Sugars and Cancer

      45 Comments on Sugars and Cancer

A reader asked me for some information on cancer and sugar, so I pulled up some items from my research database.  As long as I had the articles in front of me, I thought I’d share them.

Nothing listed here proves absolutely that sugars drive cancer or that a ketogenic diet will prevent cancer, but taken together, the articles do paint a picture.  Let’s take a look.

Cancer cells slurp up fructose, US study finds

Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.

Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.

They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types.

“These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA’s Jonsson Cancer Center and colleagues wrote.

“They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”

I found some suggested meal plans on the USDA’s official My Plate site, which I’ll share in another post.  Whole milk isn’t on the meal plan for breakfast, but orange juice and strawberry-flavored (i.e., sugary) skim milk are.  Remind me again … which of those drinks contains fructose and which doesn’t?

Compound That Blocks Sugar Pathway Slows Cancer Cell Growth

Scientists at Johns Hopkins have identified a compound that could be used to starve cancers of their sugar-based building blocks. The compound, called a glutaminase inhibitor, has been tested on laboratory-cultured, sugar-hungry brain cancer cells and, the scientists say, may have the potential to be used for many types of primary brain tumors.

The Johns Hopkins scientists, inventors on patent applications related to the discovery, caution that glutaminase inhibitors have not been tested in animals or humans, but their findings may spark new interest in the glutaminase pathway as a target for new therapies.

Glutaminase is an enzyme that controls how glucose-based nutrients are converted into the carbon skeleton of a cell. Additional enzymes that help construct the so-called “bricks” of the carbon skeleton are controlled by a gene called IDH1. In some brain cancer cells, IDH1 is mutated and the resulting enzyme grinds up the bricks into nutrients that feed cancer cells.

Yes, yes, I know what you’re thinking:  if blocking the glucose pathway slows cancer growth, why not just tell people to stop eating foods that spike glucose?  Well, I’m pretty sure the answer lies in the fact that scientists have applied for patents.  You can’t patent dietary advice, but you can patent a drug.

Diabetes Medication May Get New Life as Cancer Treatment

The drug metformin, a mainstay of diabetes care for 15 years, may have a new life as a cancer treatment, researchers said.

In a study in mice, low doses of the drug, combined with a widely used chemotherapy called doxorubicin, shrank breast-cancer tumors and prevented their recurrence more effectively than chemotherapy alone.

The findings add to a growing body of evidence that metformin, marketed as Glucophage by Bristol-Myers Squibb Co. and available in generic versions, could be a potent antitumor medicine.

In the report, being published in the Oct. 1 edition of Cancer Research, a journal of the American Association for Cancer Research, researchers said the combination of metformin and doxorubicin killed both regular cancer cells and cancer stem cells.

In contrast, doxorubicin alone had limited effect on the stem cells.

Mice that grew tumors generated from human breast-cancer cells have remained tumor-free for nearly three months on the combined treatment, while tumors have recurred in those not given the diabetes remedy.

Researchers said the results have potentially broad implications for cancer treatment.

Hmmm, now why would a drug given to type 2 diabetics be effective against cancer?  You have to read pretty far down the article to find out:

How metformin affects cancer isn’t certain, but one possibility is that it deprives tumor cells of sugar.

“Cancer cells are gluttons for glucose,” said George Prendergast, president and chief executive officer of Lankenau Institute for Medical Research, Wynnewood, Pa. “It is likely that metformin is taking advantage of this gluttony of the cancer cell in order to attack it.”

Cancer cells are gluttons for glucose … I’ll be sure to think about when I’m drinking my USDA-approved skim milk with added sugar.

Dietary glycemic load and colorectal cancer risk

The link above is to an observational study based on food questionnaires, so it doesn’t exactly meet the gold standard for research.  Nonetheless, here’s the conclusion:

The positive associations of glycemic index and load with colorectal cancer suggest a detrimental role of refined carbohydrates in the etiology of the disease.

The next time some vegan zealot trots out an observational study showing a weak association between meat and cancer, you can reply with this one and explain that since glycemic load is strongly associated with colorectal cancer, you’re sticking with a low-glycemic diet – meat included.  If the vegan zealot starts quoting the China Study, you can reply with this (sort of) China study of Chinese Americans:

Carbohydrates and colorectal cancer risk among Chinese in North America

Here’s the conclusion:

These data indicate that increased eCarb (non-fiber carb) and total carbohydrate consumption are both associated with increased risk of colorectal cancer in both sexes, and that among women, relative risk appears greatest for the right colon, whereas among men, relative risk appears greatest for the rectum.

So get T. Colin Campbell’s high-carb diet out of my face.

Effects of a ketogenic diet on tumor metabolism

This one isn’t a study; it’s a case report from 1995 of two pediatric cancer patients put on ketogenic diets.  Here are some quotes from the abstact:

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient’s overall nutritional status.

So all the way back in 1995, at least some doctors suspected that depriving cancers of glucose might help.  Sheesh.  Anyway …

RESULTS:  Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression.

Improvements in mood and skill development?  No, no, no … low-carb diets make you depressed and irritable.  I know that’s true, because I read it on Yahoo Health.

Glucose deprivation activates feedback loop that kills cancer cells

Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.

Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.

In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose —activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.

Hey, I don’t care if it’s an amplification loop that does the job or if the cancer cells just die off from a lack of fuel.  The point is, once again we see that depriving cancer cells of sugars can kill them.

Keep starving those cancer cells, folks.


45 thoughts on “Sugars and Cancer

  1. Macca - from New Zealand

    Hi Tom,
    I’m a big fan and frequently read your blog.
    About 3 and a half years ago’ I lost both parents within 6 weeks of each other to cancer – Dad to bowel and Mum to lymphoma. That was what sent me on my journey which led me to you! Dad was 86 and had been in poor health since a massive heart attack in his early 50’s. I now attribute that poor health to a high grain/carb diet with very low fat – kicked off initially by the Pritikin diet. Both parents wasted away to skeletons and you could just about watch the flesh melt from them. Their diets in hospital and prior to – both high carb with very little fat!
    I personally believe that this low fat high carb nonsense is the biggest rort since the Y2K and global warming. If 1% of the funds went in to proper diet studies to dispel the low fat myth, the world would be a happier place!

    Thank heavens for people like you who are prepared to do what you do! This is the first time I have written to you and got through but there must be thousands of people like me whose lives you have enriched and extended. Keep up the great work Tom!

    Thank you. I don’t plan on retiring any time soon.

  2. js290

    Dr. Eugene Fine is doing more contemporary research in this area. In his interview with Jimmy Moore, he pointed out that cancer won’t be starved of glucose for fuel per se with a ketogenic diet. Apparently, the magic of the ketogenic diet is the insulin response (or lack thereof).

    You also posted the talk by Dr. Craig Thompson, head of Sloan-Kettering, where he talked about why we all don’t get cancer.

    It shouldn’t be surprising that the unnecessary nutrient would be the one causing metabolic problems. Nature would not have squandered fat, the better energy source that provides more ATP, only to torment us with health problems. That is, nature would not have selected for the inability to metabolize a better fuel source. That’s not how natural selection works.

    Lipophobia is a religious dogma not based in any rational understanding of metabolism and science. As you pointed out with the patents, it’s rather convenient which privileged industries lipophobia has benefited.

    There are different theories as to how a ketogenic diet may kill cancer cells … feedback loop (the last study I quoted), less glucose uptake, lower insulin levels, perhaps some combination. I don’t care which theory is correct; I’m just happy to know we can (probably) reduce the odds of developing cancer by avoiding foods that spike glucose.

  3. Aaron Lucas

    From Gary Taubes “Good Calories Bad Calories” aka “The Diet Delusion”
    To discuss cancer, we need to first return to the subject of cancer in isolated populations eating traditional diets. The modern incarnation of these observations begins with John Higginson, who was the founding director of the World Health Organization’s International Agency for Research on Cancer (IARC), a position he would hold for two decades. In the 1950s, Higginson studied cancer incidence in native African populations and compared them with incidence in the United States and Denmark, the two nations for which equivalent data existed. With a few exceptions, Higginson reported, cancer in African natives was remarkably uncommon. This led Higginson to conclude that most human cancers were caused by environmental factors, and that diet and lifestyle factors were the primary suspects. “It would seem, therefore, that the majority of human cancer is potentially preventable,” as the World Health Organization concluded in 1964, a view that evolved into the new orthodoxy.

    Cancer epidemiologists then tried to establish what proportion of cancers these might be. Higginson suggested 70 to 80 percent of all cancers could be prevented; others said as many as 90 percent. In 1981, the Oxford epidemiologists Richard Doll and Richard Peto published the seminal work on this subject: a 120-page analysis in the Journal of the National Cancer Institute that reviewed the existing evidence on changes in cancer incidence over time, changes upon migration from one region of the world to another, and differences in cancer rates between communities and nations. (Colon cancer, for example, was ten times more common in rural Connecticut than in Nigeria; breast cancer was diagnosed eight times more often in British Columbia than in the non-Jewish population of Israel.) Based on this evidence, Doll and Peto concluded that at least 75 to 80 percent of cancers in the United States might be avoidable with appropriate changes in diet and lifestyle.

    In the quarter-century since Doll and Peto published their analysis, it has been cited in nearly two thousand journal articles, and yet the fundamental implications have been largely lost. The two most important conclusions in their analysis were that man-made chemicals—in pollution, food additives, and occupational exposure—play a minimal role in human cancers, and that diet played the largest role—causing 35 percent of all cancers, though the uncertainties were considered so vast that the number could be as low as 10 percent or as high as 70 percent.

    Higginson had repeatedly remarked on these two points during his tenure as director of IARC. In early reports, Higginson and the World Health Organization had referred to “extrinsic factors” and “environmental factors” as the cause of most cancers, by which they meant lifestyle and diet. The public and the environmental movement had perceived this to mean almost exclusively “man-made chemicals”—the “carcinogenic soup,” as it was known in the 1960s and 1970s. “It appears that only a very small part of the total cancer burden can be directly related to industrialization,” Higginson wrote. The release of industrial chemicals into the environment could not explain, for example, why the nonindustrial city of Geneva had more cancer than Birmingham, “in the polluted central valleys of England,” or why prostate cancer was ten times more frequent in Sweden than in Japan.*61

    Nonetheless, this focus on carcinogenic chemicals as the primary cancer-causing agents in the environment also carried over to nutrition-related cancer research in the laboratory. It was assumed that whatever components of diet were responsible for cancer worked the same way that chemicals did: by inducing mutations and genetic damage in cells. When cancer researchers from around the world met in September 1976 at the Cold Spring Harbor Laboratory to discuss the origins of human cancer, the talks focused on those chemicals shown to be carcinogens in animals, and the possibility that they might be found in infinitesimal or greater amounts in human diets, drinking water, or pharmaceuticals.

    By the mid-1970s, when cancer epidemiologists began to convince politicians and the public that many cancers were caused by what Peto and Doll had called the “gross aspects of diet,” rather than “ingestion of traces of powerful carcinogens or precarcinogens,” the focus was almost exclusively on fat, fiber, and red meat, or smoked-or salt-cured meat, as well as the possibly protective nature of vitamins, vegetables, and fruits. The low incidence of cancer in vegetarians and Seventh-day Adventists was often cited as evidence that meat is carcinogenic and that green vegetables and fruit are protective. (Although the incidence of colon cancer, for instance, among Seventh-day Adventists was no lower than among Mormons, described by Doll and his colleague Bruce Armstrong as “among the biggest beefeaters in the United States.”) For the next twenty years, conferences, textbooks, and expert reports on nutrition and cancer continued to focus exclusively on these factors, although now aided by the advances in molecular biology.

    By the end of the 1990s, clinical trials and large-scale prospective studies had demonstrated that the dietary fat and fiber hypotheses of cancer were almost assuredly wrong, and similar investigations had repeatedly failed to confirm that red meat played any role.*62 Meanwhile, cancer researchers had failed to identify any diet-related carcinogens or mutagens that could account for any of the major cancers. But cancer epidemiologists made little attempt to derive alternative explanations for those 10 to 70 percent of diet-induced cancers, other than to suggest that overnutrition, physical inactivity, and obesity perhaps played a role.

    Throughout these decades, refined carbohydrates and sugars received little or no attention in discussions of cancer causation. Peter Cleave had suggested in The Saccharine Disease that the refining of carbohydrates might be involved in colon cancer. John Yudkin had noted that the five nations with the highest breast-cancer mortality in women in the late 1970s (in descending order: the United Kingdom, the Netherlands, Ireland, Denmark, and Canada) had the highest sugar consumption (in descending order: the United Kingdom, the Netherlands, Ireland, Canada, and Denmark), and those with the lowest mortality rates (Japan, Yugoslavia, Portugal, Spain, and Italy) had the lowest sugar consumption (Japan, Portugal, Spain, Yugoslavia, and Italy). But in 1989, when the National Academy of Sciences published its 750-page report on Diet and Health, the authors spent only a single page evaluating the proposition that carbohydrates might cause cancer. “There is little epidemiologic evidence to support a role for carbohydrates per se in the etiology of cancer,” they noted. They did add two caveats. One was that “no definitive conclusion is justified…because carbohydrates have often been reported in epidemiologic studies only as a component of total energy and not analyzed separately.” The other was that Richard Doll and Bruce Armstrong had found sugar intake in international comparisons to be “positively correlated with both the incidence of and mortality from” colon, rectal, breast, ovarian, prostate, kidney, nervous-system, and testicular cancer, and that “other investigators have produced similar findings.”

    The patterns of cancer incidence, for many cancers, are similar to those of heart disease, diabetes, and obesity, which alone suggests an association between these diseases that is more than coincidental. This was the basis of Cleave’s speculation, of Dennis Burkitt’s, and of those cancer epidemiologists who argued that dietary fat caused breast cancer. But if dietary fat, red meat, man-made chemicals, or even the absence of fiber cannot explain the “strikingly similar” patterns of disease distribution, as the Harvard epidemiologist Edward Giovannucci remarked about colon cancer and Type 2 diabetes in 2001, then something else most likely does.

    Those cancers apparently caused by diet or lifestyle and not related to tobacco use are either cancers of the gastrointestinal tract, including colon and rectal cancer, or cancers of what are technically known as endocrine-dependent organs—breast, uterus, ovaries, and prostate—the functions of which are regulated by hormones. This connection between these diet-and life-style-related cancers and hormones has been reinforced by the number of hormone-dependent factors linked to cancers of the breast and the endometrium (the lining of the uterus). All suggest that estrogen plays an important role. All these cancers, with the possible exception of pancreatic and prostate cancer, appear to increase in incidence with weight gain. These associations together imply both a metabolic and a hormonal connection between diet and cancer. This in turn led breast-cancer researchers to focus their attention on the likely possibility that obesity increases the incidence of breast cancer by increasing estrogen production.

    The most direct evidence linking overweight or overnutrition to cancer comes from animal experiments. These date back to the eve of World War I, when Peyton Rous, who would later win a Nobel Prize, demonstrated that tumors grow remarkably slowly in semi-starved animals. This line of research lapsed until 1935, when the Cornell University nutritionist Clive McCay reported that feeding rats just barely enough to avoid starvation ultimately extended their lifespan by as much as 50 percent. Seven years later, Albert Tannenbaum, a Chicago pathologist, launched a cottage research industry after demonstrating that underfeeding mice on very low-calorie diets, as McCay had, resulted in a dramatic inhibition of “many types of tumors of divergent tissue origin.” In one experiment, twenty-six of fifty well-fed mice developed mammary tumors by a hundred weeks of age—the typical lifespan of lab mice—compared with none of fifty that were allowed only minimal calories. Tannenbaum’s semi-starved animals not only lived longer, but were more active, he reported, and had fewer “pathologic changes in the heart, kidneys, liver, and other organs.”*63

    To explain this inhibitory effect, Tannenbaum considered an idea that had originated in the 1920s with Otto Warburg, a German biochemist and later Nobel Prize winner. Warburg had demonstrated that tumor cells quickly develop the ability to survive without oxygen and to generate energy by a process of fermentation rather than respiration. Fermentation is considerably less efficient, and so tumors will burn perhaps thirty times as much blood sugar as normal cells. Incipient tumors in these calorie-restricted lab animals, it was thought, cannot obtain the huge amounts of blood sugar they need to fuel mitosis—division of the nucleus—and continue proliferating.

    Insulin was not considered a primary suspect until just recently, but the evidence has existed for a while. The earliest such link between a dysfuntion in carbohydrate metabolism and cancer dates to 1885, when a German clinician reported that sixty-two of seventy cancer patients were glucose-intolerant. One common observation by clinical investigators over the years was that women with adult-onset (Type 2) diabetes or glucose intolerance had a higher-than-average incidence of breast cancer. By the mid-1960s, researchers were reporting that insulin acts as a promoter of growth and proliferation in both healthy and malignant tissues. Howard Temin, who later won a Nobel Prize for his cancer research, reported that cells turned malignant by a chicken virus would cease to proliferate in the laboratory unless insulin was added to the serum in which they were growing. This growth-factor effect of insulin was also demonstrated in adrenal and liver-cell cancers. Insulin “intensely stimulated cell proliferation in certain tumors,” noted one 1967 report. In 1976, Kent Osborne and his colleagues at the National Cancer Institute reported that one line of particularly aggressive breast-cancer cells were “exquisitely sensitive to insulin.”

    By the late 1970s, researchers had also reported that malignant breast tumors had more receptors for insulin than did healthy tissue. The more insulin receptors on the surface of a cell, the more sensitive it will be to the insulin in its environment. Having a greater number of insulin receptors than healthy cells, as one report noted, might confer “a selective growth advantage to tumor cells.”

    “Selective growth advantage” speaks directly to the process of Darwinian evolution that is considered the controlling force in tumor development. We can think of human cells as existing in a microscopic ecosystem, living in harmony with their environment, and balanced, as are all species, between the opportunities for growth and proliferation and the processes that lead to aging and death. In such an environment, the billions of cells that eventually constitute a tumor will be the descendants of a single cell that has accumulated a series of genetic mutations, each adding to its proclivity to proliferate unfettered by any of the normal inhibitions to growth. The process in which a healthy cell eventually results in malignancy is a gradual evolution driven by a series of mutations in the DNA of the genes, each bestowing on the cell either the inclination to multiply or a breakdown in the control and repair mechanisms that have evolved to counter precisely such potentially deleterious mutations. The descendants of such a mutant cell would inherit this fitness advantage over other cells in the tissue, and so, within a few years, a single such mutant cell will leave millions of descendants. As one of those descendants in turn gains, purely by chance, yet another advantageous error or mutation, its descendants will now come to dominate.

    Each new mutation-bearing cell constitutes a new species, in effect, that is better suited to prevail in its local cellular environment. Eventually, with this continued accumulation of what to the body as a whole is simply bad luck, a single cell will come to possess precisely that set of mutant genes that drive it and allow it to grow and proliferate without limit. Because each single hit of genetic damage alone is not sufficient to produce a cancer cell, the accumulation of just the right half-dozen hits (actually, the wrong half-dozen hits) takes years or decades, which is why virtually all cancers become more common as we age.

    Cancer researchers now believe that these cancer-causing mutations occur as errors in the replication of DNA during the process of cell division and multiplication. Each one of us is likely to experience some ten thousand trillion cell divisions over the course of our lives, constituting an “enormous opportunity for disaster,” in the words of the MIT molecular biologist Robert Weinberg, author of the textbook The Biology of Cancer. This suggests that cancer-causing mutations are another unavoidable side effect of aging, which is why our cells have also evolved to be exceedingly resistant to genetic damage. They have sophisticated mechanisms to search out defects in newly replicated DNA and repair them, and other mechanisms that actually prompt a cell to commit suicide—programmed cell death, in the technical terminology—if the repair mechanisms are incapable of fixing the damage that occurred during replication. Alas, with time, these programs, too, can be disabled by the proper mutations.

    Within this Darwinian environment, insulin provides fuel and growth signals to incipient cancer cells. Its more lethal effects, however, might come through the actions of insulin-like growth factor (IGF). Growth hormone itself is secreted by the pituitary gland and works throughout the body; IGF is secreted both by the liver and by tissues and cells throughout the body, and it then works locally, where concentrations are highest. Most tissues require at least two growth factors to grow at an optimal rate, and IGF is almost invariably one of the two, and perhaps the primary regulator.

    Insulin-like growth factor is sufficiently similar in structure to insulin that it can actually mimic its effects. IGF can stimulate muscle cells to take up blood sugar, just as insulin does, though not as well. Researchers now believe that IGF serves as the necessary intermediary between the growth hormone secreted by the pituitary gland, and the actual amount of food that is available to build new cells and tissues. If insufficient food is available, then IGF levels will stay low even if growth-hormone levels are high, and so cell and tissue growth will proceed slowly if at all. Add the necessary food and IGF levels increase, and so will the rate of growth. Unlike insulin, which responds immediately to the appearance of glucose in the bloodstream and so varies considerably from hour to hour, IGF concentrations in the circulation change only slowly over days or weeks, and thus better reflect the long-term availability of food in the environment.

    Since the mid-1970s, researchers have identified many of the molecules that play a role in regulating the strength of the growth and proliferation signals that IGF communicates to the cells themselves. There are several different insulin-like growth factors, for instance, and they bind to specific IGF receptors on the surfaces of cells. The more IGF receptors on a cell’s surface, the stronger the IGF signal to the cell. If insulin levels are high enough, insulin will stimulate the IGF receptors and send IGF signals into cells as well as insulin signals.*64

    IGF and its receptors appear to play a critical role in cancer. In mice, functioning IGF receptors are a virtual necessity for cancer growth, a discovery that Renato Baserga of Thomas Jefferson University says he “stumbled” upon in the late 1980s, after nearly forty years spent studying the growth processes of normal and cancerous cells. Shutting down the IGF receptor in mice will lead to what Baserga calls “strong inhibition, if not total suppression of [tumor] growth” it is particularly lethal to those tumors that have already metastasized from a primary site elsewhere in the body.

    In the bloodstream, virtually all insulin-like growth factors are attached to small proteins that ferry them around to various tissues where they might be needed. But the IGFs, when attached to these proteins, are too large and unwieldy to pass through the walls of blood vessels and get to the tissues and cells where the IGF might be used. At any one time, only a small percentage of IGF in the circulation is left unbound to stimulate the growth of cells.

    These binding proteins constitute yet another of the mechanisms used by the body to regulate hormonal signals and growth factors. Insulin appears to depress the concentration of IGF-binding proteins, and so high levels of insulin mean more IGF itself is available to effect cell growth—including that of malignant cells. Anything that increases insulin levels will therefore increase the availability of IGF to the cells, and so increase the strength of the IGF proliferation signals. (Insulin has been shown to affect estrogen this way, too, one way in which elevated levels of insulin may potentially cause breast cancer.)

    The role of IGF in cancer appears to be fundamental, albeit still controversial. As is the case with insulin, IGF has been found in the laboratory to enhance the growth and formation of tumor cells directly; IGF signals prompt cells to divide and multiply. (This effect seems to be particularly forceful with breast-cancer cells when IGF and estrogen are acting in concert.) IGF has an advantage over other growth factors that might play a role in cancer because it can reach tumors either through the bloodstream—after being secreted by the liver—or as a result of production by nearby tissue. There’s even evidence that tumors can stimulate their own further growth and proliferation by secreting their own insulin-like growth factors. In the early 1980s, cancer researchers discovered that tumor cells also overexpress IGF receptors, just as they overexpress insulin receptors. The surfaces of tumor cells have two to three times as many IGF receptors as healthy cells, which makes them all that much more responsive to the IGF in their immediate environment.

    This is another way in which cancer cells gain their all-important survival growth advantage, suggests Derek LeRoith, whose laboratory at the National Institute of Diabetes and Digestive and Kidney Diseases did much of this research. The extra insulin receptors will cause cancerous cells to receive more than their share of insulin from the environment, which will convey to the cell more blood sugar for fueling growth and proliferation; the extra IGF receptors will assure that these cells are supplied with particularly forceful commands to proliferate. Another critical role of IGF in the development of cancer may be its ability to inhibit or override the cell suicide program that serves as the ultimate fail-safe mechanism to prevent damaged cells from proliferating.

    In the past decade, LeRoith and others have demonstrated that the various molecules involved in the communication of the IGF signal from the bloodstream to the nucleus of cells—the insulin-like growth factors themselves, their receptors, and their binding proteins—work together with insulin to regulate both the growth and metastasis (the spread of tumors to secondary sites) of colon and breast cancer. LeRoith has done a series of experiments with mice genetically engineered so that their livers do not secrete IGF. As a result, these mice have only a quarter as much IGF in their circulation as normal mice. When colon or mammary tumors are transplanted into these mice, both tumor growth and metastasis are significantly slower than when identical tumors are implanted in normal mice with normal IGF levels. When insulin-like growth factor is injected back into these genetically engineered mice, tumor growth and metastasis accelerate. David Cheresh, a cancer researcher at the Scripps Institute in La Jolla, California, has demonstrated that both insulin and insulin-like growth factor will prompt otherwise benign tumors to metastasize and migrate through the bloodstream to secondary sites.

    The working hypothesis of cancer researchers who study IGF is not that these molecules initiate cancer, a process that occurs through the accumulation of genetic errors, but, rather, that they accelerate the process by which a cell becomes cancerous, and then they work to keep the cells alive and multiplying. At a 2003 meeting in London to discuss the latest work on IGF, researchers speculated that the development of cancerous cells and even benign tumors is a natural side effect of aging. What’s not natural is the progression of these cells and tumors to lethal malignancies. Such a transformation requires the chronically high levels of insulin and IGF induced by modern diets. This hypothesis is supported by epidemiological studies linking hyperinsulinemia and elevated levels of IGF to an increased risk of breast, prostate, colorectal, and endometrial cancer.

    This hypothesis, if not refuted, would constitute a significant shift in our understanding of the development of malignant cancer. It would mean that the decisive factor in malignant cancer is not the accumulation of genetic damage in cells, much of which is unavoidable, but how diets change the environment around cells and tissues to promote the survival, growth, and then metastasis of the cancer cells that do appear. “People were thinking a bit too much that diet could be a risk factor for cancer almost exclusively based on the idea that it contained carcinogenic substances,” explains Rudolf Kaaks, director of the Hormones and Cancer Group at the International Agency for Cancer Research. “Now the idea is that there is a change in the endocrine and growth-factor environment of cells that pushes cells to proliferate further and grow more easily and skip the programmed cell-death events.”

    IGF and insulin can be viewed as providing fuel to the incipient fire of cancerous cells and the freedom to grow without limit. The critical factor is not that diet changes the nature of cells—the mutations that lead to cancer—but that it changes the nurturing of those cells; it changes the environment into one in which cancerous and precancerous cells can flourish. Simply by creating “an environment that favored, even slightly, survival (rather than programmed cell death),” says the McGill University oncologist Michael Pollak, insulin and IGF would increase the number of cells that accumulate some genetic damage, and that would increase the number of their progeny that were likely to incur more damage, and so on, until cancer is eventually achieved. “When applied simultaneously to large numbers of at-risk cells over many years,” notes Pollak, “even a small influence in this direction would serve to accelerate carcinogenesis.”

    I have one question: did you copy and paste from an e-version of the book, or did you actually type all that? Thanks either way.

  4. CNC

    “but taken together, the articles do paint a picture”

    Sure does, I will stay with my ketogenic diet. Thanks for another great article.

  5. gallier2

    You said:
    So all the way back in 1995, at least some doctors suspected that depriving cancers of glucose might help. Sheesh. Anyway …

    Ts, ts, ts, why don’t you look back to 1931 Nobel prize for medicine?
    It’s quite clear (from reading Taubes about obesity and this) that the Germans had more or less already nailed it before WWII. It looks like that after WWII, when US science with its puritanic undertone and corporatic fixation, there was a big regression in research.

    Sure, but as Taubes explained, American scientists pretty much ignored the work of the Germans after WWII. I’m thinking in terms of what was known in recent decades, when the USDA has been pushing sugary skim milk over whole milk.

  6. Tomas Blesa

    Ketogenic diet cannot guarantee curing cancer. Isn’t it because of body can make its own glucose? I hope my body cannot make its own fructose. 😉
    BTW, it sucks that many authors doesn’t clearly use word “sugar”. I often don’t know if they mean table sugar, glucose, fructose, any single molecule sugar.

    No diet or drug is 100% effective against cancer, but the preliminary studies are showing benefits for quite a few people. The body can make its own glucose from protein, but on a ketogenic diet, you’re not overdoing protein either. Bottom line is that if glucose levels are lower, there’s less glucose uptake by the cancer cells.

  7. BobG

    I literally got angry reading this, because I pay *attention* to health and nutrition news, and I had never heard of most of these studies. Any time there’s a new “Red Meat Will Kill Your Family” study, there are practically newsboys on street corners yelling “EXTRA EXTRA” about it – but a “Stop Eating Sugar And Your Cancer Might Get Less Bad” study gets ignored?

    Thanks for shining some light on this.

    Yup, the selection bias among most media health reporters is amazing. You don’t have to do much digging to find studies where meat was NOT associated with cancer, and I’ve even found a couple where eating meat was associated with LOWER cancer rates. But those don’t make the headlines.

  8. Elenor

    Argh. The daughter of a friend is … following the usual route … for treatment of an aggressive breast cancer. (She’s an RN, so mired in “the system” alas.) I’ve been trying SO hard to keep my nose out of their business, to NOT scream: “O!M!G! will you just READ this stuff!! Do NOT ignore all the modern — unacceptable to Big Pharma and the FDA/USDA — science that is being done!”

    Then, this morning… oh, you did it, Tom, you tipped me over the edge and I sent a wee bit of the above and a plea that they PLEASE read this and add it to their considerations … even outside of any considerations of treatment.

    Yes gods ! How DO we not just scream at people when we can see they’re missing or leaving out something SOOOOOOO important that might — if not save them — at least provide support that might save them! I’ve been trying so hard not to proselytize, and I’m actually getting better at leaving people alone. (Okay, so I DID send an email full of links to a guy suffering badly with psoriatic arthritis.) But, in three weeks, I’ve only handed out one “business card” of links to a girl weighing some 300 pounds suffering with thyroid and adrenal problems. (I point out they should start with “Science for Smart People on YouTube” and follow it up with Mark Sisson’s blog.)

    It’s heart-rending … I describe as sitting on top of a mountain of jewels and trying to give these life-saving GEMS to people, and they don’t want them!!

    (Anyway, thanks for letting me rant… My friend is just distraught (no surprise) and I cannot do anything beyond just be supportive and, for the most part, keep my mouth shut about possibly saving this girl’s life! ARGH!!!)

    I feel ya. It’s tough to stay out of it when you see people suffer needlessly.

  9. JEY

    Thanks, Tom…a good short summary of the studies.
    For more studies, some specific to breast cancer, readers might find this recent review study by Dr Colin Champ and Jeff Volek of interest. It has 88 excellent references, many with direct links to the study.

    Is there a link?

  10. NM

    Dr Champ (of Relentless Roger and the Caveman Doctor) is researching ketogenic diets as an adjunct to chemotherapy. It’s looking hopeful.

  11. Matt

    Thanks Tom. I , like many people, have had quite a few friends/family members die from cancer. Reading stuff like this frustrates me to no end. I hope by the time my 1 year old son is an adult, we will have seen a shift away from all the sugars in our life.

    If society hasn’t made that shift, at least your son will know better.

  12. Weezy

    Great group of studies! When I was diagnosed with breast cancer about a year ago, I started doing research and found these (among others). I knew I was already on the right path to avoid reoccurrence. DNA testing of my tumor showed that it had a low chance to reoccur (yippee!), but the doctors STILL recommended a 5 year course of drugs. I declined because of side effects and I knew that eating a ketogenic diet was my best course of action.

    A year later every time I see one of the docs for a followup, they chide me for not doing the horrible meds. At first I tried to explain to them about a ketogenic diet/glucose/tumors, but NONE of them believed me. Now I don’t say anything. They simply cannot see past their hide-bound prejudices…and I remain absolutely amazed that people specializing in cancer do not know that glucose feeds tumors. All three of them said outright that glucose has nothing to do with tumor growth.

    As you so eloquently put it, Tom: Head. Bang. On. Desk.

    Glucose has nothing to do with cancer growth? That means they’re not even reading the literature in their field of (supposed) expertise.

    Here’s to you remaining cancer-free.

  13. cancerclasses

    Dang Aaron Lucas, I thought some of my posts were long…

    The answer to why carbohydrates cause and feed cancer can be found just within the relevant pages on Wikipedia, I’ve found it but it requires the type of 30,000 foot view thinking that allows a person to ‘connect the dots’ which people specializing in cancer lack since they’re trained to find the answers by peering through microscopes. Much too narrow a focus, it’s no wonder to me as Weezy says “that people specializing in cancer do not know that glucose feeds tumors.”

    Forget or fail to ever learn how the body partitions foods for energy production and you’ll never figure it out or be able to explain it, but you can make a lot of money “treating” it.

  14. Becky

    The hardest part of the paleo diet is the anger you feel about being hoodwinked for so long by the “experts,” and about so many people suffering and dying early, needlessly.

    In my generation, countless women cooked for their heart patient husbands, using canola oil or no oil or fat at all, thinking they were prolonging their husbands’ lives, when probably the reverse is true. There is also a prevailing “belief” that fat is bad for cancer. We must, as the commenter above said, gently share these studies with people who might be receptive.

    Yup, I remember when my mom switched to vegetable oils and Egg Beaters because my dad’s cholesterol was high. If only we’d known.

  15. Janelle

    “Yes gods ! How DO we not just scream at people when we can see they’re missing or leaving out something SOOOOOOO important that might — if not save them — at least provide support that might save them! I’ve been trying so hard not to proselytize, and I’m actually getting better at leaving people alone.” (Elenor)

    One of my closest friends has been ignoring me for years. Now they’re reaping the whirlwind, so to speak. I finally did resort to screaming, but I don’t believe it did anything more than momentarily get their attention. I have to back off for the sake of my own health.

    I’ve found that friends are often the hardest to convince. So I back off rather than risk the friendship.

    1. Walter Bushell

      “When the student is ready the teacher will appear.” Just can’t teach people who can’t handle the truth.

  16. David

    The whole talk on sugar feeding cancer, definetely sounds like Steve Jobs how he had so much fruit juice and other stuff, leading to pancreatic cancer.

    I believe too that my aunt beat or stabalized her cancer when she went on the Atkins diet. At first she went vegan and that didn’t last after my uncle grilled some steak fajitas. She then decided to try the Atkins diet and she kept saying how great she felt and even took the weight off despite my grandma saying “so bad for you!!!” But since then, we haven’t even heard about if her cancer went away or not since she hasn’t talked about it. But I did see a news video on a man who had 3 months to live and heard about the Ketogenic diet. So he gave it a try and what do you know?…no more cancer and he is still living!

    1. cavenewt

      I have always wondered about Steve Jobs, his pancreatic cancer, and his being practically a fruitarian. I know it isn’t refined fructose, but according to what I’ve read he ate an awful lot of fruit, and probably wheat also.

  17. Kristin

    As usual not only a great post but great comments. So much information. I have a friend whose breast cancer is in recovery and I’ve sent her this article.

    I sure commiserate with all the comments from folks who just want to shake their friends to make them listen. Seems to be a common feeling among us who figured out how to eat to truly be healthy. It has now been about a year for me. My weight has stabilized and I while I’m not skinny with my genetics I’m not likely to be. I’m a healthy weight, even by government guidelines.

    Just yesterday I had a friend over to help in my yard. She expressed how great I looked and would I PLEASE help her learn how to eat better, cook better and give her some tools to help a third friend see the light. He lives on junk food, tons of soda and has type 2 diabetes which he assumes he can do nothing about. I showed her the first few minutes of Big Fat Fiasco and then sent her the link suggesting she and our other friend share it (they are housemates right now.) I told her my lunch was easy to make and scratch cooking need not be fancy; grass fed hamburger patty smothered in onions and cauliflower roasted in coconut oil. So now she wants me to basically hold a weekly cooking class for her.

    I’ve also overheard at a gathering last week three people who I had mentioned my diet to a long time ago and got that familiar glazed look, talking about how they were all eating low carb and getting results. I was rather floored and just let them be. And finally I saw a month or so ago a friend who has always been very heavy with that big belly indicative of his high carb diet. He had lost over 30 lbs! I remember he had asked me for some links which I provided as usual and got not even an acknowledgement of receipt which also seems to be usual. But he had made use and had changed his diet. He buttonholed me with concerns about his new diet and cholesterol. I had things to say.

    I’m getting some amazing lessons on the value of being a silent example and loving my friends as they are. Of course none of them are dying of cancer right now. That would make it a whole lot harder.

    Sounds as if you’re getting to at least a few of them. For those who don’t want to believe you, all you can do is wish them well and let them go.

  18. Mike P

    I agree with Becky. When I read through GCBC and when Gary Taubes goes into detail of the McGovern Committee, I found myself getting very angry. After all the posturing and interviews and testimonies, to hear a senator say ‘congress doesn’t have time to wait for all the data’…WTF?!?!?

    It reminds me of the scene in The Matrix when he has to choose between the red pill and the blue pill. We’ve all chosen to ‘wake up’ and it’s hard to walk around and not see the mis-information, special interests, etc. everywhere you look.

    Maybe you should get neat shades and a trenchcoat like Morpheus 🙂

    Keep on doing what you’re doing Tom!!

    Perhaps another film titled “The Fatrix.”

  19. Wil B

    Tom, here is a video presentation that is on topic and may be of interest to your readers. It was presented by Dr. Robert Lustig in 2009. Dr. Lustig is a neuro endocrinologist affiliated with U. Cal. at San Francisco. His lecture was entitled “Sugar: The Bitter Truth.” Here are two links that should work.

    Sure, great lecture. I posted it a long time ago.

  20. alexandra

    I have never heard the expression dietary refined fructose before, I thought all fructose was the same, anyone know what they mean? HFCS? does the body treat it differently from “regular” fructose?

    Probably HFCS as opposed to fructose in fruit, yes. I don’t think the body treats it differently, but it would be difficult to eat enough whole fruit to give yourself the same fructose load you’d get from eating sugar, drinking sodas or juices, etc.

  21. Kathy

    A close friend has just recently informed me she’s being treated for bladder cancer. She knows something about how I eat and we talk about diet and such, but like my husband, I’m sure she thinks I’ve gone over the edge. 🙂

    I have a draft in my email to send her links to the information on cancer and sugar. I just haven’t had the courage to send it yet. I know she won’t be mad, but I don’t want her thinking I’m meddling in her very private health issues. Maybe I can rationalize that she shouldn’t have told me about the cancer if she didn’t want my opinion? Uncharted territory here.

    I sent some information once to a friend who was suffering from an autoimmune disorder commonly linked to wheat. I prefaced it with “I’m going to make this one attempt to share what I know with you because I believe it could help. Then I promise to butt out and not mention it again.”

    My advice went unheeded, and I kept my promise.

  22. Sky King

    In trying to see the forest for the trees so to speak, or say, in taking all the pieces of the puzzle (information regarding nutrition) I’ve gathered over the years and trying to make sense of what the BIG PICTURE actually might look like…I’m going to postulate my hypothesis here and now by stating that everything essentially boils down to….those gut bacteria!

    Feed them right (no processed carbs for the most part) with a little fasting (intermittent or other) thrown in for good measure, and they’ll keep you very healthy for a very long time. But feed them crap, then you’ll feel like crap, and you’ll eventually end up down the toilet.

    Now if you’ll all excuse me…I’m going to get my phone out and get ready to answer a certain phone call from Stockholm, Sweden that I’m sure to receive anytime now!

    And when I’m giving my acceptance speech after receiving the Nobel Prize, Tom, I promise to acknowledge you and to give you some of the credit, not to mention a portion of the prize money! :0P

    As a matter of fact, a couple of studies about gut bacteria and health just landed in my inbox this weekend.

    Start working on that acceptance speech.

  23. gollum

    I don’t think pure fructose goes any other pathways either but as Tom hinted at, it’s a question of concentration.
    I suppose stuffing your face with let’s say 3 lbs of oranges any day is not *very* much better (yo the purine golly!),
    however with fruit and possibly some other things eaten in between
    you have to chew it, your intestines have to process it, wiggle it around, to get the fructose even out of the fruit pulp matrix.
    This is in effect rate-limiting, like eating 200 g of rice accompanying a huge steak meal, compared to drinking 200 g glucose.

    Already if you pre-digest the fruit into juice, the rate limit is gone.

    Fruit also tends to be available during 2 months in summer, then not as much, unless you’re stupid enough to pay a premium to have strawberries in November. Yay healthy lifestyle. See my “endless summer” pet theory.

    In fruit, other nice micronutritients come with it, some of which may offset some of the damage; also glucose is commonly accompanying fructose, which a) gives you about only 60% of fructose for the same sweetness and b) may actually help processing it in the liver, which I hear, actually depletes some energy sources (the overall balance is positive of course)
    That’s not the case if you use isolated fructose. Guess which people were told to use this. Three guesses and “diasthenics” don’t count.

  24. Jim Butler

    Quick update O/T…
    I just put on my first pair of 36″ waist jeans in over 10yrs 😉 Down from 44″. This site is a great contributor to that result.

    Thanks Tom and all who contribute.


    Outstanding, Jim.

  25. JEY

    Tom, that is a perfect way to introduce the information, I wish you had been my friend seven years ago. Instead I followed the heavily promoted “Cancer Project Diet” backed by the vegan PCRM. I don’t blame overwhelmed oncologists who just hand out their glossy brochure or the low fat guidelines from the ACS. As you said in a speech, any change will need be a crowd sourced effort to share the benefits of a low carb diet, and that includes possible cancer control.

    I gained 55 pounds on the Cancer Project plan with all those carby protein substitutes. Too much organic hearty oatmeal and bean dishes galore because I could not use soy. Reading the Gary Taubes GC,BC chapter quoted above started me on the road to low carb paleo. It took a few months more of reading all I could find on the subject of cancer and diet, before doing a nutritional about face in August 2010.

    Kathy, at three years post treatment, I had the time and interest to dig into the science. But at the time of diagnosis, your friend is likely overwhelmed with more immediate decisions and long term nutrition is a low priority. But I would have appreciated an email from a friend who distilled some of the studies for me, and may have at least given more consideration to the impact of my diet choice rather than following the first brochure handed to me.
    Dr. Champ’s keto intro is good Dr. Edes wrote with more detail:

  26. Cristina

    As an RN (Renegade Nurse!), I am constantly shaking my head at the establishment. I work in an outpatient oncology unit and the resident oncologist and her entourage eat [fat-free!] candies and jelly beans all day long. The food offered to patients is fat-free or low-fat, chemical-laden, processed, sugar-loaded “food stuffs”. Graham crackers, Lorna Doone “butter” cookies, Jello-brand jello, sugary yogurts and sodas and juices. And if that ain’t bad enough, the American Cancer Society has a program called “Survive and Thrive” which promotes the standard dogma, ensuring people are “informed” that butter, saturated fats, and meats are pro-inflammatory and pro-cancer. (According to them, grains are anti-inflammatory, so make sure you eat plenty.)
    Keeping people sick and getting sicker so that they stay in the system.

    “Wealth made in medical science is always contaminated, as it comes from the suffering of others.” Ayurveda documentary.

    Jeez. Even if they’re unaware of the link between sugar and cancer, hasn’t it occurred to anyone that candies aren’t good for patients in other ways?

  27. Kathy

    Thanks for your input on this difficult situation. My email draft actually prefaces the links with something similar. I just want her to be well.

  28. Kathy

    JEY – thank you for taking the time to share your thoughts. Hearing from someone who has “been there” has helped me choose to go ahead and send her the info – with a promise not to bring it up again – leaving the ball in her court, as they say.

  29. Galina L.

    I was very unhappy after applying the anty-inflammatory diet recommended by Dr. Andrew Weill , also a member of PCRM. it caused me 26 lb of a weight gain during one year and worsening of all medical conditions, more frequent flues and infections. The diet required elimination of a red meat and saturated fats, sugar,but more tofu, chicken breasts,beans, whole grains, fruit and veggies. I am on a LC diet since Nov.2007.

  30. Kristin

    I just got back from a camping work party weekend clearing land for the community. There was a couple there I had not met before. Very friendly. I met the man first. He offered me potato salad which I declined. I said I didn’t really eat potatoes. That initiated a discussion about our diets. He had become a raw vegan a few years ago and just loves his diet. Says he feels better than he ever has. His girlfriend got him on the diet. Then he says he has heart disease and can’t really exercise for getting out of breath too easily. He then hastens to mention that is isn’t the diet, though. The diet is great. I don’t think he had heard of a LC/HF diet before because he seemed rather puzzled at what I ate. But he was tactful and pleasant.

    Then his girlfriend came out of the trailer…a breast cancer ball cap covering her bald head and her t-shirt baggy over an emaciated body. Yes, she is currently in aggressive chemo treatment for breast cancer…and a long time vegan.

    I have to admit I was a bit stunned. I was thinking to myself “Geez guys. Do you have to be such perfect poster children for everything I’ve been studying?” The next morning the camp kitchen served pancakes and pancake syrup and someone had generously brought several boxes of donuts. I just pulled out the jar of egg salad I brought for myself. That stuff doesn’t even tempt me anymore. I did notice the woman with cancer eating a plate of pancakes. It just made me ache inside.

    Head. Bang. On. Desk.

    Reminds of a vegan friend of mine in L.A. who also loved her diet, but had to undergo major dental surgery because she’d lost half the bone mass in her jaw. I wanted to shake her and yell, “For Pete’s sake, woman, eat a steak!”

  31. Tammy

    Tom – You don’t know how timely this post is for me. My 34 year old sister is getting ready to start chemotherapy tomorrow (4/2) and on my advice about two months ago she changed her diet when she first found out about the cancer. She switched to a whole foods diet but now I am trying to get her to go full blown ketogenic for at least next several weeks. I want to give her every chance possible to get better. I’m not telling her to not have the treatment, but I’m trying to convince her to give herself the best possible chance of it being successful. I truly believe changing her diet would do just that.

    Thanks !

    I wish your sister a full recovery.

  32. Liz

    Galina, I followed a similar diet and was about 20 lbs overweight as a result. Very hard time building muscle, too. I even got my thyroid checked (it was normal), so I new it had to be my diet. Very frustrating when naturally lean vegans/vegetarians brag about their superior diet. Now I just say, “Show me your before picture.” Then they have to admit to not having a weight problem to begin with, like those authors of Skinny Bitch.

  33. Ron Keith

    Doctors sometimes use a PET scan to get a good image of the cancer cells. The patient is fasted for a period of time, which slows the tumor activity. Then the patient is given a large amount of radioactive glucose to get the tumor very active. Presto, they get a good image.

    If this isn’t proof sugar feeds cancer, I do not know what is. How can doctors claim otherwise?

    Hard to believe they haven’t put two and two together.

  34. Galina L.

    I just wanted to pass on you to article Short-Term Fasting Before Chemotherapy in Treating Patients With Cancer,

    and another one is about the combining of ketogenic diet with traditional methods of cancer treatment, according to the article, “the /ketogenic/diet may enhance the effectiveness of chemotherapy”.
    At the end of the article it was said “Dr. Scheck notes that the rigors of the diet can make it unappealing. “With the ketogenic diet, you face the same dilemma that patients sometimes face with traditional chemotherapy and radiation, that is, just how detrimental the therapy is to the patient’s quality of life,” she says.”

    Apparently, Dr.Scheck thought that ketogenic diet was as bad for a quality of life as a chemotherapy.

  35. JEY

    If you define a “ketogenic diet” as one that results in Dr. Thomas Seyfried’s “zone of metabolic managment for cancer” or glucose of 55-65mg and blood ketones of 2.5-7mm, that diet is rather rigorous with high fat intake and almost no carbs. The more common definition of a “ketogenic diet” as one with less than 50g total carbs, resulting in blood ketones over .5mm, can easily be part of a high quality of life. The KetoNutrition website is another good resource that discusses the difference on its first page with links to how to acheive true metabolic managment:

  36. Rocky Angelucci

    If there’s any remaining doubt that cancer cells love glucose, just take a look at the contrast agent employed when detecting cancer using a PET scan: radioactive glucose.

    The procedure is simple:

    1) Start glucose IV
    2) Run PET scan
    3) Bright spots on scan are cells that gobbled up glucose and are principal suspects for cancer

  37. Brenda

    Directly from the Mayo Clinic website:

    Myth: People with cancer shouldn’t eat sugar, since it can cause cancer to grow faster.

    Fact: Sugar doesn’t make cancer grow faster. All cells, including cancer cells, depend on blood sugar (glucose) for energy. But giving more sugar to cancer cells doesn’t speed their growth. Likewise, depriving cancer cells of sugar doesn’t slow their growth.

    This misconception may be based in part on a misunderstanding of positron emission tomography (PET) scans, which use a small amount of radioactive tracer — typically a form of glucose. All tissues in your body absorb some of this tracer, but tissues that are using more energy — including cancer cells — absorb greater amounts. For this reason, some people have concluded that cancer cells grow faster on sugar. But this isn’t true.

    *So, tumors use sugar, but it doesn’t cause them to grow.

    I wonder if they’ll change their tune now that pilot studies are showing that ketogenic diets put some cancers in remission.

  38. gollum

    Revisited the post after reading about glutamine on Wheat Belly Blog.
    Glutamine btw. is not a sugar, it’s an amino acid.

    Uncle’s pet theory seems to go like this. In DM2 cell is insulin resistant. Cell starves swimming in sugar. Cell goes into panic mode and turns to glutaminolysis. Glutaminolysis makes lots of bad compounds mutating cell. Cell goes cancer. The end.
    That’s very interesting, even more so in regards to the glutaminolysis blocking drug, above.

    There’s just one problem with that theory: cells can indeed take up (a bit of) glucose without insulin, by osmosis (I hear lots of cells like nervous system are not insulin dependent at all). The “need insulin to use glucose” is oversimplified PR from, uh, insulin PR. I mean, education. Insulin is in the big picture more for protecting your body from BG (in healthy subject, 60..100 even if cells certainly wouldn’t starve at 300) and anabolic phase into glycogen storage, fat pad and muscles.


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