Some studies that warn about silicion dioxide/silica

[Mufasa]

@Hans I saw that you sometimes recommend supplements with silicon dioxide (sometimes called silica) in it.
Here are some studies that explain why that is a bad idea.

All silicon dioxide on the market is likely toxic. Even when it is listed as non-nano. The reason is that it just uses aggregates of nano particles that in the body are going back to their nano form:

Is aggregated synthetic amorphous silica toxicologically relevant? - Particle and Fibre Toxicology

Background The regulatory definition(s) of nanomaterials (NMs) frequently uses the term ‘agglomerates and aggregates’ (AA) despite the paucity of evidence that AA are significantly relevant from a nanotoxicological perspective. This knowledge gap greatly affects the safety assessment and...

particleandfibretoxicology.biomedcentral.com

"The regulatory definition(s) of nanomaterials (NMs) frequently uses the term ‘agglomerates and aggregates’ (AA) despite the paucity of evidence that AA are significantly relevant from a nanotoxicological perspective. This knowledge gap greatly affects the safety assessment and regulation of NMs, such as synthetic amorphous silica (SAS). SAS is used in a large panel of industrial applications. They are primarily produced as nano-sized particles (1–100 nm in diameter) and considered safe as they form large aggregates (> 100 nm) during the production process.

This study aimed to assess the impact of aggregation on cytotoxic/biological activities in submerged cell cultures and the toxicological relevance of SAS aggregates of different sizes. In general, aggregation resulted in reduced toxicological activity of SAS. Looking closer, the large, quickly precipitating aggregates (PREC) exhibited the lowest cytotoxicity/biological activity in vitro. On the other hand, an important fraction (25% of the mass of AGGR) of non-precipitating aggregates (SuperN), which contains aggregates larger than 100 nm, exhibited similar activities as nano-sized aggregates (DE-AGGR). We conclude that aggregates with size greater than 100 nm should not be necessarily considered as less toxic than their nano-sized counterparts. This study suggests that aggregates of SAS are toxicologically relevant and should be part of the definition of NMs."

https://pubs.acs.org/doi/10.1021/nn204728k

"The presence, dissolution, agglomeration state, and release of materials in the nano-size range from food containing engineered nanoparticles during human digestion is a key question for the safety assessment of these materials. We used an in vitro model to mimic the human digestion. Food products subjected to in vitro digestion included (i) hot water, (ii) coffee with powdered creamer, (iii) instant soup, and (iv) pancake which either contained silica as the food additive E551, or to which a form of synthetic amorphous silica or 32 nm SiO2 particles were added. The results showed that, in the mouth stage of the digestion, nano-sized silica particles with a size range of 5–50 and 50–500 nm were present in food products containing E551 or added synthetic amorphous silica. However, during the successive gastric digestion stage, this nano-sized silica was no longer present for the food matrices coffee and instant soup, while low amounts were found for pancakes. Additional experiments showed that the absence of nano-sized silica in the gastric stage can be contributed to an effect of low pH combined with high electrolyte concentrations in the gastric digestion stage. Large silica agglomerates are formed under these conditions as determined by DLS and SEM experiments and explained theoretically by the extended DLVO theory. Importantly, in the subsequent intestinal digestion stage, the nano-sized silica particles reappeared again, even in amounts higher than in the saliva (mouth) digestion stage. These findings suggest that, upon consumption of foods containing E551, the gut epithelium is most likely exposed to nano-sized silica."

One of the reasons they are added to supplements is because it is the only way to get a hard tablet. Without silica, the tablet would fall apart easily.

In non-nano form, such as in plants etc, silicion dioxide is excreted easily. But in nano form, it just goes right through your membrane and will staple in your organs. Especially the stapling of silica in the liver is considered problematic:

Sub-chronic toxicity study in rats orally exposed to nanostructured silica - Particle and Fibre Toxicology

Background Synthetic Amorphous Silica (SAS) is commonly used in food and drugs. Recently, a consumer intake of silica from food was estimated at 9.4 mg/kg bw/day, of which 1.8 mg/kg bw/day was estimated to be in the nano-size range. Food products containing SAS have been shown to contain silica...

particleandfibretoxicology.biomedcentral.com

"Biochemical and immunological markers in blood and isolated cells did not indicate toxicity, but histopathological analysis, showed an increased incidence of liver fibrosis after 84-days of exposure, which only reached significance in the NM-202 treated animals. This observation was accompanied by a moderate, but significant increase in the expression of fibrosis-related genes in liver samples."

https://www.tandfonline.com/doi/full/10.3109/17435390.2014.940408

"This study presents novel insights in the risk assessment of synthetic amorphous silica (SAS) in food. SAS is a nanostructured material consisting of aggregates and agglomerates of primary particles in the nanorange (<100 nm). Depending on the production process, SAS exists in four main forms, and each form comprises various types with different physicochemical characteristics. SAS is widely used in foods as additive E551. The novel insights from other studies relate to low gastrointestinal absorption of SAS that decreases with increasing dose, and the potential for accumulation in tissues with daily consumption. To accommodate these insights, we focused our risk assessment on internal exposure in the target organ (liver). Based on blood and tissue concentrations in time of two different SAS types that were orally and intravenously administered, a kinetic model is developed to estimate the silicon concentration in liver in (1) humans for average-to-worst-case dietary exposure at steady state and (2) rats and mice in key toxicity studies. The estimated liver concentration in humans is at a similar level as the measured or estimated liver concentrations in animal studies in which adverse effects were found. Hence, this assessment suggests that SAS in food may pose a health risk. Yet, for this risk assessment, we had to make assumptions and deal with several sources of uncertainty that make it difficult to draw firm conclusions. Recommendations to fill in the remaining data gaps are discussed. More insight in the health risk of SAS in food is warranted considering the wide applications and these findings."

@haidut I think you will find those studies interesting as well, as you have mentioned the problems of silicon dioxide in your blog. Feel free to share those studies!

 

[DennisX]

Thank you! I stopped using many Life extension supps because of silicon dioxide in them. When I wrote them that I stopped using their supps because they had silicon dioxide in them they wrote back that silicon dioxide was safe!

 

[lamassu]

Good post

 

[Mufasa]

Another one:

https://www.tandfonline.com/doi/full/10.1080/17435390.2021.1931724

"For a long time, oral exposure to food-grade SAS has been considered safe as it was assumed that its bioavailability was neglectable and toxicity studies in which high doses were applied were usually negative (Fruijtier-Pölloth Citation2016). The induction of mild liver (periportal) fibrosis and induced gene expression in fibrosis-related gene sets as a result of subchronic exposure to a pyrogenic SAS, as demonstrated by van der Zande et al. (Citation2014) was therefore received critically. However, recently also other studies demonstrated adverse effects on the liver, already at low doses of exposure, including liver inflammation and lesions, i.e. perivascular amyloid accumulation, but also congestion of sinusoids, focal intralobular necrosis, hepatocyte vacuolization/steatosis, and indications of fibrosis (collagen deposition and increased mRNA levels indicative of apoptosis) (Boudard et al. Citation2019; Li et al. Citation2018; Tassinari et al. Citation2020). Although the toxicity data are inconsistent regarding their outcome, and contradictory studies exist (Table 1), those studies demonstrate that liver effects due to oral exposure to SAS cannot be excluded. Also the study by Hu et al. (Citation2019) adds to this weight of evidence. Though the study was not directed at liver toxicity (and therefore histopathology was not performed), ROS generation in serum and liver was studied weekly within the 90-day study in which mice were exposure to 4 different SAS (including two types of NPs; unclear whether food-grade) at 100 mg/kg bw/d. Pyrogenic SAS NPs (tested at 100 mg/kg bw/d) affected serum and liver biomarkers indicative of liver ROS after 7 weeks of exposure. This was combined with the altered expression of genes associated with ROS production and ER stress in liver, an effect also seen as a result of exposure to colloidal SAS NPs (Hu et al. Citation2019).

Chronically increased ROS could result in irreversible adverse effects, including liver fibrosis (Brand et al. Citation2020; Cichoż-Lach and Michalak Citation2014; Richter and Kietzmann Citation2016; Yu et al. Citation2020). Liver fibrosis is driven by ongoing liver injury and goes through several stages ultimately resulting in irreversible damage. This process starts with inflammation, which can be triggered by ROS generation, and continues with increased production of the extracellular matrix, and subsequently the formation of fibrotic material. Although, most of the histopathological findings in the positive studies in Table 1 do not demonstrate a definitive, irreversible adverse outcome such as liver fibrosis (or any effects at all), these findings can potentially progress to liver fibrosis due to further prolonged exposure. However, the exact mechanism of hepatic toxicity caused by SAS is unknown and a topic of present research (Kermanizadeh, Powell, and Stone Citation2020; Medina-Reyes et al. Citation2020; Murugadoss et al. Citation2017; Qi et al. Citation2020). Yet, as SAS is present in many everyday products, humans will be exposed to SAS on a daily basis over a prolonged period. This indicates that effects on liver cannot be excluded and further studies to the safety and effects resulting from chronic, oral exposure to food-grade SAS are warranted."

 

[liam183]

I've seen a study about it having negative effects on the dopaminergic system too

 

[JCastro]

Any caffeine tablets with silicon dioxide invariably give me neurological symptoms that abate when I stop using them. I have tested this dozens of times. It is a shame, as I have never been able to find any that don't have it, and the ones that claim not to, still cause those symptoms, while caffeine, tea, and cola do not.

I did a write-up about many more studies (up until 2020) supporting the above ones: Harmful Effects of Silicon Dioxide Nanoparticles, a Common Food and Supplement Excipient, on Gut Microbiota, Immunity, Inflammation, and Digestion