Category Archives: Disease - Page 9

Jay Wright’s Weight Loss Journey

Posted by on December 1, 2011 133 comments

Jay Wright, who comments as “Jaybird,” has had a remarkably successful weight loss story. He adopted our diet in March at a weight of 250 pounds, and reached his normal weight of 170 pounds at Halloween, seven and a half months later.

I met Jay at Wise Traditions in November and can attest that he is now a handsome, slender man.

Jay’s weight loss was remarkably consistent at about 2.5 pounds per week. He agreed to describe his weight loss journey in a guest post; my questions are in italic, Jay wrote everything else. Welcome, Jay! – Paul

I would like to thank Dr. Paul Jaminet and Dr. Shou-Ching Jaminet for writing a great diet book and website!  You have been instrumental in helping me achieve the long elusive goal of great health and weight. For me, this truly is the Perfect Health Diet!

Before PHD

Paul: Jay, what do you think caused your overweight condition in the first place?

1. Ignorance and confusion. I believe I would have eaten the PHD way and remained at a healthy weight if I was taught to eat this way from the beginning. Instead, the government promotes the anti-saturated fat, pro-seed “vegetable” oil, and whole grains food pyramid. The belief formed from trusting the experts is a lot to overcome. I remember a decade ago during the Atkins’ hype that I thought that he must be crazy to recommend such a dangerous diet that would go against the “entire” medical establishment.  Then, even after I stopped believing the Lipid Hypothesis, I was still confused by all of the rest of the diet claims out there. While I was uncertain, I thought I might as well enjoy a “normal” diet until I can figure it all out.

2. Eating Habits. Besides the high carbs, food toxins, and malnourishment of the food pyramid diet, a few other factors may have affected my eating habits. I was a normal weight child growing up and I could eat anything and everything in sight and not get even pudgy in the slightest. When all foods have the same effect – none – you don’t worry about whether the food is healthy. Also, I spent my childhood playing one sport after another which might have actually worsened my eating habits. At least here with Texas football, we were constantly encouraged to stuff ourselves and put on more weight.  When sports ended for me after college, normal amounts of food looked like a starvation diet on a plate!

3. Carelessness toward health.  Was I careless because I was told “healthy” meant a yucky salad and “unhealthy” meant a yummy steak?  A young boy always chooses the steak especially when I was constantly hungry from 3 hour practices!  This all started to change after my dad was diagnosed with heart disease and started eating a “healthy” low-fat diet. However, the real wake-up call came when my mother was diagnosed and eventually died of breast cancer! To fight the cancer, she put up a courageous fight by being the most dedicated eater of an “alkalizing” vegetarian diet ever! Yet, even though I began to care more about health, I continued to allow myself to eat anything while I learned more and took breaks from trying different diets.

4. Lack of exercise because of a bad back.  I have had a herniated disc in my lower back for about 10 years now. When I changed careers and became even more sedentary, my back problem only worsened from bad posture while sitting. I should have at least continued to walk short amounts, but at the end of the day, I didn’t even feel like tolerating even a little pain after dealing with it so much during the day. The recliner offered relief.

5. Convenience.  As a single guy, I relied on eating out for convenience over the years and pre-made frozen dinners when I ate at home mostly. Starting a diet always meant making big changes to my routine and giving up a lot of time to cook.

6. Diets were Too Low in Food Reward.  Looking back, all the diets I tried were much lower in food reward than the “regular” American diet with lots of sweets that kept calling to me! All of the previous diets required a Herculean will power just to fight the temptations. It was mental torture being on a diet!

Paul: Jay, what were your experiences on the various diets you tried – and what caused you to give them up?

Here is my weight history:

After college sports, I struggled with my weight. I was a yo-yo dieter – I could lose weight but it always ended up even higher. I tried meal shake replacements, frozen dinners to limit calories, no meat/meat, no dairy/dairy, acid/alkaline, exercise/no exercise while dieting, no cash or credit cards in my wallet going to work so I wouldn’t stop at a fast food, punishment where I had to eat a raw tomato if I cheat (I hate raw tomatoes), and many other vegetarian leaning and mental tricks.  A pattern emerged with these diets.  I would starve with low energy for about a week or two until my will power ran out. Then, I would go eat something “bad.”  If I continued to repeat the pattern and managed to be “successful,” I stayed hungry even once I reached my goal weight.  I tried to transition to a “regular” amount of food to stop starving and just maintain but to no avail.  My weight went right back up even higher than before even without cheating on the diets.

Paleo was finally the exception to the starving rule, but only at first.  I felt great on a very low carb paleo for a couple of months.  I ate a pound of meat a day and mostly vegetables with a little fruit and nuts and a lot of coconut oil. The extra fat and meat seemed to enable me to lose weight and not be hungry. I lost nearly 40 lbs and halfway to my goal.  However, I started to not feel so well and hunger was returning, too. I had headaches and energy fluctuated throughout the day. I never liked the taste of vegetables and I began dreading the need to eat more vegetables than I had ever cared to eat in my life. Also, the sugar cravings never stopped just like on the vegetarian diets. Eventually, will power ran out eventually on paleo just like on the other diets.

Here’s what I looked like at 250 pounds. I’m the one on the left in the gray shirt; the one on the right is my brother Craig Wright:

I knew I had better find an answer when my family and friends would laugh each time I declared, “Diet starts tomorrow!”

Paul: Jay, it’s very interesting that on pre-Paleo diets you were always hungry, and when you ate to satisfy your hunger, your weight returned to as high or higher than when you began. That’s consistent with the set-point theory of obesity: your set-point hadn’t changed, and so when you reduced weight below the set-point, you got hungry; when you ate to satisfy your appetite, you were obese. The Paleo experience could also be said to be consistent with the set-point theory: it reduced the set-point so you lost 40 pounds without hunger, but weight was still above normal and hunger returned as your weight got below the new set-point.

An interesting data point, which I see as a challenge for the setpoint theory because it suggests an alternative view, is that on VLC Paleo your hunger returned at the same time you began to feel unwell. This suggests that hunger and setpoint are really an index of health, and when the body is not being properly maintained the brain manufactures hunger. When nutrients are abundant and the body has all it needs to establish good health, the setpoint is reduced to normal weight, hunger disappears, and weight loss resumes.

Perfect Health Diet

Paul: Jay, what was your experience on PHD? I’m especially interested in whether you experienced plateaus where weight loss stalled, and whether you experienced hunger as on other diets.

I recorded my weight every day from April 15 through November, and enough days in March and early April to give a clear picture. Here is what happened:

As you can see, there was no stall in weight loss until I hit my target weight of 170 pounds.

Here’s my after photo, again with my brother Craig. This time Craig is on the left in black, I’m on the right in green:

Interestingly Craig has eaten pretty much the same foods as I have throughout life, and always maintained a normal weight. On my recommendation he adopted PHD soon after I did, and he also experienced health improvements – psoriasis, which he’s had for 20 years and used to leave red scales over much of his body, is nearly gone.

Hunger

I followed the PHD weight loss protocols and felt virtually no hunger throughout the 7 months. Intermittent fasting with one meal a day worked best for my schedule; I coconut oil fasted earlier in the day and 1 day per week.  After the first month, I coconut oil fasted for an entire week since I figured I should clean out my system. Then I dropped the calories to only 1200 to get some faster results early on to help my back. I thought I would readjust the calories up or the eating schedule according to my hunger, but I did not experience any hunger and had great energy so I left the plan alone. What little hunger I did experience was very mild and just meant it was time to drink another bottle of water or swig a tablespoon of coconut oil before the evening dinner. Interestingly, I ate some birthday cakes toward the end and experienced stronger and more uncomfortable hunger the following days than the previous months. The lack of hunger was definitely a key to my weight loss success.

Food Reward

For me, PHD is a high food reward diet. It tastes great every meal! Even in the beginning of the diet, I enjoyed the PHD meal just as much mentally as thinking about eating my old food. Later, my taste buds changed and PHD became clearly the more rewarding food. However, at least part of the PHD was bland. The coconut oil provided calories with no taste and helped keep my calories low. Yet, I really believe I would not have lasted on the diet if the food was bland. Having a neutral taste reminds me of the very low carb paleo diet that didn’t allow the safe starches and even small amounts of dairy. The white rice and white potatoes enabled me to eat vegetables regularly by buffering the taste until my taste buds adjusted and I began to like them. Avoiding milk but having small amounts of other dairy also went a long way in the enjoyment of the food and menu options. The safe starches, dairy, and a little bit of fruit also seem to be responsible for satisfying my sweet tooth cravings. I’m not sure if the high food reward PHD would have controlled my calorie intake since I counted calories. Nonetheless, compared to the other past diets I dreaded to eat, I prefer the high food reward of PHD. I use to say, “Why does all of the food that’s good for you taste so bad and all of the food that’s bad for you taste so good?” I don’t say that anymore with PHD.

Plateau

My belief is that total calories do matter. I’ve always been able to lose the fat and get back to my original weight provided that I lower my calories enough to accomplish it. However, my will power usually ran out before I accomplished it many times. The constant hunger and low energy with lower calories exhausted my desire to lose the weight on previous diets. In contrast, I experienced the opposite on PHD. While the PHD food and supplements provided satiety and energy, I controlled my calories by exercising, counting calories, eating only a single meal, and having oil fast days. Even after only a month, I experienced such a surge in energy even on lower calories that I increased my exercise to 2 hours of walking. Having established such a low calorie amount in the beginning with a challenging exercise and eating plan, I simply had to maintain the routine until the goal was reached.

I believe the key was PHD enabled me to maintain low enough calories to not experience a plateau as on other diets.

Set Point

My experience might show some truth to the concept of a set point. For instance, prior to starting PHD my weight stayed consistently within a 5 lb range for about 2 years. During this period I was eating whatever I wanted. My experience on PHD could be construed as the resetting of my set point to my normal weight – 170 lb. I was never hungry on PHD as long as my weight was above 175 lb. I started feeling more hunger once I got close to my normal weight in the 170s.  Unlike previous diets, I was able to eliminate the hunger by eating a little bit more — just upping my calories slightly.

Although other diets could get me to this weight point before, I had to stay in a perpetual starving mode to remain at this level. Unlike on PHD, on other diets adding enough calories to stop hunger always led to a rebound of weight that leveled out at a higher level than before I started.

When I started PHD my intended target weight was 175 pounds. With PHD, I actually continued to lose a little more than the 175 down to 170 without planning on it. Then, my weight slightly increased with obvious cheats like some birthday cake. While eating the normal amount the following days without the cheats, the weight returned to previous levels without an effort to compensate. After the weight loss, my weight has become more stable. The last month I have had several repeating days on the weight scale with the same exact weight number to the tenth of a point. This occurred even though I ate more on a few of the previous days. My weight history shows a stair stepping up higher with each diet attempt until PHD stabilized my weight back to its original healthy level.

Closing Thought

During the middle of my weight loss, I was at a restaurant eating a salad with balsamic vinegar and olive oil dressing, 8 oz steak, and a baked potato with butter and sour cream and some water with lemon, but without a dinner roll.  I paused and proclaimed, “I can’t believe I’m eating this and still losing weight! This is the BEST DIET EVER!”

How to Minimize Hyperglycemic Toxicity

Posted by on October 20, 2011 124 comments

In my reply to Jimmy Moore’s safe starches symposium (see Jimmy Moore’s seminar on “safe starches”: My reply, Oct 12), I didn’t quite have time to fully address the issue of hyperglycemic toxicity.

As J Stanton commented, it would have been good to note that we recommend consuming “safe starches” as parts of meals, not as isolated snacks, and to discuss how meal design mitigates risk of hyperglycemic toxicity:

I’ve written entire articles on the fact that fat content is the primary driver of glycemic index. It’s silly to demonize white potatoes due to high GI when a couple pats of butter – or simply consuming it as part of a PHD-compliant high-fat meal – will drop it far more than substituting a sweet potato.

I thought I’d delve into the factors affecting blood glucose response to meals, and how to minimize the rise in blood sugar. It’s a topic of general interest, since hyperglycemia might have a mild detrimental health effect in nearly everyone; but of special importance to diabetics, since controlling blood sugar is so crucial to their health.

Glycemic Index of Safe Starches

The glycemic index (GI) is “defined as the area under the two hour blood glucose response curve (AUC) following the ingestion of a fixed portion of carbohydrate (usually 50 g).” Pure glucose in water is used as the reference and defines a GI of 100.

Our recommended “safe starches” are significantly lower in GI than glucose.

White rice is typically listed with a GI of 70 or 72, but it varies by strain: Bangladeshi rice has a GI of 37, American brown rice of 50, Japonica (a white short-grained rice) of 48, Basmati rice of 58, Chinese vermicelli of 58, American long-grain rice of 61, risotto rice of 69, American white rice is 72, short-grain white rice is 83, and jasmine rice 89 (source).

Potatoes are a high-GI food but again the GI is highly variable. Baked white potatoes with the skin have a GI of 69, peeled their GI is 98. Yams have GI of 35 to 77 depending on how they are prepared, sweet potatoes of 44 to 94 (source).

With some foods the GI varies strongly with ripeness. Plaintains when unripe have a GI of 40 but when ripe the GI can reach 90 (source).

Taro has a GI of 48 to 56. That’s similar to many fruits, such as bananas which have a GI of 47 to 62. Tapioca has a GI of 70 if steamed, but can exceed 80 if boiled (source).

Gentle Cooking Lowers the Glycemic Index

As a rule, gentle cooking of starchy plants leads to a lower glycemic index and high cooking temperatures lead to a higher glycemic index.

In general, industrially processed foods, which are often processed at very high temperatures to speed them through factories, have high GIs. A study in the American Journal of Clinical Nutrition [1] compared home-cooked corn, rice, and potato with processed foods based on them (instant rice, Rice Bubbles, corn chips, Cornflakes, instant potato, and potato crisps), and the processed foods had consistently higher GIs:

Another study in the British Journal of Nutrition [2] looked at 14 starchy plants prepared in different ways and found that roasting and baking raised the GI:

GI value of some of the roasted and baked foods were significantly higher than foods boiled or fried (P<0.05). The results indicate that foods processed by roasting or baking may result in higher GI. Conversely, boiling of foods may contribute to a lower GI diet.

Perhaps cooking methods that dry out the plant increase the GI.

Meals Have Lower GI

GI is calculated by eating a single food and only that food.

But what happens when you eat a meal? You’re no longer eating one food, but a mixture of foods. The baked potato may come with meat and vegetables, and with butter on top.

You might think that a weighted average of the GI of the various foods might give a good indication of the GI of the meal. Then, since fat, meat, and vegetables have a low GI, you’d expect GI of the meal to be much lower.

It turns out that the GI of meals is low – in fact, it is even lower than the average GI of the foods composing the meal.

That is the result of a new study in the American Journal of Clinical Nutrition [3]. Three meals were prepared combining a starch (potato, rice, or spaghetti) that digested to 50 g (200 calories) glucose with vegetables, sauce, and pan-fried chicken. The GIs of the meals were consistently lower than the values predicted using a weighted average of GIs of the meal components:

Meal Actual GI Predicted GI
Potato 53 63
Rice 38 51
Spaghetti 38 54

So eating a starch as part of a meal reduces GI to the range 38 to 53 – below the levels of many fruits and berries.

Fat Reduces GI

J Stanton has noted that adding a little fat to a starch is very effective in lowering its GI. In a post titled “Fat and Glycemic Index: The Myth of Complex Carbohydrates,” JS states that:

  • Flour tortillas have a GI of 30, compared to a GI of 72 for wheat bread, because tortillas are made with lard.
  • Butter reduces the glycemic index of French bread from 95 to 65.
  • A Pizza Hut Super Supreme Pizza has a GI of 30, whereas a Vegetarian Supreme has a GI of 49.

JS suggests that the reason fat does this is that it lowers the gastric emptying rate, and cites a study which showed that adding fat to starches could increase the gastric emptying time – the time for food to leave the stomach – by 50%. [4]

What’s interesting to me here is that what we really care about is not the glycemic index, but the peak blood glucose level attained after a meal. It is blood glucose levels above 140 mg/dl only that are harmful, and the harm is proportional to how high blood glucose levels rise above 140 mg/dl. So it’s the spikes we want to avoid.

But another paper shows that gastric emptying rate is even more closely tied to peak blood glucose level than it is to glycemic index. From [5]:

So combining a starch with fat may reduce peak blood glucose levels even more than it reduces the glycemic index; which is a good thing.

Dairy reduces GI

Dairy is effective at reducing GI:

[D]airy products significantly reduced the GI of white rice when consumed together, prior to or after a carbohydrate meal. [6]

It is not likely that dairy fat alone was responsible, because whole milk worked better than butter. However, low-fat milk only reduced the GI of rice by 16%, while whole milk reduced it by 41%. So clearly dairy fats are part of the recipe, but not the whole story; whey protein may also matter.

Fiber Reduces GI

Fiber is another meal element that reduces the rise in blood sugar after eating.

Removing fiber from starchy foods increases their glycemic index [7]; adding fiber decreases it. For instance, adding a polysaccharide fiber to cornstarch reduced its GI from 83 to 58; to rice reduced its GI from 82 to 45; to yogurt from 44 to 38. [8]

So it’s good to eat starches with vegetables – the foods richest in fiber.

Acids, Especially Vinegar, Reduce GI

Traditional cuisines usually make sauces by combining a fat with an acid. Frequently used sauce acids are vinegars and citric acid from lemons, limes, or other citrus fruits.

It turns that sauce acids can substantially reduce the GI of meals. The best attested is vinegar. From a study in the European Journal of Clinical Nutrition [6]:

In the current study, the addition of vinegar and vinegared foods to white rice reduced the GI of white rice. The acetic acid in vinegar was thought to be responsible for the antihyperglycemic effect. The amount of acetic acid to be effective could be as low as that found in sushi (estimated to be about 0.2–1.5 g/100 g). The antihyperglycemic effect of vinegar is consistent with other studies performed earlier (Brighenti et al, 1995; Liljeberg & Bjorck, 1998). Although vinegar could lower GI vales, the mechanism has rarely been reported. Most studies accounted the mechanism to be due to a delay in gastric emptying. In animal studies, Fushimi (Fushimi et al, 2001) showed that acetic acid could activate gluconeogenesis and induce glycogenesis in the liver after a fasting state. It could also inhibit glycolysis in muscles. [6]

Other acids also work. Pickled foods, which are sour due to lactic acid released by bacteria, reduce the glycemic index of rice by 27% if eaten before the rice and by 25% if eaten alongside the rice [6].

Wines, especially red wines, are somewhat acidic. I haven’t seen a study of how drinking wine with a meal affects glycemic index, but it is known observationally that wine drinkers have better glycemic control and, often, long lives. [9]

So What’s the Healthiest Way to Eat “Safe Starches”?

One way to limit the likelihood of reaching dangerous blood sugar levels after a meal is by eating a relatively “low carb” diet. We recommend that sedentary people eat about 400 to 600 carb calories per day. This limits the amount eaten at any one sitting to about 200 calories / 50 g, which is the amount of a typical glucose tolerance test. It is an amount the body is well able to handle.

But the manner in which carbs are eaten may be just as important as the amount.

Let’s look again at the Perfect Health Diet Food Plate:

The design of a PHD meal is found in the body of the apple. Assuming two meals a day, the recipe is to combine:

  • A safe starch (roughly ½ pound, which translates to 150 to 300 carb calories);
  • A meat, fish, or egg (¼ to ½ pound);
  • A sauce made up of fats and acids such as lemon juice or vinegar;
  • Vegetables, preferably including fermented vegetables with their healthy acids;
  • (Optionally) some dairy or a glass of wine.

This is precisely the recipe which science has found minimizes the elevation of blood glucose after meals.

It seems reasonable to expect that a meal designed in this fashion will have a glycemic index around 30. The odds of 200 carb calories with a glycemic index of 30 generating blood sugar levels that are dangerous – 140 mg/dl or higher – in healthy people is very low. Even in diabetics, it may be uncommon.

So, yes, Virginia. There is a Santa Claus, and you can eat safe starches and avoid hyperglycemia too!

References

[1] Brand JC et al. Food processing and the glycemic index. Am J Clin Nutr. 1985 Dec;42(6):1192-6. http://pmid.us/4072954.

[2] Bahado-Singh PS et al. Food processing methods influence the glycaemic indices of some commonly eaten West Indian carbohydrate-rich foods. Br J Nutr. 2006 Sep;96(3):476-81. http://pmid.us/16925852.

[3] Dodd H et al. Calculating meal glycemic index by using measured and published food values compared with directly measured meal glycemic index. Am J Clin Nutr. 2011 Oct;94(4):992-6. http://pmid.us/21831990.

[4] Thouvenot P et al. Fat and starch gastric emptying rate in humans: a reproducibility study of a double-isotopic technique. Am J Clin Nutr 1994;59(suppl):781S.

[5] Mourot J et al. Relationship between the rate of gastric emptying and glucose and insulin responses to starchy foods in young healthy adults. Am J Clin Nutr. 1988 Oct;48(4):1035-40. http://pmid.us/3048076.

[6] Sugiyama M et al. Glycemic index of single and mixed meal foods among common Japanese foods with white rice as a reference food. Eur J Clin Nutr. 2003 Jun;57(6):743-52. http://pmid.us/12792658. Full text: http://www.nature.com/ejcn/journal/v57/n6/full/1601606a.html.

[7] Benini L et al. Gastric emptying of a solid meal is accelerated by the removal of dietary fibre naturally present in food. Gut. 1995 Jun;36(6):825-30. http://pmid.us/7615267.

[8] Jenkins AL et al. Effect of adding the novel fiber, PGX®, to commonly consumed foods on glycemic response, glycemic index and GRIP: a simple and effective strategy for reducing post prandial blood glucose levels–a randomized, controlled trial. Nutr J. 2010 Nov 22;9:58. http://pmid.us/21092221.

[9] Perissinotto E et al. Alcohol consumption and cardiovascular risk factors in older lifelong wine drinkers: the Italian Longitudinal Study on Aging. Nutr Metab Cardiovasc Dis. 2010 Nov;20(9):647-55. http://pmid.us/19695851.

 

An Anti-Cancer Diet

Posted by on September 28, 2011 163 comments

Our cancer series resumes today with some tentative advice for cancer patients. (Note: This post is designed for solid tumor cancers, not blood cancers. However, most of the advice would also be applicable to blood cancers.)

This series began with Toward an Anti-Cancer Diet (Sep 15, 2011). There we advocated trying to shift cells away from the cancer phenotype via 8 anti-cancer strategies.

Future posts will explore in detail how to implement those strategies via diet and lifestyle. Today, I’m just going to give a general overview of what I would do if I had cancer.

Eat the Perfect Health Diet

This may sound self-serving, but it’s my best advice. Our diet is designed to optimize health generally, and that’s exactly what you want to do against cancer.

I said in the introduction that cancer is a disease in which cells lose their “humanness” – their proclivity to collaborate with other human cells to create a human organism. Instead, they lose recently evolved features and “remember” an identity similar to that of our distant evolutionary ancestors from the early days of multicellular life. This regression is possible because we retain the genes of our primitive evolutionary ancestors, and silencing of only a few hundred genes may cause a human cell to resemble, genetically, bacteria or fungi.

Many gut bacteria can take on two modes of behavior – a commensal or harmless phenotype, or a virulent harmful phenotype – depending on whether their environment is benign. In beneficial environments, bacteria tend to be cooperative with their host; in harsh environments, bacteria begin to look out for their own interests “selfishly,” and begin to display virulence traits which harm their host but help them move to a better environment.

Something similar may happen with “proto-cancer” cells. In a healthy environment, they are pleased to cooperate with their host – to retain their “humanness.” But in a harsh environment, they are more likely to withdraw from their neighbors and go their own way. An abused cell is more likely to become a cancer cell.

This may sound like anthropomorphization, but the metaphor is probably sound. Bruce Ames has remarked upon the fact that almost every compound is a carcinogen in large enough doses. Why? Because any unbalanced environment is harsh, and any harsh environment makes the cell more likely to develop the cancer phenotype.

It’s not only by discouraging “cancer virulence” that a good diet helps. A healthy diet also optimizes immune function.

Immune function is highly variable. Under stress, we suppress immunity so that all the body’s resources are available to meet “fight or flight” needs. Contrariwise, peaceable happiness is stimulating to immune function. A nutrient-rich diet, savory meals, happiness, calm, restful time spent in conversation – all of these things tell the body it has no pressing concerns and that available resources can be devoted to immunity and healing.

After cancer diagnosis, from a similar medical condition, those who are under stress tend to succumb to cancer, while those who are happy, cheerful, and sociable tend to recover from it. It is believed that this difference is primarily due to improved immune function in those under less stress.

I believe that a healthy, tasty diet is also a stimulant for immune function. Make your food nourishing and enjoyable.

Specific Dietary Aspects

A few aspects of an anti-cancer diet deserve special mention. Let’s look at the PHD Food Plate:

Some aspects I would emphasize for cancer patients:

  • Safe starches. I recommend obtaining 400 to 600 glucose calories a day, mainly from safe starches. I believe it is important to avoid a glucose deficiency, since glycosylated proteins are the means of intercellular coordination, and defects in glycosylation are characteristic of the cancer phenotype. (See, eg, this paper.) You don’t want to aggravate this with a self-induced glucose deficiency.
  • Low omega-6 meats. Omega-6 fats can be very damaging to mitochondria and can promote metastasis. Our needs for them are minimal, and they are everywhere. It’s important to choose foods that minimize omega-6 levels. Among meats, prefer seafood, shellfish, and red meats; obtain eggs, milk, and organ meats from pastured and naturally raised animals. Eat tropical plant oils like coconut and palm.
  • Omega-3 and omega-6 balance. The diet should include some marine sources of omega-3 fats, like salmon or sardines.
  • Bone broth soups and gelatin (cooked collagen). Collagen is 30% of our body’s protein and forms much of the extracellular matrix scaffolding which is crucial to maintainance of tissue health. The extracellular matrix is broken down in cancer. An anti-cancer diet should be rich in cooked joint tissue, such as can be found in Ox Feet Broth soups. Vitamin C and sulfur, discussed below, are also required for collagen formation; be sure you’re not deficient in these.
  • Fermented vegetables, yogurt, and acids. A diverse portfolio of gut bacteria can be helpful to the fight against cancer by several mechanisms. Probiotic flora from fermented  foods help shield against the entry of cancer-promoting pathogens to the body through the gut; they generate by-products, like short-chain fats and vitamin K2, which have anti-cancer effects; and they can modulate immunity in a favorable direction. Acids such as vinegar and lemon juice can also favorably modify gut bacteria.
  • Vegetables, herbs, and spices.Fiber is probably beneficial against cancer. Butyrate, which is produced by gut bacteria from the digestion of many types of fiber including “resistant starch” from safe starches, has anti-cancer properties. Moreover, many vegetables and traditional herbs and spices have been shown to have anti-angiogenic effects. Foods with anti-angiogenic properties include:
    • Garlic.
    • Tomato.
    • Green tea.
    • Dark chocolate / cocoa.
    • Maitake mushroom.
    • Bok choy.
    • Kale.
    • Many berries.
    • Cherries.
    • Ginseng.
    • Turmeric.
    • Oregano.
    • Parsley.
    • Polyphenol-rich extra virgin olive oils.
  • Organ meats and egg yolks. It’s important to be well nourished, and organ meats like liver and egg yolks tend to be rich in micronutrients. They are much better than plant foods for compounds like phospholipids. In particular, choline (and its phospholipid form phosphatidylcholine) is important for methylation status and epigenetic functioning – an important element in cancer prevention.
  • Sea vegetables, sea salt, and seafoods. These are good sources of trace minerals such as iodine, which is a critical anti-cancer nutrient.

In general cancer patients should focus on the foods in the apple of the PHD Food Plate more than the “pleasure foods.” However, there’s nothing wrong with some berries, dark chocolate, pistachios, and whipped cream for dessert, and some red wine with dinner. Above all, it’s important to enjoy your food. Try to obtain from every meal a sense of pleasure and well being!

Supplements

Much more could be said on this topic than I’m going to say today. One could make a very long list of supplements that might help against cancer (also a long list of those that hurt). However, the crucial five from my point of view are in our recommended supplement list:

  • Vitamin D
  • Vitamin K2
  • Iodine
  • Selenium
  • Magnesium

The tricky one here is the iodine. Iodine dosage should be built up very slowly from a low level, so as not to disrupt thyroid function. (Hyperthyroidism can strongly promote cancer, and hypothyroidism can inhibit immune function and healing, so any thyroid dysfunction is a serious risk.) Start at 500 mcg or less, and increase the dose no faster than a doubling per month. If you get either hypothyroid or hyperthyroid symptoms from an increase in dose, back off a bit (eg instead of going directly from 500 mcg to 1 mg per day, go to 500 mcg and 1 mg on alternate days). Be patient, but try to build up to 12 mg/day over a 6 month period. Then stay there. Be sure to get 200 mcg/day selenium along with the iodine.

I also recommend a multivitamin, for general nourishment; and make sure there is no deficiency of vitamin C, zinc, copper, or chromium. Also, when it comes to antioxidants, more is not better. Avoid most antioxidant supplements other than glutathione, vitamin C, selenium, zinc, copper, and manganese.

For magnesium, I recommend taking a 200 mg oral supplement of magnesium citrate or a magnesium chelate. Epsom salt baths might not provide magnesium, but they can be a useful source of sulfur (in the form of sulfate) which assists collagen formation.

Vitamin C is an unusual case. It supports collagen formation, and for this purpose and to avoid a deficiency I strongly suggest taking 1 g per day. In higher doses, vitamin C may be helpful because it has anti-viral properties (see Fighting Viral Infections by Vitamin C at Bowel Tolerance, Sep 26, 2010), and most cancers are probably viral in origin. Linus Pauling, of course, advocated high doses of vitamin C – either taken orally to bowel tolerance, or intravenously. However, there are arguments on the other side. Vitamin C can protect cancer cells from immune attack, and also makes them resistant to chemotherapies. Clinical trials have not yet proven high-dose vitamin C therapy, but it may help against a subset of cancers caused by viruses sensitive to vitamin C therapy.

If sufficient amounts are not obtained from diet, then choline should be supplemented.

Intermittent Fasting, Intermittent Ketosis, Intermittent Protein Restriction

This is an extremely important cluster of strategies that are probably highly effective against cancer.

Their common trait is that all three promote autophagy, or “self-eating,” which is both a means for cells to cope with resource scarcity and a central part of the intracellular immune response.

When resources are abundant, cells allow aged organelles and junk proteins to accumulate. When resources are scarce, they turn on autophagy and digest unnecessary components, recycling the resources.

Autophagy is the dominant innate immune mechanism inside cells – the primary way cells kill bacteria and viruses.

Autophagy also recycles damaged mitochondria, which can be digested, enabling remaining healthy mitochondria to multiply. The result is a healthier mitochondrial population.

Since viruses and damaged mitochondria promote cancer, autophagy helps transform cells from the cancer phenotype back to the normal human phenotype.

Fasting, by inducing resource scarcity, promotes autophagy. Scarcity of amino acids, which can be achieved by a protein restricted diet, also promotes autophagy. And ketosis, which is part of the metabolic profile of starvation, also promotes autophagy.

Note in my section heading the shared word: “intermittent.” We don’t want to sustain fasts or protein scarcity too long; that could create malnourishment and cause more harm than good. Permanent ketosis may promote fungal infections. The most helpful course is probably to follow these strategies intermittently:

  • Engage in daily intermittent fasting: eat only within a 6 to 8 hour window each day. Within the fasting period, eat some coconut oil or MCT oil to promote ketosis.
  • Eat high protein for a few weeks while engaging in resistance exercise to build muscle; then low protein for a few weeks.

A Note on Ketogenic Diets

Since we wrote our book, we’ve become a bit less excited about the therapeutic potential of ketogenic diets.

Ketogenic diets have demonstrated effectiveness in brain cancers, and several considerations suggest that they would be helpful against all cancers:

  • Cancer cells are dependent on glucose metabolism, a phenomenon called the Warburg effect. In ketosis, blood glucose levels can be decreased – a fall from 90 to 65 mg/dl is achievable – and reduced glucose availability should retard cancer growth.
  • Mitochondria do well on ketones, and some studies had shown that provision of ketones can restore the ability of mitochondria to trigger apoptosis, or the programmed cell death of cancer cells.

It’s too early to judge, but a few scraps of data published recently have made ketogenic diets seem a bit less exciting then hoped.

First, the group of Michael Lisanti has published work suggesting that tumors can evade the metabolic restrictions of a ketogenic diet by manipulating neighboring normal cells. The idea (here is an overview) is that cancer cells release hydrogen peroxide, which causes a stress response in neighboring cells, stimulating them to release lactic acid, which the cancer cells can metabolize. This process can happen nearly as well on a ketogenic as on a normal diet, so the effectiveness of a ketogenic diet in starving the cancer cells is reduced.

The Lisanti group results are hardly conclusive – indeed so far as I know no other group has supported their claims – and there are plenty of skeptics. Jimmy Moore gathered responses from a panel of low-carb experts.

Second, clinical experience with ketogenic diets has not yet shown them to be highly effective. The sort of data we have is well represented by a recent report in Nutrition and Metabolism. Sixteen patients with advanced metastatic cancer were put on ketogenic diets. The results:

One patient did not tolerate the diet and dropped out within 3 days. Among those who tolerated the diet, two patients died early, one stopped after 2 weeks due to personal reasons, one felt unable to stick to the diet after 4 weeks, one stopped after 6 and two stopped after 7 and 8 weeks due to progress of the disease, one had to discontinue after 6 weeks to resume chemotherapy and five completed the 3 month intervention period.

The conclusion: a ketogenic diet “has no severe side effects and might improve aspects of quality of life and blood parameters in some patients.”

Clinical trials with control groups and more statistical power are needed to evaluate whether ketogenic diets have therapeutic effect. For now, I think the most prudent course is intermittent ketosis and intermittent ketogenic fasting, rather than a continuously ketogenic diet.

UPDATE: Mario makes a great point in the comments: fasting prior to chemotherapy reduces toxicity to normal cells but increases toxicity to cancer cells. It is quite likely that a ketogenic diet might have the same effect during chemotherapy. So the combination of intermittent ketogenic dieting with chemotherapy should be given consideration.

Circadian Rhythm Enhancement

Many diseases become more likely, or more severe, if circadian rhythms are disrupted. Enhancement of circadian rhythms may be therapeutic for these diseases.

I’ve blogged about circadian rhythm therapies for hypothyroidism (“Intermittent Fasting as a Therapy for Hypothyroidism,” Dec 1, 2010) and for sleep disorders, psychiatric disorders, neurodegenerative disorders, and obesity (“Seth Roberts and Circadian Therapy,” Mar 22, 2011).

Well, cancer is another disease for which circadian disruption may be damaging. The International Agency on Research on Cancer (IARC) has recently classified “shiftwork that involves circadian disruption” as “probably carcinogenic to humans.”

It’s plausible that circadian enhancement may be therapeutic for cancer. Tactics that enhance circadian rhythms include:

  • Exposure to mid-day sunlight.
  • Sleeping in total darkness during hours of darkness.
  • Confining eating to daylight hours.
  • Socializing – especially, looking at faces and talking – during daylight hours. Seth Roberts found that looking at images of human faces can substitute for actual socializing.
  • Exercising during daylight hours. Even low-level activity – like standing instead of sitting – helps.
  • In people who are melatonin deficient due to a brain immune response, supplementation of melatonin just before bedtime.

Curiously, circadian rhythm disruption seems to make chemotherapy more effective. Also, timing treatments to match circadian rhythms may double their effectiveness.

Exercise and Other Lifestyle Factors

A number of lifestyle factors are important for cancer recovery. David Servan-Schreiber’s Anti-Cancer has an excellent overview of the evidence.

A recent study in the Lancet found that every additional 15 min of daily exercise beyond 15 min a day reduced all-cancer mortality by 1%. Exercise appears to be therapeutic even for late stage cancers. A meta-review found that two and a half hours of exercise a week could lower a breast cancer patient’s risk of dying or cancer recurrence by 40 percent, and could reduce a prostate cancer patient’s risk of dying from the disease by about 30 percent.

However, exercise should not be exhausting. Rather, it should be restful and relaxing; or build muscle. Resistance exercise on the “Body by Science” model of one intense workout per week, with more time spent in restful recovery than in stress, is probably a good strategy. Long walks outdoors in nature, and relaxing exercises like yoga or tai chi, are also great approaches to cancer therapy.

Being sociable, happy, calm, and optimistic are all important factors for cancer recovery. Those who have companions they love, and a purpose for living that makes them happy, have the best prognosis. Be grateful for what you have, and make your body understand that life is worth living.

Dealing with Anorexia and Nausea

Anorexia and nausea can seriously impair the ability of cancer patients to eat a nourishing diet and maintain their strength.

I haven’t had time to research this aspect of the disease yet, but there do seem to be some dietary and lifestyle interventions that help.

For instance, exercise can correct anorexia.

Among dietary interventions, ginger has been reported to reduce chemotherapy-induced nausea, reducing incidence in one study from 93% to 55%. (Hat tip: Healthy Fellow.)

Ginger teas are a traditional Asian folk remedy. Slice some ginger root in water, boil it on the stove, add some rice syrup for sweetness, and drink up!

Under-Utilized Therapies

There are a few therapies which are rarely prescribed, but might be more helpful than chemotherapies in treating cancer:

  • Low-dose naltrexone.
  • Anti-viral drugs.
  • Anti-fungal therapies.

Low-dose naltrexone is taken at night before bed. It temporarily blocks opioid receptors, which leads the body to increase production of endorphins and enkephalins – immune compounds which interact with opioid receptors. The following day, the naltrexone is gone and the opioid receptors are working again, but the endorphins are still around. Taking LDN thus increases endorphin levels. Endorphins inhibit cancer proliferation, and may enhance anti-cancer immunity. Here is a recent paper on anti-proliferative effects of LDN against ovarian cancer: http://pmid.us/21685240. Here is a recent paper on LDN plus alpha lipoic acid as a therapy against pancreatic cancer: http://pmid.us/20042414. For a general overview, see http://lowdosenaltrexone.org/.

Viruses cause or contribute to most cancers, and thus anti-viral drugs have great potential. A few cancer-causing viruses are famous, such as the Human Papilloma Virus for which there is a vaccine; however, most of the viruses that cause cancer remain unknown, though we know they exist because genetic mutations that impair viral immunity greatly increase cancer incidence.

Mario Renato Iwakura recently sent me a link to a paper that nicely illustrates the potential of antiviral therapies against cancer. Cytomegalovirus, also known as human herpes virus 5, is a common virus that infects 40% of adults worldwide and 50% to 80% of Americans. However, it is found in almost 100% of human tumors. It seems to be difficult to get cancer if you haven’t been infected by cytomegalovirus.

From the paper abstract:

Medulloblastomas are the most common malignant brain tumors in children…. Human cytomegalovirus (HCMV) is prevalent in the human population and encodes proteins that provide immune evasion strategies and promote oncogenic transformation and oncomodulation…. Remarkably, all of the human medulloblastoma cell lines that we analyzed contained HCMV DNA and RNA and expressed HCMV proteins at various levels in vitro. When engrafted into immunocompromised mice, human medulloblastoma cells induced expression of HCMV proteins. HCMV and COX-2 expression correlated in primary tumors, cell lines, and medulloblastoma xenografts. The antiviral drug valganciclovir and the specific COX-2 inhibitor celecoxib prevented HCMV replication in vitro and inhibited PGE2 production and reduced medulloblastoma tumor cell growth both in vitro and in vivo.

Tumor growth declined by 72% when treated with Valcyte (valganciclovir) and an NSAID drug. A press release notes that these drugs have “relatively good adverse effect profiles” and that “antiviral drugs are selective and largely affect infected cells.”

Yet another antimicrobial approach that may be helpful against cancer is antifungal therapy. Most cancer patients develop systemic fungal infections, and fungal infections such as Candida promote metastasis and tumor growth, and may also suppress anti-cancer immunity. An effective antifungal therapy may significantly retard cancer progression.

Conclusion

Much more remains to be said, and it’s certain that we’ll refine these suggestions after more thoroughly studying the literature. But I think this basic approach to an anti-cancer diet can’t be too far wrong.

Our prayers and best wishes go out to all those who are battling cancer.

A Paleo Pregnancy Pitfall?

Posted by on September 22, 2011 29 comments

On Saturday’s Around the Web I linked to a study [1] that tied low-carb dieting early in pregnancy to obesity in the child at age 9. This made Ana concerned:

I’m somewhat worried about the pregnancy diet study. Actually I am trying to conceive, 3 months ago my husbund and I changed my diet to Paleo.

Now I see this study and even though I feel great, better than before, I’m not sure, how much credibility would you give it?

I presume that perhaps there could be too little fat, and with that too low calorie intake for a pregnant woman, perhaps that could be the case, opinions please!!!

We certainly don’t want Ana to be stressed out, and it’s hard to turn down three exclamation marks, so I thought I’d interrupt the cancer discussion to address her concerns.

The Study

The study [1] claimed two things:

  1. Women who ate less than a thousand carb calories per day during the early part of pregnancy were more likely to give birth to babies with an overly silenced gene for the Vitamin A receptor RXR-alpha.
  2. Babies born with an overly silenced gene for RXR-alpha were more likely to be overweight at age 9.

Let’s look at the second point, which is more solid, first.

RXR-alpha silencing is associated with obesity

Here is the data:

It looks like it’s normal to have about 50% RXR-alpha methylation in this promoter region and if you have 80% methylation, you’re likely to become a pudgy 9-year old.

How solid is the correlation? They replicated it in a second cohort. Their first study produced two epigenetic marks that were strongly associated with childhood obesity, RXR-alpha and eNOS. A replication study confirmed the RXR-alpha but not the eNOS association.

How plausible is it that RXR-alpha silencing would contribute to obesity? Very plausible, because RXR-alpha is the hub of a network of genes regulating most aspects of metabolism and cell activity.

Vitamin A binds to two types of nuclear receptor, RAR and RXR. When it binds to RXR, a vitamin A – RXR complex is imported into the nucleus. This then looks around for a partner. Partners of RXR-alpha include:

  • Vitamin A – RAR complexes.
  • Vitamin D – VDR (vitamin D receptor) complexes.
  • T3 thyroid hormone – TR (thyroid hormone receptor) complexes.
  • LXR (liver X receptor).
  • CLOCK, the circadian rhythm regulation gene.
  • PPAR-gamma (peroxisome proliferator-activated receptor), a regulator of lipids whose deficiency leads to high cholesterol and hyperglycemia.
  • MyoD, a factor that triggers muscle creation.
  • Many others; a list can be found at Wikipedia.

The vitamin A – RXR-alpha complex “dimerizes” with these other nuclear receptors, forming a new complex that acts as a transcription factor to turn on gene expression. Most of those other partners cannot act to turn on DNA transcription unless they dimerize with RXR.

This means that the absence of RXR-alpha would be functionally equivalent to being low in vitamin A, vitamin D, T3 thyroid hormone, CLOCK, and all those other partners. It is like being born a sun-starved hypothyroid with messed up circadian rhythms who can’t form muscle and is hyperglycemic and dyslipidemic.

All of those things are associated with obesity.

RXR-alpha silencing might be a universal component of the metabolic damage in obesity:

[A]n association between increased RXRA methylation and adiposity is consistent with the observation of strongly diminished RXRA expression in visceral white adipose tissue from obese mice (35).

Personally, I think it’s very likely that silencing of RXR-alpha promotes obesity. This is the most solid part of the paper. They have data, and the mechanism makes sense.

Conclusion: some babies are getting off to a bum start in life due to epigenetic silencing of an important gene.

Does maternal diet affect RXR-alpha silencing?

This is the really weak part of the paper. Here was their data:

When I say this was their data, this was all of it. No scatter plots, no information about how other characteristics of the diet correlate with RXRA methylation, no information about health or lifestyle characteristics of the various carbohydrate intake cohorts so that we can evaluate the possibility of confounding factors.

It is unlikely that low carbohydrate intake was causing the problem. Aside from the fact that dietary carbohydrate intake is only weakly correlated to any factors seen by the baby in the womb (eg blood glucose, insulin, etc), 261 g/day is a substantial amount of carbohydrate – well above physiological needs. So the low-carb quartile included women in glucose deficiency, glucose moderation, and glucose excess; the other quartiles only women in glucose excess. If a glucose deficiency caused RXRA hypermethylation and glucose excess caused RXRA, there would have been a much larger scatter in RXRA methylation levels among the low-carb quartile compared to the 3 higher-carb quartiles. But we can see from the graph that the standard deviations are the same in every quartile.

So there is likely to be some other factor besides carbohydrate intake that was responsible for the RXRA hypermethylation. What are the possibilities?

One possibility alluded to in the paper is that the women had low carbohydrate intake because they were starving. The paper notes that “famine during pregnancy is associated with obesity in the adult offspring (5).” However, I am unaware of recent famines in Southampton UK.

Another possibility is an excess of some other macronutrient. Those mothers who ate fewer carbs were eating more fat and possibly more protein. Given the ubiquity of vegetable oils in modern fats, the increased fat was probably largely omega-6. This raises two possibilities:

  • High maternal omega-6 intake causes RXRA methylation.
  • High maternal protein intake causes RXRA methylation.

Both possibilities have support from studies in rodents: maternal high protein intake and maternal omega-6 fat intake are both associated with obesity in offspring. For more on the risks of high protein, see The Danger of Protein During Pregnancy, Jul 12, 2010.

Another possibility is that the low-carb high-fat diet produced a vitamin A excess. As we discuss in the book, this is a common problem, especially among people taking a multivitamin; probably due to widespread vitamin D and vitamin K2 deficiencies, large numbers of people exhibit evidence of impaired health with vitamin A intake above 10,000 IU/day. As a fat-soluble vitamin, vitamin A intake is more or less proportional to fat intake.

If a balance between vitamin D and vitamin A is needed because the vitamin D-VDR complexes and vitamin A-RXR complexes have to be in proper proportion, then the body may respond to an excess of vitamin A and a deficit of vitamin D by upregulating VDR expression and downregulating RXR expression. Such downregulation may be achieved by RXR-alpha methylation.

Another possibility is some confounding factor that happens to be correlated with carbohydrate intake. In the US Nurses Health Study, nurses with the lowest carbohydrate intake were “rebels” who rejected not only the health advice to eat vegetable-rich and whole-grain rich diets, but also every other standard bit of health advice. The low-carb nurses smoked more, exercised less, and drank more alcohol and more coffee.

So it could be maternal smoking, lack of exercise, or drinking too much alcohol or caffeine that causes RXRA hypermethylation and childhood obesity.

Another possibility, raised in the comments by Amber, is that mothers of the obese children were obese themselves, ate low-carb diets for weight control reasons, and passed on their obesity to their children. It is indeed the case that obese mothers tend to have children who are obesity-prone, and it is suspected that epigenetics may be responsible for this “inherited” obesity. If low-carb diets have indeed become popular among the obese mothers of Southampton UK, then this is a possibility that must be considered.

Low-Carb Paleo Pitfalls?

Should Ana modify her diet because of this study?

I think it’s important to avoid a glucose deficiency. But I don’t think it’s necessary to eat 1,000 calories per day of carbs to achieve that.

I think it’s important to eat a moderate amount of protein, neither too much nor too little; and to limit the amount of omega-6 fats eaten.

I think it’s a good idea to avoid alcohol or excessive consumption of bioactive beverages like coffee during pregnancy. Also to avoid smoking, and to get some exercise and sun exposure.

If you’re doing all these things, I don’t think you need to be concerned. Ana says, “I feel great, better than before”; that’s good evidence that she’s well prepared for a healthy pregnancy.

Conclusion

The paper presents solid evidence that hypermethylation of RXR-alpha in the womb predisposes children to become obese at age 9.

The paper gives us essentially no evidence at all as to what causes hypermethylation of RXR-alpha in the womb, except that it correlates with low carbohydrate consumption in the women of Southampton UK.

I hate it when journals do this. If you’re going to link carb intake to RXRA methylation, give some real data and analysis. Probably the authors are saving their dietary analysis for a future paper. The carb graph was included as a “teaser” to make the work seem more interesting.

There are many known health dangers which are known risk factors for obesity and which correlate with low carbohydrate consumption in the general population. So until more evidence emerges, I think there’s little here for low-carb Paleo dieters to be concerned about.

References

[1] Godfrey KM et al. Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes. 2011 May;60(5):1528-34. http://pmid.us/21471513.