By now, the entire internet is furiously discussing the announcement by the IARC that processed meat raises the risk of colorectal cancer, and that red meat … well, ‘might’.
The outrage and surprise is silly, because pretty much the same evidence appears in the WCRF Food and Cancer Report in 1997. (Huge PDF warning!)
And there was quite a good meta-analysis published in 2011 which said essentially the same thing.
The evidence behind all four of these statements has been established and argued about and re-established for many years. If you pay even cursory attention to public health literature, this is very well trodden ground.
That doesn’t mean that the relationship between meat and colorectal cancer is a settled question. It’s more like an ongoing argument, one which is inevitably grounded in messy, difficult meta-analyses of population research. We don’t have the luxury of definitive answers or easy conclusions here — when it comes to saying how the meat/cancer association works, and what it might mean, and how strong it is, there are substantial arguments to be had.
So, everyone has lined up to have them.
Vegans, naturally, are delighted. This is normal. Any time someone says a pork chop made them stub their toe in a corridor, someone in a kaftan wearing cruelty-free worry beads writes a celebratory blog about it.
(I’m not linking to this snide gibberish. If you must read it, go to Twitter and search for “Bacon is literally Adolf Hitler” and I’m sure you’ll find it eventually.)
Meat councils and peak bodies, naturally, are defending their business model and livelihood.
(Not linking to this either. I think you can guess their arguments.)
People who are generally skeptical of nutritional epidemiology have weighed in (with some reasonable points).
Cancer peak bodies and NGOs have had a whirl at putting the announcement into perspective.
News outlets that care about the accuracy of their scientific reporting have produced generally good copy.
The Onion, as usual, has produced even better copy.
Oh, and websites and news organisation that normally report scientific results like irresponsible halfwits have, as might be expected, done their normal bang-up sandpit-level analysis and are proudly trumpeting crap like:
Finally, people who are awesome (OK, it’s pretty much just Ed Yong, but let’s be honest, he is awesome) are picking up the central distinction that’s the problem here:
“…these classifications are not meant to convey how dangerous something is, just how certain we are that something is dangerous.”
“Group 1 is billed as “carcinogenic to humans,” which means that we can be fairly sure that the things here have the potential to cause cancer. But the stark language, with no mention of risks or odds or any remotely conditional, invites people to assume that if they specifically partake of, say, smoking or processed meat, they will definitely get cancer.”
In other words, the association between processed meat and colorectal cancer is a) well established and b) pretty minor.
And honestly, I couldn’t give a ha’penny toss about any of it.
Because we’re arguing over a negative health message.
Negative health messages stink.
Compare the following two hypothetical claims:
- Don’t drink the water, it’s full of chemicals and it will kill you.
- Drink the juice, you’ll live longer and it tastes great.
2. works, and 1. sucks.
People prefer to be receive positive health messages (good things to do, basically), and they are markedly less affected by negative behaviours to avoid.
(For a recent and excellent omnibus reference see here.)
As far as a public health messaging goes, “don’t drink the water” is just another problem, rolled into the hundred thousand other component anxieties we have about food. This processed meat business is presently delivered through a louder megaphone than usual, but it is appending itself to the same laundry list of everything else we’re told to avoid, cut down, or cut out.
Has everyone forgotten we get dietary marching orders every other week?
Do health professionals expect people to keep listening indefinitely?
Does the average person differentiate between IARC making a recommendation or the research of three vegan professors of ancestral nutrition from a university that really should be re-classified as a kindergarten in the Pacific Northwest?
Not. At. All.
A cacophony of authoritative voices have recommended more of everything, and less of everything, and none of something for such a long time, and people could not be more sick of it. You know how many friends or friends-of-friends I’ve seen on social media who’ve said something along the lines of “GOOD I DON’T CARE I HOPE IT KILLS ME” in the last three days?
(I counted. It was boring, and it made me want a bacon sandwich.)
And these are largely health-conscious university-educated middle class people who are willing to put up with my scintillating conversation about hazard ratios and hepatic function and autonomic regulation and how Pete Evans should be turned into a man-skin rug.
So, I refuse to add to the groaning pile of scary health-bollocks, the haunted houses full of gluten, the dark alleys full of proscuitto crudo, the jeremiads of the wheat-free fun-free life-free saviours of the human species. The pile that just happens to monetise your fear and insecurity.
Let’s not talk about what we shouldn’t do, but what we should do.
Obviously, there’s lots of non-specific advice floating around right now — “Lose weight! Exercise more! OMG cancer!” — but here we’re going to establish some specific advice. Processed meat has a carcinogenic risk profile for a reason, not just because hippies don’t like it, and that risk is something we can address in positive language, and mitigate with positive activity.
What’s to follow is based on solid research, and has an established method of action — that is, we know that it works and WHY it work — and the behaviours I’m recommending are all achievable, straightforward things anyone can do.
Now, all I’ll say about what they do is that they specifically reduce the risk of colorectal cancer for the same reason that processed meats raise it. So don’t go quoting me as saying they ‘reverse the effect of bacon using science’ or any such silliness.
But, even so — this is the good stuff.
1. Give blood
What? Yes. Give blood.
Were you expecting eat more salad?
Give blood. Whole blood, not platelets. Give it away to someone who needs it.
Let’s nerd out quickly, and I’ll explain.
There are a bunch of mechanisms proposed for the carcinogenic potential of processed meat (and red meat). I think the evidence is pretty well established for two of them.
- N-Nitroso Compounds (NOCs)
(I always wondered why these are called NOCs and not NNCs, but anyway.)
These are nasty molecules produced, inconveniently, when nitrites (i.e. like curing salts that you find in processed meats) react with amines (which are parts of protein structure, as in, you can find them in meats). They’re fairly straightforwardly carcinogenic. We think this is the center of the problem with cured meats.
2. Haem iron
Haem is the bit of haemoglobin that gives it the name — it’s an iron ion trapped in a porphyrin ring, which goes in the middle of haemoglobin (the oxygen carrying molecule in red blood). When we eat external sources of haem, we end up with more of our own.
Blood and liver are the best sources of this (so, liverwurst or black pudding), and after that, game meat, steak and lamb. There are actually a few pathways by which we think excess haem can be carcinogenic, but the main one is facilitating the relationship about in 1. — it’s a catalyst for NOC formation.
Our previous studies in humans have established that red but not white meat stimulates endogenous intestinal N-nitrosation and that there is a dose response. … This could be important for carcinogenesis in the large bowel because many classes of NOCs have been identified, including nitrosamines, nitrosamides, and nitrosoguanidines, most of which are known carcinogens.
After eating meat, the large intestine is rich in nitrogenous residues and nitrosating agents from protein metabolism and bacterial dissimilatory nitrate metabolism. In the present study, we show that it is haem iron, not protein residues or inorganic iron, that stimulates endogenous NOC production.
Now, your body doesn’t make iron — it’s not an alchemist — so all the iron that you’ve got handy enters your body through your diet, and for the most part it stays there. Anaemia, or iron deficiency, isn’t much of a problem in the developed world any more. Instead, have have the other problem: too much iron.
(There are actually quite a few conditions implicated under the ‘too much iron’ umbrella — if you want to have a read, google ‘ferrotoxicity’ and prepare yourself for war.)
So, with our mechanism established, a few years ago this study landed like a bomb:
A multicenter randomized, controlled, single-blinded clinical trial … tested the hypothesis that reducing iron stores by phlebotomy [this is the fancy medical word for blood donation — JH] would influence vascular outcomes in patients with peripheral arterial disease. …
Patients were followed up for an average of 4.5 years. Ferritin levels were similar in both groups at baseline but were lower in iron reduction patients than control patients across all 6-month visits (mean = 79.7 ng/mL, 95% confidence interval [CI] = 73.8 to 85.5 ng/mL vs 122.5 ng/mL, 95% CI = 115.5 to 129.5 ng/mL; P < .001).
Risk of new visceral malignancy was lower in the iron reduction group than in the control group (38 vs 60, hazard ratio [HR] = 0.65, 95% CI = 0.43 to 0.97; P = .036), and, among patients with new cancers, those in the iron reduction group had lower cancer-specific and all-cause mortality (HR = 0.39, 95% CI = 0.21 to 0.72; P = .003; and HR = 0.49, 95% CI = 0.29 to 0.83; P = .009, respectively) than those in the control group.
In plain English, this says that the blood donor groups had approximately HALF the incidence of cancer or death. And the hypothesised reason? Well, it seems to be pulling out the haem.
Frankly, this is such a good result, it’s a little too good to be true. The study was justifiably criticised: the sample size was quite small, and it’s hard to say if the clinical outcomes they measured were specific enough.
Certainly, though, we can say two things:
- ‘iron reduction’ via blood donation is really effective, with the intervention group lowering their measured ferritin levels by about a third. This much at least was supremely reliable.
- It’s pretty goddamn compelling, isn’t it?
Soon after, the evidence connecting haem iron and carcinogenesis has been filing in gradually…
We have systematically reviewed 59 epidemiologic studies, published between 1995 and 2012, reporting information on total iron, dietary iron, heme iron, and biomarkers of iron status and cancer risk. Furthermore we conducted meta-analysis for colorectal [relative risk (RR), 1.08; 95% confidence interval (CI), 1.00–1.17], colon (RR = 1.12; 95% CI, 1.03–1.22), breast (RR = 1.03; 95% CI, 0.97–1.09), and lung cancer (RR = 1.12; 95% CI, 0.98–1.29), for an increase of 1 mg/day of heme iron intake. Globally, on the basis of the systematic review and the meta-analysis results, a higher intake of heme iron has shown a tendency toward a positive association with cancer risk.
One third of males (35%) and one fifth of females (18%) had high serum iron (≥120 μg/dL), which was associated with a 25% increase in risk for incidence of all cancers [HR, 1.25; 95% confidence interval (CI), 1.16–1.35] and with a 39% increase in risk for mortality from all cancers (HR, 1.39; 95% CI, 1.23–1.57). The relationship between serum iron and cancer risk was a J-shaped one, with higher cancer risk at both ends, either at lower than 60 μg/dL or higher than 120 μg/dL.
Oh, I haven’t even told you the good part yet.
If you go to give blood, they’ll test your iron levels for you.
(Actually, they’ll test a lot of things. It’s pretty much a free health check.)
And if your iron levels are too high, they’ll take some out for you, for free, and then you get a cookie, and then you probably end up saving someone’s life!
Where are you going to find a better deal than that?
2. Eat fiber
Yeah, you should have seen this one coming. Everyone knows fiber is good for everything, right?
Actually, the evidence is a bit of a mess overall — there are about twenty prospective cohort studies looking at the relationship between fiber and colorectal cancer, and their conclusions point every which way.
However, if we assort all of those results into a meta-analysis, we get something approximating an answer. Here’s a panel from the last paper to do this properly:
That last graph there is the money: the relative risk seems to decrease proportionally with the amount of fiber you eat.
Well, you’re not going to like it. The answer has been established for many years, and seems to lie in… I’ll put this delicately… “intestinal transit time”.
Yes, they followed young men around with a stopwatch waiting for their ‘intestinals’ to ‘transit’.
(I bet they made the work experience kids collect THAT data!)
As you can probably imagine, the village participants had a very high fiber diet, and the English boarding school participants did not.
And that’s the center of the hypothesis — that the post-intestinal contents are potentially high in carcinogens from the digestive process (see above!) and the shorter the contact time with the colon and rectum, the less likely those carcinogens are to do damage.
3. Get your dairy
Because milk is (usually) fortified with Vitamin D, and is our major dietary source of calcium.
Over to Park et al. 2007:
Total calcium intake (from foods and supplements) was inversely associated with colorectal cancer risk in both men (highest quintile vs. lowest: relative risk (RR) = 0.70, 95% confidence interval (CI): 0.52, 0.93; p for trend = 0.006) and women (RR = 0.64, 95% CI: 0.50, 0.83; p for trend = 0.003). The inverse association was also seen for total vitamin D intake in men (RR = 0.72, 95% CI: 0.51, 1.00; p for trend = 0.03) but not in women. Intake of dairy products was inversely associated with colorectal cancer risk, especially among nonusers of supplemental calcium (men: RR = 0.77, 95% CI: 0.59, 1.01; women: RR = 0.66, 95% CI: 0.49, 0.89). The findings support the hypothesis of protective roles for calcium, vitamin D, and dairy products in the risk of colorectal cancer.
(This isn’t just one study, there are about a dozen others… most of them describe a similar relationship. A recent review — Song et al. 2015 — describes the protective nature of calcium as ‘probable’ and Vitamin D as ‘limited-suggestive’. Happily, we don’t have to choose with dairy products, as they’re both in there.)
And why Vitamin D and calcium?
Well, that’s a lot more complicated. It’s also frankly a little out of my pay grade, and we’re pushing three thousand words, so I’m going to cop out entirely and hand back to Song et al. 2015:
Binding to fatty acids and free bile acids, suppression of cell proliferation, promotion of cell differentiation and apoptosis, inhibition of oxidative DNA damage, and modulation of colorectal cancer-related cell signaling pathways.
I can’t make you a prediction of what odds you get, how this will improve your life (or any other damn thing), I can’t make you taller or better looking.
I can’t tell you that these THREE WEIRD TRICKS mean you eat all the salami you like. That would be gruesomely irresponsible.
But I can give you the power back. These are things you can do, simple steps you can take towards taking responsibility for a potential health risk, and mostly importantly ensuring that the meat you do eat stays in your mind as just that — meat.
Not a carcinogen, not a risk, not a source of anxiety… just meat. A nice thing. Something we can enjoy. Not something to batter with strictures and cut up into sensible portions and lose sleep over.
This is where we should be.
Donating blood — how often should you go?
Not that often. Normal donation rates are once every 2 to 4 months.
Where are blood banks located?
I have XYZ disease, can I still donate?
Ask your local organisation, that changes depending on the site and the country, they’ve got their own rules.