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Rachel Cohen

The Effects of Protein on Cancer

Cancer is the second highest leading cause of death among adult men and women in

the United States. It is estimated that 1,600 people die of cancer each day, or on average, one

death every 60 seconds. Moreover, the probability of developing an invasive tumor is 38% for

women and 45% for men (1). Cancer is attributed to the unregulated proliferation of cells.

Cancer cells do not respond appropriately to signals that control normal cell behavior and as a

result, grow and divide uncontrollably. Eventually, the cancer cells can invade normal tissues

and organs and spread throughout the body (2). There is a vast amount of ongoing research

focusing on both the etiology of various cancers as well as potential treatments.

Epidemiological and experimental data suggest that nutrition plays a significant role in

preventing disease and promoting health. For nearly a century, studies have focused on the

effects of food intake reduction – known as calorie restriction. In a study conducted by McCay

and colleagues (1935), the authors suggest that food restriction without malnutrition increases

the average and maximal lifespan in rats (3). Subsequent research has consistently shown

similar results in yeasts, fruit flies, nematode worms, fish, hamsters, and in a wide variety of

mice and rat strains. Among these various species, it has been demonstrated that restricting

food intake without malnutrition slows aging, and results in increased lifespan. Moreover, both

the earlier onset of calorie restriction and the degree of restriction are important factors

associated with the lifespan extension (4).

Although experiments in calorie restriction among rodents and other species produce

health benefits, the impacts are dependent on other variables such as sex and type of low

calorie diet, and do not consistently translate into “longer-lived mammals” (5). For example, in

the 1980s, two longitudinal studies on non-human primates were conducted independently.

Both studies support the finding that “calorie restriction delays the onset of age-associated

diseases” (5). It should be noted that in one of the studies, the monkeys fed ad libitum did not

live longer than the monkeys in the control group, but they did display a delayed onset of age-

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related diseases. While this appears to contradict the results from the second study where the

monkeys fed a low-calorie diet lived longer than the monkeys fed ad libitum, the difference in

lifespan could be a result of differences between the diets (5). For example, the quality of

carbohydrate differed between the two studies whereby the monkeys in the first study received

significantly less sucrose in their diets than those in the second. Further, the diets for the

monkeys in the first study were considered diets rich in natural ingredients mostly derived from

plants while the diet from the second study contained semi-purified food and protein derived

from lactalbumin rather than plant sources. These differences could account for the inconsistent

results between the two studies thereby supporting the theory that the type of low calorie diet is

significant in its potential health impacts (5).

Recent studies have expanded their scope to examine the specific reduction in dietary

components such as proteins and suggest that the health benefits of calorie restriction might be

due to reducing protein intake specifically as opposed to total calorie consumption. A cross-

sectional study conducted by Levine et. al measured the effects of a low protein diet on middle-

age and older individuals. Data was collected from NHANES III on 6,381 adults over the age of

50. The subjects were categorized into three groups – high protein, moderate protein, and low

protein – depending on the percent of their calorie intake from protein. For the high protein

group, 20% or more of calories was from protein; for the moderate protein group, 10%-19% of

calories were from protein; and for the low protein group, less than 10% of calories were from

protein. These groups were further classified based on two age groups: 50-65 (middle-age) and

66+ (older population). Based on the results, researchers concluded that the middle-age group,

which consumed a high protein diet, was at a 74% increased risk of mortality. This group was

also four times more likely to die of cancer when compared to the low protein group (6).

Further analysis of protein consumption among the subjects revealed an association

between animal protein and mortality. It showed that when the calories were derived from plant-

based protein, there was a significant reduction, or even elimination, of death due to cancer. In

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contrast, diets high in animal protein showed an association between increased cancer-based

mortality. This study should not be interpreted such that plant-based protein diet has a

protective effect; rather, animal protein diets have a negative effect. (6)

Association between protein intake and mortality

The graph shows a correlation between low protein and protection against all-cause and cancer
mortality prior to age 66. Beyond age 66, low-protein becomes detrimental. The graphs also indicate
that no correlation between protein intake level and cardiovascular disease or diabetes mortality (6).

Levine et. al looked at the IGF-1 levels in the available 2,253 subjects to determine its

effect on associations between protein and mortality (6). IGF-1 is an activator of mTORC, and

mTORC regulates protein synthesis. Evidence suggests that deregulation of protein synthesis,

and thus of mTORC and IGF-1, is linked to human diseases including tumor growth and cancer.

One mechanism by which mTORC promotes protein synthesis is by negatively regulating

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autophagy (protein breakdown), which is important for recycling damaged organelles (7). When

mTORC is activated, autophagy is inhibited and cell proliferation is promoted. The exact

mechanism by which autophagy affects cancer is unclear, but studies show that it can act as

“both a tumor suppressor and a protector of cancer cell survival” (7).

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articles/83536-mtor-pathway-protein-synthesis.html

mTOR is regulated by growth factors including IGF-1, insulin, nutrients including


leucine, lysine, and arginine, as well as by cellular stress. When mTOR is activated,
protein synthesis is initiated and cell proliferation is promoted (7, 8)

The results of Levine et. al’s study revealed that “for every 10 ng/ml increase in IGF-1,

the mortality risk of cancer among subjects ages 50-65 increases for the high protein versus the

low protein group by an additional 9%.” However, when the older subjects’ IGF-1 levels were

examined, subjects with high or moderate protein diets had reduced risk of cardiovascular

disease mortality when IGF-1 was low, but no benefits were linked to increased IGF-1 (6).

Levine et. al expanded upon their previous research by conducting a mouse study that

examined a range of protein intake (4%-18%) and the correlation to levels of circulating IGF-1,

cancer incidence, and cancer progression. In the study, 18-week-old male mice were fed for 39

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days on either a high or low protein diet; calorie intake for the respective mice remained

consistent for the duration of the experiment. Both groups of mice were implanted with

melanoma cells. After 22 days, the mice consuming the high protein diet had a 100% tumor

prevalence compared to an 80% tumor rate in the low protein group. Further, after 39 days, the

mean tumor size was 78% larger in the high protein group. The researchers also found that

IGF-1 levels were 35% lower in the low protein group. An additional trial was conducted using

female mice fed the same dietary regimen as the male mice and implanted with murine breast

cancer cells. After 18 days, there was a 100% incidence of tumor growth in the high protein

group and 70% in the low protein group. Additionally, the tumors in the low protein group were

45% smaller and IGF-1 levels 30% lower. The results of this data suggest a correlation between

a lower protein intake and a decrease in cancer incidence and/or progression due to decreased

IGF-1 levels (6).

Taken together, the above results suggest that a low protein, primarily plant-based diet

can help regulate IGF-1 levels and help prevent cancer. Additionally, human and animal studies

suggest that consuming a low protein, primarily plant-based diet during middle age can help

prevent cancer, reduce overall mortality rate, and reduce the probability of diabetes by

regulating IGF-1 and insulin levels. However, once people reach the age of 65-70, they should

increase protein consumption to ensure adequate weight and prevent fragility (6).

An epidemiological study from 2006 looking at the correlation between a “modern

lifestyle and cancer” (9) further suggests that both decreased calorie and protein intake can lead

to preventative health benefits. “Modern lifestyle” is defined as a high-protein, high-calorie diet

and low physical activity. The study included three groups of middle-aged men and women:

group one participants were all vegetarians who, for the purpose of the study, altered their diets

by consuming only uncooked and unprocessed plant-based food; the second group consisted of

endurance runners consuming a low-calorie and low non-plant based calorie diet; the third

group, the control group, consisted of healthy, non-obese participants eating a Western diet.

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Certain biomarkers were measured at the start of the study, including IGF-1 levels. It is

important to note that medical evaluations of the participants revealed that all were non-smokers

and there was no evidence of chronic or autoimmune diseases, cancer, or diabetes (9).

After participating in the study for seven days, the participants in the low-protein, low-

calorie diet group had lower IGF-1 levels than those in the Western diet group. Furthermore,

there was no significant difference between the IGF-1 levels in the endurance running group

and the Western diet group. Data from the study also showed an association between

participating in regular endurance exercise training and a decrease in plasma factors such as

insulin and inflammatory markers that are linked to certain types of cancer. The results of the

study suggest that dietary factors, including plant-based low-protein diets, may provide

additional protective health effects (9).

Another
http://ajcn.nutrition.org/content/84/6/1456.long
approach to

examining the effects of plant-based protein on cancer is by comparing cancer rates and diets

between Western and Asian countries. Research suggests that one explanation for variation in

cancer rates across nations is due to diet. For example, Asian countries such as China, Japan,

and Korea, where soybean intake is exponentially higher compared to Western countries, have

lower rates of breast, colon, and prostate cancer (10). More specifically, breast cancer incidence

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among women in China and other Asian countries are almost seven times lower than in

American women. Further, there is a higher incidence of breast cancer in Asian women who

immigrated to the United State compared to women residing in Asian countries. This suggests

risk factors might be related to environmental and dietary factors and not just genetic factors

(11).

A population-based case-control study of breast cancer among Chinese, Japanese, and

Filipino-American women living in several cities in California, showed that intake of soybean

products was more than twice as high among Asian-American women born in Asia compared to

those born in the United States (12). Intake of tofu – a soy-based product – among immigrants

decreased in subsequent years after living in America. Further, breast cancer risk decreased as

consumption of tofu increased (12).

Soybeans contain all of the essential amino acids and are therefore a complete source

of protein. They are an isoflavone genistein - plant derived compound - with a high protein to

carbohydrate ratio (13). They are strong antioxidants (14) and have anti-cancer properties (10).

Genistein is found to have estrogenic properties; this is significant because high levels of

estrogen are linked to breast cancer (11). Estrogen synthesized in the body can impact gene

regulation by activating estrogen receptors in various cell types. E2, found in high levels in

malignant tumors, is structurally similar to genistein in that it has estrogenic properties;

therefore, genistein competes with E2 for binding to estrogen receptors (11). In theory,

competition for the receptors between E2 and genistein reduces the amount of estrogen.

Table 2 (see Appendix A) outlines findings from a series of 26 animal studies looking at

the correlation between dietary isoflavone-containing soy intake and breast cancer incidence

and prognosis (10). In each study, carcinogenesis was initiated and the animals were fed soy or

soybean isoflavones. Of all 26 studies, 65% reported “protective effects” (10) and no study

indicated increased tumor development. Further, results suggest that isoflavones have positive

health effects in breast cells. Eight of the studies listed involve soybean products and

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experimental mammary cancer of which four showed that soy inhibited carcinogenesis. Only

one study showed a decrease in tumor prevalence, and the other studies showed no effect.

Despite these observations, there is insufficient evidence to conclude that soy reduces cancer

risk due to discrepancies in research (10).

While several studies have begun to examine potential causes of cancer as well as

possible treatments, there remains a critical need for additional research. Diet, undoubtedly,

reveals itself as a protective or preventative factor against cancer. Current research suggests a

correlation between high-protein diets and increased risk of cancer. Furthermore, certain studies

suggest that animal-based protein increases the risk of cancer. Additional longitudinal

experiments as well as more global studies that compare the dietary practices of different

countries over time should be conducted to verify these claims.

References

1. Siegel R, Naishdham D, Jemal A. Cancer Statistics, 2013. CA: A Cancer Journal for
Clinicians [Internet]. 2013; Available from:
http://onlinelibrary.wiley.com/doi/10.3322/caac.21166/full

2. Cooper GM. The Development and Causes of Cancer [Internet]. The Cell: A Molecular
Approach. 2nd edition. U.S. National Library of Medicine; 1970 [cited 2017Nov10]. Available
from: https://www.ncbi.nlm.nih.gov/books/NBK9963/

3. McCay CM, Crowell MF, Maynard LA. The effect of retarded growth upon the length of life
span and upon the ultimate body size. 1935. Nutrition . 1989;5:155–71.

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4. Rizza W, Veronese N, Fontana L. What are the roles of calorie restriction and diet quality in
promoting healthy longevity? Ageing Research Reviews . 2013;13:38–45.

5. Solon-Biet SN, Mitchell SJ, de Cabo R, Raubenheimer D, Le Couteur DG, Simpson SJ.
Macronutrients and Caloric Intake in Health and Longevity. Journal of Endocrinology
[Internet]. 2015;226:17–28. Available from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490104/#__ffn_sectitle

6. Levine MA, Suarez JA, Brandhorst S, Balasubramanian P, Cheng C-WC, Madia F, Fontana,
L, Mirisola MG, Guevara-Aguirre J, Wan J, et al. Low Protein Intake Is Associated with a
Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not
Older Population. Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer,
and Overall Mortality in the 65 and Younger but Not Older Population. 2014;19:407–17.

7. Laplante M, Sabatini DM. mTOR signaling in growth control and disease [Internet]. Cell.
U.S. National Library of Medicine; 2012 [cited 2017Nov1]. Available from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331679/

8. mTor Pathway and Protein Synthesis [Internet]. MuscleChemistrycom Bodybuildings Best


Online Community Gear Cycles Training Discussion RSS. [cited 2017Nov8]. Available from:
http://www.musclechemistry.com/upload/bodybuilding-steroid-and-training-articles/83536-
mtor-pathway-protein-synthesis.html

9. Fontana L, Klein and S. Luigi Fontana [Internet]. The American Journal of Clinical Nutrition.
2006 [cited 2017Nov10]. Available from: http://ajcn.nutrition.org/content/84/6/1456.long

10. Messina MJ, Persky V, Setchell KDR, BarnesN S. Soy intake and cancer risk: A review of
the in vitro and in vivo data. Nutrition and Cancer [Internet]. 1994;21. Available from:
http://www.tandfonline.com/loi/hnuc20

11. He F-J, Chen J-Q. Consumption of soybean, soy foods, soy isoflavones and breast cancer
incidence: Differences between Chinese women and women in Western countries and
possible mechanisms [Internet]. Food Science and Human Wellness. Elsevier; 2013 [cited
2017Nov10]. Available from:
http://www.sciencedirect.com/science/article/pii/S2213453013000438

12. Wu AH, Ziegler RG, Horn-Ross PL, Nomura AM, West DW, Kolone LN, Rosenthal JF,
Hoover RN, Pike MC. Tofu and risk of breast cancer in Asian-Americans. [Internet]. Cancer
Epidemiology, Biomarkers & Prevention. American Association for Cancer Research; 1996
[cited 2017Nov10]. Available from: http://cebp.aacrjournals.org/content/5/11/901.long

13. Soybean Nutritional Information [Internet]. Soyconnection. 2017 [cited 2017Nov10].


Available from: http://www.soyconnection.com/soy-foods/nutritional-composition

14. Wei H, Saladi R, Lu Y, Wang Y, Palep SR, Moore J, Phelps R, Shyong E, Lebwohl MG.
Isoflavone Genistein: Photoprotection and Clinical Implications in Dermatology [Internet].
The Journal of Nutrition. 2003 [cited 2017Nov10]. Available from:
http://jn.nutrition.org/content/133/11/3811S.full.pdf html

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Appendix A
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Appendix A

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