Possible Dietary Causes of Cancer
In “What Does Eating Plants Do For Cancer? Part One” evidence for the positive correlation of the foods we eat with cancer was presented. The question that comes to mind is what mechanisms are driving this effect. Why is food so powerful both as a promotor of cancer and as a protection from it? The following summarizes current understanding about aspects of the food we eat that may be increasing our risk of cancer.
EXCESS BODY FAT AND HORMONES
According to the World Cancer Research Fund and the National Cancer Institute, there are twelve cancer types whose risk is increased by carrying excess body weight. These cancers are breast, ovarian, endometrial, prostate, colorectal, esophageal, stomach, kidney, liver, pancreatic, gall bladder and thyroid cancers (3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23). Why does the body respond so negatively to excess fat?
Fat cells can actually change their environment by releasing chemicals that alter nearby cells so substantially that they become cancerous. This happens by several different mechanisms. First of all, large collections of fat cells are a target for immune system cells who consider the fat cells a threat. This inflammatory response stimulates immune cells to release cytokines that can cause more rapid cell division and cell build-up and can ultimately result in the development and growth of cancer (1,2). Secondly fat cells release the hormone estrogen which can stimulate cells in the breasts and the uterus to divide uncontrollably resulting in cancer production. Additionally, excess fat makes cells resistant to insulin, causing the pancreas to create more insulin. A chronic high insulin level can increase body levels of growth factors which in turn increase cell division and promote the development of cancer (2).
Human beings ingest two types of iron – heme iron and non-heme iron. Non-heme iron is found in plant-based foods. Heme iron is derived only from animal foods and has, until recently, been thought of as superior to non-heme iron because it is absorbed more efficiently. However, it has been discovered that heme iron is associated with cancer (24). Heme iron can bring about the generation of cancer-causing free radicals such as unstable N-nitroso compounds (NOCs) that induce oxidation and inflammation, a common pathway contributing to cancer risk. It has been shown definitively that eating animal-based foods does increase NOC levels in the body while eating plant-based foods does not (25,26,27).
Of course, we all need iron in our bodies for good health, but iron is a double-edge sword. Too little iron means we cannot efficiently transport oxygen to our tissues; too much iron can increase the risk of heart disease and cancer. Unfortunately, humans have more of a problem with excess iron than with too little. The human body has no specific mechanism to get rid of excess iron, although it is interesting to note that removing blood from the body through regular blood donations has been shown to cut the risk of gastro-intestinal cancers in half (28). Humans do however have a means to prevent excess iron absorption…though it only works effectively on non-heme iron, the type found predominantly in plant foods. Through this mechanism, once you have enough iron in your blood, your body can effectively block further absorption of excess iron if it is of the non-heme type (29,51).
IGF-1 (Insulin-like Growth Factor-1)
IGF-1 is a growth hormone that controls the rate at which our cells increase and decrease in numbers and in size. When we are children IGF-1 levels are high to promote growth; levels go down as we become adults. We don’t want high levels of IGF-1 as adults because its message to cells to stay alive and keep growing and dividing can cause cancer to develop. Indeed, the more IGF-1 travelling in our bloodstreams, the higher our risk for cancer. IGF-1 seems to play a major role in transforming normal cells into cancer cells and then helping them to survive and proliferate and even to migrate through the body to grow new tumours (metastasize). (31,31,32,33)
Excess IGF-1 comes from eating animal protein. The more animal protein consumed, the higher the circulating IGF-1 in the bloodstream. Conversely, studies show that eating plant protein lowers IGF-1 levels (34,35). The less animal protein ingested the better. Only completely plant-based diets (no animal protein at all) show significantly lower blood IGF-1 levels and higher levels of a protein called IGF-Binding-Protein (IGFBP) that binds IGF-1 and limits its availability to the body (36,37,38). In one study, after only eleven days of eating no animal protein, IGF-1 levels dropped by 11% and levels of IGFBP increased by 50% (34). Tellingly, adding IGF-1 back into the diet of study subjects caused the beneficial effect on IGF-1 to completely disappear. A 2014 study followed 6000 American adults for eighteen years and found that those who ate the most animal protein had a 75% increased risk of death from all causes and a four-fold increase in cancer-related death. In those whose protein sources were plant-derived the increased risk of death from cancer was diminished or absent (39).
CARNITINE, CHOLINE AND TMAO
The relatively recent discovery of TMAO (trimethylamine-n-oxide) is an astounding illustration of the major role that the tiny bacteria in our digestive tract play in our health. This story begins with a couple of components found in our food; carnitine (an amino acid found in red meat) and choline (a similar molecule found in eggs, milk, liver, red meat, poultry and fish, including shell fish). Within 24 hours of consumption of either of these food constituents, certain gut bacteria metabolize them into a toxic substance called trimethylamine which then gets oxidized by the liver to TMAO. TMAO increases the build-up of cholesterol and inflammatory cells in atherosclerotic plaques within our arteries, making it a risk factor and a link between our gut microbes and cardiovascular and kidney disease. (40,41).
Further to this is another suspected consequence of TMAO production. The intake of animal-based foods is associated with the development of insulin resistance and gastrointestinal cancers and the research on the mechanism of this increased risk is pointing to the influence of TMAO (42,43). Further research is needed to provide more clear evidence that this is the case (45).
As individuals we do have some control over our production of this harmful molecule. Because our gut microbiota are greatly influenced by what we eat, the relative populations of our microbes rapidly respond to our particular diet (50). People who do not eat any animal protein do not produce any TMAO simply because their diet does not encourage the growth of the bacterial species that thrive on animal-based foods (45). Our bodies can produce all the carnitine we need for health, however we do need a source of choline. Plants contain ample choline for human requirements and, fortunately for us, because a plant-based diet selects for gut bacteria that do not produce TMAO, plant-based eaters need not worry about TMAO. (40)
Neu5Gc is a member of the sialic acid family, a diverse group of sugars that has been identified in the meat of mammals, especially that of carnivores. Neu5Gc is produced naturally by many mammals but not by humans due to a gene mutation that occurred about 2 or 3 million years ago during the evolution of human beings. Our closest relatives, the great apes including chimpanzees, gorillas, orangutans and bonobos, still produce Neu5Gc (45). Yet in spite of our inability to form Neu5Gc it can be found incorporated onto the surface of human cells. Where does it come from?
It appears that our Neu5Gc source is the meat, animal organs and dairy products that we eat (47). A problem arises when humans eat a source of Neu5Gc. Because our bodies do not recognize the molecule, we create antibodies against it. The resulting chronic inflammation encourages the formation of cancers and the onset of cardiovascular disease (48,49,29).
This is a huge topic, too large for one blog article. Stay tuned for “What Does Eating Plants Do For Cancer? Part Three”.
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