Toward an Anti-Cancer Diet

Since starting the blog, I’ve gotten a number of emails from cancer patients or their family members. When the Q&A page started last week, the second question was from Lindsay, asking for a cancer diet:

In the past 3 weeks my partner has been diagnosed with stage 3 breast cancer. She is 28 and there is no family history….

Do you have suggestions aside from vit d and green tea that might be therapeutic?…

In my mind she simply needs to be extremely well nourished, but that is proving tricky due to nausea. I made a batch of chicken broth the other day and the smell alone sidelined her. Any thoughts on a way to sneak in dense nutrients without a strong odor?

I’ve delayed blogging about cancer and diet because of the complexity of the issue. Research has not yet determined the optimal diet for cancer patients, and there is reason to believe that the optimal diet may differ for different cancer patients. It is not easy to balance the many factors that should influence a cancer patient’s diet.

Today I’ll lay out my general perspective on cancer. The goal is to identify aspects of the disease that we can influence through diet. In subsequent posts, I’ll discuss foods, nutrients, and eating strategies. I hope the manner in which I’m addressing the issue will help cancer patients to understand the issues better and to design an effective personal eating strategy.

Cancer as a Progression of Diseases

Cancers often develop over long periods of time – typically decades. They usually cannot be detected or diagnosed at early stages. This is just as well, because most early cancers resolve spontaneously; they disappear or return to a normal state. Perhaps we should have a distinct name for these early and usually harmless cancers – “proto-cancers” perhaps.

Proto-cancers develop through a series of stages into life-threatening cancers. At each stage, the character of the disease changes. The purpose, and perhaps the nature, of dietary interventions may change with it.

Origins of Cancer

What characterizes these proto-cancers is that one or more cells develop an abnormal state of gene expression that I’ll call the cancer phenotype.

What causes a cell to develop the cancer phenotype? I believe the most common are:

  1. Infections, especially viral infections (since viruses are good at modifying gene expression).
  2. Toxins, especially DNA-modifying toxins such as those generated by peroxidation of polyunsaturated fats.
  3. Malnutrition, especially nutrient deficiencies that impair the ability to maintain epigenetic regulation of DNA.

The Wikipedia page “Infectious Causes of Cancer” says that 18% of human cancers are known to have infectious causes, but I suspect the fraction will get much larger. Read through our story of XMRV and chronic fatigue syndrome (“Retroviruses and Chronic Fatigue Syndrome, Aug 24, 2010) for an example of how difficult it is to identify the viruses that cause cancers. In this instance, a new human retrovirus may (it is still disputed) have been discovered because men with genetic impairments to anti-viral immunity have much higher rates of prostate cancer, and scientists searched prostate tumors of men with this genetic impairment for viruses. If finding the cancer-causing virus is so difficult when we know it is present in the tested tissue, you can easily imagine how many other viruses may have escaped scientific notice.

Interventions to prevent the original causes of cancer are great for cancer prevention, but they may also be therapeutic. Removing cancer-causing viruses may enable the body to defeat a cancer it otherwise could not.

Proto-Cancers and the Evolution of Cancer Cells

The cancer phenotype has various characteristics, but at early stages important characteristics may include:

  • Suppression of mitochondrial activity, especially apoptosis (programmed cell death).
  • Metabolic changes toward metabolism of glucose and away from metabolism of fatty acids or ketones.
  • Isolation of the cell from the rest of the body. Normal human cells closely coordinate their activities with the rest of the body, especially with neighboring cells, and respond to hormonal and other signals. Cancer cells tend to be more “individualistic,” less responsive to the body and to their neighbors.

Every once in a while one of these cells with a cancer phenotype will divide, creating two daughter cells. Perhaps in part because after metabolic impairment the cell has difficulty providing sufficient ATP to handle the complex motor tasks involved in cell division, these cancer cells often fail to divide properly, resulting in daughter cells with altered genetic state. Common changes include:

  • Aneuploidy. Most genes have two copies, one inherited from the mother and one from the father. In cell division, genes are first duplicated, and then divided among two daughter cells, so that each cell gets two copies. In aneuploidy, chromosomes are improperly separated so that one cell gets three copies of a chromosomal strand, the other one. Genes on that strand then become expressed 1.5-fold in the cell with three copies, half-fold in the cell with one copy.
  • Translocations. Chromosomes have a certain gene order. However, they can be re-assembled in an improper order, with one segment translocated to another place. This changes gene expression.
  • Epigenetic modifications. DNA comes with a protein scaffold that packages and organizes it, and can be modified so that gene expression is silenced (via methylation) or enhanced (via acetylation). Epigenetic modifications are usually inherited by daughter cells – but dividing cancer cells may experience less stability in the epigenome.

These changes mean that cell division causes cells with a cancer phenotype to evolve. Let’s say aneuploidy occurs affecting a gene that stimulates cell division. One daughter cell gets 3 copies and becomes more likely to proliferate; the other cell gets only 1 copy and becomes less likely to proliferate. Of course, every time a cell divides it creates two daughters, so a decade later the first cell may have thousands of descendants while the first cell has few. A proliferative phenotype has become more common in the “tumor.”

The Middle Stages of Cancer Development

As a result of cellular evolution, the early cancer phenotype becomes a later cancer phenotype with new traits, such as:

  • A tendency to proliferate. This is the trait people most commonly associate with cancer cells.
  • A tendency to stay alive indefinitely. Some cancer cells become “immortal.” For instance, HeLa cells are immortal cells taken from the cervical cancer of Henrietta Lacks, who died in 1951. So resistant to death were these cells, they were the first human cells ever to survive in vitro.

Both traits are promoted by infections. Viruses and other germs want to stay alive, and to do that they need to keep their host cell alive, since cell death typically kills any germs in the cell (thus programmed cell death is a major part of human immune defense). Viruses also want to replicate, and to do that they often piggyback on human DNA replication. So viruses have evolved ways to promote proliferation and immortality of host cells. Cancers caused by viruses, therefore, often have a head start on acquiring these traits. Cancers that appear at young ages are probably almost always viral in origin.

Once these traits are acquired, the cancer cells proliferate and form a tiny tumor. These micro-tumors can reach a size of about 0.5 mm in diameter. At that point, growth stalls for lack of oxygen and nutrients. Cells inside the tumor cannot get enough resources to continue their growth.

Often this is the end of the cancer; it never develops beyond this point. It’s been estimated that most adults have thousands of these microtumors, and most never go on to develop clinical cancer. It is generally impossible to diagnose the presence of these microtumors.

However, cells in the microtumor are still evolving. Cells, when nutrients are available, divide, and one daughter cell survives to divide again while another cell in the tumor dies to make room. There is a “survival of the fittest” contest in which cells become more adapted to the environment of the tumor.

Progression to Diagnosable Disease

At some point, one or more cells may gain the ability to manipulate neighboring cells to their own benefit. This is a crucial stage in the development of cancer: when the cancer phenotype extends to give the tumor new abilities to exploit its human host. A key capability is:

  • the ability to induce the formation of blood vessels. This process is called angiogenesis.

This process involves manipulation of the immune system, which is responsible for wound healing as well as defense against foreign bodies. Angiogenesis is part of the normal wound healing process, and when it becomes angiogenic, a tumor (in the famous phrase of Hal Dvorak) becomes a “wound that never heals.” That is, it acts like a wound to call forth the blood vessel generation process, but it never allows the wound healing process to terminate.

Once cancer cells can call forth new blood vessels from surrounding tissue, they have access to all the body’s nutrient and oxygen resources. There is no longer any limit to the tumor’s growth. This evolution of an angiogenic capability could be said to create the disease of cancer.

One of the interesting findings of recent research is that foods can significantly influence the likelihood that tumors will develop an angiogenic capability. A number of plant compounds from foods such as garlic, tomato, green tea, and turmeric have been shown to inhibit angiogenesis. If you read the excellent book Anti-Cancer by David Servan-Schreiber, you’ll find that these anti-angiogenic foods form the essence of his dietary advice.

Once tumors can induce angiogenesis, they can grow quite large. But even large single tumors are usually not deadly.

Progression to Deadly Disease

Cancers become deadly when another change evolves:

  • Some cancer cells become metastatic.

Metastatic cells migrate away from the tumor, interact with non-cancer cells, and may travel through the blood to distant sites where they establish new tumors. When cancer metastasizes, many tumors can develop and the cancer can become a devastating drain on the host.

Immune Suppression and Co-Infections

Other new cancer capabilities may also evolve. For instance:

  • Suppression of anti-cancer immunity.

When the immune system successfully attacks and destroys cancers, it is usually through an innate immune response involving natural killer cells and macrophages. Interestingly, this is also the same immune response which defends against fungal infections.

One of the interesting aspects of the evolution of cancer cells is that they often end up with many genes silenced, such that they lose many distinctively “human” genes and probably come to resemble our primitive evolutionary ancestors. In other words, cancer cells evolve to look more like fungal cells, so that a tumor may biologically resemble a mold colony.

Suppose cancer cells evolve a capability to suppress the NK cell and macrophage immune response. Then the tumor will flourish more readily – but so also will fungal infections.

It happens that late-stage cancer patients commonly develop systemic fungal infections.

It also works the other way: fungi that have evolved into obligate parasites of human hosts, like Candida, are good at suppressing human anti-fungal immunity. In doing so they also suppress human anti-cancer immunity. Thus, fungal infections are a risk factor for cancer. I saw a study recently in which a large fraction of people treated for systemic fungal infections were diagnosed with cancer in the following five years.

There is evidence that fungal infections of cancer cells increase the rate of metastasis. So the combination of cancer and fungal infections may be particularly deadly. This suggests that cancer patients might benefit from anti-fungal therapies.

There may be great variability in human immunity against cancer. Biologist Zheng Cui has found such variability in mice, and estimates that 10-15% of humans may be highly resistant to cancer. It is likely that diet can modulate this resistance, which suggests looking for dietary tactics that promote anti-cancer immunity.

Cachexia and Anorexia

Cachexia is the wasting syndrome that afflicts late-stage cancer patients. The tumors become a large drain on resources, their nutrient consumption is not met by diet, and the rest of the body is cannibalized in order to provide resources to the tumors. Muscle and other tissue wastes away until they can no longer sustain life.

Cachexia is often what kills cancer patients.

Now, if the cancer patient could eat sufficient food, even very large tumor burdens might be tolerable. Olympic swimmers eat 12,000 calories a day; pregnant women support 8 pound growths in their abdomen without risk.

Unfortunately, cancer also tends to diminish appetite. One of the consequences of cancer’s interactions with the immune system is that late-stage cancer generates a lot of inflammatory cytokines which can be imported into the brain where they affect the food regulatory systems that Stephan Guyenet has written about, causing anorexia.

Cancer-related anorexia makes food distasteful and causes cancer patients to cease eating. Lindsay mentioned her partner’s anorexia as one of the problems she hoped I could help her address.

Exercise and dietary strategies that promote muscle and tissue growth (“anabolic” strategies) such as those employed by bodybuilders and strength athletes might increase appetite, protect tissue, and delay the negative effects of cachexia. They might also have an anti-cancer effect by depriving the cancer of resources.

Interaction with Chemotherapies

Yet another complexity is that the standard therapies for cancer involve poisoning the body with chemotoxins.

This raises a conundrum. A healthy diet makes the body, and all its cells including cancer cells, more resilient to toxins. So a healthy diet may undermine the effectiveness of chemotherapies.

Some diet-chemotherapy interactions are well documented. Supplementation of vitamin C, glutathione, and omega-3 fats are all known to protect cancer cells against chemotherapies.

If beneficial foods reduce the effectiveness of chemotherapy, it might also be the case that toxic foods could increase their effectiveness. Thus, the optimal diet during chemotherapy might be quite different from the optimal diet when off chemotherapy.

I will not say much about these interactions, other than to advise that before undergoing chemotherapy cancer patients discuss their diet and supplement regimen with the oncologist.

Summary: Our Path to an Anti-Cancer Diet

So, we’ve identified a number of possible levers for attacking cancer. We can look for dietary steps to:

1)      Defeat viral or other infections that originally caused the cancer.

2)      Remove toxins and improve nutrition in order to promote DNA and epigenome stability.

3)      Deprive cancer cells of their favored glycolytic metabolic pathways, slowing their growth.

4)      Restore mitochondrial function, promoting apoptosis (programmed cell death) of cancer cells.

5)      Inhibit angiogenesis.

6)      Inhibit metastasis.

7)      Promote anti-cancer and anti-fungal immunity.

8)      Mitigate anorexia and cachexia.

Those who are trying to prevent cancer will want to focus on (1)-(5); those with early stage cancers on (1)-(7); those with late stage cancers on (1)-(8).

Our mission: understand how diet and nutrition can affect each of these; and then try to integrate various dietary tactics into an optimal anti-cancer strategy.

Conclusion

I think this gives us plenty to work on. Next week, I’ll provide short provisional answers. Over the next year, I’ll examine each type of cancer-diet interaction in detail and see if we can refine and improve our anti-cancer strategy.

Leave a comment ?

47 Comments.

  1. paul:

    Great stuff.

    I am curious about your opinion of fasting and resulting autophagy as a possible preventive measure. I friend of mine brought it up and I also saw it talked about by a lecturer with the Sloan Kettering Cancer research department.

  2. Hi Chuck,

    Autophagy is promising from a number of angles. Fasting should be a cancer preventative, and an ingredient in anti-cancer diets. I favor daily intermittent fasting as long as that is tolerable.

  3. Thank you for an interesting post.

    Thought this video about angiogenesis might be interesting: http://www.ted.com/talks/lang/eng/william_li.html
    Also, Eugene Fine told me their article on the effect of 1 month Atkins diet is submitted so there might be some interesting data to come soon.

  4. Hi Pal,

    Thanks. I’ve cited the William Li talk before and will cite it again in this series. Also, I’ll be citing your excellent recent post on Carbs and Cancer.

    Thanks for the news about the Fine study, more data will be very interesting.

  5. Paul,

    Thanks for the great post. Are you familiar with the work of Dr. Emanuel Revici?

  6. @ Paul

    Re: Fasting

    I haven’t found much in regard to the optimal amount of time a fast should last for a relatively healthy individual for preventative measures. How did you come up with your fasting protocol?

  7. Hi Matt,

    No, but I see he worked on the lytic effects of blood serum on cancer cells (http://www.ncbi.nlm.nih.gov/pubmed/13844813). I’ve gotten interested in blood-cancer cell interactions thanks to the work of Zheng Cui.

    Chuck,

    There isn’t much. My general view is:
    1) The benefits of fasting begin after about 14 hours.
    2) You want to maximize the total number of hours of fasting benefit per month, while avoiding the negative effects of glucose deficiency, etc.
    3) Daily intermittent fasting (~16-18 hours) gives maybe 80 hours/month fasting benefits. That’s equivalent to 4 36-hour fasts per month, which is more than I can do.
    4) Daily intermittent fasting restores glycogen and protein resources in the daily feeding period, so avoids any deficiency effects that might arise on long fasts.

    I’m aware that some others including Thomas Seyfried take the opposite view: that occasional long fasts provide the greatest benefits. I’m not aware what evidence they base that view on.

  8. Thank you, Paul for beginning to explore this issue. I actually had a sort of epiphany the other day that falls in line with your mentioning that a toxic diet may actually be more beneficial for cancer cell death. I was doling out daily vitamins and it occurred to me that “nourishing,” the cancer cells is probably not a good tactic. But at the same time not supplementing with vitamins could contribute to malnutrition. It’s a slippery slope.

    My partner has had a fever for the past few days, but otherwise feels fine. This suggests to me that she is in fact fighting an infection.. An infection that could have been somewhat dormant, but is now brought to the surface because of her compromised immunity. I wonder if antibiotic treatment would be a good strategy for cancer patients.

    I look forward to future posts on this issue.

  9. I will follow this series with extreme interest.

  10. Paul,

    One more thing… I am wondering what your method of research is–what sources you use, etc. I know that you’re a scientist and so this line of thinking might come more naturally to you, but I think it would be helpful to know your process so that we (your loyal readers) may take on some research independently. Aside from just empowering ourselves I can imagine it might be nice for you to not be inundated with questions ;). I get most of my information from blogs, nih, a little pub med and book recommendations made by my favourite bloggers.

    As you have probably noticed in many of my comments and e-mails I am always looking for the “core,” issue. So my interest in knowing your process seems like a natural progression :).

    Thanks!

    Lindsay

  11. Cancer really is a tough subject like you said. Most other diseases seem pretty heavily influenced by diet, but cancer seems like it can pop up in almost anyone.

    Look forward to seeing your next post on this subject.

    Josh

  12. I lost my mother to aggressive B-Cell NHL, she went from a healthy, fit 62 year-old who hiked/ walked and gardened every day, to dying in an ICU from NHL within a span of one year. Blood cancers such as Lymphomas are NOT diet related; there are many mechanisms which cause cancers not mainly attributable to diet or even lifestyle.

    My mom never smoked, drank; and she followed a diet of mostly vegetables, some fruits, fish, stews/ soup stock made with organic meats like chicken, and rice, but her diet was very high in carbs. Her one guilty pleasure was bread, but she didn’t eat it regularly because she ate mainly rice. However, she did have gastric symptoms when she did eat bread, which in retrospect makes me suspect that she was gluten-intolerant. I did read research study implicating gluten to increased rates of Cancer, specifically Lymphoma, so this is an area that deserves studies. We need to educate the public about adverse effects of gluten, because I honestly feel this is a public health issue.

    Before becoming a CRNA (Nurse-Anesthetist), I was a pediatric oncology and pediatric ICU RN. Besides personal experience with cancer, I also have had clinical experience with it. Most inpatient cancer patients unfortunately eat foods high in sugar/ carbs and low in nutrients. They given sugary foods by medical team/ caregivers, often in the form of protein shakes which are nothing but artificially flavored drinks made with corn syrup, vegetable oils, and vitamins. If that’s not bad enough, caregivers are encouraged by medical team (physicians, RNs, dietitians, etc..) to feed these young cancer patients candy, ice-cream, greasy chicken nuggets, Doritos/ potato chips, in other words junk food, because of their calorically-dense advantage.

    I saw many kids succumb to infections due to nonexistent WBC counts as consequence to chemotherapy. But I’d always wondered what, if any, did the high sugar/ carb intake do to further weaken their already fragile immune systems. I believe diet to be just as important as an adjunctive therapy for various types of cancers, regardless of whether they may be diet-induced or not.

  13. Glad you have taken this one.

    Epigenetic stability is fascinating stuff…

    I’ve been collecting studies for a while building a thesis that cancer results from excess folate/folic acid and too little choline, betaine, B-12. PUFAs also have epigenetic effects that interrelate with the methyl donors.

    People need to eat less LA, consume less folate (by avoiding fortified foods) and eat more n-3 fats, choline.

  14. are you familiar with the concept of systemic enzymes in facilitating cancer therapy? described here: http://www.totalityofbeing.com/FramelessPages/Articles/EnzymesFightCancer.htm.

  15. I have always thought of cancer as the result of something the body(esp brain) senses as stress. this stress trigger could happen 20 yrs before someone actually gets diagnosed with cancer but the body is working up for the tumor growth and replication. it makes sense sort of to think of cancer as a sort of darwinism. i know that sounds horrible but many of the problems in health and disease would still be nonexistent as they were in the past if it were not for the medical industries ability to keep everyone alive and thus including what darwinism would have knocked out. if your body cant hack the stress, you get a disease sent by a signal in your brain far beyond our understanding, IMO. then you get doctors who throw lots of meds your way to keep you alive. i also remember reading the apoe4 gene is very interlinked to cancer. there was a german doctor who talked about stress being the determinant in cancer vs cancer free bodies

  16. I dont know about the whole chemotherapy antioxidant thing. I mean look at the Gerson therapy which has a 50% cure rate and its eating all plant foods and tons of fresh veggie juices plus some other things like liver extract and coffee enemas. There is also Dr. Gonzales who is reversing cancers nutritionally and they have many different diets for every type of cancer. Some diets are meat and fat, and some pretty much vegan.

  17. Go to http://www.lef.org and search the site for “curcumin cancer”. Very encouraging articles. They also have a new form of curcumin that is up to 7 times more bio-available than regular curcumin.

  18. CURCUMIN seems to be a win on many levels i have read so much about that stuff.

  19. You might also check out lactoferrin and modified citrus pectin on the http://www.lef.org website. Both have positive implications with cancer.

  20. About the infectious causes of cancer: when I went through RN training in the early 1970’s, much time was spent talking about the stigma of cancer. People dx with it saw friends disappear. People instinctively fear that cancer is infectious. It was stressed how foolish people are that it had been proved without a doubt that there was no infectious agent.

    So would you say we are swimming in a sea of infectious agents and therefore avoidance of cancer patients doesn’t matter? That’s how it strikes me. The important effort is to get your own body in optimum health to fight off the steady assault of cancerous cells.

    • Thanks, everyone, for the tips on anti-cancer agents! Keep them coming.

      Hi Melinda,

      Yes, that’s more or less my view. Most of these infections probably don’t spread easily. Also, most people who are infected don’t develop cancer. Most people probably acquire dozens of cancer-causing pathogens by mid-adulthood. The main issue is whether they multiply, gain control of cells, and are allowed to generate severe disease.

      I do think a life spent in a bubble would reduce cancer risk, as the risk of contagion is not zero, but the risks of interaction with other people are far smaller than the benefits. Certain risky activities, like promiscuous sexuality and blood sharing, should be minimized I think. But casual contact poses minimal risk. With a spouse, I still wouldn’t worry. You probably got infected long ago, and anyway the transfer of a few germs isn’t the main issue. The key is your immune system controlling it.

  21. But infection, toxin, and malnutrition can’t fully explain why a 6 months-old baby gets diagnosed with neuroblastoma, or how a previously healthy teenager develops osteosarcoma shortly after getting injured in same limb or part of body. These two are just some of the common types of pediatric cancers without obvious roots in the aforementioned, hypothetical causes or triggers. Genetics play a huge role in cancer, especially in pediatric oncology.

  22. I’m following this with great interest as well. My mother died of breast cancer. She was convinced there was a fungal angle to cancer. Unfortunately, the vegan route to fight it proved fatal.

  23. Great info “Cancer-related anorexia makes food distasteful and causes cancer patients to cease eating.”

    Let us know if fasting (what amount of dose/time) and autophagy help or hurt preventative measures for cancer…or maybe I’ll just browse through your archives.

  24. Perfect Health Diet » Toward an Anti-Cancer Diet | The Angelove - pingback on September 16, 2011 at 10:56 pm
  25. What to make of IGF-1 and these raw food diets?: “Note that Fontana’s group that had the lowest IGF-1 levels also ate a raw food vegetarian diet.” http://www.futurepundit.com/archives/003952.html

    “Fontana explains. “But we know there are two major influences on IGF-1 levels: calorie intake and protein intake. So we decided to look at the influence of protein.”
    Again, Fontana had a ready-made study group. His team has been following a population of strict vegans for several years. They tend to eat less protein than the CRONies from the CR Society, so he compared IGF-1 levels between the two groups.
    “The vegans had significantly less circulating IGF-1, even if they were heavier and had more body fat than CRONies,” he says. “Protein in the diet seemed to correlate with the lower levels of IGF-1. ”
    http://www.facebook.com/permalink.php?story_fbid=175762895834634&id=666889531

  26. wonderful! thanks.
    (i have a personal interest in cancer)

    your book arrived; will read them on my trip.

    warm regards,

  27. A few studies on nutrients and chemotherapy:

    Kunnumakkara AB, Sung B, Ravindran J, Diagaradjane P, Deorukhkar A, Dey S, Koca C, Yadav VR, Tong Z, Gelovani JG, Guha S, Krishnan S, Aggarwal BB. {gamma}-Tocotrienol Inhibits Pancreatic Tumors and Sensitizes Them to Gemcitabine Treatment by Modulating the Inflammatory Microenvironment. Cancer Res. 2010 October

    Elena J. Ladas, David J. Kroll, Nicholas H. Oberlies, Bin Cheng, Deborah H. Ndao, Susan R. Rheingold, Kara M. Kelly. A randomized, controlled, double-blind, pilot study of milk thistle for the treatment of hepatotoxicity in childhood acute lymphoblastic leukemia (ALL) Cancer 2009 December

    Du G, Lin H, Yang Y, Zhang S, Wu X, Wang M, Ji L, Lu L, Yu L, Han G. Dietary quercetin combining intratumoral doxorubicin injection synergistically induces rejection of established breast cancer in mice. Int Immunopharmacol. 2010 May

    Borska S, Sopel M, Chmielewska M, Zabel M, Dziegiel P. Quercetin as a potential modulator of P-glycoprotein expression and function in cells of human pancreatic carcinoma line resistant to daunorubicin. Molecules. 2010 February Feb 9;15(2):857-70.

  28. Very interesting series. Paul you have a knack for writing and explaining topics to make it understandable to all.
    What do you think of mammograms and early detection of breast cancers? Do you think some may not develop further if left alone?

  29. Dr. Jaminet,

    sorry me again,

    your take on the “evolution” of cancer cells reminds me of the concept of “micro-evolution” of the fittest (cancer cells) within the body by Dr. S. Hickey & H. Roberts.
    http://www.amazon.com/Cancer-Nutrition-Survival-Steve-Hickey/dp/141166339X/ref=sr_1_1?ie=UTF8&qid=1316320474&sr=8-1

    but i’d probably call it “devolve” rather than “evolve” as a cancer cell lost its identity & differentiation.

    the connection of fungal infection is new to me. thanks.

    regards,

  30. Hi Jana,

    Genetics play a role, but also maternal diet and infection in the womb. It’s not easy to disentangle all the causal factors.

    Hi Jaybird,

    Sorry to hear about your mom. I think there are several fungal angles to cancer, it is an interesting topic.

    Hi hggh,

    We don’t have a lot of archives on cancer, but I think intermittent fasting is definitely beneficial and ketosis (at least intermittent ketosis) probably is too.

    However, they’re not a cure for anorexia, unfortunately.

    Hi Lance,

    Thanks for the links. I do think low protein is often beneficial. Intermittent low protein may be an excellent strategy for life extension.

    Hi Peter,

    Thanks much.

    Hi Sue,

    Yes, some will not develop if left alone, so you have to try to judge the odds. There is a lot of controversy trying to figure out what the odds are.

    Hi pam,

    Thanks, that is interesting. I hadn’t heard of that book.

  31. Things That Interested Me This Week: 9-20-11 « Bare 5 - pingback on September 20, 2011 at 4:49 pm
  32. Paul, This is good but I have Leukemia, CLL. As it is a blood borne metastic type cancer, is there anything you would do differently vs a tumor type cancer?
    deb

  33. Hi deb,

    I would focus on eating a healthy, well-nourishing diet and on anti-viral steps, since CLL is mostly likely caused by a virus. So intermittent fasting, occasional ketogenic dieting, occasional low protein dieting. Not all of those at the same time!

  34. Hey Paul
    Great, thank you. That is somewhat the style I have right now. I need to look further into anti viral steps. I do use IF, some keto days and low protien meals/days as well. I do eat lots of fresh fruit, cooked veggies and keep my oils to olive oil and coconut oil.
    Looking forward to more posts re; cancer!
    Deb

  35. Hello Paul,

    cancer is definitely one of those things that can be (at least partly) prevented with a healthy diet and lifestyle, but I’ve been hesitant to do much research on it until I’ve finished learning about the pathology of cancer in medical school, due to the complexity of it.

    You have definitely provided a very good explanation of how cancers develop in this article. This is very important to me personally, since I have two grandparents that died from cancer, which might make me genetically susceptible.

    I’ve ordered your book, still waiting for Amazon to ship and can’t wait to read it 🙂

  36. I developed ovarian cancer (surgery w/chemo 6 rounds) and tested positive for BRCA1 gene. Any thoughts on how to fight this? I’m trying long fasts, IF, low carbs… haven’t tried low protein yet. Preventative skin sparing double masectomy is high on my agenda. Thank you for anything you can offer. V

  37. Hi Violet,

    I’ll post on that this week.

  38. Hi Paul. Did you post on this somewhere? I couldn’t locate the post. Thank you very much. V

  39. Melannie Allen

    Hi,
    I have been reading the cancer related articles on the website. I found the info about the cancer and fungal stuff interesting. I have heard read about some people having success with treating cancer with anti fungal medications. I was wondering if you would please comment on this.

    Thanks,
    Melannie

    • Hi Melannie,

      I haven’t heard of antifungals being effective against cancer, but cancer patients do commonly develop fungal infections, and they may become healthier by treating the infections. The same white blood cells (neutrophils) kill fungi and cancer, so there’s a chance that activating neutrophils by helping them kill fungi might promote immunity to cancer, but no one’s ever observed that so far as I know.

  40. Thanks designed for sharing such a nice thinking, post
    is nice, thats why i have read it entirely

  41. Cancer | Creative Coherence - pingback on December 4, 2015 at 6:08 pm

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