door bhrw | okt 31, 2024 | B12, gezondheidszorg
Zo nu en dan zie ik nog oude blogs van mijn hand op LinkedIn verschijnen, zoals recent gebeurde met een stukje dat ik in 2016, dus alweer ruim 8 jaar geleden, schreef over de combinatie van vitamine B12 tekort en de schildklierziekte van Hashimoto.
In dat stukje beschrijf ik twee mensen met vitamine B12 tekort. De eerste is een man met klassieke pernicieuze anemie, bij wie het even duurde voordat de ernstige hypothyreoïdie die hem ook parten speelde werd vastgesteld. Een klassieke situatie, waarin twee auto-immuun aandoeningen hand in hand gaan.
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door bhrw | aug 3, 2024 | Geen categorie, gezondheidszorg, hypofyse
Dit is mijn column in het blad HYPO Nieuws van mei 2024.
door bhrw | mei 6, 2024 | gezondheidszorg, schildklier
SON Kenniscongres mei 2019: Schildklierzorg, nu en in de toekomst
Op zaterdag 25 mei 2019 vierde SON het 1e jubileum in haar huidige vorm. Samen met vele partijen. Een vol huis! Het was een meer dan geslaagd congres met, zoals de bedoeling was, veel ruimte voor dialoog tussen arts en mens met een schildklierziekte. Het gevoel dat achter blijft: de oprechte wens bij alle betrokkenen te werken aan het verbeteren van de kwaliteit van leven van mensen met een schildklieraandoening. Zeer bemoedigend en inspirerend!
Ruim 80% van de mensen met een schildklierziekte is vrouw. En veel schildklier aandoeningen worden (mede) veroorzaakt door ons eigen immuunsysteem.
Mijn lezing op deze dag was getiteld: “Draait het om de hormonen of om de antistoffen?” Niet het meest simpele onderwerp om op zo’n dag toe te lichten. Maar, er was veel interesse in het onderwerp, en er waren heel veel vragen na afloop.
Download de volledige presentatie HIER.
door bhrw | mrt 31, 2024 | gezondheidszorg, hypofyse
Mijn meest recente column in het HYPOnieuws van Februari 2024.
door bhrw | mrt 28, 2024 | gezondheidszorg, wetenschap
Autoimmune gastritis (AIG) is characterized by the destruction of gastric parietal cells, resulting in hypochlorhydria and eventual achlorhydria, as oxyntic glands in the corpus are destroyed and become atrophic. The permanent loss of gastric acid has many impacts—both theoretical and documented. The most concerning of these are hypergastrinemia and increased N-nitroso compounds, both of which increase the risk of gastric cancers. While known deficiencies of B12 and iron are often replaced in AIG, acid is not. Moreover, patients with AIG are often prescribed acid suppression for a stomach that is decidedly no longer acidic, worsening the sequelae of gastric atrophy. Betaine hydrochloride (BHCL) is a short-acting acidifying agent, available over the counter in capsule form. Mealtime acid supplementation has an historic basis and could ameliorate many AIG-related gastrointestinal symptoms. Theoretically, acidification could also reduce the potential for hypergastrinemia and the production of N-nitroso compounds, consequently reducing the risk of gastric cancers. Supplemental vitamin C may also help in preventing gastric N-nitroso formation, regardless of the gastric pH. This narrative review describes the functions of gastric acid in gastrointestinal and immune health, documents the effects of hypochlorhydria in AIG, and proposes potential options for safely re-establishing the acid milieu of the stomach for patients with AIG.
You can download the article HERE.
door bhrw | mrt 1, 2024 | diabetes, gezondheidszorg, wetenschap
Endocrine-Disrupting Chemicals and type 2 diabetes: what is their relationship?
Summary of all research performed in the Department of Endocrinology of the UMCG, on endocrine disruptors, obesity and type 2 diabetes through a personal researcher grant awarded by DiabetesFonds Nederland to dr Jana van Vliet-Ostaptchouk.
Endocrine disrupting chemicals (EDCs) are exogenous compounds with the potential to disturb hormonal regulation and the endocrine system, consequently affecting health and reproduction in animals and humans (1). EDCs can interfere with the production, release, metabolism, and elimination of or can mimic the occurrence of natural hormones. Parabens, bisphenols and phthalates are EDCs which have in common that even though having lipophilic properties, they are quickly metabolized into more water-soluble chemicals. These chemicals in turn are easily excreted via the kidneys from the body. Due to their short half-lives of less than 24 hour, these chemicals are considered to be non-persistent (2-4). In contrast, persistent EDCs are often more resilient to metabolic degradation, making it harder to excrete these chemicals. For example, polychlorinated biphenyls (PCBs) contain chlorine atoms, which make hydroxylation by the liver much harder and leads to half-live times of months to decades. As a result, PCBs are still widely detected in blood regardless of the fact that they have been banned at least in part in Europe in 1985. Even though non-persistent EDCs are easily metabolized and excreted, their use in a wide variety of daily used consumer products has led to an ubiquitous exposure around the world.
For example, bisphenol A (BPA), 2,2-bis(4-hydroxyphenyl)propane, is a synthetic compound that is widely used as a monomer in polycarbonate plastics and epoxy resins, being one of the world’s highest production volumechemicals (Source: paper #13, Environ Int 2015). This means that humans are widely exposed to chlorinated derivatives and structural analogs of bisphenol A.
Exposure to EDCs may play an important role in the global escalating incidence of type 2 diabetes observed in the last few decades (5). Based on the observations that EDCs interfere with the body’s endocrine system, a connection between EDC and altered glucose metabolism and increased risk for T2D is proposed. This project aimed to investigate how EDC determine the risk of T2D and to pinpoint the underlying pathophysiological mechanisms. Our hypothesis was that chronic daily exposure to EDC increases the risk of developing T2D through a cascade of adverse metabolic changes. We performed systematic analysis of EDC-related changes (single and multiple EDC effects) in metabolic functioning, epigenetics and gene expression patterns, combined with an analysis of individual genetic profiles and lifestyle. This strategy aimed to uncover mechanisms underlying EDC-induced metabolic dysregulation. Our main objectives were:
- To investigate whether exposures to EDC as measured in urine increase the risk of T2D and how this risk is modified by lifestyle and genetic predisposition
- To examine the effects of EDC on metabolism and to establish EDC-related alterations in gene function (i.e. DNA methylation and gene expression)
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