Betaine
Regulatory sources consulted
Contraindications
Absolute
- Hypersensitivity to the product.
Clinical warnings
- Boxed warning · Hypermethioninaemia may be associated with cerebral oedema; monitor methionine and neurological symptoms with the metabolic team. — FDA CYSTADANE prescribing information
Drug interactions
- ModerateVigabatrina
Mechanism: May reduce vigabatrin concentrations; specialist assessment is required.
Recommendation: Co-administration requires assessment by the treating team.
FDA CYSTADANE prescribing information
- ModerateMedicines that affect GABA
Mechanism: Co-administration requires specialist review for possible clinical relevance.
Recommendation: Co-administration requires assessment by the treating team.
FDA CYSTADANE prescribing information
Pregnancy and lactation
During pregnancy and breastfeeding, use must be individualised by the treating team.
Recent literature (PubMed)
The relationship between nutrition and brain health is intricate. Studies suggest that nutrients during early life impact not only human physiology but also mental health. Although the exact molecular mechanisms that depict this relationship remain unclear, there are indications that environmental factors such as eating, lifestyle habits, stress, and physical activity, influence our genes and modulate their function by epigenetic mechanisms to shape mental health outcomes. Epigenetic mechanisms act as crucial link between genes and environmental influences, proving that non-genetic factors could have enduring effects on the epigenome and influence health trajectories. We review studies that demonstrated an epigenetic mechanism of action of nutrition on mental health, focusing on the role of specific micronutrients during critical stages of brain development. The methyl-donor micronutrients of the one-carbon metabolism, such as choline, betaine, methionine, folic acid, VitB6 and VitB12 play critical roles in various physiological processes, including DNA and histone methylation. These micronutrients have been shown to alter gene function and susceptibility to diseases including mental health and metabolic disorders. Understanding how micronutrients influence metabolic genes in humans can lead to the implementation of early nutritional interventions to reduce the risk of developing metabolic and mental health disorders later in life.
Excessive alcohol consumption is a global healthcare problem with enormous social, economic, and clinical consequences. While chronic, heavy alcohol consumption causes structural damage and/or disrupts normal organ function in virtually every tissue of the body, the liver sustains the greatest damage. This is primarily because the liver is the first to see alcohol absorbed from the gastrointestinal tract via the portal circulation and second, because the liver is the principal site of ethanol metabolism. Alcohol-induced damage remains one of the most prevalent disorders of the liver and a leading cause of death or transplantation from liver disease. Despite extensive research on the pathophysiology of this disease, there are still no targeted therapies available. Given the multifactorial mechanisms for alcohol-associated liver disease pathogenesis, it is conceivable that a multitherapeutic regimen is needed to treat different stages in the spectrum of this disease.
Choline is an essential micronutrient critical for cellular and organismal homeostasis. As a core component of phospholipids and sphingolipids, it is indispensable for membrane architecture and function. Additionally, choline is a precursor for acetylcholine, a key neurotransmitter, and betaine, a methyl donor important for epigenetic regulation. Consistent with its pleiotropic role in cellular physiology, choline metabolism contributes to numerous developmental and physiological processes in the brain, liver, kidney, lung and immune system, and both choline deficiency and excess are implicated in human disease. Mutations in the genes encoding choline metabolism proteins lead to inborn errors of metabolism, which manifest in diverse clinical pathologies. While the identities of many enzymes involved in choline metabolism were identified decades ago, only recently has the field begun to understand the diverse mechanisms by which choline availability is regulated and fuelled via metabolite transport/recycling and nutrient acquisition. This review provides a comprehensive overview of choline metabolism, emphasizing emerging concepts and their implications for human health and disease.
Testosterone boosters are heavily marketed on social media and marketplaces to men with claims to significantly increase testosterone. Lax industry regulation has allowed sales of supplements to thrive in the absence of verification of their purported benefits. Our primary objective was to systematically review all data published in the last two decades on testosterone boosters and determine their efficacy. Our outcome of interest was total testosterone increase versus placebo in four different populations: male athletes, men with late-onset hypogonadism infertile men and healthy men. Following search and screening, 52 studies were included in our review, relating to 27 proposed testosterone boosters: 10 studies of cholecalciferol; 5 zinc/magnesium; 4 Tribulus terrestris and creatine; 3 Eurycoma longifolia and Withania somnifera; 2 betaine, D-aspartic acid, Lepidium meyenii and isoflavones; while the remainder were single reports. Our findings indicate that most fail to increase total testosterone. The exceptions were β-hydroxy β-methylbutyrate and betaine, which can be considered effective for male athletes. Eurycoma longifolia, a blend of Punica granatum fruit rind and Theobroma cacao seed extracts (Tesnor™) and purified Shilajit extract (PrimaVie™) can be considered possibly effective for men with late-onset hypogonadism; Eurycoma longifolia and Withania somnifera possibly effective for healthy men; and a non-hormonal aromatase inhibitor (Novadex XT™) possibly effective for male athletes.
Reef-building corals, recognized as cornerstone species in marine ecosystems, captivate with their unique duality as both symbiotic partners and autotrophic entities. Beyond their ecological prominence, these corals produce a diverse array of secondary metabolites, many of which are poised to revolutionize the domains of pharmacology and medicine. This exhaustive review delves deeply into the multifaceted world of coral-derived lipids, highlighting both ubiquitous and rare forms. Within this spectrum, we navigate through a myriad of fatty acids and their acyl derivatives, encompassing waxes, sterol esters, triacylglycerols, mono-akyl-diacylglycerols, and an array of polar lipids such as betaine lipids, glycolipids, sphingolipids, phospholipids, and phosphonolipids. We offer a comprehensive exploration of the intricate biochemical variety of these lipids, related fatty acids, prostaglandins, and both cyclic and acyclic oxilipins. Additionally, the review provides insights into the chemotaxonomy of these compounds, illuminating the fatty acid synthesis routes inherent in corals. Of particular interest is the symbiotic bond many coral species nurture with dinoflagellates from the Symbiodinium group; their lipid and fatty acid profiles are also detailed in this discourse. This exploration accentuates the vast potential and intricacy of coral lipids and underscores their profound relevance in scientific endeavors.