It has been known for some time that there is an apparent correlation between red meat consumption and cancer. As well as a correlation between dairy products and cancer (see references below).
Correlation Does not Imply Causation
But the word here is the research indicates correlation and correlation does not necessarily imply causation. As people who eat much red meat may also be prone to eat more processed meat and “junk” food in general.
The notion that protein is the source of this cancer correlation is also what has motivated some people to adhere to the recent fasting trends. For which intermittent fasting only allow protein intake for shorter periods of time and this lowers IGF-1 levels and thereby improves health and longevity.
A recent study “Dietary protein restriction inhibits tumor growth in human xenograft models” examines the direct relationship between different amounts of protein, the sources of protein, and certain intracellular signaling pathways (IGF, AKT, mTOR) important in apoptosis and hence cancer.
The researchers used mice as human xenograft cancer models (human tumors in mice). It is therefore contrary to the above research, not a population study that indicates correlations, but although done on mice, this type of study provides more compelling direct evidence for both correlation and causation. For both ethical and practical reasons as it is impossible to follow humans for an equal amount of time (mice live much shorter lives) mice are the perfect subjects.
The researchers found compelling evidence for inhibition of cancer growth with dietary protein reduction. A high protein diet did promote a growth of human tumors in mice, but what is perhaps even more interesting is the fact that they found indications that plant proteins partially inhibited prostate cancer growth independently of caloric or protein intake.
Protein is necessary for life and without it, we would certainly die. But in the western world today we certainly love our meat and the population share that develops prostate or breast cancer is relatively high compared to other parts of the world. According to the World Health Organization; “the WHO Regions for Europe and the Americas had the highest incidence of all types of cancer combined for both sexes”.
Those parts of the world where cancer incidence is the lowest they often eat a more traditional diet composed of less protein and more plant-based proteins. Such as the Okinawan diet in Japan which is strongly correlated with less cancer (see references).
So, what does this imply?
Well, it certainly would be a good idea to eat a little more plant-based protein (beans, lentils, hemp, soy etc.) and a little less meat. After all, these food items are not only healthy, they are also often more energy efficient than cattle farming and thereby reduces the stress on our shared planet.
Data from epidemiological and experimental studies suggest that dietary protein intake may play a role in inhibiting prostate and breast cancer by modulating the IGF/AKT/mTOR pathway. In this study, we investigated the effects of diets with different protein content or quality on prostate and breast cancer.
To test our hypothesis we assessed the inhibitory effect of protein diet restriction on prostate and breast cancer growth, serum PSA and IGF-1 concentrations, mTOR activity and epigenetic markers, by using human xenograft cancer models.
Our results showed a 70% inhibition of tumor growth in the castrate-resistant LuCaP23.1 prostate cancer model and a 56% inhibition in the WHIM16 breast cancer model fed with a 7% protein diet when compared to an isocaloric 21% protein diet. Inhibition of tumor growth correlated, in the LuCaP23.1 model, with decreased serum PSA and IGF-1 levels, down-regulation of mTORC1 activity, decreased cell proliferation as indicated by Ki67 staining, and reduction in epigenetic markers of prostate cancer progression, including the histone methyltransferase EZH2 and the associated histone mark H3K27me3. In addition, we observed that modifications of dietary protein quality, independently of protein quantity, decreased tumor growth. A diet containing 20% plant protein inhibited tumor weight by 37% as compared to a 20% animal dairy protein diet.
Our findings suggest that a reduction in dietary protein intake is highly effective in inhibiting tumor growth in human xenograft prostate and breast cancer models, possibly through the inhibition of the IGF/AKT/mTOR pathway and epigenetic modifications.
The results from our studies may have a rapid translation into the clinic. We envision that patients with recurrent PCa and BC could be offered diet modifications involving protein dietary content at different stages of their disease with appropriate monitoring. The absence of a differential effect in the AS and CR LuCaP23.1 models suggest that the androgen status does not affect the response of PCa to protein restriction. Furthermore, intratumor androgen receptor expression was not inhibited in the 7% protein diet group (data not shown). An ongoing clinical study in patients with newly diagnosed PCa will provide important information on the biological changes following this dietary intervention before prostatectomy.
In summary, a high-protein diet promoted the growth of human LuCaP23.1 and WHIM16 tumors in mice, and a reduction in protein intake resulted in a significant inhibition of tumor growth even when the diet was started after the formation of measurable tumors, possibly through inhibition of the IGF/Akt/mTOR pathway and epigenetic modifications. Moreover, our findings indicate that plant proteins partially inhibit prostate cancer growth independently of caloric or protein intake, suggesting that protein quality plays a key role in the progression of prostate and breast cancer. Clinical studies in patients with prostate and breast cancer are warranted to confirm the impact of dietary modifications in protein content and quality on tumor progression.
Oncotarget. 2013 Dec;4(12):2451-61. Dietary protein restriction inhibits tumor growth in human xenograft models.
Pubmed: Dietary protein restriction inhibits tumor growth in human xenograft models