Gabor Szendi:
Why You shouldn't follow Angelina Jolie's example?

Angelina Jolie, together with millions of other women, has been mislead by the statement that BRCA gene mutations inevitably cause breast cancer. It is proven that by appropriate lifestyle changes the risk of breast cancer can be reduced to virtually zero even in the high-risk group of BRCA mutation carriers.

 

 

Angelina Jolie's double mastectomy and removed ovaries again brought the question of breast cancer prevention to the center of attention, especially in regard to those carrying a BRCA1 or BRCA2 mutation. The barbaric practice of these preventive surgeries is a sign of the defeatist attitude of Western medicine. The actress's case once again gives rise to the question of why are the findings of the extensive ongoing research, revealing that breast cancer is preventable, or at worst its risk is greatly reducible, kept confidential, so to speak. All women living the typical Western lifestyle, which means constant vitamin D deficiency and inordinate consumption of refined carbohydrates, have a notable risk of developing breast cancer during their lifetime. These non-specific risk factors can be eluded and the risk of breast cancer reduced to near zero by switching to the paleo diet and by ensuring a blood vitamin D level that is at least twice the current recommendation in the U.S.

People carrying a breast cancer predisposing gene mutation have a highly increased risk of this disease.

In this article, I will briefly review the results of research revealing that BRCA1 and BRCA2 gene mutations alone do not bear significant cancer risks-they only do so in the context of the typical Western lifestyle.

The research of the BRCA1 and BRCA2 tumor suppressor genes has gone a long way since their first description in 1994-95. It is apparent by now that these genes are vulnerable, and almost every race and region has its own specific mutations of them, of which more than 300 are of the cancer predisposing kind [1]. Since the so-called founding mutations in different ethnic groups are believed to be thousands of years old, it is reasonable to assume that these mutations have been with us all along our history and been present even earlier in the other mammalians as there exists a mouse model for BRCA1- and BRCA2-mutation-related cancer [2], and the mutation of these two genes can cause breast cancer in dogs [3].

From the fact that cancer, including breast cancer, was virtually non-existent among ancient hunter-gatherers and still is within modern tribes of the like [4], arises the question of why BRCA1 and BRCA2 mutations did not and do not cause cancer in these people. Back in the 1800's, when refined flour and sugar had not yet engulfed the Western world, cancer was surprisingly rare, and those having cancer lived long without treatment. The average survival time of people with metastatic breast cancer was 4 years, and some lived for up to 18 years [5].

The graph below shows the trend of breast cancer mortality in Sweden during the 20th century.

(Source: [6])

 

Vitamin D and Breast Cancer

The connection between vitamin D deficiency and different types of cancer, especially breast, colon, and prostate cancer, can now be considered proven [7]. In a 12 years follow-up study subjects having a vitamin D level above 25 ng/ml had 72% lower mortality from breast cancer than those with a level below that figure, as indicated by the graph below [8].

(Source: [8])

 

Initially, it appeared that vitamin D, which can, in case of sufficiently high blood levels, reduce the risk of breast cancer by up to 60-70%, is ineffective if a deleterious mutation of the BRCA1 tumor suppressor gene is present [9]. But a 2013 study conducted by David Grotsky et al. revealed that there is an alternate way in which vitamin D is capable of inhibiting tumor growth even in the presence of a BRCA1 mutation. There is a protein known as tumor suppressor p53-binding protein 1 (p53BP1) that is able to keep cell proliferation and differentiation under control even if the BRCA1 gene has lost its regulating function. Cancer cells inhibit this compensatory mechanism by inducing accumulation of a protein called Cathepsin L, which hinders the production of p53BP1. Grotsky's team has shown that in the presence of vitamin D p53BP1 production is restored, which, on one hand, reduces the risk of cancer associated with BRCA1 mutations and, on the other, improves the effect of chemotherapy in triple negative cancer [10]. The finding that the absence or inadequate presence of p53BP1 is associated with an increased risk of developing metastasis once more underlines the importance of vitamin D not only in the prevention but also in the treatment of cancer [11]. It has thus been proven that a sufficiently high (70-100 ng/ml) blood vitamin D level can provide significant protection against breast cancer even in the presence of a BRCA1 mutation and can play a critical role in cancer recovery as well.

BRCA Mutations and Increasingly Earlier Age of Cancer Onset

In the case of breast cancer, as with many other types of cancer, obesity, high blood sugar, insulin resistance, hyperinsulinemia, and high levels of whole-body inflammation are of the foremost risk factors (summarized by Szendi in 2011).

But of course, these risk factors cannot be mechanically applied to people with a BRCA mutation. If we are to phrase cancer prevention recommendations for those carrying a BRCA mutation, we have to examine this specific group of people and find out whether factors generally found protective in breast cancer are also so in their case. We have already looked at the protective effect of vitamin D.

The fact that lifestyle factors affect the penetrance (proportion of carriers with clinical symptoms) of BRCA mutations has been unequivocally proven by studies that compared different age groups in terms of age of breast cancer onset. These studies revealed that in the 20th century the later a BRCA mutation carrier was born, the younger the age of them developing breast cancer was. In a 15 years study a noticable shift in the age of breast cancer onset was observed among BRCA mutation carriers even during this short time period [12].

(Source: [12])

 

As can be seen from the graph above, the average age of breast cancer onset did not change within the 15 years of the study among non-carriers, while in the case of BRCA1 and BRCA2 mutation carriers it decreased by about 11 and 5 years respectively.

Litton et al. compared the parent and child generations in BRCA mutation carrier families. They found that while in the parent generations breast cancer developed at a median age of 48 years, it manifested 6 years earlier in the child generations. A negative relationship was also found between the time of birth and the age of breast cancer diagnosis: subjects born between 1970-80 were diagnosed positive 10.5 years earlier in the parent generations and 21.5 years earlier in the child generations as compared to those born between 1930-39 [13]. The results of the study are summarized below.

(Source: [13]

According to a study by Narod et al., BRCA mutation carriers born before 1930 were diagnosed with breast cancer at an average age 14 years older than carriers born after that year [14], as is shown below.

(Source: [14])

 

The above graph also reveals that at the age of 45 people of the first group had a 20% prevalence of breast cancer, while in the second group this number reached 65% at the same age. Thus, it has been confirmed by numerous studies that what we are dealing with is a generation-related phenomenon, i.e. the younger a BRCA mutation carrier is, the earlier they are likely to develop breast cancer [15].

This clearly implies that the adverse lifestyle changes brought by the 20th century-rapid urbanization and the escalating epidemic of obesity resulting from the ever-increasing consumption of refined carbohydrates-significantly augment the carcinogenic effect of BRCA mutations.

BRCA Mutations and Diet

Focusing on the consequences of lifestyle changes solely from the aspect of BRCA mutation carriers, the first study worth looking at is one conducted by King et al. on Ashkenazi Jewish women. The dangerous mutations of the BRCA1 and BRCA2 genes are quite common among these women with a prevalence of 1-2% [16]. According to the study, subjects born during times of limited food supply and thus consuming less calories and being slimmer in their younger years developed breast cancer at a relatively older age. The same was true for those who were involved in intense sports as a teenager. These can be seen in the graphs below.

(Source: [16])

 

In 2006 Nkondjock et al. studied BRCA1 and BRCA2 mutation carriers with respect to physical activity and energy consumption and found that the upper third of them in terms of energy consumption had a 2.76 times greater risk of breast cancer than the lower third. This number was 4.46 among subjects who became overweight or obese after the age of 18 and 4.11 among those who gained extra weight after 30 [17].

Others also found connection between excess weight gain and cancer risk. People weighing above 160 pounds were shown to have a 2.1 times higher risk of breast cancer than those below that body weight [18].

In a 2005 study Kotsopoulos et al. found a 34% reduction in breast cancer risk among BRCA mutation carriers who lost at least 10 pounds between the age of 18 and 30 [19].

During the 20th century an increasing proportion of people in Western countries became overweight or obese. Cancer statistics revealed that this increase in weight was accompanied by a parallel growth in the prevalence of different types of cancer. Based on these facts, BRCA mutation-carrying women, who are at an increased risk of breast cancer, can significantly cut their risk by living a physically active life and reducing their intake of calories. Moreover, the risk can be further mitigated by maintaining a sufficiently high vitamin D blood level.

Angelina Jolie was duped by her doctors when they painted a picture of her situation as if breast and ovarian cancer were almost inevitable fate for her. This does not have to happen to you! Now we know many things about the causes and prevention of breast cancer and the risks of conventional diagnostic methods and treatment. You can read more about these in my other articles on this website.

 

References

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2. Evers B, Jonkers J. Mouse models of BRCA1 and BRCA2 deficiency: past lessons, current understanding and future prospects. Oncogene. 2006 Sep 25;25(43):5885-97.

3. Rivera P, Melin M, Biagi T, Fall T, Häggström J, Lindblad-Toh K, von Euler H. Mammary tumor development in dogs is associated with BRCA1 and BRCA2. Cancer Res. 2009 Nov 15;69(22):8770-4.

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8. Garland, CF; Gorham, ED; Mohr, SB; Garland, FC: Vitamin D for cancer prevention: global perspective. Ann Epidemiol, 2009, 19(7):468-83.

9. Campbell MJ, Gombart AF, Kwok SH, Park S, Koeffler HP (2000) The anti-proliferative effects of 1alpha, 25(OH)2D3 on breast and prostate cancer cells are associated with induction of BRCA1 gene expression. Oncogene 19:5091-5097

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19. Kotsopoulos J, Olopado OI, Ghadirian P, Lubinski J, Lynch HT, Isaacs C, Weber B, Kim-Sing C, Ainsworth P, Foulkes WD, Eisen A, Sun P, Narod SA. Changes in body weight and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Breast Cancer Res. 2005;7(5):R833-43.