Wednesday, February 20, 2008

Fiber, inulin and cancer

Just a quickie,

It has come up off blog on a number of occasions that inulin, a fructose polymer completely indigestible to humans but edible by bacteria, is a potential carcinogen. Couple of refs here and here. I was a bit dubious of this model as it showed beef to be carcinogenic too. That upsets my biases!!!! And slightly odd as this different model showed bacon, yes you read that correctly as bacon, to be protective. Beef and chicken were neutral in this chemical carcinogen based model. I decided that playing with mice, especially bowel cancer prone mice like ApcMin/+ engineered mice, might say relatively little about humans. Still not sure.

Now this dropped out of Pubcrawler today. If you are a ApcMin/+ mouse you can choose you carcinogen from wheat bran or apple pulp (that's the healthy fiber from healthy fruit, apples):

"In conclusion, both types of resistant carbohydrates increased polyp number and tumour burden and this was associated with elevated epithelial cell proliferation and crypt fission."

Because my access account doesn't allow me the full text I can't see what the fiber did to the wild type control mice. Always the most interesting bit and not in the abstract.

Crypt fission is bad, it's what wheat germ agglutinin and insulin do. Looks like all sorts of fiber do too. Just an extreme mouse model, but next time someone extolls their belief in the benefits of resistant starches or fiber, maybe they should read and think!

Peter

21 comments:

Chainey said...

Re. Bacon

Doesn't Dr Kwasniewski claim that the flesh of the pig is most ideal, being "closest to human tissues biochemically"?

(No, I haven't read his book yet)

Peter said...

Hi Chainey,

Yes he does, but I'm a little uncomfortable with the omega 6 fatty acid concentration in lard compared to beef dripping. I don't go as far as Bruce in my dislike of all PUFA, but the cow's rumen gets rid of an awful lot of omega 6 fats which tend to end up in pork lard (pigs do limited hind gut fermentation, most PUFA hit the blood stream via the small intestine). I do wonder whether pigs in Poland in the 1970s were swill/potato/whey fed. This would give a fat better lipid profile than modern pork which is grain fed and lean anyway! I just try and keep thinking...

Peter

Glenice said...

Peter, Thanks for your blog, I am enjoying it.

What about outdoor reared Pork ala Sainsbury and my local outdoor reared only butcher. Who by the way gives me all his leaf fat which I render myself to Lard. Would this too be too high in PUFA?

In your opinion, is the Britannia Beef dripping okay to use?

Sorry about all these questions?

Glenice

Peter said...

Hi Glenice,

I doubt indoor/outdoor affects the PUFA levels, all grain fed, but the outdoor stuff does seem to taste better (probably just being influenced by marketing here???). I certainly still eat quite a lot of pork full stop. Britannia is the dripping I buy too, now my local butcher can't get suet any more (grass fed scottish beef is his speciality). This weekend we've got lamb for this Sunday. Looking forward to it...

Peter

Sasquatch said...

Hi Peter,

Interesting post, thanks for the info. I wonder if anyone has ever studied people who eat jerusalem artichokes (sunchokes), which are packed with inulin. I do eat them from time to time, and I can confirm that they're full of indigestible fiber because they give me massive gas.

About the lard, I agree the drawbacks are that it has more PUFA than suet/butter/coconut oil, and it has a poor n-6 to n-3 ratio. The advantage however is that it's the second-richest natural source of vitamin D, after cod liver oil. Suet doesn't seem to contain much vitamin D from what I can tell.

That's only if it's raised outdoors of course. I agree that the n-3/n-6 ratio wouldn't change whether it were indoors or outdoors, since even outdoor pigs aren't really doing any foraging. However, I'm sure the diet does affect the ratio. Smaller farms might be more likely to feed the pigs vegetable waste and/or alternative starches.

Also, the amount of n-6 in lard isn't any worse than in olive oil, and is easily overcome with a little fish oil, cod liver oil or flax.

Dave Lull said...

You might find Bix’s take on resistant starch interesting:

Resistant Starch

Types of Resistant Starch

Resistant Starch May Reduce the Risk of Colon Cancer

Bacteria and Blood Sugar

Anna said...

Sasquatch,

I agree about the sunchokes. They tasted nice, but wow, worst gas ever! Ugh, hot and smelly. After several years on a low carb diet and enjoying nearly no gas, it was too simply much. Heck, wikipedia.org even says this:

The inulin is not well digested by some people, leading to the misconception that sunchokes are not edible or an assumption that they cause flatulence and gastric pain. Gerard's Herbal, printed in 1621, quotes the English planter John Goodyer on Jerusalem artichokes:
"which way soever they be dressed and eaten, they stir and cause a filthy loathsome stinking wind within the body, thereby causing the belly to be pained and tormented, and are a meat more fit for swine than men." [4]

So let the pigs eat sunchokes, and I'll eat the pig :-).

Sasquatch said...

Haha, I don't want to be around the pig while it's eating sunchokes though.

Peter said...

Hi Dave,

Just had a read of your links. In the first link what struck me was that RS at low doses increased fat oxidation (15g/d RS) but at 30g/d it completely obtunded fat oxidation to the equivalent of zero g/d. Why? The SCFA made by gut bacteria belong to the gut bacteria. They're not ours. The microbiota will allow us a little of their butyrate but the bulk is sent directly to our liver and converted to tryglycerides. These are then stored as fat by activation of lipoprotein lipase. The whole cascade is controlled by Fiaf (Fasting induced adipose factor), which is to a significant extent controlled by the gut bacteria. Feed the bacteria and they make fat (butyrate), but they FORCE you store it. Now I like butyrate, it's a fat after all, it will induce fat oxidation, and I LOVE fat oxidation. I'll eat butter 'til I'm not hungry (I was going to say 'til the cows come home but...). Of course butyrate from butter feeds me directly, not via my bacteria, and via my small intestine not my colon. No gas! No Fiaf suppression either. I put it up in detail, first post is here , just check those with Fiaf at the start of the title.

The protein causes cancer links are interesting. You can see that many researchers are interested in this and also that you can seriously influence the results you get by the model you use. These models do not always represent life. Counting DNA breaks in a wild type mice MIGHT be closer to reality than counting cancers in an ApcMin/+ mouse. Who knows. Certainly not me. But I have to ask, what on earth is anyone doing putting protein in to their colon anyway? The protein I eat is for me. I choose it as highly digestible, especially eggs (WHO standard for maximum protein quality). After that I eat enough to meet by needs, probably 60-70g/d in total. If my small intestine cannot cope with this something is wrong (probably gluten damage from healthy whole grains, or damage from the lectins in pulses!).

I noticed that the Greenland eskimo do not seem to have a colon cancer problem on 299g of protein, 169g fat but only 10g carbohydrate per day. I have the paper, it's in Norwegian (or possibly Danish) and I only have it as a pdf. I got it from a Norwegian friend via email. The macronutrient table translates easily just by looking at it (no, I don't speak Norwegian).

Also, while I have no problem with high protein diets per se for weight loss or anything else, they are not my choice. I eat high fat. Fat equals flat line glucose, flat line insulin.

Re the paper on barley or white bread for supper:

"Eating barley for dinner almost halved total blood glucose (area under the curve) during the 2 hours following breakfast the next day when compared to eating white bread for dinner.

(There was an almost 10 mg/dl lower blood sugar at 30 and 45 minutes after breakfast.) Barley also resulted in lower blood sugars the morning after dinner meals of spaghetti or spaghetti+wheat bran."

I read through this and I simply don't recognise any of the things discussed (barley, white bread, wheat bran or spaghetti) as food! I don't have to take the point off of a glucose spike after breakfast because scrambled egg yolks in butter does not produce a spike in the first place.

I've mentioned before, I like butyrate. Butter sourced butyrate that is.

Peter

PS due to a broken nose from a childhood accident I tend to snore occasionally. That's bad enough. Given the effects of boiled barley on gut flora I would end sleeping on the sofa.

migraineur said...

Peter - thank you so much for your analysis of the resistant starch studies that Bix posted. She recently posted something about how a vegan diet lowered A1c more than the standard ADA diet, and attributed the "success" of the vegan diet to resistant starch. I took one look at the study numbers and almost had a cow right in my office. A1c levels in both groups were at around 7! She didn't post my comments, to the effect that an A1c of 7 corresponds to average blood glucose of around 180 mg/dl or 10 mmol/dl; and that many diabetics can get their A1c down to normal or near-normal levels without medication by cutting out the exact foods that a vegan diet promotes.

Peter said...

Hi migraineur,

I see you read Dr Bernstein. Apparently Bix doesn't!

Peter

Bruce said...

I mainly dislike PUFAs when they're the predominant fat in a food. Pork is about average, IMO - like goose, duck, olive oil, avocado, eggs, and hazelnuts. I choose to restrict the PUFAs more heavily because it seems to promote greater lifespan/health.

I think it's best to keep as high a ratio of SFA/PUFA, and MUFA/PUFA as possible. Things like beef, mac nut oil, foie gras, coconut oil, kidney suet, butter, cocoa butter... Maybe unrefined red palm oil.

You'd probably be better off eating fatty chicken and pork than most of the vegetable fats. I focus on lean seafood, esp shellfish, with butter or other acceptable fats. They have high nutrient density and extremely low PUFA content. I'm trying to get more omega-9 PUFAs, which your body makes under low-PUFA intake.

Mead Acid (omega-9) is more stable, and less reactive, because the last double bond is shielded by 8 carbon atoms. Omega-6 fats are shielded by 5 carbon atoms and omega-3 are only shielded by 2. So they are the most reactive of all. I feel, like Peat, fats should be limited according to chain length and unsaturation.

Bruce said...

Glenice: pork leaf fat is best IMO. It's similar to lamb fat. About 48% SFAs and <8% PUFAs. Normal pork fat is about 40% SFAs and 12% PUFAs. As Peter noted, pigs would have better fat (less PUFAs) if they were fed a diet of potatoes, milk, fruits, and other low-PUFA foods.

http://www.nutritiondata.com/facts-C00001-01c20ZO.html

The amount of PUFAs in the animal's fat tends to correspond to the % of calories from PUFAs. If you feed an animal corn (5% PUFAs) and soybeans (19% PUFAs), those will average out to 12% PUFAs overall in the body. A ruminant animal will have less than this, because they have enzymes and bacteria to saturate PUFAs.

The ratios of SFAs and MUFAs aren't as static as PUFAs, because animals can make them from carbs.

Bruce said...

migraineur: "...A1c of 7 corresponds to average blood glucose of around 180 mg/dl or 10 mmol/dl..."

The problem is that a1c and average blood sugar do not really correlate that well. The graph looks like the graph for heart disease for all the countries which Ancel Keys ignored. Some people had low A1c and a high blood sugar and others had high A1C and low blood sugar.

http://care.diabetesjournals.org/cgi/content/full/25/2/275/F1

We need a better theory. Blaming it all on carbs, blood sugar, insulin just doesn't work. According to the data, PUFAs are involved in damages to protein attributed to carbs. The PUFAs damage proteins 23x faster in vitro, where the carbs are free and the PUFAs are mostly bound. If Peat is correct, there should be a huge drop in A1c by cutting PUFAs.

http://tinyurl.com/ytng7r

Aspirin and salicylates in food are also known to block glycation, and function as anti-oxidants. Markers and risk factors (like A1c) may be irrelevant in another context.

http://raypeat.com/articles/aging/aspirin-brain-cancer.shtml
http://raypeat.com/articles/articles/unsaturatedfats.shtml

Dave Lull said...

Hi Peter,

Thanks for taking the time to comment on Bix's postings: very interesting. And most of it is very new to me: a lot to think about. I read your blog daily to keep up with the new postings and to make my way through the older ones, including the comments. Your blog's intelligent and knowledgeable commenters certainly increase its value for me.

Best,
Dave

gunther gatherer said...

Hi Dave and Peter,

The resistant starch question keeps coming up for me too. I notice Peter that your main vegetable seems to be potato. This is also what JK prescribes, but can you please tell me why?

I'm trying to find a low-fiber vegetable as a vehicle for fat with low fructose, as well as to make my life a bit more interesting amongst all this fat...

Thanks,
Gunther

hopeful geranium said...

And here the carcinogenic effect of inulin plus rye (fibre from healthy wholegrains, so to speak) is taken for granted...
But it is modified by lignans, similar to what you might find in flaxseed or sesame...
So if you must eat bread, eat the seeded varieties?
But why not just eat the seeds...

Cancer Lett. 2000 Dec 20;161(2):253-8.
Chemopreventive activity of crude hydroxsymatairesinol (HMR) extract in Apc(Min) mice.
Oikarinen SI, Pajari A, Mutanen M.
Source
Department of Applied Chemistry and Microbiology (Nutrition), University of Helsinki, P.O. Box 27, FIN-00014, Helsinki, Finland.
Abstract
We studied the effects of a lignan, hydroxymatairesinol (HMR), and rye bran on intestinal tumor development in adenomatous polyposis colimultiple intestinal neoplasia (Apc)(Min) mice. HMR showed a strong chemopreventive effect in this animal model. The mean number of adenomas in the small intestine was significantly lower (26. 6+/-11.0, P<0.05) in mice fed the inulin and HMR when compared with the inulin and inulin/rye bran fed mice (39.6+/-8.9 and 36.0+/-7.4, respectively). HMR resulted in normalization of beta-catenin levels in adenoma tissue, indicating that HMR mediates its chemopreventive effect through the Apc-beta-catenin pathway. In the cytosolic fraction, beta-catenin level in adenoma tissue was significantly elevated (P=0.008-0.013) in all the diet groups as compared with that of the surrounding mucosa. In the nuclear fraction, beta-catenin in the inulin (3.15+/-2.9 relative units) and inulin/rye (5.17+/-6.94 relative units) groups was also significantly higher (P=0.003-0.009) in the adenoma tissue when compared with the surrounding mucosa (0.5+/-0.5 and 0.35+/-0.39 relative units). However, HMR was able to restore nuclear beta-catenin level of the adenoma tissue (0.41+/-0.25 relative units) to the level found in the surrounding mucosa (0.36+/-0.28 relative units).

PMID: 11090976 [PubMed - indexed for MEDLINE]

hopeful geranium said...

The thing about protein...
The protein does not cause the cancer in these experiments; that is done by a drug.
Restricting some nutrients thereafter might induce a stress response that promotes apoptosis, or helps the immune system suppress any tumours, or is selectively cytotoxic.
Overfeeding certain nutrients may promote the tumour in various ways.
But the foods are NOT the carcinogens in these models; they are cancer-promotors.
Look at folic acid; this will reduce the rate of carcinogenesis in models like cervical cancer, and probably colon cancer, but once colon cancer is progressing, folic acid supplementation can then promote it.
There are multiple stages of cancer development and at different stages the same nutrients can have opposing effects on the final outcome.

hopeful geranium said...

The problem with pork, as I read the limited research, may be that the fat of the meat contains some of its omega 6 as arachidonic acid, and the ratio of AA to EPA and DHA is considerably higher than it is in beef fat.
This would make the fat in pork - especially "lean" pork - more inflammatory than olive oil.

Lipids. 1998 Apr;33(4):437-40.
Contribution of meat fat to dietary arachidonic acid.
Li D, Ng A, Mann NJ, Sinclair AJ.
Source
Department of Food Science, RMIT University, Melbourne, VIC, Australia.
Erratum in
Lipids 1998 Aug;33(8):837.
Abstract
Arachidonic acid (AA) in the diet can be efficiently absorbed and incorporated into tissue membranes, resulting in an increased production of thromboxane A2 by platelets and increased ex vivo platelet aggregability. Results from previous studies have shown that AA is concentrated in the membrane phospholipids of lean meats. However, the concentration of AA in the visible fat portion of meats also may be significant despite being ignored in most studies. The aim of this study was to accurately quantitate the AA content of visible fat and the lean portion of beef, lamb, pork, chicken, duck, and turkey. The visible fat of meat contained a significant quantity of AA, ranging from 20 to 180 mg/100 g fat, whereas the AA content of the lean portion of meat was lower, ranging from 30 to 99 mg/100 g lean meat. Beef and lamb meats contained lower levels of AA in both the visible fat and lean portion than that from the other species. The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat

jpatti said...

I'm not sure where the assumption that pork eats mostly grain when pastured is coming from.

The pork I buy is from a dairy farm and it eats mostly skim milk and whey. In fall, it cleans up the orchards and also gets a lot of nuts, that being what it is "finished" on.

I'm not sure what that does to their omega ratio.

The bit about it being on pasture means little in terms of diet, as pigs don't eat a whole lot of grass, being omnivores (though probably SOME, even my carnivore cats eat some lawn).

But it does mean they're in the sun and thus have lots of vitamin D in their fat.

Still, I'd not expect good things if raised primarily on grain - but that isn't the only option.

George Henderson said...

what pigs evolved to eat is no mystery; roots and shoots, burrowing animals (e.g. worms, grubs, beetles) and snails, windfall nuts and fruits, and some carrion.
Pigs on smallholdings get a lot of restaurant leftovers.