Let me introduce myself. My name is Mark Sisson. I’m 63 years young. I live and work in Malibu, California. In a past life I was a professional marathoner and triathlete. Now my life goal is to help 100 million people get healthy. I started this blog in 2006 to empower people to take full responsibility for their own health and enjoyment of life by investigating, discussing, and critically rethinking everything we’ve assumed to be true about health and wellness...Tell Me More
For today’s edition of Dear Mark, I’m answering three questions from readers. First, what do I make of the recent study showing a link between lung cancer in men and supplementation with vitamin B6 and vitamin B12? Next, how stable is folate in liver? Other foods with high folate content before cooking, like legumes and greens, lose a lot during cooking. And finally, what’s my take on the old study where subjects’ markers of oxidative damage improved after eating a diet bereft of produce?
Mark, I wonder if you’ve seen the study linking lung cancer in men with vitamin B supplementation: http://ascopubs.org/doi/abs/10.1200/JCO.2017.72.7735
What do you think?
Interesting study, thanks.
Supplementation with vitamin B6 or B12 was not associated with lung cancer risk in women.
Supplementation with vitamin B6 or B12 was associated with lung cancer risk in men, but only if those supplements were taken separately. If they supplemented with either vitamin as part of a multivitamin, the risk disappeared.
In other studies, vitamin B6 appears to be protective against most types of cancer, including lung cancer. Circulating levels of vitamin B6 protect against lung cancer. People with low “functional” vitamin B6 status—meaning they have low levels of active vitamin B6—have a greater risk of lung cancer.
Here’s what I think is going on: The study is capturing people with vitamin issues and disorders that cause deficiencies. People who take high dose vitamin B6 or B12 are more likely to have those disorders. They’re more likely to have low levels of the vitamins. They’re more likely to be prescribed vitamin supplements to make up for the deficiency. They’re probably even more likely to be unhealthy; many people take vitamins as an antidote to poor health.
Maybe supplementing isn’t good enough to overcome the inherent deficiency, or the condition causing the deficiency. Maybe these people aren’t converting supplemental vitamin B6 into the active, “functional” form that protects against cancer. Many of the participants were smokers at baseline, and the vitamin-mediated risk of cancer went up in those who smoked. Maybe they’re taking vitamins in response to an underlying disease state.
Those underlying disease states change how vitamin B6 acts in the body. In one study, “functional” B6 status was protective against lung cancer, while another type of biomarker measuring the catabolism of B6 due to inflammation, was linked to a rise in lung cancer. Low-grade inflammation is often high in states of disease or general unhealthiness, and B6 catabolism is a strong predictor of all-cause mortality.
It does seem that cooking affects these folate sources differently. If you compare cooked (boiled, drained) legumes, lentils come out on top! (Although liver is still king.)
This is true.
Animal-sourced folate is quite stable whether you freeze it or cook it.
I should say that overcooking your liver will deplete the folate. 12 minutes of frying in corn oil until 158°F/70°C caused a 50% loss of folate. 16 minutes of broiling until 158°F/70°C caused a 40% loss. That’s an obscene amount of cooking. Cooked liver should be pink inside. Creamy, not grainy. Even then, you still maintain at least half of the already generous amount of folate.
Older studies got better results, with fried beef liver losing between just 11-15% of folate. They probably weren’t overcooking it.
A ghost said:
I’d love to hear your opinion on this study:
Man, I wish I could get my hands on the full study. I’ll comment, but keep in mind that I’m only going off the abstract. Consider this fun speculation, not iron-clad conclusion.
Researchers took 8 smokers and 8 non-smokers, removed all concentrated sources of flavonoids from their diet, and fed them meat patties dosed with green tea extract for 10 weeks. This amounted to a “fruit-and-vegetable-free diet,” as produce is the richest source of flavonoids.
Green tea extract had some positive effects on postprandial oxidative stress, but they didn’t last. The half life of the extract in the body was 2 hours. As the subjects peed it out, the antioxidant capacity returned to normal.
What’s weird is that oxidative damage to DNA, lipids, and blood proteins all decreased over ten weeks despite the subjects eating no produce and the green tea extract only improving antioxidant capacity for a few hours postprandial.
Maybe the diet was dense with vitamins and minerals. After all, vitamins and minerals serve antioxidant functions and provide building blocks for the production of endogenous antioxidants like glutathione.
Maybe most of the oxidative damage our DNA, lipids, and blood proteins face occurs immediately after eating. If so, the postprandial increase in antioxidant capacity could have made all the difference.
We don’t know enough about the rest of the diet to say anything else or do anything but make guesses. They weren’t only eating the green tea meat patties. They ate other stuff, too—a “strictly controlled diet” absent fruits and vegetables. I really wish I could get my hands on the full paper.
That’s it for today, folks. Help out down below if you have anything to add, ask, or proclaim!
Take care, be well, and Grok on.