One of the great things about our growing community is how people like Denise Minger have emerged from near obscurity to become recognized leaders in certain areas. When it comes to parsing the scientific studies, very few people have the combination of skills, understanding of the scientific method and probability, AND the willingness to dig deep into the minutiae to get to the essence of a study. Denise is one of those rare people. If you haven’t read Denise’s take-down of the China Study, you owe it to yourself to do so.
Lucky for us, Denise has taken the time to dig into the latest research on diet and breast cancer in today’s guest post. (Thank you!) Without further ado, Denise…
If you’ve been scanning the health news lately (or live within earshot of some gloating low-fat adherents), you might’ve noticed a flurry of recent headlines linking fat and cholesterol to breast cancer. In case you haven’t, this should get you up to speed:
Catch the drift?
These doomful blurbs sprang from a mouse study published earlier this month in the American Journal of Pathology, showing that mice fed a higher-fat, cholesterol-enriched diet developed bigger and more aggressive tumors than mice eating their normal “chow” diet. According to the researchers, this suggests that “cholesterol accelerates and enhances tumor formation.” And if the news stories are to be trusted, that means we should curb the fat and toss back some statins with our Healthy Whole Grain dinners.
Even if you’re not a woman, chances are good that you’ve encountered one before, and maybe even spent some time inside one’s womb. And considering about one out of every seven women will face breast cancer in her lifetime, dietary links with this disease tend to be a hot topic for health-minded folks of either gender. So what’s going on with this study? Can it tell us anything important, or is it another one for the lame-research slush pile?
If you don’t want to trudge through the full text of the study linked above, here’s the rundown. The researchers took two groups of mice: one wild, ordinary-mouse-on-the-street strain and one special strain that’s predisposed to developing mammary tumors. For both the wild and the tumor-prone mice groups, half got a standard chow diet and half got a Western diet. These are the only food details offered in the paper:
Female mice hemizygous for the PyMT transgene were given either a Western diet (57BD; LabDiet, Richmond, IN) containing 20.2% fat, 16.8% protein, and 48.0% carbohydrate, or a chow diet (5010; LabDiet) containing 4.5% fat, 23.0% protein, and 50.1% carbohydrate, at age 4 weeks and thereafter ad libitum. Although fat content of the diet was increased, carbohydrate content was not altered. Moreover, energy values of the 2 diets were similar (4.43 kcal/g and 4.14 kcal/g for Western and chow diets, respectively).
Fair enough. From this description, you’d think the main difference between the diets was fat content: 4.5 percent in one and 20.2 percent in the other (with slightly lower protein and carbohydrate levels to compensate). But whenever we hear a diet described only in terms of macronutrient ratios with no assurance that the food variables are controlled, it’s usually a bad sign (and an inevitable slush pile omen). Fortunately, Google exists. Even though the paper’s lips are zipped about the actual ingredients of the diets, the spec sheets for both the chow diet 5010 and “Western diet” 57BD are posted online, so we can figure out exactly what these mice were eating.
It turns out the chow-diet mice—the ones who got fewer tumors—were feasting on a mix of:
Not exactly a five-star cuisine, but most of these ingredients aren’t alien substances to mice. It’s passable fare.
But what about the high fat diet that promoted so much tumor growth? Was it the same as above, just slathered in a few pats of butter? Alas, the “Western diet” mice weren’t even eating food. Along with a small amount of added cholesterol, their diet consisted of:
It’s a marvel the Western diet got labeled “high fat and cholesterol” when it’s only 21 percent fat and nearly a third pure table sugar. It’s also a marvel that the researchers pegged the tumor-enhancing effects of the Western diet on its cholesterol content rather than on any of the other differences it had with the chow diet (for example: everything). In fact, the protein source alone might play a role in spurring the big, speedy tumors found in the Western diet rats, since so much of their diet was casein. Dare I reference my old pal T. Colin Campbell, whose research showed isolated casein tends to boost tumor growth in rodents when it exceeds 5 percent of their diet? I dare. There may be something uniquely cancer-promoting about isolated complete proteins (like casein) in a purified diet, probably due to the fact that they promote growth in general but lack the matrix of protective substances found in whole foods.
But the most interesting thing here is that hefty dose of sucrose in the Western mouse diet. Even back in the 80s, researchers were noting an association between sugar consumption and breast cancer, speculating that:
A possible connecting link between sugar consumption and breast cancer is insulin. This is an absolute requirement for the proliferation of normal mammary tissue and experimental mammary tumours may regress in its absence. Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake.
There’s a growing body of research addressing the insulin-breast cancer link, and unlike with fat, the findings are more consistent. High insulin is associated with a greater risk of death from breast cancer, may lead to a greater risk of breast cancer in postmenopausal women, and may be a risk factor for breast cancer independent of estrogen. Although insulin responses to sugar vary between mouse strains, there’s some evidence that mice fed sucrose as their primary carbohydrate (opposed to other foods like cornstarch) have higher levels of insulin and insulin-like growth factor 1. Both insulin and IGF-1 can potentially stimulate the growth of breast cancer cells and hike up testosterone levels (which also has some compelling links with breast cancer). And one study examining the effects of different sources of protein, fat, and carbohydrate on mammary tumors in mice showed that the sucrose-eating mice had 100 percent tumor incidence by the end of the study.
Since the researchers were mostly concerned with fat and cholesterol in this study, they didn’t examine potential pathways between tumor growth and insulin, or consider whether the high sugar and casein content of the Western diet had anything to do with cancer promotion. I’ve got a hunch there are some untapped clues there, but from this study, we’ll never know for sure.
Although most of the media outlets pounced on the “high fat” part of this study, the researchers themselves were more intrigued by the effects of cholesterol. Interestingly, the mice exhibited lower cholesterol as their tumors grew—suggesting that the tumors seemed to guzzle cholesterol and use it for cell proliferation, causing a drop in serum levels. (This jibes with a trend we’ve seen in humans, where certain cancer patients have significantly lower cholesterol than the rest of the population.) The researchers speculate that lowering blood cholesterol could help limit tumor growth in humans, and they conclude: “Drugs that target cholesterol metabolism could be used in addition to drugs that may facilitate the elimination of breast cancer cells.” (Did you hear that? Could it be the joyous clinking of the statin companies’ wine glasses?)
Even if tumors (breast or otherwise) do hoard cholesterol, there’s no way to tell from this study whether cholesterol actually promotes their growth, and if deliberately lowering your levels would do a darn thing for cancer prevention. In fact, the researchers note that “it is not unreasonable to assume that liver function may be affected in this disease” and that “plasma lipoprotein levels could be influenced by reduced hepatic lipoprotein secretion”—in which case the breast tumors might not be reducing cholesterol by using it for their own growth, but the body is simply producing less of it.
This study might’ve uncovered an interesting role of cholesterol in tumor growth, but it’s hard to tell what the significance would be even if that’s the case. Given the total lack of a control diet and the sketchy assembly of ingredients in the Western cuisine, we can’t glean much of anything about the role of fat or cholesterol in human breast cancer. The only things saving this study from that slush pile are the three nuggets of wisdom it confers: Don’t be born a tumor-prone mouse, don’t eat a foodless diet based on table sugar and casein, and read the full text of studies before letting news headlines make you nervous.