Saturday, January 08, 2011

Two Studies That Link Dietary Fat To Cancer

They're both mouse studies. Both from the same research team at Jefferson University in my hometown of Philadelphia. One study linked fat to breast cancer (and lung cancer), the other to prostate cancer (and lung cancer).

The first appeared in The American Journal of Pathology this month:

Role of Cholesterol in the Development and Progression of Breast Cancer, The American Journal of Pathology, January 2011

The PyMT mouse was used because its cancer is similar to human breast cancer. Mice were fed either a diet mimicking the standard American diet or a control diet.

Western Diet:
20.2% fat
0.2% cholesterol

Control Chow diet:
4.5% fat
<0.03% cholesterol

There were more breast tumors, they were larger, they appeared sooner, and they metastasized more easily in the mice eating the higher-fat diet:
"In summary, administration of a Western-type diet resulted in accelerated tumor onset, and increased tumor incidence, multiplicity, and burden. These data suggest an important role for dietary cholesterol in tumor formation."
They also found a link to lung cancer:
"The results suggest a trend toward an increased number of metastases in the lungs of PyMTg mice fed a Western diet compared with mice fed a chow diet."

The second appeared in the same journal last month:

A Western-Type Diet Accelerates Tumor Progression in an Autochthonous Mouse Model of Prostate Cancer, The American Journal of Pathology, December 2010

Here's a Jeff press release:

High Dietary Fat, Cholesterol Linked to Increased Risk of Prostate Cancer, Thomas Jefferson University - Kimmel Cancer Center, December, 2010

The TRAMP mouse was used in this case because its cancer parallels human prostate cancer. The mice were fed diets similar to those above. Again, there were larger tumors that grew faster and metastasized more easily to the lungs:
"They found that the Western diet accelerated prostate tumor development and progression. These tumors also produced increased levels of receptors that bind to lipoprotein carriers of cholesterol, and they were more aggressive. The researchers further discovered that the TRAMP mice fed a Western diet appeared to experience greater incidence of cancer metastasis to the lungs, compared to the control group."
This was interesting ... In both studies, mice experienced a sudden drop in serum cholesterol after tumors formed, suggesting uptake and use of cholesterol by the tumor. Another hypothesis is an alteration of fat metabolism by the liver after cancer develops.

The leader of the team, Dr. Philippe Frank, said:
"Cells need cholesterol to produce androgen hormones, and androgen hormones promote prostate cancer growth,” he explains. “Perhaps more importantly, we also believe that tumors feed on cholesterol, and the more blood cholesterol is accessible, the more is available for tumor growth."
Photo of mice from January study. "Note the increased number of large and bulky tumors in the PyMT mouse fed a high cholesterol diet compared with the mouse fed a regular chow diet."


Frederick said...

"Cells need cholesterol to produce androgen hormones, and androgen hormones promote prostate cancer growth."

Only if the cancer is already established. Low testosterone levels are actually a significant risk factor for prostate cancer.

Frederick said...

Dihydrotestosterone May Not Affect Prostate Growth But May Reduce BMD:


"It has been noticed that the administration of estradiol both stimulates prostatic growth (Suzuki et al. 1994) and increases the incidence of prostatic carcinoma in rats (Shirai et al. 1994). Rats treated with DHT plus estradiol did not develop tumors (Shirai et al. 1994). In a 1.8-year open survey of 37 men aged 55–70 years treated with daily percutaneus DHT treatment, high plasma levels of DHT (> 8.5 nmol/l) effectively induced clinical benefits in andropausal symptoms, while slighly but significantly reducing prostatic size (de Lignieres 1993). It has been concluded in many studies that estrogens play an important role in the pathogenesis of BPH. Estradiol but not DHT acts in concert with SHBG to produce an 8-fold increase in intracellular cAMP in human BPH tissue, causing growth of the prostate, while DHT, which blocks the binding of estradiol to SHBG, completely negates the effect of estradiol (Nakhla et al. 1994)."

I don't think it is any coincidence that risk of prostate cancer climbs with age, and that older men also have higher levels of estrogens/lower levels of androgens. Today, especially in the western world, we are also exposed to more estrogenic substances than at any other point in history. Men are definitely not supposed to be maintaining levels of estradiol similar to those found in women and experiencing gynecomastia/proliferation of breast tissue.

DHT is often demonized, but in actuality, it is absolutely essential for male sexual development, virilization, libido, sperm count/motility, et cetera.

Bix said...

Good point about estrogenic substances and other endocrine disruptors. Men were never exposed to these substances, at these levels, historically.