ALUMINUM – IS IT A BRAIN TOXIN ?

Steven Lippmann, M.D. Emeritus Professor, University of Louisville School of Medicine 

For decades there have been concerns about whether aluminum is toxic for humans. Does it cause dementias? No conclusive answers, but many people have gotten rid of aluminum cookware, despite still using aluminum foil. Lots of us remember the past frequency of pots and pans made of aluminum. There were questions about whether aluminum incorporation into the body, by oral or dermal means, might induce cognitive declines or other neurological conditions, like parkinsonism, autism, or others.           

There are investigations suggesting that aluminum toxicity is related to early-onset dementia of an Alzheimer disease-like state. However, other research documents no clear etiological leakage. Studies provide no definitive answer. There is much speculation, but a literature review leaves one realizing how little we truly understand. Exposure is widespread because aluminum is the third commonest element in the earth’s crust, and thus, it is in our food supply, medications, and cosmetics.           

Aluminum, in acceptably low levels, is naturally present in many fruits, vegetables meats, fish, and cheeses, etc., but without noting dangerous consequences. Toxicity from this is not recognized. In addition, aluminum is used to facilitate some food preparations like in baking and/or pickling. Baking powder is one of the ingredients of concern, but fortunately aluminum-free baking powders that only contain sodium bicarbonate are ubiquitously available and safe. Exposure can also come through water purification processes and might leach into beverages via aluminum can containers.           

There are many industrial and medical applications. Besides widely available aluminum containing antacids, its hydroxide can also be a vaccine adjuvant. Fear of vaccines has long been an issue; yet, not all vaccines contain aluminum. Our currently available COVID-19 vaccinations contain no aluminum; good news now adays during this pandemic. Reportedly, there is no aluminum in Pfizer, Moderna, Johnson & Johnson, or AstraZeneca vaccines.           Aluminum has antibacterial and antiperspirant qualities, thus it is present in some underarm odor-suppression products. Antiperspirants diminish sweating and that differentiates them from deodorants. Some cosmetic and skin care products also contain aluminum traces, and that also includes styptic pencils or powders, because of their potential to diminish bleeding from small abrasions or cuts, like from razor shaving.           

What about the safety of antiperspirants that contain aluminum? Some marketed products, state clearly up-front in bold lettering that they do not contain aluminum chlorohydrate. That prominent disclosure is sometimes followed in small print on the back label, saying that this product contains potassium alum. Yes, alum is an aluminum salt with potassium, sulfate, sodium, or ammonium. Potassium alum is sometimes called potash alum, proclaimed to be safe, and used in place of aluminum chloride or chlorohydrate.Apparently, this form of chlorohydrate is a small molecule and is easily absorbed through skin, while alum is larger and is thus with less dermal penetration. The implications of these statements opens a question because the product labeling appears to be deceptive. It seemed that the marketers want to convey that their product contains no aluminum and counts on people not reading or understanding potassium alum’s relationship to this metallic element. It might still be safe, but the product labeling prompts concern.           

The pathophysiology of many neurodegenerative conditions remains unknown and proven aluminum toxicity is not obvious. One possible explanation from some sources suggests that aluminum-induced dementias may be due to a physiological predisposition to retain aluminum in the body and/or brain. Thus, vulnerable persons might become toxic while other people evidence no ill effects. However, anyone with a family history of early-onset dementia, probably ought to diminish aluminum exposures.           

Despite lack of clarity about brain toxicity, there are ways to reduce exposures. One can easily avoid aluminum-content antiperspirants, not employ aluminum cookware, even not cooking in its foil form, and not using aluminum-containing baking powders, antacids, and/or vaccinations. Patients and the public should be made aware that no current COVID-19 vaccinations in this country contain aluminum. Also, let people know that many popular antacid tablet brands contain aluminum salts, but calcium carbonate alone and/or with magnesium salt alternative antacids are very widely available. More difficult to identify and harder to rule out is exposure through packaged, prepared baking products. This may not be a major concern, but the degree of presence and risk is not widely known.           We should not become preoccupied with an unproven toxicity, but there are reasonable precautions to minimize adding high aluminum exposures. Time may settle this issue. For now, rely on awareness and prudence.

KPMA Town Hall Meeting

Please join us Thursday, November 11th, 2021, virtually for a Town Hall beginning at 6:30pm.  Our schedule is as follows:

6:30pm – 7:00pm    Sheila Schuster, Ph.D., will discuss assessment thus far from Severe Mental Illness Task Force and tentative recommendations for improving access and care for this patient population.

7:00pm – 7:30pm     Gagandeep Kaur, M.D, will discuss rising number of young adolescent suicidality/attempts, particularly in young girls.

7:30pm – 8:00pm     Allen Brenzel, M.D, will provide a high level overview of current mental health and SUD/OUD climate in Kentucky.  Discuss what strategies/initiative (if any) are being planned at the state level to mitigate for Kentuckians suffering from mental illness/SUD/OUD, with respect to the pandemic.

Registration is free for this virtual event.  You may register using the link below.  A calendar invite is attached as well.

Register Now

Telemedicine and COVID-19


Telemedicine technology has been around for a few decades but it was never optimally utilized until the COVID-19 pandemic. Insurance reimbursement was a big barrier in utilizing telemedicine along with other systems barriers. In March 2020, COVID-19 was declared a pandemic by WHO. After this, telemedicine was considered the preferred modality of treatment in the health care industry, and insurance supported the use of this technology. This was a big change for all of us as physicians. We all had to adapt to this new technology within days. This transition had its pros and cons, there was a lot of uncertainty about the usage of telemedicine at that time. When the pandemic started, we were worried if we would be able to continue to safely provide care for our patients or not. With telemedicine as a preferred modality, several of us started working from home. It’s been more than a year now since we have been doing Telemedicine and it has been an interesting experience. Some of us love it and some not so much.


Now most of us are comfortable with this technology and some of us prefer virtual over in-person visits. We never thought that we would be able to build therapeutic rapport and feel connected with patients via telemedicine but I have to say that I feel connected. Research supports this as well. A systematic review by Guaiana and et al published in October 2020 in the Community Mental Health journal showed that the efficacy of Telemedicine and in-person visits were similar (1). Several patients prefer using Telemedicine over in-person visits. There are several advantages of Telemedicine visits. From the patient perspective, 1) They can overcome the geographical barrier and save the transportation cost. 2) They don’t have to worry about bad weather. 3) Several patients are very anxious about waiting in the doctor’s office so they like virtual visits. 4) Mobility is another barrier. As with any technology, there are disadvantages of telemedicine as well. Some patients don’t have access to video technology, some patients are not tech-savvy and it intimidates them to use this platform. As physicians, we see several advantages and disadvantages as well. One of the biggest advantages has been the ability to continue patient care during the COVID- 19 pandemic. Patients’ show rate has been better as compared to in-person visits. Psychiatry is more equipped to do Telemedicine as compared to other specialties where physicals are needed to diagnose and treat patients. With the COVID-19 pandemic, research is showing worsening of mental health so demand for mental health treatment is increasing. Maxime. T et al did a retrospective cohort study on 236379 patients who were COVID survivors. They found out that estimated evidence of neurological and psychiatric diagnosis was 33.62 % in the following 6 months post-COVID (2). 


At this time Telemedicine continues to grow in Psychiatry but we still don’t know what would be the future of Telemedicine once the COVID-19 pandemic is over. Will we as physicians and our patients struggle with virtual “ fatigue” or will we continue to like this? Will this pandemic be over or is COVID- 19 here to stay? Will this be a “ new normal” or not? It is hard to answer these questions at this time. It would be appropriate to have a hybrid model where patients and physicians can have the choice to have either virtual or in-person visits depending on what’s best for the patient. As with any other decision-making in health care, we have to weigh the risks and benefits and make our best decision. 

 References-1.Guaiana, G., Mastrangelo, J., Hendrikx, S. et al. A Systematic Review of the Use of Telepsychiatry in Depression. Community Ment Health J 57, 93–100 (2021). https://doi.org/10.1007/s10597-020-00724-22.6-month neurological and psychiatric outcomes in 236379 survivors of COVID-19: a retrospective cohort study using electronic health records Maxime Taquet, John R Geddes, Masud Husain, Sierra Luciano, Paul J Harrison 

Ruchita Agrawal MD, FAPA
Board Certified Adult Psychiatrist
Associate Chief Medical Officer Adult Services
Seven Counties Services
708 Magazine Street
Phone no. 5025898926
Assistant Professor U of L

NEUROBIOLOGY OF SCHIZOPHRENIA: 101


Raymond Pary, M.D., VA Hospital, VA Staff Psychiatrist and Steven Lippmann, M.D., Retired PsychiatristLouisville, KY

Schizophrenia has a heterogeneous clinical prodrome and variable outcome. It usually occurs with symptoms of delusions and auditory hallucinations. Sometimes, affective presentations include depression or mania, or less often, catatonia with bradykinesia and mutism. Such presentations are often labeled schizoaffective disorder or catatonia, respectively. Clinical patterns alter over time as do lifetime diagnoses and are unpredictably identified even by accomplished psychiatrists. Agitated and/or violent behavior is occasionally observed.


A historical perspective on schizophrenia starts with Emil Kraepelin. In the early 1900s, he attributed degenerative cells in the brain as being responsible for the deteriorating course of illness. The brain pathology is likely genetic and/or related to gene expression, but there are many unanswered questions about the [RP1] role genes have in the neuropathology. Further understanding is needed to understand how the heterogeneous brain connections and circuits contribute to schizophrenia. Diagnoses, now based on subjective clinical symptoms, will in the future hopefully be determined by documentable brain changes. Some amelioration of clinical severity for many patients followed the 1960s advent of administering antipsychotic medications; yet, responses to these drugs is variable.

Sigmund Freud speculated that schizophrenia resulted from disintegration of the ego and separation from reality. Accordingly, the death of the ego produced a loss of self-identity. Unsuccessful attachment to the opposite sex parent and disordered family patterns were thought to contribute to the psychopathology. Paranoid delusions are stress-induced, based on unconscious homosexual impulses. These theories were further elaborated and included the concept of the “schizophrenogenic mother”. Such concepts might have retarded research progress about neurobiology, and there is a dearth of evidence corroborating that mothers actually cause schizophrenic illnesses in their offspring.


Pneumoencephalographic studies reveal that people with schizophrenia have abnormally large brain ventricles. Computerized tomography corroborates this finding. It also suggests that schizophrenia begins in utero as a neurodevelopmental disorder, and that manifestations vary over the life cycle. Ventricular enlargement is not static and appears to exert influence on the illness pathology.


Magnetic resonance brain imaging research among neonates at high risk for schizophrenia reveals that cortical thickness alterations, diminished gray matter volume, and white matter changes occur in the same regions as where pathology is documented in adults with schizophrenia. This supports a neurodevelopmental abnormality. However, structural investigations document non-specific gray and white matter abnormalities that differ among patients and are not diagnostic. 


Positron emission tomography measures blood flow and glucose utilization, depicting abnormalities of brain function. Such investigations evidence deficits in working memory, executive functioning, processing speed, and language production. Imaging studies reveal anatomic abnormalities in the medial frontal cortex, the posterior cingulate cortex, reduced cortical thickness, white matter abnormalities, and enlarged lateral ventricles. The subcortical amygdala, thalamus, hippocampus, and nucleus accumbens are documented to be subnormal in size.


The dopamine hypothesis involving these structures during this illness has undergone refinements over time. In short, the assumption was that hyperactivity of dopamine D2 receptors influence the presence of positive symptoms, while hypofunction of the D1 receptor in the prefrontal cortex may have a role in the negative manifestations of disease. Abnormalities of dopamine may change over different stages of illness and are dependent on other neurochemical systems. These interactive neuronal networks also at least involve glutamate, gamma-aminobutyric acid, and serotonin.


There are progressive alterations in the brains of some patients with schizophrenia. The apparent brain volume changes also might be explained to be imaging artifacts or induced by exposure to antipsychotic pharmaceuticals. The neuropathology leading to hallucinations and delusions remains unexplained. Similar questions apply to the pathological variance among individuals. It is still not established as to whether early detection and treatment mitigate disease progression. Nevertheless, antipsychotic drugs exert a positive influence on the lives of many people with this illness; withdrawing these pharmaceuticals usually yields worsening clinical outcomes for those affected.


Schizophrenia is a disease with genes influencing the development of brain structure and neuronal performance. Alteration of cortical and subcortical structures has pathological consequences for white matter function. These vary between individuals, but abnormalities in neuronal connectivity occurs in many individuals with this illness. Research continues. Antipsychotic medicines generally induce some clinical improvement; yet, there remains no means to cure or fully understand this terrible disease. The neurobiology of schizophrenia is still an enigma.
A Suggested ReadingDelisi, L. The Neurobiology of Schizophrenia. Focus 2020; 18 (4): 368-374