Cervical Dysplasia

Cervical Dysplasia: A Nutrition and Natural-Health Reference

Definition and Overview

Cervical dysplasia is a precancerous condition in which abnormal cell growth occurs on the surface lining of the cervix or endocervical canal, the opening between the uterus and the vagina. It is also called cervical intraepithelial neoplasia (CIN). Precancerous cervical cell changes are referred to as cervical dysplasia, cervical intraepithelial neoplasia (CIN), and squamous intraepithelial lesion (SIL).

It is caused by the persistent infection of human papillomavirus (HPV) into the cervical tissue. This cell growth and change can allow the entrance of human papillomavirus (HPV), the cause of more than 90% of cervical cancer. Strongly associated with sexually transmitted human papillomavirus (HPV) infection, cervical dysplasia is most common in women under age 30 but can develop at any age.

All cervical cancers begin with these cellular changes, but not all women with cervical dysplasia will go on to develop cancer. HPV virus (HPV 16 most commonly) is the most important etiological agent for the process of cervical carcinogenesis. However, HPV infection solely does not cause cervical cancer. There are various factors which act synergistically to develop cervical dysplasia and cancer.

Classification Systems

There are two different systems for classifying cervical dysplasia: the SIL (squamous intraepithelial lesion) system and the CIN (cervical intraepithelial neoplasia) system. Although what the systems describe is similar, they differ in some important respects.

In the CIN system, classification of cervical dysplasia is based both on the degree of dysplasia within the individual cells and the depth below the surface of the cervix to which the dysplasia extends. According to the CIN system, cervical dysplasia is divided into CIN1 (corresponding to mild dysplasia or LSIL), CIN2 (corresponding to moderate dysplasia or HSIL), and CIN3 (corresponding to severe dysplasia or HSIL).

Most of CIN1 will regress back to normal tissue over time, but about 11% of CIN1 will progress to CIN3. Only a very small percentage of CIN1 leads to cancer. About 43% of CIN2 will regress back to normal and 20% will progress to CIN3. Although some CIN3 will spontaneously regress, this dysplasia is almost always treated since the next step is cancer.

Body Systems Involved

The Cervical Epithelium and Squamocolumnar Junction

The cervix is the lower, narrow part of the uterus (womb) located between the bladder and the rectum. It forms a canal that opens into the vagina, which leads to the outside of the body. The Papanicolaou (Pap) smear is a collection of cells from the squamocolumnar junction of the cervix where the columnar epithelium is juxtaposed to the smooth squamous epithelium. In this area, squamous metaplasia is causing squamous cells to replace columnar cells. This transformation zone is particularly vulnerable to HPV infection.

Viral Oncoproteins and Cell Cycle Regulation

HPV gene expression becomes unlinked to the state of cellular differentiation of infected epithelial cells, and deregulation of expression of the early region of the viral genome results in a dramatic increase in the expression of the two HPV oncoproteins (E6 and E7). This results in the loss of the normal cell cycle control of the epithelium, and cells will develop morphologic features with immature "basaloid-type" squamous cells and mitotic figures in the upper half of the cervical epithelium.

The Immune System

The immune system plays an essential role in the natural history of HPV-related lesion development, persistence, and clearance. Local immunity is pivotal in the pathogenesis, spontaneous regression, and progression of cervical dysplasia; however, the underlying mechanisms are not fully known. In lesion persistence and progression, the immune microenvironment of cervical high-grade squamous intraepithelial lesions (cHSIL) is characterized by a lack of intraepithelial CD3+, CD4+, and CD8+ T cell infiltrates and Langerhans cells compared to the normal epithelium, and by an increased number of CD25+FoxP3+ regulatory T cells (Tregs) and CD163+ M2 macrophages.

Diagnosis and Presentation

HPV infection and cervical dysplasia generally cause no symptoms. Regular gynecological visits including a pelvic exam and Pap test can identify the conditions. Cervical dysplasia that is seen on a Pap test is called squamous intraepithelial lesion (SIL). Dysplasia that is seen on a biopsy of the cervix is called cervical intraepithelial neoplasia (CIN). Acetic acid applied to the cervix during colposcopy reveals the abnormal areas visually. A biopsy of this area is performed and sent to the pathologist to evaluate the degree of dysplasia present.

Contributing and Associated Factors

HPV Type and Viral Factors

Among the HPVs that infect the genital tract, certain types typically cause warts or mild dysplasia ("low-risk" types; HPV-6, HPV-11), while other types (known as "high-risk" HPV types) are more strongly associated with severe dysplasia and cervical cancer (HPV-16, HPV-18). The most common type of cervical cancer-causing HPV is HPV 16, which accounts for about half of all cervical cancers caused by this virus. Others include HPV 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68.

Cofactors of HPV infection can be classified into three groups: environmental or exogenous factors (oral contraceptive use, tobacco use, diet, and STIs), viral factors (HPV type and variant, viral load, and viral integration), and host factors (endogenous hormones, genetic factors, and immune response). In order to fully understand the risk factors that contribute to the progression of low- and high-grade cervical lesions, we must consider all three types of cofactors.

Tobacco Smoking

Among women with a chronic HPV infection, smokers are twice as likely as nonsmokers to develop severe cervical dysplasia, because smoking suppresses the immune system. Cigarette smoking, and even exposure to second-hand smoke, can triple a person's risk of developing the condition.

Tobacco smoking not only causes DNA adducts and strand breaks, but it independently causes an increased viral load in HR-HPV-infected cells. Tobacco smoking induces the heightened expression of E6 and E7 and can inhibit the immune system response to HPV. A case-control study found that for women who smoked more than 20 cigarettes per day, an adjusted odds ratio of 2.5 (95% CI: 1.6–3.9) was found for developing cervical dysplasia.

Sexual Behavior and Number of Partners

Having multiple sexual partners, especially those who have had multiple partners themselves, can increase the risk, though sometimes people can develop the condition from exposure to just one partner. In the same case-control study, for women who reported more than six sexual partners, the adjusted odds ratio was 11.5 (95% CI: 6.6–20.2).

Oral Contraceptive Use

Use of oral contraceptives for more than 10 years increased the risk, with an adjusted odds ratio of 2.3 (95% CI: 1.2–4.5). Conflicting data are observed when oral contraceptive intake is considered as a risk factor for cervical dysplasia development. Hence, further extensive studies are needed to determine the clear association between these.

Immunosuppression and HIV

People with compromised immune systems, such as those with HIV, transplant recipients, or those taking immunosuppression drugs, are also at higher risk. Women with HIV are more likely to have persistent HPV, common in low and middle-income countries. Speculation holds that HIV infection and consequent immunodeficiency negatively affects HPV clearance, consequently increasing prevalence and incidence of cervical dysplasia and cervical cancer.

Body Mass Index and Other Sociodemographic Factors

A 2025 case-control study published in PubMed found that factors significantly associated with cervical dysplasia included more than three sexual partners (odds ratio 71.4; 95% CI: 16.4–310.9), bacterial vaginosis (OR 101.2; 95% CI: 12.2–838.2), body mass index ≥ 25 (OR 12.9; 95% CI: 3.9–42.0), and grand multiparity (OR 39.0; 95% CI: 7.1–225.4).

Nutrients Studied in Relation to Cervical Dysplasia

Folate (Vitamin B9)

Background and Observational Evidence: A localized folate deficiency, which is sometimes misdiagnosed as cervical dysplasia because of morphological similarities between the cytologic features of megaloblastosis seen with folate deficiency and the changes associated with dysplasia, could be a component of the dysplastic process.

A study of 324 women with CIN and 228 women with normal cytological smears found that statistically lower levels of folic acid were found in the women with CIN-HPV-positive (OR: 7.5; 95% CI: 1.2–9.7). Studies have shown that lower levels of antioxidants coexisting with low levels of folic acid increases the risk of CIN development.

A case-control study of 726 subjects found that red blood cell folate levels at or below 660 nmol/L interacted with HPV-16 infection. Low red blood cell folate levels enhance the effect of other risk factors for cervical dysplasia, and in particular that of HPV-16 infection.

Clinical Trial Evidence: An early small trial (47 young women with mild or moderate dysplasia of the uterine cervix received oral supplements of folic acid, 10 mg, or a placebo daily for 3 months under double-blind conditions) found that before treatment the mean red cell folate concentration was lower among oral contraceptive agent users than nonusers, and that cytology scores improved in supplemented subjects. However, this result was not confirmed in later, larger trials.

A larger randomized, placebo-controlled clinical intervention trial at the Southwest Oncology Group evaluated the effect of oral folic acid supplementation on the natural history of cervical intraepithelial neoplasia (CIN) in a multi-institutional prospective, randomized, double-blind, placebo-controlled trial. Three hundred thirty-one women with biopsy-proven koilocytic atypia, mild CIN, or moderate CIN were randomized to receive oral folic acid (5 mg) or a similar-appearing placebo daily for 6 months. The conclusion was that supplementation with folic acid (5 mg/day) does not enhance the regression of early epithelial abnormalities of the cervix.

A 235-subject randomized trial likewise found that after 6 months no significant differences were observed between supplemented and unsupplemented subjects regarding dysplasia status, biopsy results, or prevalence of HPV-16 infection. Folate deficiency may be involved as a cocarcinogen during the initiation of cervical dysplasia, but folic acid supplements do not alter the course of established disease.

Evidence summary: Observational and cross-sectional studies consistently find lower folate levels associated with cervical dysplasia, particularly in the presence of HPV-16 infection. However, multiple randomized controlled trials have not demonstrated that folic acid supplementation reverses established CIN. The evidence therefore supports folate status as a potential cofactor in disease initiation but not as a therapeutic agent once dysplasia is established.

Vitamin C (Ascorbic Acid)

Observational Evidence: An early case-control study found that low vitamin C intake is an independent contributor to risk of severe cervical dysplasia when age and sexual activity variables are controlled. Analysis of matched pairs showed that 29% of cases compared to 3% of controls had vitamin C intake less than 50% of the recommended daily allowance, yielding a ten-fold increase in risk of cervical dysplasia as estimated by odds ratio (p less than 0.05).

There is substantial epidemiological evidence of a protective effect of vitamin C in cancers of the cervix, rectum, and breast. Antioxidant vitamins can inhibit the proliferation of cancer cells, stabilize the p53 protein, prevent DNA damage, and reduce immunosuppression.

Clinical Trial Evidence: A randomized, double-blind, placebo-controlled, factorial study of 141 women used a daily oral administration of 30 mg beta-carotene and/or 500 mg vitamin C in women with minor squamous atypia or CIN I. The regression rate was slightly higher, but not significantly so, in those randomized to beta-carotene compared to no beta-carotene (hazard ratio = 1.58, 95% CI: 0.86–2.93, P = 0.14) and slightly lower, but not statistically significant, for those randomized to vitamin C compared to no vitamin C (hazard ratio = 0.65, 95% CI: 0.35–1.21, P = 0.17). The currently available evidence from this and other trials suggests that high doses of these compounds are unlikely to increase the regression or decrease the progression of minor atypia and CIN I.

Evidence summary: Observational studies suggest an inverse association between dietary vitamin C intake and cervical dysplasia risk. Intervention trials using vitamin C supplementation alone have not demonstrated statistically significant clinical benefit in reversing established lesions. The overall evidence is preliminary, largely epidemiological, and inconsistent across trials.

Beta-Carotene and Vitamin A (Retinoids and Carotenoids)

Observational Evidence: Numerous observational studies have demonstrated an inverse relationship between the consumption of diets rich in fruits and vegetables and the risk of developing preinvasive neoplasia or cancer at a number of organ sites, including the cervix. Case-control studies exploring the relationship between diet and cervical dysplasia have demonstrated that a low intake of vitamins A, C, and beta-carotene was associated with an increased risk of cervical dysplasia.

A study measuring plasma micronutrient levels found that plasma beta-carotene concentrations in cigarette smokers were significantly lower regardless of cervical pathology, whereas plasma lycopene and canthaxanthin levels were significantly lower in smokers with CIN. The findings of a decrease in all plasma antioxidant nutrient levels except tau-tocopherol in women with CIN and cancer suggest a potential role for antioxidant deficiency in the pathogenesis of CIN and carcinoma of the cervix.

A Korean case-control study of 144 cervical cancer cases and 288 controls found that total intakes of vitamins A, C, and E were strongly inversely associated with cervical cancer risk: OR = 0.35 (CI = 0.19–0.65), OR = 0.35 (CI = 0.19–0.66), and OR = 0.53 (CI = 0.28–0.99), respectively.

Clinical Trial Evidence: A Phase III randomized, double-blind trial evaluated the effect of daily beta-carotene (30 mg) versus placebo over a 2-year period on CIN 2 and 3 lesions. The conclusion was that beta-carotene does not enhance the regression of high-grade CIN, especially in HPV-positive subjects.

An earlier randomized placebo-controlled trial found that no effect of beta-carotene on the regression percentages was observed (OR = 0.68, 95% CI: 0.28–1.60 using the broad definition). A secondary analysis, in which the effect of the total intake of beta-carotene (diet + medication) on the regression percentages of cervical dysplasia was studied, did not show a positive effect either.

An additional randomized double-blinded trial found that a large proportion of mild CIN lesions regress; age and HPV infection play an important role in the natural course of CIN. Supplementation of beta-carotene does not appear to have a detectable benefit in treatment of CIN.

Evidence summary: Multiple randomized controlled trials consistently find that beta-carotene supplementation does not produce significant regression of established CIN lesions, regardless of grade. Observational studies show an inverse association between dietary carotenoid and retinoid intake and risk, but this has not translated to intervention benefit. Evidence for isolated beta-carotene supplementation is negative to neutral.

Vitamin D

Evidence: Several studies have found an inverse relationship between the incidence of cervical neoplasia and vitamin D levels. A 2023 narrative review updates the current evidence supporting the notion that the vitamin D endocrine system has a preventive role in cervical cancer, mainly in the early phases. Vitamin D along with its active metabolite calcitriol and its metabolic and signaling system, known as the vitamin D endocrine system, have been widely recognized as a pivotal regulator of calcium homeostasis in addition to non-calcemic antitumoral effects in a variety of human cancers, including cervical cancer.

A systematic review published in 2023 found that women with cervical intraepithelial neoplasia may benefit from folate supplementation against oxidative stress and inflammation. Vitamin D may reduce oxidative stress and may have a therapeutic effect. However, a clinical trial on 58 women diagnosed with CIN2/3 found that supplementation with 50,000 IU vitamin D3 for six months did not affect CIN2/3.

Key uncertainties remain, including tissue heterogeneity of VDR expression, optimal dosing windows and target 25(OH)D ranges for cervical endpoints, and safety at higher exposures such as hypercalcemia.

Evidence summary: Observational data suggest an inverse relationship between vitamin D status and cervical neoplasia risk. Mechanistic data are supportive, but clinical trial evidence is limited and results are mixed. Evidence is currently preliminary and insufficient to establish clinical recommendations.

Selenium

The antioxidant activity and immunomodulatory properties of trace minerals including zinc and selenium have been shown in recent research to protect against carcinogenesis, especially in the pathogenesis of cervical neoplasia. While zinc supplementation has been attributed with better HPV clearance and lesion regression, selenium has shown positive impacts in lessening oxidative damage and encouraging CIN regression.

The 2023 systematic review referenced a randomized, double-blind, placebo-controlled trial on selenium supplementation and found favorable effects on regression of cervical tissues and metabolic profiles of patients with cervical intraepithelial neoplasia, published in the British Journal of Nutrition (2015).

Evidence summary: Early observational and one clinical trial data suggest a potential role for selenium in CIN regression, but the overall evidence base is small and preliminary. Further well-powered trials are needed.

Zinc

Zinc promotes the clearance of the human papilloma virus and reduces the chance of viral infection. A study of Korean women with cervical dysplasia and cervical cancer assessed serum selenium and zinc levels. Among the study group, 28 had CIN and 36 had invasive cervical cancer. These women were compared to 44 healthy women. Women with CIN or cancer had significantly lower selenium and zinc levels.

Evidence summary: Cross-sectional data associate lower serum zinc levels with CIN and cervical cancer. Data from clinical trials on zinc supplementation specifically for cervical dysplasia are sparse. The evidence is currently observational and preliminary.

Phytochemicals and Natural Botanical Ingredients

Indole-3-Carbinol (I3C) and Diindolylmethane (DIM)

Traditional/Background Context: I3C and its in vivo metabolite DIM are not historically documented as traditional medicines in any well-characterized botanical tradition. They are naturally occurring compounds found in cruciferous vegetables such as broccoli, cabbage, Brussels sprouts, and kale, and have attracted research interest since the late 1990s primarily through laboratory and early clinical research.

Scientific Evidence: Indole-3-carbinol (I3C) is a phytochemical derived from broccoli, cabbage, and other cruciferous vegetables with proven anticancer efficacy including the reduction of cervical intraepithelial neoplasia (CIN) and its progression to cervical cancer.

Indole-3-carbinol inhibited spontaneous or chemical-induced tumorigenesis in mammary gland, liver, lung, cervix, and gastrointestinal tract in different animal model studies. These preclinical findings have led to its human trials in cervical dysplasia, breast cancer, vulvar intraepithelial neoplasia, and recurrent respiratory papillomatosis.

In a key human clinical trial referenced across multiple sources, a placebo-controlled trial of indole-3-carbinol in the treatment of CIN (Bell et al., 2000, Gynecol Oncol) found that four of eight patients in the 200 mg/day arm and four of nine patients in the 400 mg/day arm had complete regression, compared to none in the placebo group. Data from early phase clinical trials suggested that I3C is effective against precancerous cervical dysplasia and vulvar intraepithelial neoplasia.

Mechanistically, PTEN is diminished during the transition from a low-grade to a high-grade dysplasia. I3C prevents this loss of PTEN and appears to increase its expression. As a tumor suppressor, PTEN is often inactivated during tumorigenesis, thereby giving progeny tumor cells growth and survival advantages.

In vitro, both I3C and DIM caused accumulation of DNA strand breaks in three cervical cancer cell lines. Induction of apoptosis was confirmed by nuclear morphology, nucleosome leakage, altered cytoplasmic membrane permeability, and caspase 3 activation. Neither I3C nor DIM caused apoptotic changes in normal human keratinocytes.

Evidence summary: Preclinical (in vitro and animal) evidence for I3C and DIM is compelling. Early-phase human clinical trial data show promise for I3C in regression of CIN, but results come from small, early-phase trials only. Larger, confirmatory randomized controlled trials are lacking. Evidence is currently preliminary but directionally positive.

Green Tea Catechins (EGCG / Polyphenon E)

Traditional Context: Green tea (Camellia sinensis) has a centuries-long history of use in Chinese and East Asian traditional medicine and food culture. Its use in the context of cervical lesions is a modern research application rather than one rooted in historical botanical traditions.

Scientific Evidence: In vitro studies have suggested that green tea catechins may exert chemopreventive activity for cervical cancer. Epigallocatechin gallate (EGCG, a major green tea catechin) and Polyphenon E (a decaffeinated, enriched, and defined mixture of green tea catechins) inhibited the growth of HPV-positive cervical cancer cells and HPV-immortalized cervical epithelial cells in a dose-dependent fashion.

An early non-randomized clinical study investigated the clinical efficacy of green tea extracts (Polyphenon E and EGCG) delivered in a form of ointment or capsule in patients with HPV-infected cervical lesions. Fifty-one patients with cervical lesions (chronic cervicitis, mild, moderate, and severe dysplasia) were divided into four groups, compared with 39 untreated patients as a control. Poly E ointment was applied locally to 27 patients twice a week; for oral delivery, a 200 mg capsule was taken daily for eight to 12 weeks. In the study, 20 out of 27 patients (74%) under poly E ointment therapy showed a response. Six out of eight patients under ointment plus capsule therapy (75%) showed a response, and three out of six patients (50%) under capsule therapy showed a response.

However, the largest confirmatory trial yielded different results. A randomized, double-blind, placebo-controlled trial of Polyphenon E (decaffeinated and enriched green tea catechin extract) was conducted in women with persistent human papillomavirus (HPV) infection and low-grade CIN1. Ninety-eight eligible women were randomized to receive either Polyphenon E (containing 800 mg epigallocatechin gallate) or placebo once daily for 4 months. The primary study outcome was oncogenic HPV clearance and clearance of CIN1. Results showed that there was no difference in the response rate by treatment allocation. Complete response, defined as negative for high-risk HPV and normal histopathology, was noted in 7 (17.1%) and 6 (14.6%) women in the Polyphenon E and placebo groups, respectively.

Evidence summary: EGCG and Polyphenon E show clear anti-HPV and antiproliferative activity in cell culture and animal models. An early uncontrolled clinical study suggested benefit, particularly from topical application. The single largest randomized, placebo-controlled trial, however, found no statistically significant difference from placebo. Evidence remains preliminary and, as of the latest available trials, does not support efficacy in clinical use for CIN1 regression.

Dietary and Lifestyle Factors

Overall Diet Quality and Fruit and Vegetable Intake

There is evidence that diet and nutrition are modifiable risk factors for several cancers. In recent years, attention paid to micronutrients in gynecology has increased, especially regarding HPV infection. A comprehensive 2023 review of the literature found that different oligo-elements and micronutrients demonstrated a potential protective role against cervical cancer by intervening in different stages of the natural history of HPV infection, development of cervical dysplasia, and invasive disease.

Regarding nutrients, different antioxidants may have differing abilities to intervene in the natural history of cervical diseases associated with HPV infection. Regarding foods, the intake of both vegetables and fruits containing multiple vitamins may widely suppress cervical cancer development. A 2023 systematic review and meta-analysis found that there is an ongoing association between decreased HPV persistence, decreased likelihood of cervical intraepithelial neoplasia (CIN), and weakened inflammation with adequate intake of vitamins A, C, D, and E, as well as carotenoids.

Vitamin A (retinol), vitamin D, and papaya might be more effective in preventing early dysplasia, CIN 1. In contrast, vitamin E and lycopene might be more effective in preventing late dysplasia, CIN 2/3. Both fruits and carotenoids might widely prevent HPV infection, CIN 1–3, and cervical cancer.

Tobacco Smoking as a Dietary/Lifestyle Antagonist

The negative effects of tobacco smoking may be stronger than the positive effects of vitamins, vegetables, and fruits on the regression of cervical disease such as cervical intraepithelial neoplasia (CIN). A relatively low intake of vitamins, vegetables, and fruits in combination with tobacco smoking was most associated with a high incidence of cervical neoplasia.

Physical Activity

Investigators have suggested that physical activity could decrease the risk of CIN through promotion of cell-mediated immunity. Physical activity and abstaining from smoking could benefit the regression of CIN and the decreasing of DNA viral load of HPV. However, the roles of physical activity and abstaining from smoking on the regression of CIN and viral load are not fully clarified.

Calcium and Dairy

Researchers evaluated 405 women, 333 with invasive cervical cancer and 72 with CIN III, and compared them with 2025 healthy women of a similar age. They found that women who had a diet high in milk, yogurt, and fish were much less likely to have invasive cancer, while women whose diet was high in tofu and green leafy vegetables had a moderately decreased risk of CIN III. These researchers concluded that higher dietary calcium and vitamin D intake was associated with lower cervical cancer risk among this group of women.

Limitations in the Evidence Base

Numerous studies have attempted to determine associations between micronutrients and risk of CIN and cervical cancer. Studies that were conducted before a reliable test for assessing HPV infections was available may have resulted in misclassification because of differences in assay sensitivity, which could have led to residual confounding. Another limitation in previous studies may be related to methodologic limitations such as the proper choice of controls for case-control studies. Since cervical cancer does not develop in the absence of HR-HPV infections, only controls exposed to HR-HPV should be included in studies that investigate cofactors for CIN or cervical cancer.

Most previous papers have described epidemiological studies. Thus, further research using in vitro and in vivo approaches will be needed to clarify the effects of dietary and nutrient intake in detail.

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