Everyone knows that modern high-fat processed diet lead to obesity. Obesity is associated with several health issues, including cancer.

But since this fact is popular, even doctors, now prescribe low-fat diet. They force patients to get rid of even traditional fat-focused diet like Ghee.

At this juncture, it is important to know different dietary fat and their role in health and diseases.

Different Types of Dietary Fats

Fatty acids are long, straight-chain molecules categorized as:

1. Saturated : Animal far
2. Monosaturated
3. Polyunsaturated

Difference between them is their chemistry. Since our focus is cancer, we will consider only those fat types which affects cancer etiology upto some extent (In reality, there is no single cause for cancer. There are always multiple factors working together, causing cancer).

Omega-6 fat, Estrogen and Cancer

In 1982, National research council, USA, identified fats (Omega-6 fatty acids) as the single dietary component most strongly related to cancer risk. This report was based on studies that suggested correlations between fats consumption and incidence of GI, Prostate and breast cancers.

But these reports did not provide specific detail. Later it was realized from more studies that intake of omega-6 fatty acids may promote cancer progression partly by increasing the production of availability of estrogen. [1][2][3][4][5][6]

Estrogen is a growth factor for a number of cancers, including breast cancer. High-fat diets and associated increase in fat tissuecan increase estrogen by number of ways:

1. Fat tissue is a major source of estrogen production in postmenopausal women.
2. Obesity and insulin resistance can decrease the levels of sex hormone binding globulin in men and women and increase cancer risk. Decreased binding protein means more biologically active estrogen.
3. Obesity can alter estrogen metabolism in the liver
4. High-fat diet may reduce the amount of estrogen excreted through the feces.

If you have not read old post, we have covered here (http://prachodayat.in/fast-food-estrogen-storm/), how fast-food diet leads to high serum estrogen level. And as per this post, it plays critical role in cancer progression.

Make your teen kids aware about this and help them love their life. Stop being suicidal. Stop fast food, processed food and high-fat diet full of Omega-6 fat.

Solution is to replace Omega-6 fat by Omega-3 fat. In Indian context, it is desi cow ghee.

 

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References

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[1] Dwyer JT. Dietary fat and breast cancer: Testing interventions to reduce risks. In Exercise, calories, fat and cancer. Jacobs MM, ed. New York: Plenum Press, 1992.

[2]

Possible Mechanisms through which Dietary Lipids, Calorie Restriction, and Exercise Modulate Breast Cancer

Though the exact cause of breast cancer still remains a mystery, years of investigations have suggested that several dietary and endocrine-related factors may induce and/or could modulate the growth of breast cancer. Epidemiologic and experimental evidence have indicated a close association between high-fat diets and increased incidence of breast cancer.^1–3 Furthermore, several immunologic functions, including the levels of growth factors, cytokines, and sex steroid hormones, may be altered or regulated by dietary lipids.^4,5 Excessive fat in the diet has been reported to enhance the growth of both spontaneously occurring and chemically induced colon and mammary tumors, as well as accelerated growth of transplantable carcinomas.^6–8 Diets containing high levels of ω-6 fatty acids derived from vegetable fats appear to enhance tumorigenesis, while ω-3-containing lipids, either from vegetable or marine origin, or low levels of fat in the diet can diminish tumorigenesis. Recently, a number of mechanisms have been proposed to explain the modulation of mammary tumorigenesis in experimental animals by increasing the levels of dietary fats.^9,10 Initiation and promotion have been linked to immune suppression,¹¹ prostaglandin production,^12,13 free radical formation,¹⁴ membrane fluidity changes,¹⁵ intracellular transport system modulation,¹⁶ increased caloric utilization,¹⁷ increased mammotrophic hormone secretion,¹⁸and cytokine changes.^19,20 Over-expression of oncogenes and certain growth factors are other mechanisms that have been linked to dietary changes that may influence mammary tumori-genesis.

https://link.springer.com/chapter/10.1007%2F978-1-4684-7953-9_15

[3]

Meta-analysis: Dietary Fat Intake, Serum Estrogen Levels, and the Risk of Breast Cancer

Abstract

BACKGROUND: There is compelling evidence that estrogens influence breast cancer risk. Since the mid-1980s, dietary fat intervention studies have been conducted to investigate the effect of fat intake on endogenous estrogen levels. To further our understanding of the possible relationship between dietary fat and breast cancer, we conducted a meta-analysis of dietary fat intervention studies that investigated serum estradiol levels, and we reviewed the nature of the evidence provided by prospective analytic studies of fat consumption and breast cancer risk. METHODS: A computerized search of the English language literature on estrogen/estradiol and dietary fat intervention studies published from January 1966 through June 1998 was conducted using the MEDLINE® database. Pooled estimates were derived from the change in estradiol levels associated with fat reduction from 13 studies. Analyses were conducted separately for premenopausal and postmenopausal women and in both groups combined. RESULTS AND CONCLUSIONS: Statistically significant reductions in serum estradiol levels of − 7.4% (95% confidence interval [CI] = − 11.7% to −2.9%) among premenopausal women and − 23.0% (95% CI = −27.7% to −18.1%) among postmenopausal women were observed, with an overall −13.4% (95% CI = −16.6% to −10.1%) reduction observed. The greatest reductions occurred in two studies in which dietary fat was reduced to 10%-12% of calories compared with 18%-25% of calories in the other studies. A statistically significant reduction in estradiol levels of −6.6% (95% CI = −10.3% to −2.7%) remained after exclusion of these two studies. Review of prospective analytic epidemiologic studies that allowed for dietary measurement error suggests that the possibility that reducing fat consumption below 20% of calories will reduce breast cancer risk cannot be excluded. IMPLICATIONS: Dietary fat reduction can result in a lowering of serum estradiol levels and such dietary modification may still offer an approach to breast cancer prevention.

https://academic.oup.com/jnci/article/91/6/529/2549361

[4]

Western nutrition and the insulin resistance syndrome: a link to breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10099938

[5] https://www.ncbi.nlm.nih.gov/pubmed/8391818

[6]

Sex hormone-binding globulin, its membrane receptor, and breast cancer: a new approach to the modulation of estradiol action in neoplastic cells.

The role of human Sex Hormone-Binding Globulin (SHBG), the plasma carrier of sex steroids, and its membrane receptor, SHBG-R, in estrogen-dependent breast cancer has been investigated in our laboratory in the past few years. SHBG-R is expressed in MCF-10 A cells (not neoplastic mammary cells), MCF-7 cells (breast cancer, ER positive) and in tissue samples from patients affected with ER positive breast cancer, but not in estrogen-insensitive MDA-MB 231 cells. The SHBG/SHBG-R interaction, followed by the binding of estradiol to the complex protein/receptor, causes a significant increase of the intracellular levels of cAMP, but does not modify the amount of estradiol entering MCF-7 cells. The estradiol-induced proliferation of MCF-7 cells is inhibited by SHBG, through SHBG-R, cAMP and PKA. Similarly, the proliferation rate of tissue samples positive for SHBG-R was significantly lower than the proliferation rate of negative samples. SHBG and SHBG-R could thus trigger a ‘biologic’ anti-estrogenic pathway. In order to get a more detailed knowledge of this system, we first examined the frequence of the reported mutated form of SHBG in 255 breast cancer patients. The mutated SHBG is characterized by a point mutation (Asp 327 –> Asn) causing an additional N-glycosylation site, which does not affect the binding of steroids to SHBG. The frequence of the mutation was significantly higher (24.5%) in estrogen-dependent breast cancers than in healthy control subjects (11.6%). This observation confirms the close relationship between SHBG and estrogen-dependent breast cancer and suggests that the mutation could modify SHBG activity at cell site. Lastly, the possibility of using SHBG to modulate the estradiol action in breast cancer was further studied by transfecting MCF-7 cells with an expression vector carrying the SHBG cDNA (study in collaboration with G.L. Hammond). Transfected cells are able to produce significant amount of SHBG in their medium, but their SHBG-R is reduced to undetectable levels. The SHBG produced by transfected MCF-7 cells is, however, able to inhibit estradiol-induced proliferation of MCF-7 cells expressing a functional receptor. Thus, the local production of SHBG obtained with transfection could be a useful tool to control cell growth in estrogen-dependent breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10419027