Yearly Archives: 2011 - Page 24

An Osteoarthritis Recovery Story

Posted by on May 17, 2011 84 comments

Jacqueline wrote us in late March asking for tips for osteoarthritis.

She had experienced continuous pain and stiffness in her thumbs for the last year, and occasional pain when gardening for more than 10 years. Her younger sister also has joint pain and can’t turn her neck. Her father, now 73, has had pain in his thumbs for decades which eventually spread to his fingers, and a shoulder spur which had required surgery. Jacqueline’s dad says that osteoarthritis “runs in the family.”

Of course, even if there is some sort of genetic basis for osteoarthritis, it will be modifiable through diet and nutrition.

Jacqueline had been eating low-carb since 2003: meat and vegetables for dinner, fruit and yogurt or eggs, bacon, and sausage for breakfast, but an occasional sandwich for lunch. Around 2007, Fitday gave her macronutrient ratios as near 65% fat, 17% carb, 17% protein. In 2009 she gave up wheat entirely. At that point she developed dry eyes.

Upon reading our “low-carb dangers” series which discussed dry eyes (see Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers, Nov 15, 2010), she decided to add some carbs back to her diet. Potatoes and bananas cured her dry eyes.

But the joint pain remained, and she asked for any further suggestions. My reply was:

Shou-Ching had a condition like that and it got better with regular vitamin K2 supplementation. Presumably it was caused by improper calcification. Magnesium, vitamin D, and vitamin C are the next most likely to be important.

I think malnutrition is probably the major cause of osteoarthritis. (We know it can cause it in moose!)

For rheumatoid arthritis the cause is usually infectious. Low-dose antibiotics, as suggested by the Road Back Foundation, often work.

The dry eye indicates a glucose and/or vitamin C deficiency. Either will contribute to joint problems too, since the joint lubricants are all made from essentially the same materials as tear lubricants / mucus. So it’s good you’ve re-introduced starch, but I would add more than just some potatoes and tubers. After you’ve gotten used to very low-carb it can be hard to re-orient yourself to the quantities you may need. If glucosamine helps, that suggests you don’t have enough glucose to make your own glucosamine. I would eat more starches and take more C also.

I think you’re probably close and a little more diet experimentation should be able to fix the problem. Rice and vitamin K2 are probably your best friends.

Jacqueline implemented that advice. She wrote back in early May:

What I did:

I kept on taking the 1.5g glucosamine daily and tried, really tried to up my carbs (as starch) intake – you’re right, once you get used to not eating them, it can be quite hard to do. I seem to have succeeded somewhat as I have gone back to using Fitday a bit and have managed (on the days I was checking) about 100g carbs a day. If I didn’t manage with the carbs, I consciously tried to eat a bit more protein on the day instead.

I have increased the frequency with which I take magnesium and vitamin K2 … and started taking a vitamin C (1g) every day. I’m easing off on vitamin D though as summer and some sunshine is finally here. I’ve also pretty much stopped the fish oil – this is of course related to your recent posts – because I do eat oily fish weekly and other fish and seafood regularly….

I have also cut out my addiction to cashew nuts since I was in Paris for a few days before Easter….

Results:

The aching and stiffness has been receding steadily. The right thumb was already improving with my trying to increase carbs (because of the dry eyes) and taking the glucosamine. The right thumb now feels pretty much back to normal. The left thumb has also stopped aching especially over the last 2-3 weeks although it is still a bit prone to ‘catching’ with sudden pain – and a sort of pulling in the ligaments  – as if it can’t react quickly enough to a sudden move e.g. when driving. I am now – over the last few days – playing the piano a lot more (got a bit out of practice with the Paris trip etc.)  – and my thumbs are recovering well – not sore the next day like they were before.

Conclusion

There are basically three kinds of arthritis:

  • osteoarthritis, which I associate with nutrient deficiencies, is a loss of cartilage and lubricating fluid in the joints, or an improper calcification or ossification of the soft tissue;
  • reactive arthritis, which is due to infections; and
  • rheumatoid arthritis, which is an autoimmune disorder but the autoimmunity is usually caused by an infection and clearing the infection will usually clear the autoimmunity.

Food toxins can also collect in the joints and cause immune reactions that produce arthritis-like joint symptoms. Foods that frequently cause allergies, such as tree nuts, may be worth eliminating as a test, as Jacqueline eliminated cashew nuts.

Since diagnosing the cause of arthritis symptoms is an art more than a science, and nutrient deficiencies are easily remedied, they’re almost always a good place to start with any joint pain and stiffness.

I’m glad they’re working for Jacqueline! It’s nice when the easy fixes work.

Kimchi

Posted by on May 15, 2011 64 comments

UPDATE: For our recipe for kimchi, see “Homemade Kimchi” (June 26, 2011).

While the Chinese stir-fry vegetables, Koreans pickle them. Wikipedia explains the history of kimchi:

Early kimchi was made of cabbage and beef stock only. Red chili, a New World vegetable not found in Korea before European contact with the Americas, was added to kimchi recipes some time after 1500. Red chili pepper flakes are now used as the main ingredient for spice and source of heat for many varieties of kimchi. In the twelfth century other spices, creating flavors such as sweet and sour, and colors, such as white and orange, were added.

There are many varieties of kimchi. The Kimchi Field Museum in Seoul has documented 187 varieties of kimchi, and there are an almost infinite number of variations upon the basic varieties.

Kimchi’s Health Benefits

Kimchi is a natural probiotic. At early stages in its pickling, lactic acid bacterial species such as Leuconostoc mesenteroides and Lactobacillus plantarum dominate. [1] As kimchi ages, more species appear and the bacterial environment diversifies.

There is evidence that eating kimchi helps against autoimmune disorders and allergies. [2, 3] It’s also plausible that kimchi would help against bowel conditions, since those often feature a limited repertoire of gut flora. (See Bowel Disease, Part IV: Restoring Healthful Gut Flora, July 27, 2010.)

Kimchi Side Dishes

Kimchi is usually served as a side dish when fresh. Here are a few photos from our local Asian supermarket.

When most people think of kimchi they think of cabbage. Here is a whole row of cabbage kimchi:

Cabbage kimchi is made by soaking the cabbage in salt, squeezing the water out, and layering the salted cabbage with a marinade. Marinades may contain shredded radish, chili powder (which gives the red color), garlic, garlic sprouts, and green onion.

Often the marinade will include oyster or anchovy as a flavor enhancer: you can see a sign for oyster cabbage kimchi in the above picture. These are better quality kimchi; poor quality kimchi may use MSG.

However, there are many other types of pickled kimchi besides cabbage. Here is another picture from our local supermarket:

Along the bottom and upper left are pickled vegetables, on the upper right are fermented seafood. In this picture are probably about 80 different varieties of kimchi.

Here are some examples of what we eat:

On the left is Napa cabbage kimchi, which is for Koreans what salad is to Americans. It includes Korean radish, pepper powder, onion, green onion, apple, pear, sugar, salt, ginger, garlic, salted shrimp, salted anchovy, and oyster sauce. On the right is a spicy radish kimchi.

This is another extremely popular flavor, cucumber kimchi. It’s seasoned with chives, Korean radish, hot red pepper powder, onion, carrot, sugar, salt, ginger, garlic, salted anchovy, and sweet rice flour.

Pickled white radish. One of Paul’s favorites, with a very mild taste; seasoned with cayenne, fish sauce, and salt.

Clockwise from upper left: pickled seaweed (seasoned with vinegar, wine, sugar, cayenne, scallion, oil, green pepper, garlic, and ginger); pickled garlic cloves (seasoned with vinegar, salt, sesame, panicum, black bean, and miso); seasoned sesame leaves (with cayenne and garlic); pickled yellow radish; and garlic stem kimchi (flavored with garlic, sesame, and pepper paste).

This last picture illustrates how we often eat vegetables with dinner. We’ll cook an entrée and starch, but serve the vegetables family-style in their original plastic containers; everyone can serve themselves. It makes for a nice buffet of vegetables with very little labor.

Kimchi Soups and Stews

As kimchi gets older, it becomes sour as acidic fermentation products build up, and the mix of bacterial species tends to change to a less probiotic mix.

Older kimchi will therefore be put in soups and stews and boiled to remove bacteria and dilute the sour taste.

Some examples can be seen in this trailer for an upcoming US public television series, “Kimchi Chronicles”. First, a promo introducing the series:

This longer trailer shows an example of using older kimchi as an ingredient in a stew:

How to Make Kimchi

Here’s a video showing how to make kimchi at home:

Conclusion

It’s a good idea to find some flavors of kimchi, or other fermented vegetables like pickles or sauerkraut, that you like. It’s an inexpensive and nourishing way to obtain probiotic bacteria; and a convenient and easy way to eat vegetables!

References

[1] Cho J et al. Microbial population dynamics of kimchi, a fermented cabbage product. FEMS Microbiol Lett. 2006 Apr;257(2):262-7. http://pmid.us/16553862.

[2] Won TJ et al. Modulation of Th1/Th2 Balance by Lactobacillus Strains Isolated from Kimchi via Stimulation of Macrophage Cell Line J774A.1 In Vitro. J Food Sci. 2011 Mar;76(2):H55-H61. http://pmid.us/21535768.

[3] Won TJ et al. Oral administration of Lactobacillus strains from Kimchi inhibits atopic dermatitis in NC?/?Nga mice. J Appl Microbiol. 2011 May;110(5):1195-202. http://pmid.us/21338447.

Around the Web; Morgellons Edition

Posted by on May 14, 2011 32 comments

Here’s what caught my eye this week:

[1] Interesting posts this week: Stephan Guyenet’s discussion with Chris Kresser is sure to be fascinating, because the material left on the cutting room floor is great. I especially liked Stephan’s observations about insulin’s contributions to weight loss, via promoting satiety and leptin sensitivity.

Chris Masterjohn refutes an old canard: The cannibals of New Guinea preferred fishermen, not missionaries. Of course – fishermen are more nutritious, they have more iodine.

Apropos this week’s post (Can Endurance Exercise Promote Cancer?, May 11, 2011), Keith Norris of Theory to Practice discusses the relation between fitness and health:


Personally, I’ve never gotten to the right of the part of the curve labeled “Health” and “Performance,” and spent too much time in the area off the chart called “Unhealth” and “Non-performance.”

Via Obesity Panacea’s Travis Saunders, exercise induces weight loss in controlled laboratory conditions but not in real life. Scientists discover that Vancouver bedbugs are carrying antibiotic-resistant staph (MRSA). Chronic acetaminophen (Tylenol) use doubles the risk of blood cancers. Aspirin is better.

Via Dr Cobb at Z-Health, a study showing that walking barefoot decreases stress on the knees and hips of people with osteoarthritis. Charles Poliquin defends his high-dose fish oil recommendation with a study showing that 7 people were able to take 60 g/day fish oil for 12 weeks without “serious adverse events.”

Finally, Richard Nikoley has some mouth-watering food photos.

[2] Post-Mother’s Day music:

[3] Morgellons, a medical mystery: Via The Guardian, a mysterious complaint:

Morgellons was named in 2001 by an American called Mary Leitao, whose son complained of sores around his mouth and the sensation of “bugs”. Examining him with a toy microscope, Leitao found him to be covered in unexplained red, blue, black and white fibres. Since then, workers at her Morgellons Research Foundation say they have been contacted by more than 12,000 affected families….

Optical image of what sufferers are adamant are morgellons fibres in skin samples – are they made up of alien ­matter, or are ­everyday materials the more likely explanation? Photograph: Vitaly Citovsky/Suny at Stony Brook

Back in London, I find a 2008 paper on morgellons in the journal Dermatologic Therapy that describes patients picking “at their skin continuously in order to ‘extract’ an organism”; “obsessive cleaning rituals, showering often” and individuals going “to many physicians, such as infectious disease specialists and dermatologists” – all behaviours “consistent with DOP”. (For treatment, the authors recommend prescribing a benign antiparasitic ointment to build trust, and supplementing it with an antipsychotic.)

These dermatologists don’t know much, but they know an antipsychotic drug is the treatment.

Fortunately there is an excellent doctor looking into the matter:

I contact Dr Anne Louise Oaklander, associate professor at Harvard Medical School and perhaps the only neurologist in the world to specialise in itch. I email her describing morgellons, pointing out it’s probably some form of DOP. But when we speak, she knows all about morgellons already. “In my experience, morgellons patients are doing the best they can to make sense of symptoms that are real. They’re suffering from a chronic itch disorder that’s undiagnosed. They have been maltreated by the medical establishment. And you are welcome to quote me on that,” she adds….

“That they have insects on them is a very reasonable conclusion because, to them, it feels no different from how it would if there were insects on them. To your brain, it’s exactly the same. So you need to look at what’s going on with their nerves. Unfortunately, what can happen is a dermatologist fails to find an explanation and jumps to a psychiatric one.”

[4] Let’s ride:

Via Yves Smith

This picture reminds me of a story. I once was on a long airplane flight seated next to two girls who demanded piggy-back rides around the cabin. They asked me to guess their ages. After I had guessed every age from 3 to 13, I gave up. Can you guess how old they were?

Select for the answer: They were 5½ and 7½!

[5] Does it cure being a lawyer?: A “therapy dog” is available for checkout at the Yale Law School library. But he can’t be removed from the library, because he’s a rufference work. (Via Tom Smith.)

[6] They’re born and they’re off to college, just like that: Via John Durant, a robin raises her chicks:

Robins: 4 Eggs, 4 Weeks from Fred Margulies on Vimeo.

[7] The raccoon who will live forever in our memories: Stabby has been immortalized:

It’s only the beginning, I believe. That raccoon has great things ahead of him!

[8] Those were the days: The medicines weren’t that great, but the advertising posters were cool. Via The Scientist, a slideshow of mostly 19th century medicinal posters:

[9] The old mannequin head drop prank: This one always works.

via Amy Alkon.

[10] Shou-Ching’s photo-art:

© 2011 Shou-Ching Jaminet.

[11] Video of the week: Polar photographer Paul Nicklens shares some remarkable photographs. Don’t miss the part where the friendly leopard seal tries to feed him penguins:

Can Endurance Exercise Promote Cancer?

Posted by on May 11, 2011 50 comments

I got into a bit of trouble in the comments a few weeks back when I joked that Grete Waitz may have died from marathoning. Steve replied:

Paul, you said “… marathoning (from which Grete Waitz just died at 57)”

Gee. The news said cancer. How confident are you that she died “from” running marathons?

Of course, not confident at all. Maybe if she’d been a sprinter she would have died at 54. Maybe if Lance Armstrong had been a couch potato he would still have had testicular cancer metastasized to his brain and lung at age 25.

A few days ago I got an email. Two highly fit endurance athletes, both of whom have always tended to their health and been careful to eat “healthy” (i.e. vegetable and whole grain rich, meat and fat poor) diets, have contracted cancers in the prime of life and been given less than a year to live. My correspondent asked, “Why?”

Let’s look into this. Is it possible that endurance exercise, especially if combined with a high-carb diet, may promote cancer?

Oxidative Damage to DNA and Cancer

Human DNA is constantly being damaged and repaired. It’s been estimated that over the course of a cell cycle – that is, from the time a cell is formed to the time it divides into two daughter cells – a human cell develops 5,000 single-stranded DNA breaks due to oxidative damage from reactive oxygen species (ROS). The vast majority are repaired by the body’s DNA repair machinery. [1]

However, in typical human cells 0.1% or 5 are not successfully repaired; instead a corresponding break is created in the complementary DNA strand, resulting in a double-strand break. In people with Bloom syndrome, an inherited condition which creates a strong predisposition to cancer, fully 1% or 50 are not successfully repaired. [1]

The double-strand break leads to a re-arrangement or “translocation” of parts of the chromosome. Usually, this does not break the coding region for a protein, but it does break non-coding regions resulting in changes to gene expression.

These sorts of genetic changes are observed both in cancer and in aging. [1] In short, oxidative damage to DNA is considered a risk factor for cancer development.

Oxidative Damage to DNA Has Been Specifically Linked to Endurance Exercise

Diets and activities that increase oxidative stress – for instance, diets deficient in antioxidant minerals – can therefore increase cancer risk. And diets and activities that minimize oxidative stress can minimize cancer risk and facilitate recovery.

Endurance exercise generates oxidative stress. Marathon running “caused a large increase in the tissue content of oxidized glutathione (189%) at the expense of reduced glutathione (-18%).” [2]

Moreover, endurance exercise damages DNA:

Both a systemic inflammatory response as well as DNA damage has been observed following exhaustive endurance exercise….

Extremely demanding endurance exercise has been shown to induce both a systemic inflammatory response [15, 42, 53, 71] as well as DNA damage [21, 36, 58, 62, 80]….

Exercise-induced DNA damage in peripheral blood cells appear to be mainly a consequence of an increased production of reactive oxygen and nitrogen species (RONS) during and after vigorous aerobic exercise [58]. Besides oxidative stress, other factors such as metabolic, hormonal and thermal stress in addition to the ultra-structural damage of muscle tissue are characteristic responses to prolonged strenuous exercise, that can lead to the release of cytokines, acute phase proteins and to the activation or inhibition of certain lines of the cellular immune system [15, 29]. [3]

There seems to be a big difference between moderate exercise and exercise to exhaustion. Moderate exercise actually protects DNA by upregulating DNA repair:

Sato et al. showed that acute mild exercise as well as chronic moderate training does not result in DNA damage, but rather leads to an elevation in the sanitization system of DNA damage [66]. [3]

However, endurance exercise leads to increased DNA damage:

Increased levels of DNA strand breaks were observed after exhaustive treadmill running in subjects of different training status [22, 45]….

In conclusion, there is growing evidence that strenuous exercise can lead to DNA damage that with few exceptions [36] is predominantly observed not before 24 h after the resolution of exercise [21, 44, 45, 80]. [3]

In addition, strenuous endurance exercise induces hormonal and other changes which might promote cancer. An Ironman triathlon has significant effects on hormones and inflammatory markers, some of which persist for more than 19 days post-race:

Briefly, as described in details elsewhere [42], there were significant (P<0.001) increases in total leukocyte counts, MPO, PMN elastase, cortisol, CK activity, myoglobin, IL-6, IL-10 and hs-CRP, whereas testosterone significantly (P<0.001) decreased compared to pre-race. Except for cortisol, which decreased below pre-race values (P<0.001), these alterations persisted 1 d post-race (P<0.001, P<0.01 for IL-10). Five days post-race CK activity, myoglobin, IL-6 and hs-CRP had decreased, but were still significantly (P<0.001) elevated. Nineteen days post-race most parameters had returned to pre-race values, with the exception of MPO and PMN elastase, which had both significantly (P<0.001) decreased below pre-race concentrations, and myoglobin and hs-CRP, which were slightly, but significantly higher than pre-race [42]. [3]

In the opinion of the authors of this review, the biggest problem is production of reactive oxygen and nitrogen species (RONS) by damaged immune cells:

The most conclusive picture that emerges from the available data is that oxidative stress seems to be the main link between exercise-induced inflammation and DNA damage…. DNA damage in peripheral immuno-competent cells, indeed, most likely resulted from an increased generation of RONS due to initial systemic inflammatory responses or the delayed inflammatory processes in response to muscle damage (Fig. 1). [3]

What About High-Carb Diets?

Do high-carb diets contribute?

During strenuous exercise mitochondria produce oxidation products:

The mitochondrial electron transport system can trigger the formation of superoxide leading to increased production of H2O2 by superoxide dismutase [49], [50]. [4]

In a normal person at rest, about 1-2% of the oxygen utilized by mitochondria ends up in superoxide. [4]

Before we go further let’s take a brief detour into mitochondrial chemistry: specifically, something called the electron transport chain.

Here’s a stylized view:

Source: Wikipedia.

The main point for our purposes is that there are two points of entry into the chain, one that goes through complex I and one that bypasses it.

Glucose metabolism favors entry via complex I, while fatty acid metabolism is relatively more favorable to entry via complex II. Quantitatively, glucose metabolism produces 5 NADH molecules (entering at complex I) for every one succinate molecule (entering at complex II), while fatty acid metabolism produces only 2 NADH for every one succinate.

High-carb dieting tends to habituate the body to metabolism of glucose. Therefore, it increases utilization of complex I.

This is significant because complex I is vulnerable to production of excess oxidative stress under some circumstances.

In principle, every mitochondrial complex has the potential to operate cleanly with minimal production of superoxide. However, if mitochondrial function is in any way impaired, so that operation of a complex is inhibited, then ROS production can rise substantially.

If for some reason electrons cannot flow properly through the electron transport chain, then they leave as superoxide:

One factor which may sensitise cells to increased DNA damage is impaired mitochondrial function [74]…. Reduced electron flow through the mitochondrial respiratory chain, particularly through the inhibition of complex I or complex III, favours the enhanced production of superoxide and H2O2 [75]. Together, with the age-dependent increase in oxidative stress and decline in NAD+ and ATP content, we found a tendency to the reduction in the activity of the respiratory complexes with age in all organs. Sipos et al. (2003) showed that mitochondrial formation of H2O2 due to complex I inhibition is more clinically relevant than ROS production due to inhibition of complex III and IV in situ [76]. [4]

What exactly did Sipos et al. find?  They state:

ROS formation was not detected until complex III was inhibited by up to 71 +/- 4%, above that threshold inhibition, decrease in aconitase activity indicated an enhanced ROS generation. Similarly, threshold inhibition of complex IV caused an accelerated ROS production. By contrast, inactivation of complex I to a small extent (16 +/- 2%) resulted in a significant increase in ROS formation, and no clear threshold inhibition could be determined. [5]

Basically, superoxide can be generated in complexes I, III, and IV. However, in complexes III and IV, there is a high threshold of inhibition of electron transport before any superoxide is produced. In complex I, there is no threshold:  even very slight inhibition will generate ROS. This means that during practical living, the great majority of excess ROS is produced from complex I.

This means that high-carb dieting, which increases utilization of complex I, will tend to generate oxidative stress if there is any inhibition of complex I.

But in endurance exercise, there is inhibition of complex I. To name just one pathway, exercise increases levels of the hormone DHEA, and DHEA inhibits complex I. [6]

It looks like high-carb diets and endurance exercise may be a bad combination.

Are Whole Grains Especially Bad?

There may be specific problems with grain toxins. For instance, wheat germ agglutinin, a wheat toxin that is very effective at distributing itself through the body through transcytosis, is able to damage mitochondria:

WGA induced a loss of transmembrane potential, disruption of the inner mitochondria membrane, and release of cytochrome c and caspase-9 activation after 30 min of cell interaction. [7]

At high doses in test tubes this can lead to cell death. It’s conceivable that at physiological levels WGA damage to mitochondria might mildly inhibit complex I and increase oxidative stress.

Of course, any deficiency in antioxidant minerals zinc and copper, which dismutate superoxide to hydrogen peroxide which is then disposed of by glutathione peroxidase (a selenium containing enzyme), would increase oxidative stress. Wheat contains phytic acid which chelates minerals and reliance on wheat as a calorie source may impair antioxidant status.

Conclusion

I don’t want to exaggerate the risks of endurance sports. With the exception of melanoma [8], there isn’t a clear increase in cancer incidence among marathon runners. And if this post seemed a bit tortuous, it’s because there’s no simple “smoking gun” pathway connecting endurance exercise to cancer.

On the other hand, endurance exercise is probably not as healthy, in terms of cancer risk, as shorter-duration activities. Also, the risk may rise substantially on high-carb or wheat-based diets. There are at least a few plausible mechanisms, not all of which I’ve discussed here, that might connect endurance exercise on grain-based high-carb low-fat diets to cancer.

References

[1] Vilenchik MM, Knudson AG. Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer. Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12871-6. http://pmid.us/14566050.

[2] Cooper MB et al. The effect of marathon running on carnitine metabolism and on some aspects of muscle mitochondrial activities and antioxidant mechanisms. J Sports Sci. 1986 Autumn;4(2):79-87. http://pmid.us/3586108.

[3] Neubauer O et al. Exercise-induced DNA damage: is there a relationship with inflammatory responses? Exerc Immunol Rev. 2008;14:51-72. http://pmid.us/19203084.

[4] Braidy N et al. Age related changes in NAD+ metabolism oxidative stress and sirt1 activity in wistar rats. PLoS One. 2011 Apr 26;6(4):e19194. http://pmid.us/21541336.

[5] Sipos I et al. Quantitative relationship between inhibition of respiratory complexes and formation of reactive oxygen species in isolated nerve terminals. J Neurochem. 2003 Jan;84(1):112-8. http://pmid.us/12485407.

[6] Safiulina D et al. Dehydroepiandrosterone inhibits complex I of the mitochondrial respiratory chain and is neurotoxic in vitro and in vivo at high concentrations. Toxicol Sci. 2006 Oct;93(2):348-56. http://pmid.us/16849397

[7] Gastman B et al. A novel apoptotic pathway as defined by lectin cellular initiation. Biochem Biophys Res Commun. 2004 Mar 26;316(1):263-71. http://pmid.us/15003540.

[8] Ambros-Rudolph CM et al. Malignant melanoma in marathon runners. Arch Dermatol. 2006 Nov;142(11):1471-4. http://pmid.us/17116838.