habits with good ones.  The most powerful of these changes is switching from the meat-, dairy-, and junk food-based Western diet to the McDougall starch-based diet.  I have seen what I believe to be spontaneous remissions in my patients several times. Ruth Heidrich, reported as a Star McDougaller, is one remarkable example of metastatic breast cancer diagnosed over 26 years ago—and she lives cancer free today.

*I believe there are minor benefits to be had from PAP smears every 3 to 5 years until age 50, one routine colon exam (polyps) at age 55 to 60, exams of the mouth (leukoplakia), and skin exams (pre-melanoma).

1) Zahl PH, Maehlen J, Welch HG. The natural history of invasive breast cancers detected by screening mammography. Arch Intern Med. 2008 Nov 24;168(21):2311-6.

2) Larsen SU, Rose C. Spontaneous remission of breast cancer. A literature review.Ugeskr Laeger. 1999 Jun 28;161(26):4001-4.

3) Baxter N; Canadian Task Force on Preventive Health Care. Preventive health care, 2001 update: should women be routinely taught breast self-examination to screen for breast cancer? CMAJ. 2001 Jun 26;164(13):1837-46.

4) Gøtzsche PC, Nielsen M. Screening for breast cancer with mammography.Cochrane Database Syst Rev. 2006 Oct 18;(4):CD001877.

Scientists Seek to Rein In Diagnoses of Cancer

By TARA PARKER-POPE
A group of experts advising the nation’s premier cancer research institution has recommended changing the definition of cancer and eliminating the word from some common diagnoses as part of sweeping changes in the nation’s approach to cancer detection and treatment.
The recommendations, from a working group of the National Cancer Institute, were published on Monday in The Journal of the American Medical Association. They say, for instance, that some premalignant conditions, like one that affects the breast called ductal carcinoma in situ, which many doctors agree is not cancer, should be renamed to exclude the word carcinoma so that patients are less frightened and less likely to seek what may be unneeded and potentially harmful treatments that can include the surgical removal of the breast.
The group, which includes some of the top scientists in cancer research, also suggested that many lesions detected during breast, prostate, thyroid, lung and other cancer screenings should not be called cancer at all but should instead be reclassified as IDLE conditions, which stands for “indolent lesions of epithelial origin.”
While it is clear that some or all of the changes may not happen for years, if it all, and that some cancer experts will profoundly disagree with the group’s views, the report from such a prominent group of scientists who have the backing of the National Cancer Institute brings the discussion to a higher level and will most likely change the national conversation about cancer, its definition, its treatment and future research.
“We need a 21st-century definition of cancer instead of a 19th-century definition of cancer, which is what we’ve been using,” said Dr. Otis W. Brawley, the chief medical officer for the American Cancer Society, who was not directly involved in the report.
The impetus behind the call for change is a growing concern among doctors, scientists and patient advocates that hundreds of thousands of men and women are undergoing needless and sometimes disfiguring and harmful treatments for premalignant and cancerous lesions that are so slow growing they are unlikely to ever cause harm.
The advent of highly sensitive screening technology in recent years has increased the likelihood of finding these so-called incidentalomas — the name given to incidental findings detected during medical scans that most likely would never cause a problem. However, once doctors and patients are aware a lesion exists, they typically feel compelled to biopsy, treat and remove it, often at great physical and psychological pain and risk to the patient. The issue is often referred to as overdiagnosis, and the resulting unnecessary procedures to which patients are subjected are called overtreatment.
Cancer researchers warned about the risk of overdiagnosis and overtreatment as a result of new recommendations from a government panel that heavy smokers be given an annual CT scan. While the policy change, announced on Monday but not yet made final, has the potential to save 20,000 lives a year, some doctors warned about the cumulative radiation risk of repeat scans as well as worries that broader use of the scans will lead to more risky and invasive medical procedures.
Officials at the National Cancer Institute say overdiagnosis is a major public health concern and a priority of the agency. “We’re still having trouble convincing people that the things that get found as a consequence of mammography and P.S.A. testing and other screening devices are not always malignancies in the classical sense that will kill you,” said Dr. Harold E. Varmus, the Nobel Prize-winning director of the National Cancer Institute. “Just as the general public is catching up to this idea, there are scientists who are catching up, too.”
One way to address the issue is to change the language used to describe lesions found through screening, said Dr. Laura J. Esserman, the lead author of the report in The Journal of the American Medical Association and the director of the Carol Franc Buck Breast Care Center at the University of California, San Francisco. In the report, Dr. Esserman and her colleagues said they would like to see a multidisciplinary panel convened to address the issue, led by pathologists, with input from surgeons, oncologists and radiologists, among others.
“Ductal carcinoma in situ is not cancer, so why are we calling it cancer?” said Dr. Esserman, who is a professor of surgery and radiology at the University of California, San Francisco.
Such proposals will not be universally embraced. Dr. Larry Norton, the medical director of the Evelyn H. Lauder Breast Center at Memorial Sloan-Kettering Cancer Center, said the larger problem is that doctors cannot tell patients with certainty which cancers will not progress and which cancers will kill them, and changing terminology does not solve that problem.
“Which cases of D.C.I.S. will turn into an aggressive cancer and which ones won’t?” he said, referring to ductal carcinoma in situ. “I wish we knew that. We don’t have very accurate ways of looking at tissue and looking at tumors under the microscope and knowing with great certainty that it is a slow-growing cancer.”
Dr. Norton, who was not part of the report, agreed that doctors do need to focus on better communication with patients about precancerous and cancerous conditions. He said he often tells patients that even though ductal carcinoma in situ may look like cancer, it will not necessarily act like cancer — just as someone who is “dressed like a criminal” is not actually a criminal until that person breaks the law.
“The terminology is just a descriptive term, and there’s no question that has to be explained,” Dr. Norton said. “But you can’t go back and change hundreds of years of literature by suddenly changing terminology.”
But proponents of downgrading cancerous conditions with a simple name change say there is precedent for doing so. The report’s authors note that in 1998, the World Health Organization changed the name of an early-stage urinary tract tumor, removing the word “carcinoma” and calling it “papillary urothelial neoplasia of low malignant potential.” When a common Pap smear finding called “cervical intraepithelial neoplasia” was reclassified as a low-grade lesion rather than a malignancy, women were more willing to submit to observation rather than demanding treatment, Dr. Esserman said.
“Changing the language we use to diagnose various lesions is essential to give patients confidence that they don’t have to aggressively treat every finding in a scan,” she said. “The problem for the public is you hear the word cancer, and you think you will die unless you get treated. We should reserve this term, ‘cancer,’ for those things that are highly likely to cause a problem.”
The concern, however, is that since doctors do not yet have a clear way to tell the difference between benign or slow-growing tumors and aggressive diseases with many of these conditions, they treat everything as if it might become aggressive. As a result, doctors are finding and treating scores of seemingly precancerous lesions and early-stage cancers — like ductal carcinoma in situ, a condition called Barrett’s esophagus, small thyroid tumors and early prostate cancer.
But even after years of aggressively treating those conditions, there has not been a commensurate reduction in invasive cancer, suggesting that overdiagnosis and overtreatment are occurring on a large scale.
The National Cancer Institute working group also called for a greater focus on research to identify both benign and slow-growing tumors and aggressive diseases, including the creation of patient registries to learn more about lesions that appear unlikely to become cancer.
Some of that research is already under way at the National Cancer Institute. Since becoming director of the institute three years ago, Dr. Varmus has set up a list of “provocative questions” aimed at encouraging scientists to focus on critical areas, including the issue of overdiagnosis and molecular tests to distinguish between slow-growing and aggressive tumors.
Another National Cancer Institute program, the Barrett’s Esophagus Translational Research Network, or Betrnet, is focused on changes in the esophageal lining that for years have been viewed as a precursor to esophageal cancer. Although patients with Barrett’s are regularly screened and sometimes treated by burning off the esophageal lining, data now increasingly suggest that most of the time, Barrett’s is benign and probably does not need to be treated at all. Researchers from various academic centers are now working together and pooling tissue samples to spur research that will determine when Barrett’s is most likely to become cancerous.
“Our investigators are not just looking for ways to detect cancer early, they are thinking about this question of when you find a cancer, what are the factors that might determine how aggressively it will behave,” Dr. Varmus said. “This is a long way from the thinking 20 years ago, when you found a cancer cell and felt you had a tremendous risk of dying.”

Too Much Breast-Cancer Treatment?

Every few months, another study reports that many breast cancers are being “overdiagnosed”—that is, detected and treated even though they would never cause problems if they were left alone. In one article, epidemiologists in Norway estimated that 15% to 25% of breast cancers found by mammograms were being treated unnecessarily.

A study in Norway fuels the debate over whether breast cancer can be overtreated. Melinda Beck on The News Hub discusses the debate over the concept of too much breast-cancer treatment. Photo: Bloomberg.

The study in the Annals of Internal Medicine in April calculated that for every 2,500 women offered mammograms over 10 years, one breast-cancer death was averted, but six to 10 women were subjected to surgery, radiation and/or chemotherapy unnecessarily.

The researchers in Norway compared breast-cancer rates in counties where a government mammogram program had begun with those without such screening, as well as with past years. They found that detecting and treating many early-stage breast cancers reduced the number of late-stage cancers and deaths only slightly, prompting them to conclude that much of the treatment was unnecessary—in some cases because the cancers wouldn’t have progressed, and in some cases because they were fatal despite being treated early. Other studies have estimated that the overdiagnosis rate falls in a wide range, anywhere from 2% to 52%.

There is currently no way to tell which patients diagnosed with breast cancer—200,000 a year in the U.S.—could safely forgo treatment, breast-cancer specialists say. “When you can tell me which cancers need to be treated and which don’t, then I will consider this argument” about overdiagnosis, says Clifford Hudis, chief of the Breast Cancer Medicine Service at Memorial Sloan-Kettering Cancer Center in New York City.

Clinicians say leaving breast cancer untreated is a gamble they can’t take. “I don’t know anyone who offers women the option of doing nothing,” says Eric Winer, director of the breast cancer program at Dana-Farber Cancer Institute in Boston. “On the one hand, we are aware of the overtreatment, all of us. On the other hand, there are still 40,000 women every year who die of breast cancer.”

Otis Brawley, an epidemiologist and breast-cancer specialist who heads the American Cancer Society, notes such estimates are all statistical presumptions. “Even if we overdiagnose 1 in 5, we have numerous studies showing that by treating all these women, we save a bunch of lives,” he says.

A 2011 Cochrane review of seven trials in which 600,000 women were randomly assigned to get mammograms or not estimated that while 30% were overdiagnosed, breast cancer deaths were reduced by 15%.

Even in the precancerous stage, called ductal carcinoma in situ (DCIS) when abnormal cells are confined to a milk duct, physicians almost always advise women to have a lumpectomy or mastectomy along with radiation, because about 20% of the 65,000 cases of DCIS found every year in the U.S. become invasive cancer.

A few women do opt to monitor their DCIS to see if it progresses. A study in the journal The Breast last year of 14 such women, who took hormone-blocking drugs, found that after two years, eight decided to have surgery, with five of them having progressed to stage 1 invasive breast cancer. Six remained on active surveillance with no evidence their DCIS had worsened.

The authors, from the University of California, San Francisco, noted that even when DCIS becomes an invasive cancer, it’s treatable when found at an early stage: The odds that a 60-year old woman with a 7 millimeter breast tumor, would die from it in the next 10 years are less than 3%, half the risk she faces of dying from another cause during that time.

Physicians say it would be far riskier to leave invasive breast cancers untreated. “At this point, any breast cancer does need to be removed,” says Bhuvaneswari Ramaswamy, a breast cancer researcher at the Ohio State University Comprehensive Cancer Center in Columbus, Ohio. “We do more than we need to because we don’t know how to do less.”

Scientists have made progress in analyzing individual breast cancers and tailoring treatment accordingly. About two-thirds of tumors have estrogen receptors that make them vulnerable to hormone-blocking medications. About one-third test positive for a protein called HER2 that makes cancers particularly aggressive, but susceptible to the drug Herceptin.

A new wave of tests can predict how tumors will behave based on their genetic profile. The most commonly used test is Oncotype DX, which analyzes 21 genes. Cells from about half the breast tumors in the U.S. are now sent to Genomic Health Inc. in Redwood City, Calif., which developed the test. The company’s technicians determine how likely the cancer is to recur in 10 years and whether the patient would benefit from chemotherapy as well as radiation and surgery. Company officials say the test has reduced the number of U.S. breast-cancer patients on chemotherapy by 20% since it became available in 2004.

A new Oncotype DX test can predict whether a patient with DCIS would benefit from radiation in addition to surgery. But there is no test that can determine whether a breast tumor can be left untreated. “That’s a dream that we would all have for the future,” says Steven Shak, co-founder of Genomic Health, who led the development of Herceptin.

The company is testing a version of Oncotype DX that may be able to tell which prostate cancers don’t need treatment. More than 60% of prostate cancers are thought to be so slow-growing that they would never be life-threatening, but as of now, there is no way to tell those apart from the fast-growing ones that kill 28,000 men in the U.S. every year. About 20% of prostate cancer patients opt for “active surveillance” rather than immediate treatment—in part because the side effects of radiation and surgery can be severe, including impotence and incontinence.

Biostatisticians argue that fewer mammograms would reduce the number of small, early cancers found, as well as the rate of false positives that require additional scans and biopsies. That’s the rationale the U.S. Preventive Service Task Force used in 2009 when it recommended that women get mammograms every two years starting at age 50, instead of annually starting at age 40.

“I’m certainly not asking anyone to stop getting mammograms. I am asking my profession to tell women the truth about the [overdiagnosis] deal,” says H. Gilbert Welch, professor of medicine at Dartmouth Institute for Health Policy & Clinical Practice.

Patients are seldom even told about the overdiagnosis issue and there is very little data on the long-term side effects of cancer treatments, which can include chronic pain, debilitating fatigue, “chemo brain” or foggy thinking, and additional cancers linked to radiation treatments, says Fran Visco, president of the National Breast Cancer Coalition, a nonprofit advocacy group. “We shouldn’t not tell them the truth because we are worried they’ll be confused.”

Many physicians who treat breast cancer patients are loath to stop looking so hard for cancer, and hope for additional tests that can better predict which breast tumors will stay harmless. Meanwhile, says Memorial Sloan-Kettering’s Dr. Hudis, “we are quibbling over whether everyone benefits or only some people. Let’s not lose sight of the fact that we are saving lives.”

The Facts About Breast Cancer

A look at data about the disease in the U.S. and the typical treatments.

•Estimated new cases in 2012: 226,870 women; 2,190 men

•Estimated deaths in 2012: 39,510 women; 410 men

•Median age of diagnosis: 61

•Median age at death: 68

•Percentage diagnosed as Stage IV (metastasized): 5%

•Five-year survival by stage: local 98%; regional 83%; metastasized 23%

•Five year survival overall: 89%

•Diagnosed in lifetime with breast cancer: 1 in 8 women

Sources: NCI/SEER data from 2005-2009; National Cancer Institute

Typical Treatments by Stage:

•Stage 0 (noninvasive DCIS): lumpectomy or mastectomy and radiation, sometimes hormone therapy

•Stage I or II: lumpectomy or mastectomy, radiation and often chemotherapy

•Stage III: chemotherapy and radiation before or after mastectomy, underam lymph nodes removed, often targeted therapy

•Stage IV and recurrent: surgery (depending on where cancer has spread), chemotherapy, radiation, hormone, other therapies

Is Sugar Toxic?

Kenji Aoki for The New York Times
By GARY TAUBES
Published: April 13, 2011
 On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.
Multimedia

What the average American consumes in added sugars:

Kenji Aoki for The New York Times

Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have alsoportrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not themajor, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (v.titunik-MagGroup@nytimes.com).

Good question Finlay

Why is the school nurse promoting dairy as a necessary and good food choice for the children?

Good question Finlay.

The very simple answer is that your mind has been captured by your parents’ acceptance of milk as a great food. Your Dad assumed it was a good product because his mom and I made it available to him.

Why do we accept milk, or any other product, as being good for us? Because, we trust our Mom and Dad to make the right choices for us.

Unfortunately, the Dairy industry has been brain washing school children for years. Even when your Bumpa went to school, we had a nurse come around and tell us how good milk was 67 years ago.

So, you can see we have been listening to the dairy industry for too long without questioning them.

It is hard to believe that we have all been deceived by this one group. The problem gets worse if you consider the nurse truly believes that she is telling you the truth. She and her parents were misled as well.

So we now have a belief system that says milk is good for you no matter what.

So, again, your mind has just accepted that milk is good for you without question. This is not because you are complacent, or not thoughtful. It is because you are trusting of your parents’ choices and of what the nurse is telling you.

The dairy industry wants us to be complacent, docile and subservient and not to question them or their products.

I know that you will make an informed decision on this topic as you make yourself aware of the real facts. The facts are as follows:

Dairy products will make you fat, they will clog your arteries with plaque, promote heart disease, obesity, and, worst of all, cancer. The protein in milk is a known carcinogen, that is, it promotes the growth of cancer once cancer is initiated. Most sinful of all, milk contributes to diabetes in infants and reduces the lives of many children to a life-long disease dependent on insulin medications to stay alive. The dairy industry has been warned and prohibited from promoting cows’ milk for consumption by children under 2 years old.

So, you see Finlay, there are other opinions but generally dissenting views are not published or supported by the establishment. By the way, acne and facial pock marks can be attributed to milk consumption by teenagers. Look good, avoid dairy.

That is why it is up to you to do one very important thing.

“THINK”

Breast Cancer
By Robert Cohen Executive Director Text Only

B = Breast Cancer


The following ten references provide converging lines of evidence that focus upon one central point.There are hundreds of millions of different proteins in nature, and only one hormone that is identical between any two species. That powerful growth hormone is insulin-like growth factor, or IGF-I. IGF-I survives digestion and has been identified as the KEY FACTOR in breast cancer’s growth.

IGF-I is identical in human and cow.

If you believe that breast feeding “works” to protect lactoferrins and immunoglobulins from digestion (and benefit the nursing infant), you must also recognize that milk is a hormonal delivery system. By drinking cow’s milk, one delivers IGF-I in a bioactive form to the body’s cells. When IGF-I from cow’s milk alights upon an existing cancer…

“Human Insulin-like growth factor (IGF-I) and bovine IGF-I are identical. Both contain 70 amino acids in the identical sequence.”

Judith C. Juskevich and C. Greg Guyer. SCIENCE, vol. 249. August 24, 1990.

“IGF-I is critically involved in the aberrant growth of human breast cancer cells.”

M. Lippman. J. Natl. Inst. Health Res., 1991, 3.

“Estrogen regulation of IGF-I in breast cancer cells would support the hypothesis that IGF-I has a regulatory function in breast cancer.”

A.V. Lee, Mol-Cell- Endocrinol., March, 99(2).

“IGF-I is a potent growth factor for cellular proliferation in the human breast carcinoma cell line.”

J.C. Chen, J-Cell-Physiol., January, 1994, 158(1)

“Insulin-like growth factors are key factors for breast cancer growth.”

J.A. Figueroa, J-Cell-Physiol., Nov., 1993, 157(2)

“IGF-I produces a 10-fold increase in RNA levels of cancer cells. IGF-I appears to be a critical component in cellular proliferation.”

X.S. Li, Exp-Cell-Res., March, 1994, 211(1)

“IGF-I plays a major role in human breast cancer cell growth.”

E.A. Musgrove, Eur-J-Cancer, 29A (16), 1993

“IGF-I has been identified as a key factor in breast cancer.”

Hankinson. The Lancet, vol. 351. May 9, 1998

“Serum IGF-I levels increased significantly in milk drinkers, an increase of about 10% above baseline but was unchanged in the control group.”

Robert P. Heaney, Journal of the American Dietetic Association, vol. 99, no. 10. October 1999

“IGF-1 accelerates the growth of breast cancer cells.”

M. Lippman Science, Vol. 259, January 29, 1993

Recombinant Bovine Growth Hormone

Recombinant Bovine Growth Hormone, Public Servants and Trust

Call me idealist, but I give our elected officials and public servants the befit of the doubt – that they are acting in our best interests to the best of their (sometimes limited) knowledge. This interview both confirms and explodes that belief. From the CBC’s public affairs show of Nov 22 2012, two Canadian scientists from Health Canada’s Food Inspection Agency explain the pressures they felt (to the point of being fired) to allow the use of Eli Lilly and Monsanto’s Recombinant Bovine Growth Hormone (RBGh) in Canadian dairy cattle.

RBGh is a synthetic, laboratory produced version of a hormone that cattle produce cyclically during their growth, maturation and lactation. It is administered to increase milk production in adult cows. RBGh has been strongly linked to several metabolic diseases both in dairy cattle and in humans consuming milk produced by cattle being treated with RBGh. Luckily, Canadian dairy farmers are not allowed to use RBGh on their animals.


The bad news – the Canadian government has slowly changed Canadian dairy regulations (in the face of pressures from GATT and NAFTA agreements) to allow freer access to Canada’s markets for American dairy products (including those from cows treated with RBGh). In an effort to reduce “protectionism” and to allow “market forces” to dictate what’s best for us, our dairy marketing laws have been slackened to allow access to our grocery shelves to U.S. dairy products. The American products allowed access to Canadian markets are dehydrated products. They are listed as “milk ingredients”, “concentrated skim milk”, “whey protein concentrate” or “milk protein concentrate”. Using milk products from cows treated with RBGh is a sneaky way to help keep the cost of your yogurt and other dairy products artificially low. Even in the U.S.A., many small farmers have stopped using RBGh on their cattle because they noticed the negative health effects. Most industrial farming operations (factory farms) still use this hormone as a way to keep production up and costs down. When you consume products with RBGh milk, you expose yourselves to serious health risks (cancer, thyroid and gonadal problems, allergy and inflammation problems) and you indirectly encourage poor animal welfare practices.

Read the ingredients and think don’t buy dairy products labelled with “milk ingredients”, “concentrated skim milk”, “whey protein concentrate” or “milk protein concentrate”. It’s that simple. Vote with your wallet, and when the next election comes to your neighbourhood – ask questions of those vying for office. Don’t blindly trust their good intentions.

Health Protection Branch, Health Canada
April 21, 1998

This volume consists of the submission by Consumers International, a 230- member organization in 100 countries: supplementary information dated Sept 25/97

Identified potential public health impacts were as follows:

  1. Levels of IGF-I are significantly elevated in milk from rBST treated cows and will continue to rise with increased use of BST.It is the IGF-I, not the BST per se. that is the main cause for concern regarding possible adverse effects on human health. It is indicated that IGF levels are substantially increased in the latest Monsanto study and in 5/7 studies previously reviewed by JECFA. US FDA concurs that BST treatment leads to statistically significant increases in IGF-I levels in milk. Another study (Prosser et al, 1989) was cited which was reviewed neither by JECFA nor FDA, which reported very high levels (3.6x normal) – much higher than what had been presented in the submitted data. Table I is a good summary of the data.
  3. IGF-I, in the presence of casein and other protective factors, is not destroyed by digestion in the stomach and can pass into the intestine, where it may produce local harmful effects. Epithelial cells in the colon grow more rapidly in response to IGF-I at the levels typically found in milk. Acromegaly, a disease involving high endogenous IGF-I levels, is associated with increased risk of colon cancer and pre-cancerous colon polyps.
  5. It is suggested that toxicity studies with free IGF and the fact that endogenous levels of IGF levels are higher than what is found in the milk of BST treated cows is irrelevant because the IGF is not associated with any protective factors that would ensure bioactivity. IGF binds to receptors lining the GI tract and will stimulate the synthesis of its own receptors. It is also suggested that IGF -1 can be absorbed in the systemic circulation where it may affect the levels of other hormones.
  7. Increased mastitis leads to higher antibiotic residues exacerbating antibiotic resistance. The FDA’s “safe” limits of up to 150 ppb can select for disease resistance in S. aureus.
  9. It is speculated that IGF-I plays a role in the expression of genes that encode for prion synthesis and that increased IGF-I shortens the incubation period for Bovine Spongiform Encephalopathy (BSE). Thus, the use of BST might increase the risk of exposure to BSE infection.


  • local effects on GI tract: both paracrine and autocrine in nature – growth factor for colon cancers -conclude that the colon is at special risk
  • strong role in breast cancer
  • may play a role in osteosarcoma, the most common bone tumor in children, usually occurring during the adolescent growth spurt
  • implicated in lung cancer
  • possess angiogenic properties – important to tumors some of which secrete their own growth factors to promote angiogenesis,
  • e.g., retinal neovascularization in mice

In November of 1993, the FDA approved rBST zinc suspension to enhance milk production in lactating dairy cows, declaring that the milk from treated cows is safe for human consumption. The United States is the only developed country permitting the use of BST, of which there are four manufacturers. There are reports on file that Monsanto pursued aggressive marketing tactics, compensated farmers whose veterinary bills escalated due to increased side effects associated with the use of rBST, and covered up negative trial results. All the four US manufacturers refused to disclose the lists of their research grants to US universities.

 

  • WHAT WAS DONE

    For the purpose of approving ESCs, HSD concluded that the milk and meat from BST treated cows was safe for human consumption as early as 1986, without providing any rationale as why this conclusion was reached. Studies submitted in support of this conclusion were not described until 1990.

    1990: 4-page review by D.R. Casorso completed within two weeks of the filing of the submission.

    1995: more detailed review by M.S. Yong which presented, for the first time, the rationale for concluding that meat and milk from BST -treated cows is safe for human consumption; first mention of the potential adverse health effects of IGF-I.

    1998 reviews by M.S. Yong: rationale for waiving the need for chronic toxicity testing; discussion of potential allergenicity.


    WHAT WAS NOT DONE

    Studies indicated by manufacturer as being available upon request were never requested by HSD reviewers.

    Importance of the 3-month rat toxicology study as an indicator of potential oral absorption of rBST, i.e., the demonstration of immunoglobins in rat serum, was not mentioned. This is an important omission in that the lack of oral bioactivity formed the basis for waiving chronic toxicity study requirements. The human health implications of the immunological findings in rats should have been thoroughly evaluated and dismissed only if adequately justified by the evidence available at the time (e.g., binding of rBST to HG receptor is negligible; antibodies raised to rBST will not cross react with HG, primary response was induced in only 30% of animals at high doses, etc.). IGF-I production in liver of rats was not examined. Species specificity issues and possible threshold effects (dose -response) should have been discussed. Secondary challenge bioassays should have been requested to further characterize the immunological response.

    The fact the rBST can be absorbed, albeit at high doses, calls into question the decision not to request additional chronic toxicity studies. The evaluator should have explored the physiological effects of such high oral doses (and effects on hypophysectomized rats further (e.g., effects on peripheral growth and metabolism).

    The 1990 evaluation was largely a theoretical review taking the manufacturer’s conclusions at face value. No details of the studies nor a critical analysis of the quality of the data was provided.

    The requirement for a 3-month study in a nonrodent species (e.g,, dog) was not requested. No long-term toxicology, teratology or reproductive/fertility studies were requested. Definitive studies demonstrating the lack of absorption of rBST or IGF-I upon oral administration were neither conducted nor requested.

    Potential adverse effects of IGF-I on human health were not discussed until 1995. When discussed, rationales were based purely on speculative reasoning and not on substantive data or studies. The rationale for not requiring chronic toxicity or teratology/reproductive studies was described in more detail in the 1998 reports but again is based on the assumption that there are no physiological consequences of oral absorption of rBST. This ignores the fact that the 3-month rat study did show a physiological response.

    Evidence from the animal safety reviews were not taken into consideration. These studies indicated numerous adverse effects in cows, including birth defects, reproductive disorders, higher incidence of mastitis, which may have had an impact on human health. This observation should be qualified by the poor quality of the data package. Similar observations were recorded in the FDA FOI summary and the company label. These findings should have stimulated the need for requesting additional teratology and reproduction studies in laboratory animals. This should have prompted HSD evaluators to re-examine the accuracy of their data and the assumptions based thereon.

    The mastitis issue should have raised concerns regarding increased use of antibiotics with consequent exacerbation of resistance to antibiotics.

    The nature of the product (being a hormone) and its chemistry should have prompted more exhaustive and longer toxicological studies in laboratory animals.