A high intake of saturated fats, found mainly in foods of animal origin, stimulates the progression of prostate cancer cells.
We already know that replacing saturated fats with unsaturated fats (in particular monounsaturated and polyunsaturated omega-3 fatty acids) reduces the risk of cardiovascular disease and premature mortality. This protection is due to the opposite effect of these two types of dietary fat on LDL-cholesterol levels. It is an important risk factor for heart attack and stroke. While saturated fats increase the amount of LDL-cholesterol in the blood, unsaturated fats lower the levels of this form of cholesterol.
Saturated Fat: Rise in Cholesterol and Cancer
The majority of saturated fats come from foods of animal origin: meat, eggs, dairy products. While unsaturated fats are mainly found in plants: vegetable oils, nuts, certain seeds. A simple way to achieve a good balance between the intake of saturated and unsaturated fats is therefore to increase the dietary intake of plants and at the same time reduce the consumption of animal products.
The negative effect of saturated fat on health is not limited to an increase in LDL cholesterol levels. Several studies have shown that these fats also have a pro-inflammatory action. They would contribute to the development of certain serious pathologies such as insulin resistance or the progression of certain cancers in the form of metastases.
Stimulate or block the progression of prostate cancer
A link between saturated fat and cancer progression is also suggested by a recent study. Using a mouse model expressing the oncogene MYC and genetically predisposed to developing prostate cancer, these researchers observed that a diet enriched in saturated fat was associated with major changes in the metabolism of prostate cells. This led to the activation of several genes involved in tumor growth. Animals fed saturated fat had larger tumors than those fed a normal diet. Strongly suggesting that these genes activated by saturated fat are involved in the progression of prostate cancer.
Interestingly, this activation is reversible. Because a reduction in saturated fat intake cancels the increase in gene expression and abolishes tumor progression. A very important point of the study is that this genetic signature, associated with a high intake of saturated fat, is also observed in patients with prostate cancer. The researchers used data on the consumption of saturated fat acquired during epidemiological studies (Health Professionals Follow-up Study and the Physicians’ Health Study). They noted that patients with prostate cancer who had the greatest gene activation in their cancer were four times more likely to die from their disease.
However, this increase is not observed for unsaturated fatty acids (monounsaturated and polyunsaturated). This confirms that it is the genetic activation induced by saturated fats that is responsible for tumor progression.
At 40, 1/3 of men already have micro-tumors in the prostate
A decrease in dietary saturated fat intake may slow the progression of prostate cancer. But also reduce the risk of mortality associated with advanced forms of this disease. This is an important discovery. Because from the age of 40, a third of men already have microscopic tumors of the prostate. They are therefore at very high risk of developing cancer of this organ in the decades that follow.
Favor unsaturated fats of vegetable origin while limiting those of animal origin. This could therefore allow these prostatic microtumors to remain in a dormant state. This dietary orientation is a promising way to reduce the high incidence of prostate cancer. With the added bonus of better cardiovascular health!
Boren J et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur. Heart J. February 2020.
Labbé DP et al. High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program. Nat. Common. 2019; 10:4358.
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