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A bumpy transition to ketosis

Fasting for more than 36 hours proved challenging in ways that took me completely by surprise so I decided to break my fast on Day 4 and continue my transition to ketosis while eating food. My goal remains to reach Prof. Seyfried’s recommended “zone of metabolic management”: blood glucose between 55 and 65 mg/dL and blood ketone levels of at least 4.0 mM. How much protein should I eat to try to get there? How many calories?

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To see what happened on Days 1-3, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.”

A funny thing happened on the way to ketosis . . .

Day 4 (2/3/13)—fourth day of fasting

Notes: Only slept from 2 am to 5:30 am. Big jump in ketones this morning, but hungrier. Numerous unhappy symptoms: difficulty concentrating, tired but couldn’t sleep, mild headache, low energy, a little cold, heartbeat a little stronger than usual, dark circles under eyes, stomach growly, and slight tinnitus (ringing in the ears). At this point, I considered breaking the fast, but then something happened that convinced me it was time to eat.

My cell phone rang at about 2 pm [my ringtone is a harp playing a lovely arpeggio; you may be familiar with it]. Anyway, I answered the call, spoke for a few minutes, and then hung up. But the harp kept playing, very faintly and mysteriously, in the distance, nowhere near where my phone was located . . . over and over again. Uh-oh. I realized that I must be having a mild auditory hallucination—certainly something I had never experienced before in my whole life. While absolutely fascinating to me on one level, it was a clear indication that my brain was not getting the nutrients it needed to function properly, so quite concerning on another level.

This hauntingly beautiful harp call was either a sign that my ascension was drawing nigh, or it was time to have some lunch. I chose lunch:)

What does this mean for cancer patients?

What does this mean for people with cancer who may have been considering fasting up to 5 days to rapidly establish ketone levels of 4.0 mM? It may mean nothing. It may be my own unique response to fasting. Perhaps some people tolerate fasting for more than 3 days beautifully. However, at least for me, fasting for longer than 3 days was not tolerable, and to have continued the fast would have been unwise.

Now, if I had continued another day or two until my ketones had risen to 4.0 mM, would all of the side effects have gone away? I don’t know. If I had already been keto-adapted (at lower ketone levels), would I have tolerated the fast better? Maybe, I don’t know. But since the point of the fast is to change from a regular diet to ketosisk as rapidly as possible, people who try this plan aren’t expected to be keto-adapted already. In most cases, I think it may be wiser to try Dr. Seyfried’s alternative initiation plan instead of fasting (see details in the “Dietary Treatment of Cancer” post).

I certainly could never have accomplished his recommendation of an annual 7-day fast, so my cells will not have the opportunity to cannibalize each other after all. I am just going to have to hope that my healthy diet naturally reduces my risk for developing pre-cancerous cells in the first place.

The transition to a ketogenic diet

What’s next? I will continue to try to reach Seyfried’s “zone of metabolic management” while eating a carefully measured, mostly meat, ketogenic diet.

First, I need to calculate my protein requirements. Based on my personal stats:

• Dr. Seyfried recommends I eat between 62 and 92 grams of protein per day.
• Phinney and Volek recommend I eat between 75 and 156 grams of protein per day.
• Dr. Rosedale recommends I eat 77 grams of protein per day based on my body measurements, but 47 grams of protein per day based on my body fat percentage.

Hmmmm . . . since protein requirements are clearly difficult to estimate (see my protein page for more details), and one size does not fit all, I’m just going to start with 75 grams of protein per day, and if I need to adjust it along the way, I will.

If I were trying to treat cancer, Dr. Seyfried would want me to reduce my calorie intake significantly below my daily requirements (resting/basal metabolic rate or “BMR”). My estimated BMR is 1400 cals/day, so I’ll try to keep my calories to a maximum of 1400 per day.

Day 4, continued:

Notes: I felt much better about an hour after eating some food. It was especially wonderful to regain my powers of concentration. And surprisingly, despite having not eaten a thing for nearly 4 days, once I started eating, my appetite was actually fairly low. Therefore my calories for the day were also pretty low. Was this the effect of high ketone levels/low insulin levels?

Day 5 (2/4/13)

Notes: Got very hungry at dinnertime but a very small amount of food was required to feel better (8 g protein + 13 g fat).

Reflections on my transition to ketosis, week 1

• Fasting certainly does jump-start ketosis, but fasting for more than 36 hours may not be safe for everyone, and was no fun.
• Appetite is generally much lower as ketones rise.
• Hunger feels different in ketosis than on a standard diet. I experienced mild headache, stomach growls, calm thoughts of food, can still go hours without eating and function fine. Zero emotional component. Compare this to hunger on a standard diet, which (for me) = irritability, anxiety, distractibility, emotional longing for food, sense of urgency, carbohydrate cravings, and wish to stop whatever I’m doing and find something to eat right away.
• My blood sugar is still pretty high despite high ketones, but I think all bets are off during first few weeks, as “keto-adaptation” can take 3 weeks or more. [Keto-adaptation refers to the body’s adjustment to the efficient use of ketones for fuel instead of glucose.]
• Do I need to eat more fat to get higher ketones, or is it just a matter of time? If I were to eat more fat, that would mean more calories—would weight loss slow down or stop?
• I am hesitant to do any experiments within my experiment until after a month of this plan, so for now I’m going to stick with: 75 g protein, 1400 cals max, carbs less than 30 g/day, mostly meat, no dairy, no caffeine, no artificial anything.

Check out “Keto for Cancer: Week 2—Protein and Ketosis” to see how I got my ketones way, way up. For information about starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

A bumpy transition to ketosis

Fasting for more than 36 hours proved challenging in ways that took me completely by surprise so I decided to break my fast on Day 4 and continue my transition to ketosis while eating food. My goal remains to reach Prof. Seyfried’s recommended “zone of metabolic management”: blood glucose between 55 and 65 mg/dL and blood ketone levels of at least 4.0 mM. How much protein should I eat to try to get there? How many calories?

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To see what happened on Days 1-3, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.”

A funny thing happened on the way to ketosis . . .

Day 4 (2/3/13)—fourth day of fasting

Notes: Only slept from 2 am to 5:30 am. Big jump in ketones this morning, but hungrier. Numerous unhappy symptoms: difficulty concentrating, tired but couldn’t sleep, mild headache, low energy, a little cold, heartbeat a little stronger than usual, dark circles under eyes, stomach growly, and slight tinnitus (ringing in the ears). At this point, I considered breaking the fast, but then something happened that convinced me it was time to eat.

My cell phone rang at about 2 pm [my ringtone is a harp playing a lovely arpeggio; you may be familiar with it]. Anyway, I answered the call, spoke for a few minutes, and then hung up. But the harp kept playing, very faintly and mysteriously, in the distance, nowhere near where my phone was located . . . over and over again. Uh-oh. I realized that I must be having a mild auditory hallucination—certainly something I had never experienced before in my whole life. While absolutely fascinating to me on one level, it was a clear indication that my brain was not getting the nutrients it needed to function properly, so quite concerning on another level.

This hauntingly beautiful harp call was either a sign that my ascension was drawing nigh, or it was time to have some lunch. I chose lunch:)

What does this mean for cancer patients?

What does this mean for people with cancer who may have been considering fasting up to 5 days to rapidly establish ketone levels of 4.0 mM? It may mean nothing. It may be my own unique response to fasting. Perhaps some people tolerate fasting for more than 3 days beautifully. However, at least for me, fasting for longer than 3 days was not tolerable, and to have continued the fast would have been unwise.

Now, if I had continued another day or two until my ketones had risen to 4.0 mM, would all of the side effects have gone away? I don’t know. If I had already been keto-adapted (at lower ketone levels), would I have tolerated the fast better? Maybe, I don’t know. But since the point of the fast is to change from a regular diet to ketosisk as rapidly as possible, people who try this plan aren’t expected to be keto-adapted already. In most cases, I think it may be wiser to try Dr. Seyfried’s alternative initiation plan instead of fasting (see details in the “Dietary Treatment of Cancer” post).

I certainly could never have accomplished his recommendation of an annual 7-day fast, so my cells will not have the opportunity to cannibalize each other after all. I am just going to have to hope that my healthy diet naturally reduces my risk for developing pre-cancerous cells in the first place.

The transition to a ketogenic diet

What’s next? I will continue to try to reach Seyfried’s “zone of metabolic management” while eating a carefully measured, mostly meat, ketogenic diet.

First, I need to calculate my protein requirements. Based on my personal stats:

• Dr. Seyfried recommends I eat between 62 and 92 grams of protein per day.
• Phinney and Volek recommend I eat between 75 and 156 grams of protein per day.
• Dr. Rosedale recommends I eat 77 grams of protein per day based on my body measurements, but 47 grams of protein per day based on my body fat percentage.

Hmmmm . . . since protein requirements are clearly difficult to estimate (see my protein page for more details), and one size does not fit all, I’m just going to start with 75 grams of protein per day, and if I need to adjust it along the way, I will.

If I were trying to treat cancer, Dr. Seyfried would want me to reduce my calorie intake significantly below my daily requirements (resting/basal metabolic rate or “BMR”). My estimated BMR is 1400 cals/day, so I’ll try to keep my calories to a maximum of 1400 per day.

Day 4, continued:

Notes: I felt much better about an hour after eating some food. It was especially wonderful to regain my powers of concentration. And surprisingly, despite having not eaten a thing for nearly 4 days, once I started eating, my appetite was actually fairly low. Therefore my calories for the day were also pretty low. Was this the effect of high ketone levels/low insulin levels?

Day 5 (2/4/13)

Notes: Got very hungry at dinnertime but a very small amount of food was required to feel better (8 g protein + 13 g fat).

Reflections on my transition to ketosis, week 1

• Fasting certainly does jump-start ketosis, but fasting for more than 36 hours may not be safe for everyone, and was no fun.
• Appetite is generally much lower as ketones rise.
• Hunger feels different in ketosis than on a standard diet. I experienced mild headache, stomach growls, calm thoughts of food, can still go hours without eating and function fine. Zero emotional component. Compare this to hunger on a standard diet, which (for me) = irritability, anxiety, distractibility, emotional longing for food, sense of urgency, carbohydrate cravings, and wish to stop whatever I’m doing and find something to eat right away.
• My blood sugar is still pretty high despite high ketones, but I think all bets are off during first few weeks, as “keto-adaptation” can take 3 weeks or more. [Keto-adaptation refers to the body’s adjustment to the efficient use of ketones for fuel instead of glucose.]
• Do I need to eat more fat to get higher ketones, or is it just a matter of time? If I were to eat more fat, that would mean more calories—would weight loss slow down or stop?
• I am hesitant to do any experiments within my experiment until after a month of this plan, so for now I’m going to stick with: 75 g protein, 1400 cals max, carbs less than 30 g/day, mostly meat, no dairy, no caffeine, no artificial anything.

Check out “Keto for Cancer: Week 2—Protein and Ketosis” to see how I got my ketones way, way up. For information about starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Dr. Seyfried’s book, Cancer as a Metabolic Disease, inspired me to attempt a fasting jump-start to ketosis to see how long it takes to achieve his “zone of metabolic management.” Read on to see how it’s going so far! (I’m still alive . . . )

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

Dr. Seyfried’s ketogenic diet for cancer

Caution: dietary experiments with fasting and ketosis are best done under medical supervision, particularly if you have a medical condition or take any daily medications. Everyone’s metabolism is different, so results will vary. Please see my post “Is the Ketogenic Diet Safe for Everyone?“

After reading Dr. Seyfried’s book,1 I immediately felt sympathy for those of you out there who have cancer now, or who are cancer survivors worried about recurrence—were you hoping for a simple nutritional strategy, such as “eat more broccoli” or “add chia seeds to your morning smoothie?” Had I led you down a road of hope and then left you feeling disheartened when you saw how difficult Dr. Seyfried’s diet appeared to be? Let me try to make it up to you by trying his diet myself while you watch from the comfort of your living room.

Seyfried’s fasting jump-start to ketosis

Dr. Seyfried says the fastest way to achieve optimal blood glucose and ketone levels is to begin with a water-only fasting jump-start to ketosis for 3-5 days. Then embark on a low-calorie “ketogenic” diet, aiming for blood sugar levels of 55-65 mg/dL and blood ketone levels of at least 4.0 mM (see article 3 of my cancer series for more details). As a reminder, average blood glucose levels for most healthy people eating a standard diet run between about 70 and 95 mg/dl, and blood ketone levels are usually 0.3 mM or less.

His plan sounded extreme even to me. However, fasting is supposed to be rather comfortable once you get used to it, and ketogenic diets are known for reducing appetite and improving people’s sense of well-being in most cases. Thankfully I do not have cancer, but nevertheless, in an attempt to rekindle the hope that some of you may have lost, I thought I’d take one for the team and try his recommendations myself.

Goals of this experiment

• To see if I can reach Dr. Seyfried’s “zone of metabolic management.”
• To see if I can maintain high ketone levels and low blood sugar levels using my mostly-meat diet [standard ketogenic diets tend to rely heavily on high-fat dairy products, eggs, and coconut oil, none of which I tolerate well].
• To explore the impact of protein: fat ratios, calories, and exercise on ketone and blood sugar levels.
• To compare urine ketones to blood ketones and see if there is any correlation.
• To document effect of this diet on mood, energy, concentration, weight, sleep, etc.
• To document any side effects of this diet.

My N=1 experiment, phase I: fasting jump-start to ketosis

“N=1” refers to an experiment with only one subject (in this case, me). Everyone’s metabolism is different, so please take my experience with a big grain o’ salt. Please note that, just because Dr. Seyfried suggests that a water-only fast is the fastest way to get into ketosis does not mean that it is required. I also can’t say whether faster is necessarily better for your health or easier than a gradual transition to ketosis.

Supplies:

Note on the ketone meter: When I conducted this experiment, the most affordable, accurate ketone meter was the Precision Xtra®. Unfortunately the “affordable” ketone strips cost $2.22 each! I have since found a meter just as accurate, with an array of great features—and the strips are a much more reasonable 99 cents. You can read more about why I recommend the Keto-Mojo glucose/ketone meter on my ketogenic diet and mental health resources page. Because I like their meter and their mission, I’ve partnered with them to offer my readers 15% off of the purchase of any new meter kit. Just click the link here; no coupon code necessary.

Day 1 (1/31/13)

Notes: Much easier day than I had expected. Stomach a little growly, slightly lightheaded, minor difficulty concentrating, vision slightly blurry, low energy. Slept well, but had a funny dream about a granola bar—something I haven’t eaten in nearly six years! Since exercise confuses things, none for now.

Day 2 (2/1/13)

Notes: Fascinating that blood sugar this morning was higher than last night, without any food. This may be due to cortisol and adrenaline reactions to falling blood sugar—these hormones kick in when blood sugar falls to pull it back up again. Mild headache in the morning. More difficulty concentrating today—”spacey” would be the right word—but it only affected my efficiency in doing paperwork. I was otherwise fine and able to work a full day, run errands, drive, etc. Sleep was terrible—slept from 10pm to 1:30 am, then wide awake until 5am, then back to sleep until about 7:30 am. Sleep quality itself was very light and dream-filled, but no granola bar visions tonight. I can’t believe how much easier this is than I thought it would be—I’m not experiencing distressing levels of hunger or cravings.

Day 3 (2/2/13—Happy Groundhog’s Day!)

Notes: Finally, we have the appearance of (modest) ketones and blood sugar is stabilizing. Concentration was better today, but still not back to normal. Hunger was more noticeable in the morning and afternoon but again, not distressing. Would it have been nice to eat something? Yes, but it didn’t preoccupy my mind. By late evening, hunger is stronger, there is a very mild headache, slight lightheadedness, and stomach growling—this may represent blood sugar falling?—but I was productive late into the evening. I am motivated to keep going by 1) intellectual curiosity and 2) hope that once the ketones are nice and high and the blood glucose is nice and low, hunger will disappear and I’ll feel great. We shall see! I sure am saving a lot of time and money this week…

How much longer did my fasting jump-start to ketosis last? What happened on Day 4 took me completely by surprise! Read about days 4-7 in the next post in this series “Keto for Cancer: Week 1—My Transition to Ketosis.” If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Dr. Seyfried’s book, Cancer as a Metabolic Disease, inspired me to attempt a fasting jump-start to ketosis to see how long it takes to achieve his “zone of metabolic management.” Read on to see how it’s going so far! (I’m still alive . . . )

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

Dr. Seyfried’s ketogenic diet for cancer

Caution: dietary experiments with fasting and ketosis are best done under medical supervision, particularly if you have a medical condition or take any daily medications. Everyone’s metabolism is different, so results will vary. Please see my post “Is the Ketogenic Diet Safe for Everyone?“

After reading Dr. Seyfried’s book,1 I immediately felt sympathy for those of you out there who have cancer now, or who are cancer survivors worried about recurrence—were you hoping for a simple nutritional strategy, such as “eat more broccoli” or “add chia seeds to your morning smoothie?” Had I led you down a road of hope and then left you feeling disheartened when you saw how difficult Dr. Seyfried’s diet appeared to be? Let me try to make it up to you by trying his diet myself while you watch from the comfort of your living room.

Seyfried’s fasting jump-start to ketosis

Dr. Seyfried says the fastest way to achieve optimal blood glucose and ketone levels is to begin with a water-only fasting jump-start to ketosis for 3-5 days. Then embark on a low-calorie “ketogenic” diet, aiming for blood sugar levels of 55-65 mg/dL and blood ketone levels of at least 4.0 mM (see article 3 of my cancer series for more details). As a reminder, average blood glucose levels for most healthy people eating a standard diet run between about 70 and 95 mg/dl, and blood ketone levels are usually 0.3 mM or less.

His plan sounded extreme even to me. However, fasting is supposed to be rather comfortable once you get used to it, and ketogenic diets are known for reducing appetite and improving people’s sense of well-being in most cases. Thankfully I do not have cancer, but nevertheless, in an attempt to rekindle the hope that some of you may have lost, I thought I’d take one for the team and try his recommendations myself.

Goals of this experiment

• To see if I can reach Dr. Seyfried’s “zone of metabolic management.”
• To see if I can maintain high ketone levels and low blood sugar levels using my mostly-meat diet [standard ketogenic diets tend to rely heavily on high-fat dairy products, eggs, and coconut oil, none of which I tolerate well].
• To explore the impact of protein: fat ratios, calories, and exercise on ketone and blood sugar levels.
• To compare urine ketones to blood ketones and see if there is any correlation.
• To document effect of this diet on mood, energy, concentration, weight, sleep, etc.
• To document any side effects of this diet.

My N=1 experiment, phase I: fasting jump-start to ketosis

“N=1” refers to an experiment with only one subject (in this case, me). Everyone’s metabolism is different, so please take my experience with a big grain o’ salt. Please note that, just because Dr. Seyfried suggests that a water-only fast is the fastest way to get into ketosis does not mean that it is required. I also can’t say whether faster is necessarily better for your health or easier than a gradual transition to ketosis.

Supplies:

Note on the ketone meter: When I conducted this experiment, the most affordable, accurate ketone meter was the Precision Xtra®. Unfortunately the “affordable” ketone strips cost $2.22 each! I have since found a meter just as accurate, with an array of great features—and the strips are a much more reasonable 99 cents. You can read more about why I recommend the Keto-Mojo glucose/ketone meter on my ketogenic diet and mental health resources page. Because I like their meter and their mission, I’ve partnered with them to offer my readers 15% off of the purchase of any new meter kit. Just click the link here; no coupon code necessary.

Day 1 (1/31/13)

Notes: Much easier day than I had expected. Stomach a little growly, slightly lightheaded, minor difficulty concentrating, vision slightly blurry, low energy. Slept well, but had a funny dream about a granola bar—something I haven’t eaten in nearly six years! Since exercise confuses things, none for now.

Day 2 (2/1/13)

Notes: Fascinating that blood sugar this morning was higher than last night, without any food. This may be due to cortisol and adrenaline reactions to falling blood sugar—these hormones kick in when blood sugar falls to pull it back up again. Mild headache in the morning. More difficulty concentrating today—”spacey” would be the right word—but it only affected my efficiency in doing paperwork. I was otherwise fine and able to work a full day, run errands, drive, etc. Sleep was terrible—slept from 10pm to 1:30 am, then wide awake until 5am, then back to sleep until about 7:30 am. Sleep quality itself was very light and dream-filled, but no granola bar visions tonight. I can’t believe how much easier this is than I thought it would be—I’m not experiencing distressing levels of hunger or cravings.

Day 3 (2/2/13—Happy Groundhog’s Day!)

Notes: Finally, we have the appearance of (modest) ketones and blood sugar is stabilizing. Concentration was better today, but still not back to normal. Hunger was more noticeable in the morning and afternoon but again, not distressing. Would it have been nice to eat something? Yes, but it didn’t preoccupy my mind. By late evening, hunger is stronger, there is a very mild headache, slight lightheadedness, and stomach growling—this may represent blood sugar falling?—but I was productive late into the evening. I am motivated to keep going by 1) intellectual curiosity and 2) hope that once the ketones are nice and high and the blood glucose is nice and low, hunger will disappear and I’ll feel great. We shall see! I sure am saving a lot of time and money this week…

How much longer did my fasting jump-start to ketosis last? What happened on Day 4 took me completely by surprise! Read about days 4-7 in the next post in this series “Keto for Cancer: Week 1—My Transition to Ketosis.” If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

The future of cancer prevention and treatment may not be in sexy, high-tech, gene-targeting therapies, but in our own hands . . . or rather, on our own plates. Which diets work best for cancer treatment and prevention?

[This is the 4th in a 4-part article inspired by Dr. Thomas Seyfried’s book Cancer as a Metabolic Disease. Go to “What Causes Cancer? Part I” to begin with the first article.]

Cancer treatments: Standard therapies vs. dietary therapies

Standard therapies

• Conventional treatments can help in the short-term but can cause problems in the long-term.
• Chemotherapy is toxic to healthy cells and can breed resistance among cancer cells, increasing the risk of more aggressive cancers if relapse occurs.
• Radiation turns up the activity of the tumor growth pathway (PI3K/Akt/HIF), which promotes not only tumor growth, but also recruitment of new blood vessels (angiogenesis) and drug resistance.
• Radiation increases fusion activity between cells, which means that normal and healthy cells can merge into hybrid cells and become more aggressive.
• Radiation directly damages mitochondria, which increases risk for cancer in the future.
• Both radiation and immunosuppression therapy (drugs that suppress the immune system) can increase the incidence of metastatic cancers (cancers that spread).
• Steroids such as dexamethasone (Decadron), often used to reduce inflammation, raise blood sugar levels, feeding tumor cells and enhancing their survival.

Dietary therapies

• DER (dietary energy restriction) triggers cancer cell death via apoptosis(programmed cell suicide), which is a natural, noninflammatory process that happens from within the cell, causing no collateral damage. Conventional treatments kill cancer cells via necrosis, an inflammatory process that happens from the outside and is locally destructive. Tumor cells that are being fed glucose/glutamine are resistant to apoptosis, but under ketogenic conditions, they become better able to undergo apoptosis again.
• DER and chemotherapy can both cause weight loss. However, the weight loss associated with DER is healthy and does not weaken people, whereas chemotherapy-induced weight loss is unhealthy and weakens people.

Dr. Seyfried wonders if some of the benefit that some people obtain from chemotherapy may be due to the calorie restriction that occurs due to loss of appetite. He notes that drug studies don’t usually take this possibility into consideration.

“DER (dietary energy restriction) can be considered a broad-spectrum, nontoxic metabolic therapy that inhibits multiple signaling pathways required for progression of malignant tumors regardless of tissue of origin. It is not clear to me why so many oncologists have difficulty appreciating this concept.

“Therapies that reduce glucose and elevate ketones can starve glucose-dependent cancer cells while protecting and fueling healthy cells. There is no other cancer therapy that can do this.”

Complementary cancer-fighting strategies

Dr. Seyfried does not think that dietary restriction alone is sufficient to fight most cancers, so he proposes some additional strategies that can be used in combination with dietary measures to optimize results:

• “Anti-glycolytic” drugs that reduce the activity of the glycolysis (fermentation) pathway, which is the primary energy pathway for most cancer cells.

“Anti-glycolytic drugs together with energy-restricted diets could act as a powerful double ‘metabolic punch’ for the rapid killing of glycolysis-dependent tumor cells.”

• “CR-mimetic” drugs that mimic the effects of calorie restriction by lowering glucose levels. These drugs should not be used without diet, because they lower glucose without raising ketones. Without ketones, healthy cells could die of energy failure—they would have neither glucose nor ketones for fuel.
• Hyperbaric (high pressure, 100%) oxygen. Excess oxygen reduces the activity of an enzyme called hexokinase II, which grabs onto glucose after it enters cells and traps it inside so it can be burned for energy.

But standard treatment sometimes works and diet doesn’t always work . . .

We all know people who have undergone successful standard treatments and who have not had a recurrence of cancer. My own mother had cancer twice, decades ago, and has had no cancer since. In both cases surgery was curative for her. If you are lucky enough to have a simple form of cancer in a body part that can be completely removed, and you catch it before it spreads, your prognosis is probably pretty good.

Chemotherapy and radiation can kill many cancer cells because (as discussed in article #1), they are more vulnerable to these agents than healthy cells, and if you have a healthy enough immune system, your own body may be able to take care of the rest. Some people never get cancer again—they may change their lifestyle after a cancer scare and start taking better care of themselves (my mother stopped smoking, for example). Some adopt a healthier diet or start exercising. Some may just be lucky. But clearly modern cancer therapies have made a difference for some people, including my own mother.

So my mom is a cancer success story, but a close family friend of ours who was diagnosed with glioblastoma multiforme (brain cancer) was not so lucky. She lived for only a few months, and those final months were of very poor quality. She had smoked for years, but had quit long before her diagnosis. She loved candy. As kids we always looked forward to her visits, because she always walked through the door with a big package of red licorice and a king-sized bag of m&m’s. And as soon as she ran out of treats, she’d say to my mother: “Ain’tcha got somethin’ sweet?”

I have no idea why she got brain cancer, of course, but modern treatments certainly were not able to help her. I do find it interesting that the second most common type of cancer among young people is brain cancer, and the brain just happens to be the organ most heavily dependent on glucose. Could it be that the brain is especially sensitive to the damaging effects of high sugar/high flour diets?

Ketogenic diet for cancer case studies

First study of ketogenic diet with human brain malignancy

Linda Nebeling, PhD, MPH, RD (now with the National Cancer Institute) authored the first-ever study of a ketogenic diet in human brain malignancy [Nebeling 1995]. This was a landmark study of two young girls with advanced-stage, inoperable brain tumors that had not responded to traditional therapies. A three-year-old girl with stage IV astrocytoma and an eight year old girl with grade III astrocytoma were treated with a ketogenic diet. Both children responded well, and experienced long-term tumor management without further chemotherapy or radiation. PET scans revealed a 22% reduction in glucose uptake by tumors in both girls.

Low-calorie/ketogenic diet with brain tumors

Giulio Zuccoli MD (Italian neuro-radiologist) and Thomas Seyfried PhD published a case report [Zuccoli 2010] of a middle-aged woman with glioblastoma (a form of brain cancer) who was treated with a 600-calorie/day ketogenic diet. Upon diagnosis, steroids (to control inflammation) and anticonvulsant medication (to control seizures) were given. She underwent surgery, fasted briefly, and then began the diet. After 14 days on the diet, steroids were stopped, and chemotherapy and radiation treatments were started. After two months, chemotherapy and radiation were discontinued. One week later, PET scan and MRI were performed and no tumor tissue or swelling was detected.The patient stopped the diet, and 10 weeks later, MRI showed evidence that the tumor had come back.

This case report demonstrated that a) the ketogenic diet was well-tolerated; b) the diet may be a useful add-on therapy, as most tumors of her type do not respond as well as hers did to standard treatments alone, and c) inflammation was well-controlled without the usual need for steroids, supporting the anti-inflammatory properties of the diet.

Very low-carb diet in ten patients with incurable cancers

Eugene Fine, MD, professor of nuclear medicine at Albert Einstein College of Medicine just published a 28-day pilot study [Fine 2012] of a very low carbohydrate diet in ten men and women ages 53-73 with incurable, advanced cancers of a variety of types (3 colon, 2 breast, 2 lung, 1 ovarian, 1 esophageal, 1 fallopian tube). Carbohydrate intake was about 9%, but protein and fat were not restricted. Interestingly, those with high ketone levels (and low insulin levels) were the only ones whose tumors either stopped growing or got smaller as evidenced by PET scan. His video presentation is below in the resources section. Dr. Fine’s study is groundbreaking because it may pave the way for additional studies, which are badly needed. Below is his video presentation from the 2012 Ancestral Health Symposium entitled: “Dietary Insulin Inhibition as a Metabolic Therapy in Advanced Cancer.”

Ketogenic diet in four patients with brain cancer

Beth Zupec-Kania, RD is a nutritionist with the Charlie Foundation (an organization dedicated to raising awareness of and providing support for the use of ketogenic diets in children with epilepsy). Ten glioma (brain cancer) patients contacted her for help in using ketogenic diets in the treatment of their cancer. Four of them ultimately committed to a strictly supervised ketogenic diet. Three of the four patients had stable or atrophied (reduced) tumor size documented by MRI. Two had been on the diet for several years and were still alive despite having initially been given only a few months to live. One patient died; he had had advanced stage metastatic cancer prior to starting the ketogenic diet. He remained active and alert until the last two months of his life, and outlived his prognosis by a year.

Obstacles to dietary treatments

Ketogenic diets are hard to follow. They require careful monitoring, tremendous self-discipline, and essentially require that people turn their usual diet completely upside-down. You’ve got to be very motivated, and have the full support of everyone who lives with you. Even if everyone on the planet were 100% convinced that a ketogenic diet is the best diet for cancer, I would eat my hat if everyone with cancer followed it. That would be unrealistic—changing one’s diet is hard.

Ketogenic diets are, by nature, high-fat diets, and this will bother some people on a psychological level, due to (unnecessary) fear of eating fat. For more information, see my fats page and my cholesterol page.

Most physicians are taught next to nothing about nutrition during medical training, and once in practice, are too busy to learn. Nutritional treatments are not particularly sexy or high-tech and may not be of interest to some physicians. Nutritional treatments may be viewed as slower to take effect, and as time-consuming to implement.

But here is the most important obstacle: if a particular treatment is not sanctioned by the medical establishment and does not have solid studies behind it, most doctors will be afraid to recommend it or even support it, due to discomfort with uncertainty and fears of medical malpractice. Doctors take their responsibilities very seriously and want to provide the best treatment they can. In today’s world, that means applying the “standard of care.” Currently surgery, chemotherapy, and radiation are the standard of care. And what’s more, is that the standard of care is what insurance companies will pay for. They are unlikely to cover ketone meters, testing strips, special nutritional counseling, etc.

Is your doctor simply keeping up with the standard of care or is he or she interested in being on the cutting edge? Would your doctor be willing to read Dr. Seyfried’s book, or at least his journal article? [see references below]

The good news is you do not need your doctor’s permission to eat a ketogenic diet, only his or her support and willingness to monitor your progress. Open-minded, patient-centered physicians should be on board with your efforts so long as you are willing to take responsibility for your care.

Do ketogenic diets really need to be so strict?

If you read article 3, you may have been disheartened to see how tough Dr. Seyfried’s dietary recommendations are. Yet as draconian as his diet is, he doesn’t think it will work very well on its own without chemotherapy. While no treatments of any kind are perfect, if Dr. Seyfried’s hypothesis about mitochondria and diet are correct, shouldn’t they have the potential to work better than he thinks they will?

Having read his book and heard him speak, I believe Dr. Seyfried is a brilliant scientist and thinker. The only (gentle, constructive, but wicked important) criticism I have is the same one I have of most scientists who study diet—he thinks about diet as a simple collection of proteins, carbohydrates, and fats, and neglects the actual foods in the diet.

Dr. Seyfried compared two different types of chow in mice with cancer—one high-carb “standard” chow and one high fat “ketogenic” chow. He found that the ketogenic chow did not work against cancer if you let the mice eat as much as they wanted. Their little blood sugar levels stayed high and their cancers grew. He had to lower their calories to see benefits. He concluded that both diets worked equally well as long as you lowered calories—a lot. This made me suspicious, so I visited the chow manufacturers’ websites to see what the diets actually contained. I wonder if it will shock you as much as it shocked me.

Dr. Seyfried’s standard high-carb chow:

ProLab RMH 3000 (LabDiet)—62% carbohydrate, 22% protein, 5% fat, 5% fiber

Ingredients: ground wheat, dehulled soybean meal, wheat middlings, ground corn, fish meal, pork fat, alfalfa meal, calcium carbonate, brewer’s yeast, soybean oil, salt, vitamins, and minerals.

The first four ingredients are refined grains and legumes. Nearly 100% refined junk (including lots of refined carbohydrate) that no self-respecting mouse would naturally consume. No wonder he had to limit how much of this stuff the mice ate by 30-60% in order to lower blood glucose.

Dr. Seyfried’s ketogenic chow:

Ketocal (Nutricia)—90% fat, 1.6% carbohydrate, 8.4% protein

Ingredients: hydrogenated soybean oil, dry whole milk, refined soybean oil, soy lecithin, corn syrup solids.

Nice. Processed soy, dairy, and corn syrup. Poor little mice.

If you have read my dairy page, you will know that the whey proteins in milk raise insulin levels, which can prevent ketosis. This may have been why he had to limit how much of this stuff the mice ate to get good results.

To Dr. Seyfried’s credit, he points out in his book that other researchers have been able to achieve good results in their animal cancer experiments without having to restrict calories and he is unable to explain why. Let’s look at a mouse diet that worked without restricting calories:

Unrestricted ketogenic chow:

Ketogenic Bio-Serv F3666—8.36% protein, 0.76% carbohydrates and 78.8% fat

Ingredients: lard, butter, corn oil, casein, cellulose, mineral mix, vitamin mix, dextrose

Look, ma, no whey protein and no refined carbohydrate! The mice could eat as much of this (admittedly very weird) chow and get good results [Stafford 2010]. It makes me hopeful that even this odd diet, which is a far cry from a healthy mouse diet, delivered positive results.

Dr. Seyfried also referred to another study that used a high-protein, low-carb diet with unrestricted calories that also worked, but I could not locate the article in time to include it here. [Ho 2011]

I can’t help but wonder how these little mice would have fared had they been fed real food that mice are actually supposed to be eating.

So, do we need to restrict calories or not? It may depend on the composition of the diet . . . I think the jury is still out. However, people who eat well-formulated ketogenic diets report a substantial reduction in appetite and tend to naturally find themselves eating quite a bit less without having to count calories.

Metastatic cancer is different

Ninety percent of all cancer deaths are due to metastatic disease (cancer that has spread to more than one organ). These are the bad boys. Once cancer is on the move it’s very hard to stop, which is why prevention is so important. But before we get to that, one of the most fascinating topics in Dr. Seyfried’s book is his theory of how and why some cancers travel through the body to distant organs. He makes a compelling argument for the role of a particular kind of immune cell called a macrophage in helping cancers to spread.

The normal role of macrophages (macs) in our immune system is a very complicated and special one. These are amazing cells, with the ability to change their personality, shape, and behavior whenever necessary, depending on the local circumstances. Every macrophage begins its little life as monocyte, a round cell that can cruise the bloodstream. When trouble is lurking anywhere in the body—if there is injury or inflammation or infection—monocytes heed the call of damaged tissues and travel to the troubled area. Once they are close enough, they squeeze themselves out of the blood vessel and into local tissue, where they magically morph into macrophages so they can to get to work.

Macrophages assess the situation and release all kinds of special chemical signals to help recruit other types of immune cells to the scene. But the coolest thing about macrophages is that they can swallow stuff whole. MAC ATTACK!! Macs engulf our own used-up, damaged, or dead cells, and devour bacteria that can do us harm.

When macs run amok . . .

Now these cells are our best friends in infection or wound healing, but if they become cancerous, they can become our worst enemy, because they are very active, can fuse with other cells, and they are mobile. Now you’ve got macs gone amok. Metastatic tumor cells of many types have been observed to have phagocytic behavior (i.e. they eat other cells…just like macs do). Macs are often found mixed in among tumor cells, contributing to chronic inflammation in the area by triggering local immune reactions. These macs are called TAM’s, or tumor-associated macrophages. Tumors containing TAM’s have a poorer prognosis.

Macs tend to hang out more often in their favorite organs—they are especially drawn to lung, liver, and bone. These also happen to be favorite places for cancer to migrate to, as well. Some cancers also like to spread to injured or inflamed parts of the body, just like a mac would. Plants and certain lower animals, which do not have macrophages, can also get cancer, but their cancers never metastasize. Fascinating.

How best to prevent cancer in the first place?

Since 90% of all cancer deaths are due to metastatic cancers (cancers that have spread to more than one organ)—and this estimate has not changed in 50 years—early detection and prevention of spread plays a MAJOR role in prognosis. But the good news is that most cancer IS preventable.

About 5% of cancers are caused by mutations that are inherited at birth. About 15% of cancers are caused by viruses. The rest—a full 80%—are associated with the following risk factors:

• Smoking
• Alcohol
• Obesity
• Age
• Radiation exposure
• Carcinogenic chemical exposure

This means that the vast majority of cancers are preventable using lifestyle modifications. Dr. Seyfried writes (and I have read many papers supporting this logic), that the best way to prevent cancer (and most chronic diseases, for that matter), is to avoid exposure to things that cause tissue inflammation. All of the above risk factors are directly associated with inflammation. Two of the above risk factors are dietary—alcohol and obesity, so let’s zero in on those. This is a nutrition website, after all.

What is the connection between obesity and inflammation?

The road to inflammation is paved with refined carbohydrates. To fully explain the science behind these connections here would take us too far off track, but suffice it to say for now that refined carbohydrates (such as sugar and flour) lead to high blood sugar and high insulin levels. These, in turn, increase the production of damaging free radicals within the mitochondria. They also increase the production of a molecule called NF-kappa-B, which turns on genes that promote inflammation. It would therefore make sense, whether you are overweight or not, to minimize your exposure to refined carbohydrates.

Obesity is a major risk factor for cancer, and there is no question that diet is the most powerful tool available to manage weight. If you have been paying attention to thought leaders in the field of obesity, or you are familiar with the information on this website about obesity, or you have learned through your own experiences what works best, you know that the single most effective dietary strategy for preventing and managing weight gain (as well as for preventing and managing most chronic diseases of civilization) is avoiding refined carbohydrates. Refined carbohydrates keep blood sugar and insulin levels high, promoting inflammation and oxidation throughout the body. They also encourage overeating due to loss of control over appetite, which continues the vicious cycle.

Yet we all know people with cancer who are not overweight and who seem to take excellent care of themselves. We even know of athletes who don’t drink, don’t smoke, and are in excellent physical condition, who nevertheless have come down with cancer. Could it be that refined carbohydrate is the hidden risk factor in people like this? To learn more about the connection between carbohydrates and cancer, there is an excellent review article available free on line.

In addition to avoiding inflammation, Dr. Seyfried recommends a 7-day, water-only fast once a year. His reasoning is that a total fast forces the body to rid itself of damaged and weakened cells that may be pre-cancerous. With nothing else to eat, healthy cells turn to cannibalism, eating their vulnerable neighboring cells. How’s that for an image?

The bottom line

The bottom line is that diet clearly makes a huge difference, but we don’t yet know what the ideal diet for cancer treatment is. There is no question in my mind at this point that carbohydrates are bad for cancer. To what degree calories, protein and fat need to be restricted is unclear. We need more studies, and they need to be more thoughtfully designed. It seems that ketogenic diets have tremendous potential, but I don’t know if they need to be as strict as Dr. Seyfried recommends. Might people who design their ketogenic diet around healthy, whole foods and avoid dairy be able to get away with more calories?

I do think it makes sense for those of us who want to reduce our risk for cancer to minimize refined carbohydrates, minimize dairy products (particularly those with high whey content), maintain our weight in a healthy range, and choose whole foods over processed foods. Since that dietary pattern is already quite an improvement from the standard American diet, I have hope that it could make a big difference in our risk for cancer (as well as many chronic diseases).

However, if I already had cancer or were a cancer survivor, I wouldn’t touch a carbohydrate with a 10-foot pole. Dairy, being a growth formula (for baby cows), would also be off the menu.

Taking one for the team

Dr. Seyfried’s book, Cancer as a Metabolic Disease,inspired me to attempt a fasting jump-start to ketosis to see how long it takes to achieve his “zone of metabolic management.” To read about my 5-week experiment with Dr. Seyfried’s dietary recommendations, start with the first post: Seyfried’s Cancer Diet: My Fasting Jump-Start to Ketosis.

The future of cancer prevention and treatment may not be in sexy, high-tech, gene-targeting therapies, but in our own hands . . . or rather, on our own plates. Which diets work best for cancer treatment and prevention?

[This is the 4th in a 4-part article inspired by Dr. Thomas Seyfried’s book Cancer as a Metabolic Disease. Go to “What Causes Cancer? Part I” to begin with the first article.]

Cancer treatments: Standard therapies vs. dietary therapies

Standard therapies

• Conventional treatments can help in the short-term but can cause problems in the long-term.
• Chemotherapy is toxic to healthy cells and can breed resistance among cancer cells, increasing the risk of more aggressive cancers if relapse occurs.
• Radiation turns up the activity of the tumor growth pathway (PI3K/Akt/HIF), which promotes not only tumor growth, but also recruitment of new blood vessels (angiogenesis) and drug resistance.
• Radiation increases fusion activity between cells, which means that normal and healthy cells can merge into hybrid cells and become more aggressive.
• Radiation directly damages mitochondria, which increases risk for cancer in the future.
• Both radiation and immunosuppression therapy (drugs that suppress the immune system) can increase the incidence of metastatic cancers (cancers that spread).
• Steroids such as dexamethasone (Decadron), often used to reduce inflammation, raise blood sugar levels, feeding tumor cells and enhancing their survival.

Dietary therapies

• DER (dietary energy restriction) triggers cancer cell death via apoptosis(programmed cell suicide), which is a natural, noninflammatory process that happens from within the cell, causing no collateral damage. Conventional treatments kill cancer cells via necrosis, an inflammatory process that happens from the outside and is locally destructive. Tumor cells that are being fed glucose/glutamine are resistant to apoptosis, but under ketogenic conditions, they become better able to undergo apoptosis again.
• DER and chemotherapy can both cause weight loss. However, the weight loss associated with DER is healthy and does not weaken people, whereas chemotherapy-induced weight loss is unhealthy and weakens people.

Dr. Seyfried wonders if some of the benefit that some people obtain from chemotherapy may be due to the calorie restriction that occurs due to loss of appetite. He notes that drug studies don’t usually take this possibility into consideration.

“DER (dietary energy restriction) can be considered a broad-spectrum, nontoxic metabolic therapy that inhibits multiple signaling pathways required for progression of malignant tumors regardless of tissue of origin. It is not clear to me why so many oncologists have difficulty appreciating this concept.

“Therapies that reduce glucose and elevate ketones can starve glucose-dependent cancer cells while protecting and fueling healthy cells. There is no other cancer therapy that can do this.”

Complementary cancer-fighting strategies

Dr. Seyfried does not think that dietary restriction alone is sufficient to fight most cancers, so he proposes some additional strategies that can be used in combination with dietary measures to optimize results:

• “Anti-glycolytic” drugs that reduce the activity of the glycolysis (fermentation) pathway, which is the primary energy pathway for most cancer cells.

“Anti-glycolytic drugs together with energy-restricted diets could act as a powerful double ‘metabolic punch’ for the rapid killing of glycolysis-dependent tumor cells.”

• “CR-mimetic” drugs that mimic the effects of calorie restriction by lowering glucose levels. These drugs should not be used without diet, because they lower glucose without raising ketones. Without ketones, healthy cells could die of energy failure—they would have neither glucose nor ketones for fuel.
• Hyperbaric (high pressure, 100%) oxygen. Excess oxygen reduces the activity of an enzyme called hexokinase II, which grabs onto glucose after it enters cells and traps it inside so it can be burned for energy.

But standard treatment sometimes works and diet doesn’t always work . . .

We all know people who have undergone successful standard treatments and who have not had a recurrence of cancer. My own mother had cancer twice, decades ago, and has had no cancer since. In both cases surgery was curative for her. If you are lucky enough to have a simple form of cancer in a body part that can be completely removed, and you catch it before it spreads, your prognosis is probably pretty good.

Chemotherapy and radiation can kill many cancer cells because (as discussed in article #1), they are more vulnerable to these agents than healthy cells, and if you have a healthy enough immune system, your own body may be able to take care of the rest. Some people never get cancer again—they may change their lifestyle after a cancer scare and start taking better care of themselves (my mother stopped smoking, for example). Some adopt a healthier diet or start exercising. Some may just be lucky. But clearly modern cancer therapies have made a difference for some people, including my own mother.

So my mom is a cancer success story, but a close family friend of ours who was diagnosed with glioblastoma multiforme (brain cancer) was not so lucky. She lived for only a few months, and those final months were of very poor quality. She had smoked for years, but had quit long before her diagnosis. She loved candy. As kids we always looked forward to her visits, because she always walked through the door with a big package of red licorice and a king-sized bag of m&m’s. And as soon as she ran out of treats, she’d say to my mother: “Ain’tcha got somethin’ sweet?”

I have no idea why she got brain cancer, of course, but modern treatments certainly were not able to help her. I do find it interesting that the second most common type of cancer among young people is brain cancer, and the brain just happens to be the organ most heavily dependent on glucose. Could it be that the brain is especially sensitive to the damaging effects of high sugar/high flour diets?

Ketogenic diet for cancer case studies

First study of ketogenic diet with human brain malignancy

Linda Nebeling, PhD, MPH, RD (now with the National Cancer Institute) authored the first-ever study of a ketogenic diet in human brain malignancy [Nebeling 1995]. This was a landmark study of two young girls with advanced-stage, inoperable brain tumors that had not responded to traditional therapies. A three-year-old girl with stage IV astrocytoma and an eight year old girl with grade III astrocytoma were treated with a ketogenic diet. Both children responded well, and experienced long-term tumor management without further chemotherapy or radiation. PET scans revealed a 22% reduction in glucose uptake by tumors in both girls.

Low-calorie/ketogenic diet with brain tumors

Giulio Zuccoli MD (Italian neuro-radiologist) and Thomas Seyfried PhD published a case report [Zuccoli 2010] of a middle-aged woman with glioblastoma (a form of brain cancer) who was treated with a 600-calorie/day ketogenic diet. Upon diagnosis, steroids (to control inflammation) and anticonvulsant medication (to control seizures) were given. She underwent surgery, fasted briefly, and then began the diet. After 14 days on the diet, steroids were stopped, and chemotherapy and radiation treatments were started. After two months, chemotherapy and radiation were discontinued. One week later, PET scan and MRI were performed and no tumor tissue or swelling was detected.The patient stopped the diet, and 10 weeks later, MRI showed evidence that the tumor had come back.

This case report demonstrated that a) the ketogenic diet was well-tolerated; b) the diet may be a useful add-on therapy, as most tumors of her type do not respond as well as hers did to standard treatments alone, and c) inflammation was well-controlled without the usual need for steroids, supporting the anti-inflammatory properties of the diet.

Very low-carb diet in ten patients with incurable cancers

Eugene Fine, MD, professor of nuclear medicine at Albert Einstein College of Medicine just published a 28-day pilot study [Fine 2012] of a very low carbohydrate diet in ten men and women ages 53-73 with incurable, advanced cancers of a variety of types (3 colon, 2 breast, 2 lung, 1 ovarian, 1 esophageal, 1 fallopian tube). Carbohydrate intake was about 9%, but protein and fat were not restricted. Interestingly, those with high ketone levels (and low insulin levels) were the only ones whose tumors either stopped growing or got smaller as evidenced by PET scan. His video presentation is below in the resources section. Dr. Fine’s study is groundbreaking because it may pave the way for additional studies, which are badly needed. Below is his video presentation from the 2012 Ancestral Health Symposium entitled: “Dietary Insulin Inhibition as a Metabolic Therapy in Advanced Cancer.”

Ketogenic diet in four patients with brain cancer

Beth Zupec-Kania, RD is a nutritionist with the Charlie Foundation (an organization dedicated to raising awareness of and providing support for the use of ketogenic diets in children with epilepsy). Ten glioma (brain cancer) patients contacted her for help in using ketogenic diets in the treatment of their cancer. Four of them ultimately committed to a strictly supervised ketogenic diet. Three of the four patients had stable or atrophied (reduced) tumor size documented by MRI. Two had been on the diet for several years and were still alive despite having initially been given only a few months to live. One patient died; he had had advanced stage metastatic cancer prior to starting the ketogenic diet. He remained active and alert until the last two months of his life, and outlived his prognosis by a year.

Obstacles to dietary treatments

Ketogenic diets are hard to follow. They require careful monitoring, tremendous self-discipline, and essentially require that people turn their usual diet completely upside-down. You’ve got to be very motivated, and have the full support of everyone who lives with you. Even if everyone on the planet were 100% convinced that a ketogenic diet is the best diet for cancer, I would eat my hat if everyone with cancer followed it. That would be unrealistic—changing one’s diet is hard.

Ketogenic diets are, by nature, high-fat diets, and this will bother some people on a psychological level, due to (unnecessary) fear of eating fat. For more information, see my fats page and my cholesterol page.

Most physicians are taught next to nothing about nutrition during medical training, and once in practice, are too busy to learn. Nutritional treatments are not particularly sexy or high-tech and may not be of interest to some physicians. Nutritional treatments may be viewed as slower to take effect, and as time-consuming to implement.

But here is the most important obstacle: if a particular treatment is not sanctioned by the medical establishment and does not have solid studies behind it, most doctors will be afraid to recommend it or even support it, due to discomfort with uncertainty and fears of medical malpractice. Doctors take their responsibilities very seriously and want to provide the best treatment they can. In today’s world, that means applying the “standard of care.” Currently surgery, chemotherapy, and radiation are the standard of care. And what’s more, is that the standard of care is what insurance companies will pay for. They are unlikely to cover ketone meters, testing strips, special nutritional counseling, etc.

Is your doctor simply keeping up with the standard of care or is he or she interested in being on the cutting edge? Would your doctor be willing to read Dr. Seyfried’s book, or at least his journal article? [see references below]

The good news is you do not need your doctor’s permission to eat a ketogenic diet, only his or her support and willingness to monitor your progress. Open-minded, patient-centered physicians should be on board with your efforts so long as you are willing to take responsibility for your care.

Do ketogenic diets really need to be so strict?

If you read article 3, you may have been disheartened to see how tough Dr. Seyfried’s dietary recommendations are. Yet as draconian as his diet is, he doesn’t think it will work very well on its own without chemotherapy. While no treatments of any kind are perfect, if Dr. Seyfried’s hypothesis about mitochondria and diet are correct, shouldn’t they have the potential to work better than he thinks they will?

Having read his book and heard him speak, I believe Dr. Seyfried is a brilliant scientist and thinker. The only (gentle, constructive, but wicked important) criticism I have is the same one I have of most scientists who study diet—he thinks about diet as a simple collection of proteins, carbohydrates, and fats, and neglects the actual foods in the diet.

Dr. Seyfried compared two different types of chow in mice with cancer—one high-carb “standard” chow and one high fat “ketogenic” chow. He found that the ketogenic chow did not work against cancer if you let the mice eat as much as they wanted. Their little blood sugar levels stayed high and their cancers grew. He had to lower their calories to see benefits. He concluded that both diets worked equally well as long as you lowered calories—a lot. This made me suspicious, so I visited the chow manufacturers’ websites to see what the diets actually contained. I wonder if it will shock you as much as it shocked me.

Dr. Seyfried’s standard high-carb chow:

ProLab RMH 3000 (LabDiet)—62% carbohydrate, 22% protein, 5% fat, 5% fiber

Ingredients: ground wheat, dehulled soybean meal, wheat middlings, ground corn, fish meal, pork fat, alfalfa meal, calcium carbonate, brewer’s yeast, soybean oil, salt, vitamins, and minerals.

The first four ingredients are refined grains and legumes. Nearly 100% refined junk (including lots of refined carbohydrate) that no self-respecting mouse would naturally consume. No wonder he had to limit how much of this stuff the mice ate by 30-60% in order to lower blood glucose.

Dr. Seyfried’s ketogenic chow:

Ketocal (Nutricia)—90% fat, 1.6% carbohydrate, 8.4% protein

Ingredients: hydrogenated soybean oil, dry whole milk, refined soybean oil, soy lecithin, corn syrup solids.

Nice. Processed soy, dairy, and corn syrup. Poor little mice.

If you have read my dairy page, you will know that the whey proteins in milk raise insulin levels, which can prevent ketosis. This may have been why he had to limit how much of this stuff the mice ate to get good results.

To Dr. Seyfried’s credit, he points out in his book that other researchers have been able to achieve good results in their animal cancer experiments without having to restrict calories and he is unable to explain why. Let’s look at a mouse diet that worked without restricting calories:

Unrestricted ketogenic chow:

Ketogenic Bio-Serv F3666—8.36% protein, 0.76% carbohydrates and 78.8% fat

Ingredients: lard, butter, corn oil, casein, cellulose, mineral mix, vitamin mix, dextrose

Look, ma, no whey protein and no refined carbohydrate! The mice could eat as much of this (admittedly very weird) chow and get good results [Stafford 2010]. It makes me hopeful that even this odd diet, which is a far cry from a healthy mouse diet, delivered positive results.

Dr. Seyfried also referred to another study that used a high-protein, low-carb diet with unrestricted calories that also worked, but I could not locate the article in time to include it here. [Ho 2011]

I can’t help but wonder how these little mice would have fared had they been fed real food that mice are actually supposed to be eating.

So, do we need to restrict calories or not? It may depend on the composition of the diet . . . I think the jury is still out. However, people who eat well-formulated ketogenic diets report a substantial reduction in appetite and tend to naturally find themselves eating quite a bit less without having to count calories.

Metastatic cancer is different

Ninety percent of all cancer deaths are due to metastatic disease (cancer that has spread to more than one organ). These are the bad boys. Once cancer is on the move it’s very hard to stop, which is why prevention is so important. But before we get to that, one of the most fascinating topics in Dr. Seyfried’s book is his theory of how and why some cancers travel through the body to distant organs. He makes a compelling argument for the role of a particular kind of immune cell called a macrophage in helping cancers to spread.

The normal role of macrophages (macs) in our immune system is a very complicated and special one. These are amazing cells, with the ability to change their personality, shape, and behavior whenever necessary, depending on the local circumstances. Every macrophage begins its little life as monocyte, a round cell that can cruise the bloodstream. When trouble is lurking anywhere in the body—if there is injury or inflammation or infection—monocytes heed the call of damaged tissues and travel to the troubled area. Once they are close enough, they squeeze themselves out of the blood vessel and into local tissue, where they magically morph into macrophages so they can to get to work.

Macrophages assess the situation and release all kinds of special chemical signals to help recruit other types of immune cells to the scene. But the coolest thing about macrophages is that they can swallow stuff whole. MAC ATTACK!! Macs engulf our own used-up, damaged, or dead cells, and devour bacteria that can do us harm.

When macs run amok . . .

Now these cells are our best friends in infection or wound healing, but if they become cancerous, they can become our worst enemy, because they are very active, can fuse with other cells, and they are mobile. Now you’ve got macs gone amok. Metastatic tumor cells of many types have been observed to have phagocytic behavior (i.e. they eat other cells…just like macs do). Macs are often found mixed in among tumor cells, contributing to chronic inflammation in the area by triggering local immune reactions. These macs are called TAM’s, or tumor-associated macrophages. Tumors containing TAM’s have a poorer prognosis.

Macs tend to hang out more often in their favorite organs—they are especially drawn to lung, liver, and bone. These also happen to be favorite places for cancer to migrate to, as well. Some cancers also like to spread to injured or inflamed parts of the body, just like a mac would. Plants and certain lower animals, which do not have macrophages, can also get cancer, but their cancers never metastasize. Fascinating.

How best to prevent cancer in the first place?

Since 90% of all cancer deaths are due to metastatic cancers (cancers that have spread to more than one organ)—and this estimate has not changed in 50 years—early detection and prevention of spread plays a MAJOR role in prognosis. But the good news is that most cancer IS preventable.

About 5% of cancers are caused by mutations that are inherited at birth. About 15% of cancers are caused by viruses. The rest—a full 80%—are associated with the following risk factors:

• Smoking
• Alcohol
• Obesity
• Age
• Radiation exposure
• Carcinogenic chemical exposure

This means that the vast majority of cancers are preventable using lifestyle modifications. Dr. Seyfried writes (and I have read many papers supporting this logic), that the best way to prevent cancer (and most chronic diseases, for that matter), is to avoid exposure to things that cause tissue inflammation. All of the above risk factors are directly associated with inflammation. Two of the above risk factors are dietary—alcohol and obesity, so let’s zero in on those. This is a nutrition website, after all.

What is the connection between obesity and inflammation?

The road to inflammation is paved with refined carbohydrates. To fully explain the science behind these connections here would take us too far off track, but suffice it to say for now that refined carbohydrates (such as sugar and flour) lead to high blood sugar and high insulin levels. These, in turn, increase the production of damaging free radicals within the mitochondria. They also increase the production of a molecule called NF-kappa-B, which turns on genes that promote inflammation. It would therefore make sense, whether you are overweight or not, to minimize your exposure to refined carbohydrates.

Obesity is a major risk factor for cancer, and there is no question that diet is the most powerful tool available to manage weight. If you have been paying attention to thought leaders in the field of obesity, or you are familiar with the information on this website about obesity, or you have learned through your own experiences what works best, you know that the single most effective dietary strategy for preventing and managing weight gain (as well as for preventing and managing most chronic diseases of civilization) is avoiding refined carbohydrates. Refined carbohydrates keep blood sugar and insulin levels high, promoting inflammation and oxidation throughout the body. They also encourage overeating due to loss of control over appetite, which continues the vicious cycle.

Yet we all know people with cancer who are not overweight and who seem to take excellent care of themselves. We even know of athletes who don’t drink, don’t smoke, and are in excellent physical condition, who nevertheless have come down with cancer. Could it be that refined carbohydrate is the hidden risk factor in people like this? To learn more about the connection between carbohydrates and cancer, there is an excellent review article available free on line.

In addition to avoiding inflammation, Dr. Seyfried recommends a 7-day, water-only fast once a year. His reasoning is that a total fast forces the body to rid itself of damaged and weakened cells that may be pre-cancerous. With nothing else to eat, healthy cells turn to cannibalism, eating their vulnerable neighboring cells. How’s that for an image?

The bottom line

The bottom line is that diet clearly makes a huge difference, but we don’t yet know what the ideal diet for cancer treatment is. There is no question in my mind at this point that carbohydrates are bad for cancer. To what degree calories, protein and fat need to be restricted is unclear. We need more studies, and they need to be more thoughtfully designed. It seems that ketogenic diets have tremendous potential, but I don’t know if they need to be as strict as Dr. Seyfried recommends. Might people who design their ketogenic diet around healthy, whole foods and avoid dairy be able to get away with more calories?

I do think it makes sense for those of us who want to reduce our risk for cancer to minimize refined carbohydrates, minimize dairy products (particularly those with high whey content), maintain our weight in a healthy range, and choose whole foods over processed foods. Since that dietary pattern is already quite an improvement from the standard American diet, I have hope that it could make a big difference in our risk for cancer (as well as many chronic diseases).

However, if I already had cancer or were a cancer survivor, I wouldn’t touch a carbohydrate with a 10-foot pole. Dairy, being a growth formula (for baby cows), would also be off the menu.

Taking one for the team

Dr. Seyfried’s book, Cancer as a Metabolic Disease,inspired me to attempt a fasting jump-start to ketosis to see how long it takes to achieve his “zone of metabolic management.” To read about my 5-week experiment with Dr. Seyfried’s dietary recommendations, start with the first post: Seyfried’s Cancer Diet: My Fasting Jump-Start to Ketosis.

Thomas Seyfried PhD, a brain cancer researcher with over 25 years of experience in the field, gave a groundbreaking presentation about cancer at the Ancestral Health Symposium held at Harvard Law School this past August. The three main take-home points of his talk:

1. Cancer is not caused by genetic mutations
2. Cancer is a mitochondrial disease
3. Cancer can be treated with ketogenic diets

The gene theory of cancer

In case your basic biology is rusty: our genes are made of DNA—coils of coded information that tell our cells exactly how to build all the proteins they need to conduct their daily business. These blueprints have to be flexible, because cells need different proteins under different circumstances. Cells must be able to adapt to various conditions, such as stress, injury, infection, temperature changes, and food supply. So, genes contain lots of special controls that can be turned on and off, depending on what’s going on in and around the cell.

I was taught in medical school that cancer is about genes going haywire—something evil comes along, like a toxic chemical or a beam of radiation, attacks your DNA, and poof—you’ve got cancer (unless you are a cartoon character, in which case you develop superpowers). Mutant cells start dividing like crazy and taking over your body. I was also taught that the way to get rid of cancer is to flood it with toxic chemicals and radiation . . . hmmm . . .

The company line is that cancer is caused by mutations (changes) in DNA that transform healthy, well-behaved cells into reckless, ravenous, immortal renegades. These mutations hijack the set of instructions encoded in the cells’ DNA, and scientists think these mutations cause cells to go wild.

Differences between healthy cells and cancer cells

Cancer cells are very different from normal cells. They grow independently, ignoring the anti-growth signals and death cues that would normally keep healthy cells from getting out of control. Cancer cells create their own blood supply and can divide forever. They lose many of the physical features of their mother cells; they are usually smaller, and may be disfigured or even shapeless. Sometimes they fuse with each other or with neighboring cells, creating strange hybrids. The most aggressive types of cancer cells invade local tissues and/or break loose and travel in the bloodstream to distant parts of the body (metastasize).

Hundreds of thousands of different mutations have been discovered in cancerous cells, but it is actually rare to find genetic mutations in healthy cells because healthy cells have stable DNA. DNA is the most important molecule in the body so evolution has made sure it is well-protected. The DNA of healthy cells is not fragile. It would not have survived all this time if it were. There are even “caretaker genes” that are designed to maintain and repair defects in DNA, because lots of things in the natural environment can injure DNA—even things we think of as healthy, such as sunlight and vegetables.

Cancer cells have unstable DNA, which mutates easily and is therefore constantly changing. This is why there are so many mutations found in cancer cells. This “genomic instability” is viewed as a strong suit by scientists who believe in the mutation theory. They think that the tumor cells keep mutating to improve themselves, and that the ones with the most clever mutations are the ones which survive best and reproduce best (Darwinism—survival of the fittest). They think of cancerous cells as invincible—as stronger, faster, and smarter than healthy cells. But this isn’t true.

Yes, most tumor cells are growing faster than most of their healthy neighboring cells, but this is not because they are speedier. It’s because they are unregulated. All the healthy cells around them are capable of growing just as fast, but there are checks and balances in place to prevent them from growing willy-nilly. When necessary, they can grow just as fast, if not faster than tumor cells do. For example, when the liver is injured and healthy cells need to grow rapidly to replace the injured cells, their growth rate is the same as for liver cancer cells during tumor progression.

Tumor cells are more vulnerable than healthy cells. This is how radiation and chemotherapy work. Radiation and chemotherapy are toxic to all cells, cancerous or not, but they are more toxic to tumor cells. If tumor cells were more robust than normal cells, these therapies would kill off all your healthy cells and only the big ugly tumor would survive. Instead, people are treated to the brink of destruction with chemicals and radiation while doctors cross their fingers hoping more tumor cells will die than healthy cells, and that patients will survive the therapy.

Fragile DNA is not flexible enough or coordinated enough to respond to challenges. It is, after all, the stability of healthy DNA that allows our cells to adapt to stressful environments. Tumor cells are also more sensitive to heat (fever) and to starvation. When the body is stressed, the tumor cells are the first ones to go. These are not supervillain clones.

Just because cancer cells have lots of mutations doesn’t necessarily mean that mutations cause cancer. Seyfried argues that mutations are just red herrings (no disrespect to the herring community intended).

Poking holes in the mutation theory

The “oncogenic paradox” refers to this puzzle:

• A huge variety of things in the world—from viruses to radiation to chemicals to oxidation—can damage DNA and cause mutations. Seyfried quotes Nobel-prize winner Albert Szent-Györgyi: “It is getting more and more difficult to find something that is not carcinogenic.”
• There are hundreds of thousands of unique mutations associated with tumors. A single colon cancer cell can contain 11,000 mutations! The sheer number and type of mutations found in cancer cells are so serious that they would cause a healthy embryo to spontaneously abort, yet cancer cells somehow soldier on.
• The transformation of a healthy cell into a cancerous cell (malignant transformation) happens in the very same specific way every time.

How can all of these different and unpredictable events leading to all of those random mutations always cause exactly the same outcome? That’s like saying no matter how you attack an orc—whether you stab him in the belly with a sword, throw a rock at his head, or push him off a cliff—his left arm always falls off. Preposterous.

No specific mutation is a reliable marker for any one type of cancer

There is not one example of a mutation that causes the same type of cancer every time. Even those mutations most strongly associated with certain cancers only cause cancer in certain people.

Cancer cells within the very same tumor can have different mutation patterns.

Mutated genes thought to be strongly associated with cancer (“oncogenes”) sometimes do promote tumor growth, but sometimes they inhibit tumor growth, and sometimes they even do both.

Transplant experiments make the strongest case

Here’s the thing: if you transplant mutated cancer cell DNA into a healthy cell, the healthy cell almost never becomes cancerous.1 Only 2 out of 24 experiments were successful in transforming normal cells into cancer cells (and scientists couldn’t be sure that viral contamination wasn’t to blame). These results essentially kill the mutation theory dead on the spot.

The war on cancer

Just think about it: if cancer is a genetic disease, based on hundreds of thousands of mutations, what are we supposed to do, create hundreds of thousands of different drugs to treat it?

President Nixon declared war on cancer 40 years ago. The mutation theory of cancer has been solidly in place and guiding research since 1981, yet despite the enormous amounts of money, time, and energy that have been poured into cancer research since, we continue to lose the war against this killer disease. Fifteen-hundred Americans die every day from cancer. Researchers now place hope in the Cancer Genome Project, which they see as the shining future of cancer treatment. They have already started using the genetic fingerprints of cancer to design expensive, high-tech drugs that specifically target the unique DNA pattern of individual cancer cells. More than 700 of these smart bombs have been developed so far, yet none of them have saved a single life. The vast majority of whatever progress we have made against cancer has been due to identification of and education about lifestyle risk factors (such as smoking), not due to advances based on genetic theories.

Seyfried argues that the reason why we are making so little progress is because we are fighting the wrong enemy. Genes, he argues, are not the enemy, and they are not in the driver’s seat. Instead, they are innocent victims of the cancer. They are damaged, destabilized, and randomly mutated by the cancerous process. But if genetic mutations do not cause cancer, what does? How do cancer cells get by with all of these mutations? What keeps them going? And what causes all of these mutations in the first place?

In the next article in the series, “What Causes Cancer: Part II,” I explain the role of mitochondria in our cells and the significant link between damaged mitochondria and cancer.

To read my detailed critique of the World Health Organization’s 2015 report claiming that red meat causes cancer: “WHO Says Meat Causes Cancer“

Thomas Seyfried PhD, a brain cancer researcher with over 25 years of experience in the field, gave a groundbreaking presentation about cancer at the Ancestral Health Symposium held at Harvard Law School this past August. The three main take-home points of his talk:

1. Cancer is not caused by genetic mutations
2. Cancer is a mitochondrial disease
3. Cancer can be treated with ketogenic diets

The gene theory of cancer

In case your basic biology is rusty: our genes are made of DNA—coils of coded information that tell our cells exactly how to build all the proteins they need to conduct their daily business. These blueprints have to be flexible, because cells need different proteins under different circumstances. Cells must be able to adapt to various conditions, such as stress, injury, infection, temperature changes, and food supply. So, genes contain lots of special controls that can be turned on and off, depending on what’s going on in and around the cell.

I was taught in medical school that cancer is about genes going haywire—something evil comes along, like a toxic chemical or a beam of radiation, attacks your DNA, and poof—you’ve got cancer (unless you are a cartoon character, in which case you develop superpowers). Mutant cells start dividing like crazy and taking over your body. I was also taught that the way to get rid of cancer is to flood it with toxic chemicals and radiation . . . hmmm . . .

The company line is that cancer is caused by mutations (changes) in DNA that transform healthy, well-behaved cells into reckless, ravenous, immortal renegades. These mutations hijack the set of instructions encoded in the cells’ DNA, and scientists think these mutations cause cells to go wild.

Differences between healthy cells and cancer cells

Cancer cells are very different from normal cells. They grow independently, ignoring the anti-growth signals and death cues that would normally keep healthy cells from getting out of control. Cancer cells create their own blood supply and can divide forever. They lose many of the physical features of their mother cells; they are usually smaller, and may be disfigured or even shapeless. Sometimes they fuse with each other or with neighboring cells, creating strange hybrids. The most aggressive types of cancer cells invade local tissues and/or break loose and travel in the bloodstream to distant parts of the body (metastasize).

Hundreds of thousands of different mutations have been discovered in cancerous cells, but it is actually rare to find genetic mutations in healthy cells because healthy cells have stable DNA. DNA is the most important molecule in the body so evolution has made sure it is well-protected. The DNA of healthy cells is not fragile. It would not have survived all this time if it were. There are even “caretaker genes” that are designed to maintain and repair defects in DNA, because lots of things in the natural environment can injure DNA—even things we think of as healthy, such as sunlight and vegetables.

Cancer cells have unstable DNA, which mutates easily and is therefore constantly changing. This is why there are so many mutations found in cancer cells. This “genomic instability” is viewed as a strong suit by scientists who believe in the mutation theory. They think that the tumor cells keep mutating to improve themselves, and that the ones with the most clever mutations are the ones which survive best and reproduce best (Darwinism—survival of the fittest). They think of cancerous cells as invincible—as stronger, faster, and smarter than healthy cells. But this isn’t true.

Yes, most tumor cells are growing faster than most of their healthy neighboring cells, but this is not because they are speedier. It’s because they are unregulated. All the healthy cells around them are capable of growing just as fast, but there are checks and balances in place to prevent them from growing willy-nilly. When necessary, they can grow just as fast, if not faster than tumor cells do. For example, when the liver is injured and healthy cells need to grow rapidly to replace the injured cells, their growth rate is the same as for liver cancer cells during tumor progression.

Tumor cells are more vulnerable than healthy cells. This is how radiation and chemotherapy work. Radiation and chemotherapy are toxic to all cells, cancerous or not, but they are more toxic to tumor cells. If tumor cells were more robust than normal cells, these therapies would kill off all your healthy cells and only the big ugly tumor would survive. Instead, people are treated to the brink of destruction with chemicals and radiation while doctors cross their fingers hoping more tumor cells will die than healthy cells, and that patients will survive the therapy.

Fragile DNA is not flexible enough or coordinated enough to respond to challenges. It is, after all, the stability of healthy DNA that allows our cells to adapt to stressful environments. Tumor cells are also more sensitive to heat (fever) and to starvation. When the body is stressed, the tumor cells are the first ones to go. These are not supervillain clones.

Just because cancer cells have lots of mutations doesn’t necessarily mean that mutations cause cancer. Seyfried argues that mutations are just red herrings (no disrespect to the herring community intended).

Poking holes in the mutation theory

The “oncogenic paradox” refers to this puzzle:

• A huge variety of things in the world—from viruses to radiation to chemicals to oxidation—can damage DNA and cause mutations. Seyfried quotes Nobel-prize winner Albert Szent-Györgyi: “It is getting more and more difficult to find something that is not carcinogenic.”
• There are hundreds of thousands of unique mutations associated with tumors. A single colon cancer cell can contain 11,000 mutations! The sheer number and type of mutations found in cancer cells are so serious that they would cause a healthy embryo to spontaneously abort, yet cancer cells somehow soldier on.
• The transformation of a healthy cell into a cancerous cell (malignant transformation) happens in the very same specific way every time.

How can all of these different and unpredictable events leading to all of those random mutations always cause exactly the same outcome? That’s like saying no matter how you attack an orc—whether you stab him in the belly with a sword, throw a rock at his head, or push him off a cliff—his left arm always falls off. Preposterous.

No specific mutation is a reliable marker for any one type of cancer

There is not one example of a mutation that causes the same type of cancer every time. Even those mutations most strongly associated with certain cancers only cause cancer in certain people.

Cancer cells within the very same tumor can have different mutation patterns.

Mutated genes thought to be strongly associated with cancer (“oncogenes”) sometimes do promote tumor growth, but sometimes they inhibit tumor growth, and sometimes they even do both.

Transplant experiments make the strongest case

Here’s the thing: if you transplant mutated cancer cell DNA into a healthy cell, the healthy cell almost never becomes cancerous.1 Only 2 out of 24 experiments were successful in transforming normal cells into cancer cells (and scientists couldn’t be sure that viral contamination wasn’t to blame). These results essentially kill the mutation theory dead on the spot.

The war on cancer

Just think about it: if cancer is a genetic disease, based on hundreds of thousands of mutations, what are we supposed to do, create hundreds of thousands of different drugs to treat it?

President Nixon declared war on cancer 40 years ago. The mutation theory of cancer has been solidly in place and guiding research since 1981, yet despite the enormous amounts of money, time, and energy that have been poured into cancer research since, we continue to lose the war against this killer disease. Fifteen-hundred Americans die every day from cancer. Researchers now place hope in the Cancer Genome Project, which they see as the shining future of cancer treatment. They have already started using the genetic fingerprints of cancer to design expensive, high-tech drugs that specifically target the unique DNA pattern of individual cancer cells. More than 700 of these smart bombs have been developed so far, yet none of them have saved a single life. The vast majority of whatever progress we have made against cancer has been due to identification of and education about lifestyle risk factors (such as smoking), not due to advances based on genetic theories.

Seyfried argues that the reason why we are making so little progress is because we are fighting the wrong enemy. Genes, he argues, are not the enemy, and they are not in the driver’s seat. Instead, they are innocent victims of the cancer. They are damaged, destabilized, and randomly mutated by the cancerous process. But if genetic mutations do not cause cancer, what does? How do cancer cells get by with all of these mutations? What keeps them going? And what causes all of these mutations in the first place?

In the next article in the series, “What Causes Cancer: Part II,” I explain the role of mitochondria in our cells and the significant link between damaged mitochondria and cancer.

To read my detailed critique of the World Health Organization’s 2015 report claiming that red meat causes cancer: “WHO Says Meat Causes Cancer“