Discuss the association of diet and cancer.
There are three major components of how a diet can influence cancer, obesity/caloric restriction,
hypermethylation of DNA and flavonoids and carotenoids. In this essay each topic will be discussed,
and evidence provided for how they are linked to the development and progression of cancer.
Obesity/Caloric restriction
Obesity has been linked to hormonal cancers such as, prostate, breast, and endometrial cancers, and
has been highly implicated in post-menopausal women developing breast cancer. In Pre-menopausal
women oestrogens are mainly synthesised in the ovaries however, post-menopausal women
synthesise most of their oestrogens via peripheral site synthesis, and in obese women this occurs in
the adipose tissue (Cleary and Grossmann, 2009). Excessive caloric intake and weight gain can lead
to hyperinsulinemia due to insulin resistance and increased production. Insulin-like growth factors
(IGF) are mitogens which control energy-dependent growth processes (Calle and Thun, 2004). IGF-1
inhibits apoptosis and stimulates cell proliferation. Leverrier et al (1999) carried out a study which
concluded that IGF-1 inhibited intrinsic apoptosis via Bcl-x inhibition and early caspase inhibition.
Another element to obesity and cancer is the recovery. The high incidence of co-morbidities in obese
patients adds further risk of complication and higher risk of mortality, alongside impaired wound
healing. In a review written by Arnold et al (2016), it was discussed how modern technology has
improved the detection of cancers and the therapies available are more effective, yet the
physiological impact of obesity is adding to the mortality rates of cancers and, how better guidance
was needed for obese patient recovery to reduce the impact of the co-morbidities.
On the other hand, caloric restriction has been shown to reduce the incidence of cancer occurrence.
A prime example of this is the Okinawa diet. Inhabitants Okinawa have been researched for their
low-calorie diet and high life expectancy. However, a recent study (Tamaki et al, 2014)
demonstrated the impacts of post-world war II US military occupancy caused westernisation of the
community and the diets. The researchers discussed how a rise in breast cancer incidence in the
female population of Okinawa was linked to an increase in BMI. They found that underweight, pre-
menopausal women had a statistically significant reduction in odds ration (used to determine the
effect of BMI on breast cancer development risk) whereas being overweight or obese resulted in a
statistically significant increase in odds ratio and therefore an increased risk of breast cancer.
Interestingly, a caloric restriction, in severe cases anorexia nervosa, has been shown to reduce the
incidence of cancer however, a study carried out by Bens et al (2018) investigated breast cancer in
women with a history of anorexia nervosa (n= 22,654) and those without (n= 224,619). They found
that the women with a history of anorexia nervosa had a worse survival rate (2.2-fold significantly
increased) than those without. The cause of this is still unknown yet there are many contributing
factors.
DNA hypermethylation
DNA hypermethylation is a hallmark of most cancers. When CpG islands in the promoter regions of
DNA are hypermethylated a silencing mechanism occurs. Tsuruta et al (2011) investigated micro-
RNA silencing due to hypermethylation and the impacts in endometrial cancer. They found that CpG
island hypermethylation caused a downregulation of miR-152 expression which they thought may
contribute to the tumorigenesis and the activation of oncogenic pathways in endometrial cancer.
There are three major components of how a diet can influence cancer, obesity/caloric restriction,
hypermethylation of DNA and flavonoids and carotenoids. In this essay each topic will be discussed,
and evidence provided for how they are linked to the development and progression of cancer.
Obesity/Caloric restriction
Obesity has been linked to hormonal cancers such as, prostate, breast, and endometrial cancers, and
has been highly implicated in post-menopausal women developing breast cancer. In Pre-menopausal
women oestrogens are mainly synthesised in the ovaries however, post-menopausal women
synthesise most of their oestrogens via peripheral site synthesis, and in obese women this occurs in
the adipose tissue (Cleary and Grossmann, 2009). Excessive caloric intake and weight gain can lead
to hyperinsulinemia due to insulin resistance and increased production. Insulin-like growth factors
(IGF) are mitogens which control energy-dependent growth processes (Calle and Thun, 2004). IGF-1
inhibits apoptosis and stimulates cell proliferation. Leverrier et al (1999) carried out a study which
concluded that IGF-1 inhibited intrinsic apoptosis via Bcl-x inhibition and early caspase inhibition.
Another element to obesity and cancer is the recovery. The high incidence of co-morbidities in obese
patients adds further risk of complication and higher risk of mortality, alongside impaired wound
healing. In a review written by Arnold et al (2016), it was discussed how modern technology has
improved the detection of cancers and the therapies available are more effective, yet the
physiological impact of obesity is adding to the mortality rates of cancers and, how better guidance
was needed for obese patient recovery to reduce the impact of the co-morbidities.
On the other hand, caloric restriction has been shown to reduce the incidence of cancer occurrence.
A prime example of this is the Okinawa diet. Inhabitants Okinawa have been researched for their
low-calorie diet and high life expectancy. However, a recent study (Tamaki et al, 2014)
demonstrated the impacts of post-world war II US military occupancy caused westernisation of the
community and the diets. The researchers discussed how a rise in breast cancer incidence in the
female population of Okinawa was linked to an increase in BMI. They found that underweight, pre-
menopausal women had a statistically significant reduction in odds ration (used to determine the
effect of BMI on breast cancer development risk) whereas being overweight or obese resulted in a
statistically significant increase in odds ratio and therefore an increased risk of breast cancer.
Interestingly, a caloric restriction, in severe cases anorexia nervosa, has been shown to reduce the
incidence of cancer however, a study carried out by Bens et al (2018) investigated breast cancer in
women with a history of anorexia nervosa (n= 22,654) and those without (n= 224,619). They found
that the women with a history of anorexia nervosa had a worse survival rate (2.2-fold significantly
increased) than those without. The cause of this is still unknown yet there are many contributing
factors.
DNA hypermethylation
DNA hypermethylation is a hallmark of most cancers. When CpG islands in the promoter regions of
DNA are hypermethylated a silencing mechanism occurs. Tsuruta et al (2011) investigated micro-
RNA silencing due to hypermethylation and the impacts in endometrial cancer. They found that CpG
island hypermethylation caused a downregulation of miR-152 expression which they thought may
contribute to the tumorigenesis and the activation of oncogenic pathways in endometrial cancer.
