Medical Bulletin 09/ August/ 2024 - Video

A study published in JAMA Network Open reveals that about 5% of adults are exposed to six potentially hepatotoxic botanicals, which are largely unregulated products typically used to improve health or treat minor health complications.

The use of herbal and dietary supplements (HDSs) is rapidly increasing worldwide due to their perceived health benefits. With over 80,000 products available at various unregulated retail outlets, these supplements can be purchased without a prescription. The most common categories include multivitamins, minerals, vitamin D, omega-3 fatty acids, and calcium. However, these products do not require approval from the Food and Drug Administration (FDA) before being marketed. As a result, there is often a lack of thorough safety and efficacy assessments.

In the current study, scientists have determined population-level estimates of exposure to six potentially hepatotoxic botanicals, including turmeric or curcumin, green tea, Garcinia cambogia, black cohosh, red yeast rice, and ashwagandha.

The study analysed data from over 9,500 adults, focusing on their exposure to prescription drugs and herbal and dietary supplements in the past 30 days.

Among 9,685 adult participants, about 58% reported consuming herbal and dietary supplements at least once within the past 30 days. The majority of participants reported consuming hepatotoxic botanicals without any recommendations from their healthcare providers. The most commonly reported reasons for the use were health improvement, disease prevention, and immunity boosting.

Given the lack of regulatory oversight on botanicals, scientists advise clinicians to obtain a complete medication and botanicals use history when evaluating patients with unexplained symptoms or liver test abnormalities.

References: Likhitsup A. 2024. Estimated Exposure to 6 Potentially Hepatotoxic Botanicals in U.S. Adults. JAMA Network Open. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2821951

A recent JAMA Network Open study assesses the role of omega-3 polyunsaturated fatty acids (PUFAs) in reducing white matter lesion (WML) accumulation and neuronal integrity degeneration in older adults.

The accumulation of cerebral white matter lesions (WML) is linked to an elevated risk of cognitive decline and Alzheimer's Disease (AD). The underlying pathophysiological mechanisms include the diminished regenerative capacity of oligodendrocytes, reduced cerebral blood flow (cerebral hypoperfusion), breakdown of the blood-brain barrier, and activation of endothelial cells.

The current placebo-controlled, quadruple-blinded, and randomised clinical trial`s treatment stratification was was carried out using the apolipoprotein E ε4 allele (APOE*E4) carrier status, and all results were compared against a placebo group.

The results showed that the group receiving omega-3 treatment showed less annual progression of crude white matter lesions (WML) compared to the placebo group. However, this difference was not statistically significant. Similar results were observed for neuronal integrity, where the omega-3 group experienced a lesser decline in diffusion tensor imaging fractional anisotropy (DTI-FA), though this was also not statistically significant. Additionally, there were no differences between the groups in the average annual changes in ventricular volume or total brain volume.

Therefore, the study concluded that a omega-3 treatment was well-tolerated and safe yet ineffective in attaining a significant reduction in WML progression and neuronal integrity breakdown in individuals at an increased risk of dementia.

References: Shinto, L. H., Murchison, C. F., Sillbert, L. C., et al. (2024) ω-3 PUFA for Secondary Prevention of White Matter Lesions and Neuronal Integrity Breakdown in Older Adults: A Randomized Clinical Trial. JAMA Network Open 7(8). doi:10.1001/jamanetworkopen.2024.26872

In a recent study published in the journal Nature Medicine, researchers review the adverse effects of Western diets on human health.

The increased consumption of processed food products that are high in refined sugars, fats, and salts has been observed throughout the world. This shift in dietary habits, which is often referred to as the ‘Westernization of diets,’ has been largely attributed to the affordability and availability of these food products.

Despite the economic advantages of a Western diet, regular consumption of these foods can significantly raise the risk of both chronic and noncommunicable diseases. These include stroke, ischemic brain disease, myocardial infarction, ischemic heart disease, obesity, type 2 diabetes, metabolic dysfunction-related fatty liver disease, inflammatory bowel disease (IBD), and colon cancer.

Several studies have highlighted the negative impact of the Western diet on the human gut microbiome. The reduced consumption of dietary fibre, replaced by additives such as emulsifiers and artificial sweeteners, has led to microbial rarefaction, a decrease in the diversity and abundance of essential microorganisms in the gut microbiome.

Ultra-processed foods, trans fats, and inflammatory ingredients, all of which are present in high concentrations in the Western diet, increase the risk of developing IBD.The rising prevalence of several liver diseases, some of which include liver steatosis, cirrhosis, and hepatocellular carcinoma, has also been attributed to the Westernization of diets.

Western diets, characterised by high sugar and fat content and low fibre, heighten the risk of chronic diseases by promoting systemic inflammation and gut dysbiosis. Hence, there is a pressing need for healthcare and public health professionals to raise awareness about the harmful effects of such diets and to engage in global discussions on the affordability and sustainability of healthier eating options.

References: Adolph, T. E., & Tilg, H. (2024). Western diets and chronic diseases. Nature Medicine. doi:10.1038/s41591-024-03165-6

In a recent study published in the journal Nature, by recruiting the immune system to combat tumour cells, immunotherapy has improved survival rates, offering hope to millions of cancer patients. However, only about one in five people responded favourably to these treatments.

With a goal of understanding and addressing immunotherapy’s limitations, researchers at Washington University School of Medicine in St Louis have found that the immune system can be its own worst enemy in the fight against cancer.

Cancer vaccines represent a new approach to personalised cancer immunotherapy. Aimed at the mutant proteins specific to a patient’s tumour, such vaccines induce killer T cells to attack tumour cells while leaving healthy cells unharmed. Schreiber’s group previously showed that more effective vaccines also activate helper T cells, another immune cell type, that recruit and expand additional killer T cells to destroy the tumours. But when they tried to add increased amounts of the helper T cell target to supercharge the vaccine they found that they had generated a different type of T cell that inhibited rather than promoted tumour rejection.

Tr1 cells normally put the brakes on the immune system to prevent it from attacking the body’s healthy cells. But their role in cancer has not been seriously explored. Looking through previously published data, the researchers found that tumours from patients who had responded poorly to immunotherapy had more Tr1 cells compared with tumours of patients who had responded well. The number of Tr1 cells also increased in mice as tumours grew bigger, rendering the mice insensitive to immunotherapy.

It is concluded that the drug effectively circumvents the suppressive immune cells that often hinder the effectiveness of immunotherapy. By doing so, it significantly enhances the ability of the immune system to target and destroy cancer cells, potentially improving the overall efficacy of immunotherapy treatments.

References: Awwad, M. & North, R. J. Immunologically mediated regression of a murine lymphoma after treatment with anti-L3T4 antibody. A consequence of removing L3T4+ suppressor T cells from a host generating predominantly Lyt-2+ T cell-mediated immunity. J. Exp. Med. 168, 2193–2206 (1988).