MEMOSINE

Memosine: natural support for healthy homocysteine management.

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Understanding Hyperhomocysteinemia

What is Hyperhomocysteinemia?
Hyperhomocysteinemia is a metabolic condition characterized by elevated plasma levels of homocysteine, a sulfur-containing amino acid that is a natural byproduct of methionine metabolism.
From Theory to Clinical Practice
Historically, homocysteine was considered primarily a biochemical marker. However, accumulating scientific evidence has established it as an independent risk factor associated with endothelial dysfunction and impaired vascular health.
Vascular Risks
The clinical significance of elevated homocysteine lies in its ability to damage the vascular endothelium and compromise the structural integrity of blood vessel walls. This process promotes vascular injury and contributes to the development and progression of atherosclerosis, highlighting the importance of appropriate clinical assessment and monitoring.

Metabolic Pathways of Homocysteine Regulation

The Role of Remethylation and Transsulfuration
Homocysteine is a key intermediate in methionine metabolism and is regulated through two major metabolic pathways.
In the remethylation pathway, homocysteine is converted back to methionine by the enzyme methionine synthase, a reaction that requires adequate levels of vitamin B12 and folate. In the transsulfuration pathway, homocysteine is converted into cystathionine and subsequently into cysteine. This process is catalyzed by the enzyme cystathionine β-synthase (CBS), which requires vitamin B6 as an essential cofactor.

The Impact of Metabolic Dysfunction
Maintaining the balance between these two pathways is essential for cardiovascular and cerebrovascular health. When either pathway is impaired or functions inefficiently, homocysteine metabolism is compromised, leading to elevated plasma homocysteine concentrations—a condition known as hyperhomocysteinemia.

The Clinical Significance of MTHFR Mutations

Enzymatic Impairment and Metabolic Efficiency
Homozygous mutations in the MTHFR gene significantly reduce the activity of the methylenetetrahydrofolate reductase enzyme. As a result, the conversion of folic acid into 5-methyltetrahydrofolate (5-MTHF), its biologically active form, is impaired. Consequently, even an adequate dietary intake of folate may not ensure sufficient production of active folate, compromising the remethylation of homocysteine.

Enzymatic inefficiency impairs remethylation, leading to chronic plasma homocysteine accumulation. This metabolic ‘clogging’ promotes hyperhomocysteinemia, exposing the patient to severe risks to vascular health.”

IN-DEPTH ANALYSIS

HYPERHOMOCYSTEINEMIA

Clinical Implications and Pathophysiology

Cerebrovascular Risk and Small Vessel Disease
Hyperhomocysteinemia is recognized as an independent risk factor for cerebrovascular disease and contributes to endothelial dysfunction, particularly affecting small cerebral vessels. Elevated plasma homocysteine concentrations have been associated with an increased risk of ischemic stroke and the progression of cerebral small vessel disease, both of which are important contributors to vascular cognitive impairment (Obeid et al., 2017; Zhang et al., 2021).

Cerebrovascular diseases: hyperhomocysteinemia is responsible for damage to small cerebral arteries. Patients with hyperhomocysteinemia exhibit a four-fold increased risk of developing cerebral venous sinus thrombosis (Martinelli, 2003). Furthermore, a strong correlation is observed between hyperhomocysteinemia and the risk of developing ischemic stroke events (Wald, 2006).

Cardiovascular Complications and Thrombotic Risk
Beyond its effects on cerebral circulation, hyperhomocysteinemia contributes to systemic vascular damage by promoting endothelial dysfunction and accelerating atherosclerotic processes. Clinical evidence supports an association between elevated homocysteine levels and an increased risk of thromboembolic events, including deep vein thrombosis and coronary artery disease. These findings highlight the importance of appropriate management strategies aimed at reducing long-term cardiovascular risk (Moretti et al., 2017; Humphrey et al., 2020).

IN-DEPTH ANALYSIS

MEMOSINE reduces the levels of HOMOCYSTEINE

Memosine tablet contains

Betaine 378.5 mg
CurQfen® 200 mg
of which 70 mg of total curminoids,
60 mg fenugreek fiber
Vitamin B6 9.5 mg
Vitamin D 25 mcg
Vitamin B12 33 mcg
Folic acid (Quatrefolic®) 400 mcg

Gluten Free

REQUEST THE ENTIRE NUTRITIONAL INFORMATION TABLE

Turmeric

Native indian plant, belong to the ginger family
Curcumin is extracted from the dried and ground root
It is one of the components of curry
Used in traditional Asian medicine
Antioxidant and anti-inflammatory properties, useful for a large group of diseases
Indian populations have low incidence of dementia
Epidemiological data suggest that the high consumption of turmeric among Indian populations is associated with a lower incidence of certain diseases, supporting the hypothesis that curcumin may play a potential role in counteracting some of the adverse vascular effects associated with hyperhomocysteinemia.

Pinto, D. S., et al. (2020). Curcumin and its potential effects on the cardiovascular system and hyperhomocysteinemia: A review of molecular mechanisms. Journal of Nutritional Biochemistry, 82, 108405.

Zullo, G., et al. (2022). Homocysteine, Endothelial Dysfunction, and Degenerative Pathologies: State of the Art. Journal of Clinical Medicine, 11(13), 3745.

Ng T.P., Chiam P.C., Lee T., Chua H.C., Lim L., Kua E.H. Curry consumption and cognitive function in the elderly. Am. J. Epidemiol. 2006;164:898-906.

CurQfen®

It is a formulation based on free curcuminoids under amorphous form, embedded within a soluble fiber matrix derived by fenugreek that allows curcuminoids absorption, in a free form, directly by the intestines.

100% natural
curcuminoids absorption under a free form
Pharmacokinetics: 24 h
Able to cross the blood-brain barrier

VITAMIN D

Vitamin D is defined as a group of fat-soluble pro-hormones consisting of 5 different vitamins: the two most important are vit.D2 (er gocalciferol, plant origin) and vit.D3, or cholecalciferol, derived from cholesterol, animal origin, the more biologically active form.
Very few foods naturally have vitamin D (fish, eggs, liver, some mushrooms). The major source of our body’s vitamin D comes from the sun exposure.
Vitamin D3 obtained through sun exposure (particularly UVB irradiation) or through the diet undergoes two hydroxylation reactions and can be transformed, in the liver and kidney, into calcitriol, its active metabolite.
The Italian Society of Osteoporosis, Mineral Metabolism and Skeletal Diseases (SIOMMMS) claims that 80% of the population in Italy is vit.D deficient and this deficient condition would increase with advancing age affecting almost the entire elderly population.

Biological functions of vitamin D

Vitamin D acts by a hormone-like mechanism of action, binding to the VDR receptor found in target cells.
One of the most important roles of vitamin D is to maintain skeletal calcium balance by promoting calcium absorption in the gut, maintaining calcium and phosphate levels for bone formation, enabling parathyroid hormone proper functioning for the correct serum calcium levels maintenance.
Recent studies have suggested that vitamin D plays a role in regulating the innate-type immune response through the reduction of pro-inflammatory cytokines release by T lymphocytes and inhibition of t cells proliferation.
In vitro experiments have shown that hydroxycitriol can stimulate the production of human cathelicidin (CAMP), a peptide with antimicrobial action in different cell cultures.
The scientific literature also contemplates a number of epidemiological and observational studies regarding the correlation between low vitamin D levels and the risk of developing specific cancers, multiple slerosis, and depression.

The Role of Vitamin D in Hyperhomocysteinemia (HHcy) Management

The Role of Vitamin D in Hyperhomocysteinemia (HHcy) Management

Metabolic Regulation: Vitamin D may contribute to the maintenance of homocysteine homeostasis, potentially helping to regulate elevated plasma homocysteine levels(Vojinovic et al., 2020).
Endothelial Protection: Vitamin D may support vascular function by reducing oxidative stress and contributing to the preservation of endothelial integrity in the context of HHcy (Zullo et al., 2022).
Neuronal Protection: Vitamin D may help counteract glutamate-mediated excitotoxicity and neuroinflammatory processes associated with elevated homocysteine levels.
Potential Protective Synergy: Through its neurotrophic and neuroprotective effects, Vitamin D may contribute to the preservation of neuronal function and blood-brain barrier integrity in conditions associated with hyperhomocysteinemia.

Recommended vitamin D daily dose

The recommended dose ranges from 400 to 1000 I.U. per day

1 I.U. corresponds to 0.025 mcg of cholecalciferol
1 mcg of cholecalciferol corresponds to 40 I.U.
MEMOSINE contains 25 mcg of cholecalciferol per tablet
25 mcg corresponds to 1000 daily units, the recommended dose

MEMOSINE contains 1000 units of VITAMIN D per tablet