Role of Nutrition in Cervical Cancer Prevention

In the United States, cervical cancer is the third most common gynecologic cancer. Squamous cell carcinoma (60 per cent of cases), adenocarcinoma (25 per cent), and various histologies are among the subtypes of cervical cancer (6 per cent). The human papillomavirus (HPV) is the cause of aberrant cell alterations that contribute to cancer formation, and HPV is found in 99.7% of cervical malignancies. Cervical cancer is frequently symptomless. Abnormal vaginal discharge, irregular bleeding, and bleeding after intercourse are the most prevalent symptoms. Advanced disease can also induce bowel or urinary cancer symptoms, as well as pain in the lower back and pelvis that radiates into the posterior legs.

Risk factors for cervical cancer, in addition to HPV infection, include:

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Age: Women under the age of 20 had the lowest incidence, while women aged 45 to 49 had the highest.

Obesity: Obesity and the risk of cervical cancer were shown to have a weak but significant link in a meta-analysis published in 2016.

Sexual activity: Early sexual intercourse, a history of multiple sexual partners (or a partner with multiple partners), a history of sexually transmitted disease, a sexual relationship with someone who has been exposed to HPV, and intercourse with an uncircumcised man are all linked to a higher risk of HPV infection.

Smoking: In those with a high-risk HPV infection, smoking raises the chance of infection with the virus as well as the risk of cancer.

Pregnancy history. Women under the age of 20 when they have their first child, as well as those who have had three or more full-term pregnancies, are at a higher risk.

Oral contraceptives: With the use of oral contraceptives for a longer period, the risk of adenocarcinoma rises.

Immunosuppression: HPV infections are more common in women who have been infected with the human immunodeficiency virus (HIV), which weakens the immune system.

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Anti-Cancer Diet: Nutritional Considerations are listed below.

Dietary variables may impact cervical cancer risk, according to epidemiological research. The suppressive impact of some micronutrients on HPV infection, notably carotenoids (both vitamin A and non-vitamin A precursors), folate, and vitamins C and E, may account for part of the dietary effect. Reduced risk has been linked to the following factors:

• Fruits and vegetables are healthy choices. In women with a high HPV virus load, poor consumption of fruits and vegetables is linked to a three-fold increased risk of cervical intraepithelial neoplasia (CIN) classes 2 and 3. Low blood levels of elements found in fruits and vegetables (such as vitamin A and lycopene) were linked to a higher risk of CIN class 3. Other carotenoids, such as alpha-carotene, beta-cryptoxanthin, lutein/zeaxanthin, and lycopene, as well as gamma-tocopherol, have been linked to a lower risk of high-grade CIN. These nutrients may help remove high-risk HPV infections, but they aren't linked to the elimination of persistent infections.
• B vitamins, such as folic acid. Cervical cancer risk appears to be influenced by interactions between folate status, mutations in the folate-dependent enzyme methylene-tetrahydrofolate reductase (MTHFR), plasma homocysteine, and HPV. Women with greater plasma folate concentrations were less likely to be diagnosed with CIN 2+, particularly when their vitamin B12 levels were within normal limits. When compared to women with the MTHFR CT/TT genotype who had greater blood folate levels, those with lower plasma folate were more likely to be diagnosed with CIN 2+.
• According to studies, women who drink alcohol daily have a considerably higher chance of HPV persistence than those who drink less or never, especially if they have a high viral load.

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Reference:

1. Hajiesmaeil M, Mirzaei Dahka S, Khorrami R, Rastgoo S, Bourbour F, Davoodi SH, Shafiee F, Gholamalizadeh M, Torki SA, Akbari ME, Doaei S. Intake of food groups and cervical cancer in women at risk for cervical cancer: A nested case-control study. Caspian J Intern Med. 2022 Summer;13(3):599-606. doi: 10.22088/cjim.13.3.599. PMID: 35974932; PMCID: PMC9348217.