Boost Your Metabolism: The Power of Vitamins!



They're considered "micro" nutrients, in spite of the amazing variety and versatility that they have, together with the fact that they’re deemed necessary to perform almost every metabolic reaction in order to be able to produce a functional product that will then of course keep feeding the train sequence of reactions needed to create a homeostatic state within you.


They speed up, couple, enhance, link and energize your whole asset of metabolic reactions. They're also essential components of key central energetic molecules of your metabolism of carbs, fats, and proteins such as Acetyl-CoA, NAD, FAD, FMN, and some of the Quinones needed for the exchange of energy in the oxidative phosphorylation pathway (1).


Vitamins, to start with are divided into two categories: fat soluble and water soluble. As the name stands for, some vitamins are easier transported by fats and they need that kind of oily consistency in order to be able to perform their functions, inside this group we find:


Vitamin A, which plays an essential role in maintaining a good health sight, now there is evidence that it also plays an essential role in the metabolism of carbs, fats and proteins as a helper on the transportation process of fats.


The main forms of vitamin A are retinol, retinoic acid and retinal, while the main liver storage form is retinyl palmitate.The re-surging interest in vitamin A relates to retinoid acid’s actions as an endocrine and paracrine hormone. Retinoic acid is thought to be essential for embryonic stem cell differentiation and development, and in maintaining healthy structure and function of epithelial cells (2).


Vitamin A has a role in the regulation of the macronutrient metabolism of carbohydrates, lipids and proteins. This vitamin is also thought to inhibit the growth of tumour cells in vitro and may play a role in controlling cell division and differentiation, as well as cell apoptosis (2).


Vitamin D is also known as a pro-hormone, meaning it will help you in the metabolism of cholesterol aiding it to regulate the production of hormones.

Is popular due to being one of the main helpers to absorb calcium, and of course related to the bone health and articulation maintenance.


However, as research advances there are now new functions associated with the availability of this Vitamin. The optimum blood level of vitamin D is associated with the overall health of bone, skin and the immune response. Vitamin D status has been correlated with risk status for cardiovascular disease and stroke.


In addition, low levels of vitamin D were observed in patients with respiratory infections and HIV, which may relate to the role of vitamin D in immunity. Low levels of vitamin D and its metabolites have also been indirectly linked to the development of breast cancer. The active form of vitamin D, (1,25-(OH)2D3), and the vitamin D receptors (VDRs) are postulated to have a regulatory effect on normal and breast cancer cell growth and differentiation. In addition, 1,25-(OH)2D is thought to have a role in TNF-α expression, which induces apoptosis of cancer cells (2).


There are two main forms of vitamin D: ergocalciferol (also called vitamin D2) and cholecalciferol (also known as vitamin D3). Vitamin D2 is provided by plants, which are subjected to ultraviolet irradiation, or by dietary supplementation. While a small quantity of vitamin D3 is obtained from food derived from animals, the greatest natural source of this vitamin is endogenous synthesis during sunlight exposure. This endogenous synthesis is influenced by many factors such as skin thickness and colour, the period of sunlight exposure and the season (2).


Vitamin E, known for its antioxidant properties, allows also to reduce the reactive oxygen species (ROS), allowing to lower inflammation and proliferation of cancerous or pre-cancerous cells.


Vitamin E is a fat-soluble antioxidant metabolite and an essential dietary factor. There are two naturally occurring groups of vitamin E: tocopherols and tocotrienols. This vitamin inhibits platelet aggregations, and therefore it may play a protective role against the atherosclerotic process and cardiovascular disease. It has also been suggested that vitamin E has a protective role against arthritis, cataracts, neurological disease and immunological disorders (2).


Vitamin E has been associated with cancer prevention, because of its involvement in a variety of biological activities, including anti-oxidation, anti-proliferation and anti- inflammation. This is thought to be through vitamin E’s role in protecting membrane polyunsaturated fatty acids and plasma lipoproteins from free radical attack and γ-tocopherol’s role in NO2 detoxification. This vitamin has also been linked with suppression of the synthesis of TNF, IL-1, IL-6 and IL-8. In addition, in human breast cancer cell lines vitamin E has been shown to have apoptotic and growth inhibitory effects on the cancer cells (2).


Vitamin E deficiency is most commonly associated with genetic or malabsorption disorders e.g. cystic fibrosis, chronic hepatitis and gastrointestinal disorders (2).


Vitamin K, known due to the relation to clotting factors, better coagulation and strengthening your wound healing processes.


It has 2 primary forms, K1 and K2. Vitamin K1 (phylloquinone) is found in green leafy vegetables, cabbage, and cauliflower. Lesser quantities are found in fish, meat, and some fruits. The gut microflora synthesizes vitamin K2 (menoquinone) (3).

Is necessary for the activation of certain clotting factors in the liver which are responsible for coagulation. For activation to occur, the clotting proteins must bind calcium. Vitamin K-dependent gamma-carboxylation of specific glutamic acid residues allows the proteins to bind calcium and carry out the coagulation cascade. Specifically, vitamin K serves as a cofactor for gamma-glutamyl carboxylase and catalyzes the post-translational synthesis of gamma-carboxy-glutamyl residues. This process activates prothrombin and factors VII, IX, X, protein C and S (3).


Vitamin-K deficiency is clinically significant due to its prevalence in a variety of patient populations. Risk factors include antibiotic use which interferes with vitamin-K production in the gut, nutritional deficiency and high ingestion of vitamins A and E. Newborns are also at risk for deficiency due to immature gut flora, poor placental transfer and low content in breast milk. The risk in newborns is further increased with a maternal history of anticonvulsant and anticoagulant use. A common clinical syndrome which results from vitamin-K deficiency is hemorrhagic disease of the newborn, a life-threatening bleeding condition in neonates (3).


Hydrosoluble Vitamins.


Vitamin B1. Important in function of nervous system. Helps release energy from foods during metabolic reactions; promotes normal appetite.


Recommended Intake: Infants: 0.2–0.3 mg, Children: 0.5–0.6 mg, Adolescents: 0.9–1.2 mg, Men: 1.2 mg, Women: 1.1 mg Pregnant/lactating

Women: 1.4 mg (4).


Pathologies: Associated with neuronal loss, gliosis (neural inflammation), vascular damage (4).


Riboflavin (Vitamin B2). Helps with vision, release energy from foods; healthy skin.

Recommended Intake: Infants: 0.3–0.4 mg Children: 0.5–0.6 mg Adolescents: 0.9–1.3 mg Men: 1.3 mg, Women: 1.1 mg

Pregnant women: 1.4 mg Lactating women: 1.6 mg.


Pathologies: Peripheral nerve demyelination in chickens. (4)


Niacin (Vitamin B3). Promotes healthy nerves, skin. Energy production from foods; aids digestion, promotes normal appetite.


Recommended Intake: Infants: 2–4 mg Children: 6–8 mg Adolescents: 12–16 mg Men: 16 mg, Women: 14 mg, Pregnant women: 18 mg Lactating women: 17 mg.


Pathologies: Chromatylic (color perception) changes in neurons of motor cortex. Degeneration of spinal cord. Patchy demyelination in peripheral nerves. Nonspecific dermatitic changes (i.e. perivascular lymphohistologic infiltrate, mild edema, fibrosis) (4).


Vitamin B5, Pantothenic Acid . Aids in formation of hormones; involved in energy production. Pantothenic acid, a component of coenzyme A, is an essential nutrient that is required in the synthesis of acetylcholine and melatonin. Coenzyme A is also used as a means of transporting carbon atoms within the cell by catalyzing the production of acetyl-CoA. Therefore, it is important in the conversion of pyruvate to acetyl- CoA and α-ketoglutarate to succinyl-CoA which is necessary for the propagation of the tricarboxylic acid cycle in energy production. It is also needed for the synthesis of fatty acids.


Recommended Intake: Infants: 1.7–1.8 mg, Children: 2–3 mg, Adolescents: 4–5 mg, Men and Women: 5 mg, Pregnant women: 6 mg, Lactating women: 7 mg.


Pathologies: Naturally occurring pantothenic acid deficiency in humans is actually very rare and has been observed only in cases of severe malnutrition. Most information comes from case reports of severe malnutrition or from experimental animal research. The symptoms of deficiency are similar to other B vitamin deficiencies, which are primarily are due to impaired energy production. Nonspecific systemic symptoms commonly seen are fatigue, irritability, apathy, malaise, nausea, and abdominal cramps (4).


Vitamin B6, Pyridoxine οr Pyridoxal. Is a collective term for the family of 2-methyl- 3-hydroxy-5-hydroxymethylpyridine compounds. There are six major derivatives; pyridoxine, pyridoxal, and pyridoxamine, and their phosphorylated derivatives, pyridoxine-5-phosphatase, pyridoxal-5-phosphatase, and pyridoxamine-5-phosphatase. Pyridoxine is a water- soluble vitamin that acts primarily as a necessary cofactor for over 100 enzymes that are mostly involved in amino acid metabolism, including transamination, deamination, and decarboxylation, in addition to being necessary in glycolysis and gluconeogenesis.


It is also needed in the decarboxylation of some amino acids into neurotransmitters. Examples of these are the conversion of histidine to histamine, tryptophan to serotonin, glutamate to γ-aminobutyric acid (GABA), and dihydroxyphenylalanine to dopamine. Pyridoxine is also needed for the synthesis of sphingolipids, hemoglobin, and gene expression.


Recommended Intake: Infants: 0.1–0.3 mg Children: 0.5-0.6 mg Adolescents: 1.0 –1.3 mg Men and women (19–50 years): 1.3 mg, Men over 50 years: 1.4 mg, Women over 50 years: 1.3 mg, Pregnant women: 1.9 mg, Lactating women: 1.2 mg.


Pathologies: Pyridoxine deficiency may present with cardiovascular, dermatologic, gastrointestinal, hematologic, or neuro- logic symptoms. Mild deficiency in B6 vitamin is a state that may be associated with an increased risk of cardiovascular disease. Cardiovascular abnormalities include early myocardial infarction, early stroke, and recurrent venous thromboembolism.


Associated with higher risk for coronary artery disease (CAD) in patients with coronary atherosclerosis. Hematologic problems include anemia. Dermatologic symptoms include erythematous itching, burning, blisters, vesicles, hyperpigmentation, and thickening of skin, similar to those observed with vitamin B2 or vitamin B3 deficiencies. Central nervous system symptoms include depression, anxiety, irritability, confusion, and generalized seizures. Gastrointestinal symptoms include nausea, diarrhea, abdominal discomfort, and pain. (4).


Vitamin B8 or B7, Biotin. Helps release energy from carbohydrates; aids in fat synthesis.


The brain is particularly sensitive to the delivery and metabolism of glucose. Biotin plays a key role in glucose metabolism and homeostasis, including regulation of hepatic glucose uptake, gluconeogenesis (and lipogenesis), insulin receptor transcription and pancreatic β-cell function.


Recommended Intake: Infants: 5–6 mg, Children: 8–12 mg, Adolescents: 20–25 mg, Men and women: 30 mg Pregnant women: 30 mg, Lactating women: 35 mg. (4).


Pathologies: Frank deficiency in biotin is rarely reported, although lower circulating levels of biotin have been reported in those suffering gluco-regulatory dysfunction, for instance Type II diabetes, alongside an inverse relationship between fasting plasma glucose and biotin levels (5).


Vitamin B9, Folate and Vitamin B12, Cobalamin.


The functions of these two vitamins are inextricably linked due to their complementary roles in the “folate” and “methionine” cycles. Indeed, a deficiency in vitamin B12 results in a functional folate deficiency, as folate becomes trapped in the form of methyltetrahydrofolate. An actual or functional folate deficiency, with an attendant reduction in purine/pyrimidine synthesis and genomic and non-genomic methylation reactions in brain tissue, leads to decreased DNA stability and repair and gene expression/transcription, which could hamper neuronal differentiation and repair, promote hippocampal atrophy, demyelination and compromise the integrity of membrane phospholipids impairing the propagation of action potentials (5).


Recommended Intake Vitamin B9: Men and women ages 19 years and older should aim for 400 mcg. Pregnant and lactating women require 600 mcg and 500 mcg, respectively. People who regularly drink alcohol should aim for at least 600 mcg of folate daily since alcohol can impair its absorption.


Recommended Intake Vitamin B12: The Recommended Dietary Allowance for men and women ages 14 years and older is 2.4 micrograms (mcg) daily. For pregnancy and lactation, the amount increases to 2.6 mcg and 2.8 mcg daily, respectively.


Pathologies: Folate related downregulation of the synthesis of proteins and the nucleotides required for DNA/RNA synthesis, has ramifications for rapidly dividing tissue in particular, and therefore underlies the foetal developmental disorders and megaloblastic anaemia (alongside aspects of neuronal dysfunction), associated with either folate or vitamin B12 deficiency. The efficient functioning of the folate cycle is also necessary for the synthesis and regeneration of tetrahydrobiopterin, an essential cofactor for the enzymes that convert amino acids to both monoamine neurotransmitters (serotonin, melatonin, dopamine, noradrenaline, adrenaline), and nitric oxide (5).


Vitamin B12 deficiency is often manifested in the form of neurological symptoms prior to the appearance of more typical hematological changes. Notably, whilst about a third of those suffering folate or vitamin B12 deficiency present only with anaemia, a similar proportion present only with neuropsychiatric symptoms. Indeed, more than a third of psychiatric admissions have been found to be suffering deficiencies in folate or vitamin B12 (5).


Finally, another important water soluble Vitamin C is Ascorbic Acid, which is known by the protection that it gives you in terms of the immune system or against common colds, however,


Ascorbic acid, also known as vitamin C, is a water-soluble vitamin that is most importantly needed as an enzymatic cofactor in the synthesis of collagen. Therefore, it is needed for the production and repair of skin, tendons, ligaments, and blood vessels. The basis of the neurologic disorders observed in scurvy is probably related to low activity of other ascorbic acid dependent enzymes. Indoleamine 2,3-dioxygenase, the first and rate-limiting enzyme in human tryptophan metabolism, has also been implicated in the pathogenesis of many diseases. This enzyme is necessary to form kynurenine, and its pathway regulates the metabolism of tryptophan to neuroactive compounds, and also seems to be a key factor in the communication between the nervous and immune systems (3).


Intracellular ascorbate serves several functions in the CNS, including antioxidant protection, peptide amidation, myelin formation, synaptic potentiation, and protection against glutamate toxicity (3).


Recommended Intake: Infants: 40–50 mg, Children: 15–25 mg, Adolescents: 45–75 mg, Men: 90 mg, Women: 75 mg, Pregnant Women: 80-85 mg, Lactating women: 115–120 mg, Smokers: +35 mg.


Pathologies: Vitamin C deficiency causes a clinical syndrome known as scurvy. Inactivation of peptidyl-prolyl-4-hydroxylase (P4H) by ascorbic acid deficiency is the first identified cause of scurvy. The elderly, alcoholics, and those who subsist on diets devoid of fresh fruits and vegetables are most vulnerable. Infants and children on restrictive diets for medical, economic, or social reasons are at risk for scurvy (3).


The symptoms of scurvy result from the breakdown of tissues dependent on collagen. The signs of the disease are caused by alteration of the extracellular matrix in the blood vessels, bones, skin, gums, and tendons, which result in skin lesions, hemorrhages, and fragile bone (Fain, 2005). Symptoms of scurvy include lassitude, vision problems, and neurologic disorders. Neurologic symptoms associated with vitamin C deficiency are unusual (3).


In summary, as depicted in all the review of Water and Fat Soluble Vitamins we could witness that they're more than essential for plenty of your metabolic reactions and as research is now pointing out, many of the neurodegenerative diseases are associated with a deficiency of any of the Vitamin B group.


Many times we don't see, to find the relationship of all of these small molecules, but they are so important that in general they are considered the oil for your whole metabolic engine. Therefore missing one of them starts disrupting one of the pathways which will in turn generate a missing link in the next pathway and that could initiate a chain reaction between your whole arsenal of metabolic intermediates. Thus, all of this metabolic disrupted cycles eventually with time will have an effect in the production of reliable chemical messengers either at the level of your nervous system, circulatory compounds or immune messengers.


Additionally the impact of a deficiency of any of these Vitamins will also be translated in a poor microbiome health that will start to produce a lousy gastrointestinal health and will give rise to leaky gut, gastroesophageal reflux, gastritis, or any of those intestinal issues.


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References.


1. Ortega D. “Sugar: The Sweet Poison!”. https://www.davidortegab.com/post/sugar-the-sweet-poison. October 15th, 2019.


2. Albahrani, A. A., & Greaves, R. F. (2016). Fat-soluble vitamins: clinical indications and current challenges for chromatographic measurement. The Clinical Biochemist Reviews, 37(1), 27.


3. Chawla, J., & Kvarnberg, D. (2014). Hydrosoluble vitamins. In Handbook of clinical neurology (Vol. 120, pp. 891-914). Elsevier.


4. Reddy P, Jialal I. Biochemistry, Vitamin, Fat Soluble. [Updated 2018 Nov 23]. In: StatPearls.


5. Kennedy, D. O. (2016). B vitamins and the brain: Mechanisms, dose and efficacy—A review. Nutrients, 8(2), 68.

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