Breast implant illness (BII), also known as systemic symptoms associated with breast implants (SSBI), is often used to describe various systemic symptoms that some patients attribute to their breast implants. The literature identifies multiple “syndromes” associated with breast implants including silicone incompatibility syndrome and autoimmune inflammatory syndrome induced by adjuvants (ASIA) syndrome. Over 100 systemic symptoms have been reported, including “brain fog,” lack of motivation, joint pain, hair loss, and fatigue. Clinical evaluation of these patients fails to show a definitive medical cause, and their symptoms remain medically unexplained. Medically unexplained symptoms is a term used only after a full medical workup fails to decipher a potential cause. We do know that some patient’s symptoms will improve with implant removal. While there have been articles showing potential association of breast implants to symptoms or autoimmune diseases, causation has yet to been proven.

BII or SSBI remains a diagnosis of exclusion. There are no specific physical or laboratory findings in these patients that could be used to make a diagnosis. It is important that other causes of their symptoms be ruled out, as not to miss a treatable condition. The preoperative evaluation would depend on the presenting symptoms and should be conducted by the patient’s primary care physician with referrals to specialists as indicated.

Ruling out a possible disease is not the same as ruling out an illness. It would be easier to determine a potential cause of the patients’ symptoms if there was substantive medical evidence, including abnormal physical findings or abnormal laboratories to support their complaints. Patients often present with a wide variety of symptoms in no specific configuration and with no abnormal laboratories or physical findings that could be used to direct the search for an etiology. Proposed causes include an adjuvant reaction to silicone, autoimmune disease, biofilms, heavy metal toxicity, allergy, and neuropsychiatric conditions.

An adjuvant is an antigen that enhances an immune response. In 1964, Miyoshi reported patients who developed diverse symptoms after injections with silicone or paraffin fillers. This led to concerns that the silicone used in breast implants could induce an immune reaction that could trigger autoimmune diseases. ASIA syndrome was first described by Shoenfeld in 2011, referring to not only silicone-induced symptoms but also aluminum in vaccines, and other potential adjuvants leading to fibromyalgia, chronic fatigue syndrome, Gulf War and Sick Building syndrome. Over 100 articles have been published on ASIA since the initial publication. Most are opinions or case studies with no clearly defined causative agent and nonspecific clusters of symptoms. To determine definitively that silicone is an adjuvant or toxin requires a defined biologic mechanism. There must be a temporal relationship between exposure and the onset of symptoms and a defined dose response, which currently has not been shown. Early generation breast implants had high rates of rupture and gel bleed inviting the comparison to silicone adjuvant injections. Newer generation silicone implants have a considerably lower incidence of gel bleed and systemic symptoms have also been reported in patients with saline implants. The symptoms reported by patients with BII, and the ASIA syndrome criteria are nonspecific common in the general population. The limitation of most of the studies linking breast implants to symptoms is the lack of data as to whether symptoms could have existed prior to implant placement, lack of control groups, and no long-term follow-up. ASIA syndrome, like BII, is not a recognized medical condition and presents with varied, nonspecific symptoms. It is not useful to use one not recognized condition to explain another.

In response to the 1992 Silicone Gel Moratorium, the Institute of Medicine (IOM) published their systematic assessment on the long-term positive and negative consequences of silicone breast implantation. The Safety of Silicone Breast Implants was published in 1999 and in the judgment of the committee, they believed there were sufficient studies to determine that silicone implants were not causally related to systemic illnesses. Despite their conclusions concerns persisted. Since this report, there have been numerous publications discussing potential associations between silicone and autoimmune diseases, and each requires careful review. Most published studies have significant selection bias, poor follow-up, and/or lack a control group. Coroneos and colleagues evaluated the Food and Drug Administration (FDA) postapproval data on 99,993 subjects from 2 United States implant manufacturers. They reported a higher rate of Sjogren’s syndrome, scleroderma, rheumatoid arthritis, melanoma, and still birth compared to the general population, and a reduced risk of fibromyalgia and birth defects. There are significant limitations with this study. The 2 manufacturers included utilized different protocols; 1 manufacturer utilized patient-reported data, the other utilized physician diagnosed data, and the follow-up was vastly different. The harms reported were derived from the manufacturer study with only 20% follow-up and used patient-reported data, which introduces the potential for significant bias. Further, the authors used normative data as the control, which was generated from physician diagnoses, rather than patient-reported information. Watad and colleagues reviewed the data from a large Israeli health system and found a higher likelihood of rheumatic and autoimmune disorders in women with breast implants than in controls. This study is limited in that no confounding variables were included in the analysis and the implant cohort consisted of patients with known, probable, and possible implants, leaving the likelihood that some patients included in the implant cohort may not have had implants. Many of the published studies show significant selection bias, short follow-up duration or lost to follow up, and a lack of control groups.

More than 25 years after the IOM report, a study by Barbosa and colleagues reviewed the medical records of 22,006 patients in a military health system, which included 513 patients with breast implants. They reported no difference incidence of symptoms, connective tissue diseases, or allergies in patients with breast implants compared to patients without a history of implants. In 2025, Jagasia and colleagues analyzed the effect of ruptured implants on systemic and local immune changes. In this prospective study, they measured peripheral antibody levels for common breast antigens and gene expression in breast parenchymal tissue in patients with intact and ruptured implants. They found no difference in genetic profiles between patients with and without ruptured implants. There was also no difference in breast-related antigens between patients with intact or ruptured implants, saline or gel, and between textured and smooth implants. Their data showed ruptured implants do not confer changes to either systemic antibody levels or gene expression in breast tissue. They state that there is no evidence of systemic or local immune changes that explain the symptoms reported by patients with BII.

Implanted medical devices and exposure to bacteria can be a recipe for disaster, potentially causing infection requiring removal of the device. Subclinical infections can also occur with implanted medical devices. In 1981, Burkhardt described subclinical infections around breast implants mostly involving species of Staphylococcus bacteria. Bacteria around implants has been associated with capsular contracture as demonstrated by the landmark studies by Adams and colleagues. In 2020, Lee and colleagues suggested biofilms may be a cause of symptoms in patients with BII. He cultured the capsules of 50 patients undergoing explant for systemic symptoms associated with their implants. Thirty six percent of the symptomatic patients had positive cultures as opposed to 6% of historic controls. This article was limited by using standard culture, which can be unreliable for biofilm analysis, as well as the use of a historic control. McGuire and colleagues evaluated capsules of patients with BII versus control nonsymptomatic implant cohort subjects using polymerase chain reaction (PCR) testing and no statistically significant difference was found in the presence or type of bacterial. No fungal DNA was identified in either cohort. Additionally, there was no difference identified in symptoms or symptom improvement in patients with positive or negative PCR results. A publication by Sinha and colleagues suggests the presence of oxylipins, lipid-derived molecules produced by bacteria, which can induce biofilm formation, in the capsules and peripheral blood of patients with BII. They suggest that biofilms may play a role in systemic symptom development. They specifically reference 10-Home oxylipin, which is associated with staphylococcal species. However, oxylipin elevation is known to be temporary and is nonspecific. The study by McGuire and colleagues evaluated peripheral blood for the presence of antibodies to Staphylococcus enterotoxins in SSBI patients versus controls. A difference could indicate a subclinical Staphylococcus infection or history of Staphylococcus infection or biofilm. While there were statistically higher Staphylococcus enterotoxin A levels in the BII cohort versus controls (36% vs 18%), the tested implants and capsules of the subjects with the higher levels did not contain PCR evidence of Staphylococcus , indicating potential Staphylococcus infection elsewhere in the body. Although interesting, the study is not conclusive and the potential for oxylipin involvement in systemic symptoms will require further study.

A prevalent theory in many of the BII social media groups is that heavy metals contained in breast implants leech from the implant into the surrounding capsule causing symptoms. This is the leading reason these sites, and the surgeons they endorse, recommend a total capsulectomy. FDA guidance for breast implant labeling requires manufacturers provide qualitative and quantitative analysis of the silicone elastomer shell and gel of silicone breast implants. They specifically request the manufacturers publish plasma-mass spectrometry analysis for metals including antimony, arsenic, barium, beryllium, cadmium, chromium, cobalt, copper, lead, magnesium, mercury, molybdenum, nickel, platinum, selenium, silver, tin, titanium, vanadium, and zinc. These levels are derived from volatile and extractable analysis of the implants after dissolution in acids or incineration. Each manufacturer must submit these data in a table published in their Summary of Safety and Effectiveness Data. The levels portrayed on the tables are presented without context. In fact, all levels reported are either nondetectable or well below levels considered safe for exposure. Unfortunately, these tables are often presented in the BII groups as a list of ingredients, which is understandably concerning for implant patients.

In a prospective, blinded cohort study by Wixtrom and colleagues, the authors measured the levels of 22 heavy metals in tissue taken from breast implant capsules. Tissue was obtained from SSBI and non-SSBI subjects, as well as breast tissue from control subjects who had no history of any implanted medical device. Heavy metals were detected in the capsules as well as the breast tissue of the control cohort, but all were well below safe levels for daily exposure. Some metals such as arsenic were statistically higher in the breast tissue of women who never had breast implants.

Allergic reactions have been suggested as a potential cause for SSBI. Eosinophilia, or elevated levels of eosinophils, is associated with allergic diseases and a marker for allergic reactions. McGuire and colleagues evaluated the peripheral blood and implant capsules in patients with self-described BII versus 2 control groups. Eosinophils were found in only 2 of 200 capsules, and no elevation of eosinophils was found in the blood of any subject. There was also no difference in measure immunoglobulin E antibodies to Staphylococcus enterotoxins and no difference in adverse type 1 hypersensitivity reactions in any of the cohorts.

Another prevalent theory to explain SSBI is that silicone causes a localized immune response, which leads to systemic inflammation producing symptoms. The presence of gel bleed and reports of silicone identified in implant capsules producing inflammation is thought to produce a systemic inflammatory process or nociceptive process leading to symptoms. However, SSBI has been reported in all implant types, including saline implants. Danino and colleagues studied silicone particles in implant capsules around implants sold in North America. They meticulously demonstrated that there were no silicone particles in the capsules surrounding saline implants. McGuire and colleagues evaluated capsules after removal in patients with BII versus controls where 64% of the BII cohort had saline implants. They found that the presence silicone was significantly higher the non-BII cohort. The same study showed a higher incidence of synovial metaplasia in the non-BII cohort associated with textured surface implants.