Symptoms of vitamin and mineral deficiencies: how to read the signs
A standard blood test does not detect most micronutrient insufficiencies. Biological reference values reflect a threshold of frank deficiency, not a functional optimum. Between the two lies a grey zone, often wide and clinically silent, in which the body nonetheless sends readable signals: persistent fatigue with no identified cause, slowed recovery, irritability, changing skin, brittle nails. These manifestations are neither chance nor hypochondria; they most often reflect a cellular deficit in precise molecules the body needs every day to function properly.
This article reviews the clinical signs associated with an insufficiency of each of the micronutrients in base One. It is not a diagnostic guide, still less an encouragement to self-medicate. It is a recognition tool: learning to read what the body expresses, before biology is forced to quantify it.
THE VITAMINS
Vitamin C — L-ascorbic acid
Vitamin C is a cofactor of about a dozen enzymes involved in collagen synthesis, the production of noradrenaline and adrenaline, and cellular protection against oxidative stress. Its depletion shows up across several distinct clinical registers.
Skin and tissue signs
The skin loses firmness and radiance. Bruises appear after minor trauma, wound healing is prolonged, and hair follicles show characteristic keratoses. Gums may bleed easily when brushing. These signs reflect insufficient collagen synthesis: without correct hydroxylation of proline and lysine, collagen's intermolecular bridges do not form.
Neuroendocrine signs
Adrenal fatigue shows up as mid-day asthenia, heightened sensitivity to stress, and poor recovery after exertion. The adrenal gland holds one of the highest vitamin C densities in the body; each episode of acute stress consumes a significant share of it.
Immune signs
Susceptibility to ENT infections rises, infection episodes last longer, and recovery is more laborious. These reflect weakened lymphocyte defence and immunoglobulin production.
Vitamin E — Mixed tocopherols (α, β, γ, δ)
Vitamin E is the main fat-soluble antioxidant of cell membranes. Its deficiency primarily affects lipid-rich structures: the nervous system, red blood cells and muscles.
Neuromuscular signs
Progressive muscle weakness, coordination problems and altered skin sensitivity can signal a prolonged deficiency. In adults the signs are often subtle: fatigue on exertion, a sense of heavy legs, slightly diminished reflexes.
Cardiovascular and haematological signs
Haemolytic anaemia can occur in marked deficiency, as erythrocytes are particularly vulnerable to lipid peroxidation without tocopherol protection. An elevated oxidised LDL without frank hypercholesterolaemia may also point to vitamin E deficiency.
Skin signs
The skin shows increased dryness, less effective healing and greater sensitivity to photo-oxidation.
Vitamin B1 — Thiamine HCl
Thiamine is the central coenzyme of entry into the Krebs cycle, that is, of cellular energy production from glucose. Its deficiency first appears in the most energy-dependent tissues: the nervous system and the myocardium.
Neurological signs
Tingling in the lower limbs, leg muscle weakness, difficulty concentrating and a failing short-term memory are the first clues. Mental fatigue disproportionate to activity, slowed information processing and irritability without obvious cause are among the signs that functional psychiatry learns to recognise.
Cardiac and general signs
Palpitations, breathlessness on moderate exertion, lower-limb oedema in advanced deficiency. Daily consumption of coffee, tea, alcohol or foods rich in thiaminase (raw fish) worsens these, as these substances degrade or inhibit the vitamin's absorption.
Vitamin B2 — Riboflavin (R5P + HCl)
Riboflavin is the precursor of the coenzymes FAD and FMN, central players in the mitochondrial respiratory chain. Its deficiency, often associated with that of other B vitamins, produces characteristic mucosal and skin signs.
Mucosal signs
The lips crack and show fissures at the corners of the mouth (angular cheilitis). The tongue becomes red, smooth and painful (glossitis). The oral and pharyngeal mucosa are irritated.
Skin and eye signs
Seborrhoeic dermatitis around the nose and ears, eye irritation and photosensitivity, and increased corneal vascularisation point to riboflavin deficiency, common in people with low intake of dairy or animal products.
Haematological signs
A normocytic anaemia can set in, as riboflavin participates in binding iron to haemoglobin.
Vitamin B3 — Niacin and Nicotinamide
Vitamin B3 is the precursor of NAD+, the coenzyme of more than four hundred metabolic reactions. Its classic deficiency, pellagra, has become rare in developed countries, but functional insufficiencies are more widespread than acknowledged.
Metabolic and cognitive signs
Persistent fatigue, difficulty concentrating, weakened memory and unstable mood can reflect insufficient NAD+ production. The sirtuins, NAD+-dependent epigenetic regulators, see their activity reduced, which affects DNA repair and cellular longevity.
Skin and digestive signs
In more pronounced deficiency: sun-sensitive skin, patchy redness on exposed areas, digestive disturbances (nausea, intermittent diarrhoea), mucosal inflammation. The lipid profile can deteriorate with a drop in HDL.
Vitamin B5 — Calcium pantothenate
Vitamin B5 is essential to the synthesis of acetyl-CoA, the universal cofactor of the Krebs cycle, hormone production and neurotransmission. Its deficiency, although rare in isolation, frequently appears within a poly-deficient picture.
Characteristic signs
The burning or tingling sensation in the soles (burning feet syndrome) is one of the most telling signs of a B5 deficit. Added to it are deep fatigue resistant to rest, sleep disturbances, muscle cramps, slow healing, morning nausea and marked irritability.
Skin and endocrine signs
Hair quality deteriorates, the skin loses its capacity to regenerate. Adrenal functions weaken, translating into poor stress management, orthostatic hypotension and reduced resistance to infection.
Vitamin B6 — Pyridoxine HCl + P5P
A cofactor of more than one hundred and sixty enzymatic reactions, vitamin B6 holds a central position in amino acid metabolism and neurotransmitter biosynthesis. Its deficiency produces a remarkably rich clinical picture.
Neuropsychological signs
Depression, anxiety, irritability and sleep disturbances are among the manifestations most frequently associated with a B6 deficit. The synthesis of dopamine, serotonin, GABA and noradrenaline depends directly on P5P as a cofactor; insufficient intake affects the whole neurochemical balance. Premenstrual water retention and premenstrual syndrome can also worsen.
Skin, mucosal and nervous signs
Seborrhoeic dermatitis, stomatitis, angular cheilitis and glossitis are common to B6 and B2 deficiency, which complicates clinical distinction. Limb paraesthesia, mild peripheral neuropathy and cognitive fatigue are other warning signals.
Metabolic signs
Plasma homocysteine rises, as B6 (P5P) is a cofactor of the transsulfuration of homocysteine into cystathionine. A biologically detected asymptomatic hyperhomocysteinaemia should systematically raise the possibility of a B6, B9 or B12 deficit.
Vitamin B8 — D-Biotin
Biotin is a cofactor of the mitochondrial carboxylases involved in the metabolism of carbohydrates, fatty acids and amino acids. Its partial production by the gut microbiota makes it particularly sensitive to flora imbalances.
Hair and skin signs
Diffuse hair loss is the best-known sign of a biotin deficit. The hair becomes dry, brittle and dull. Dermatitis around the orifices (nose, mouth, eyes), brittle nails with longitudinal ridges and dry skin complete the picture.
Neurological signs
Paraesthesia, cognitive fatigue, daytime sleepiness and mild depression can accompany the skin signs. Taking broad-spectrum antibiotics or a marked gut dysbiosis worsens this profile by reducing endogenous biotin production by commensal bacteria.
Vitamin B9 — 5-MTHF (L-5-methyltetrahydrofolic acid)
Folate governs cell replication, red blood cell formation and the methylation cycle. About 40% of the population carries a polymorphism of the MTHFR gene that reduces the conversion of ordinary folic acid into its active form (5-MTHF), making functional deficiency signs more frequent than they appear in statistics.
Haematological signs
Macrocytic (megaloblastic) anaemia is the classic manifestation: the erythrocytes, too large and too few, carry oxygen inefficiently. Marked fatigue, pallor, exertional dyspnoea and palpitations are signs that can precede the biological diagnosis.
Neuropsychological signs
Treatment-resistant depression, memory problems, chronic anxiety and unexplained irritability have been associated with an active-folate deficiency in several clinical cohorts. Folate deficiency disrupts DNA methylation and the synthesis of monoaminergic neurotransmitters.
Mucosal and obstetric signs
Glossitis, recurrent canker sores, mild chronic diarrhoea. In the periconceptional period, active-folate deficiency is the main avoidable risk factor for neural tube defects.
Vitamin B12 — Hydroxocobalamin + Methylcobalamin
B12 is a cofactor of two fundamental reactions: the methylation of homocysteine and the isomerisation of methylmalonyl-CoA in the mitochondria. Liver reserves allow the deficiency to stay clinically silent for three to five years, which systematically delays its recognition.
Neurological signs
Neuropathy through demyelination is the most serious and potentially irreversible complication. It shows up first as symmetrical paraesthesia of the extremities (tingling, burning sensations), then balance and coordination problems, muscle weakness and, in time, progressive cognitive disturbances.
Psychiatric and cognitive signs
Depression, memory problems, cognitive slowing, episodic confusion, irritability and, in advanced cases, psychosis: these often precede the biological signs. In older people, B12 deficiency is one of the most frequently underdiagnosed reversible causes of cognitive decline.
Haematological signs
Megaloblastic anaemia, identical in its clinical presentation to that of folate, is accompanied by intense fatigue, pallor and dyspnoea.
Metabolic signs
Hyperhomocysteinaemia is almost constant, with its documented cardiovascular and cognitive consequences. Vegan and vegetarian populations, older people (reduced absorption via intrinsic factor) and patients on proton-pump inhibitors or metformin have a structurally elevated risk.
Beta-carotene — Provitamin A
Beta-carotene is converted into vitamin A (retinol) according to the body's needs, eliminating the over-toxicity risk specific to preformed retinol. Vitamin A governs vision, mucosal immunity and epithelial cell differentiation.
Visual signs
Night blindness, or difficulty seeing in low light (impaired twilight vision), is the earliest and most specific sign of a vitamin A deficit. It results from insufficient rhodopsin in the retinal rods, whose synthesis depends directly on retinal.
Skin and mucosal signs
The skin shows excessive keratinisation, marked dryness (xerosis) and a rough texture. The ocular, respiratory and digestive mucosa lose their integrity, raising susceptibility to ENT and intestinal infections.
Immune signs
Increased susceptibility to bacterial and viral infections, poor mucosal healing and a weakened cellular immune response reflect vitamin A's role in lymphocyte differentiation and the production of protective mucins.
THE MINERALS AND TRACE ELEMENTS
Zinc — Zinc citrate
A cofactor of about three hundred enzymes and of zinc-finger proteins involved in gene transcription, zinc is one of the most versatile micronutrients. Its deficiency, common in vegetarians and people on prolonged antibiotic therapy, produces a rich and often underestimated clinical picture.
Immune signs
Increased susceptibility to viral and bacterial infections, slowed healing of skin wounds and recurrent canker sores are the most frequent manifestations. Zinc governs the maturation and proliferation of T lymphocytes; its deficit directly weakens cellular immunity.
Skin and appendage signs
White spots on the nails (punctate leukonychia), brittle nails, diffuse hair loss and resistant acne are warning signals. The skin heals less well; superficial wounds become infected more easily.
Sensory signs
A loss or alteration of taste (dysgeusia) and smell (dysosmia) are among the most specific signs of a zinc deficit. These also occur during viral infections, due to acute zinc depletion induced by the inflammatory response.
Reproductive and cognitive signs
Cognitive fatigue, slowing of working memory, a drop in male libido and reduced fertility (spermatogenesis) complete the picture in adults.
Selenium — L-selenomethionine
Selenium is the cofactor of the glutathione peroxidases and the thyroid deiodinases. Its deficiency primarily affects two systems: cellular antioxidant defence and thyroid function. The margin between efficacy and toxicity is narrow; both a frank insufficiency and a chronic excess produce measurable clinical signs.
Thyroid signs
A functional hypothyroidism despite a normal or sub-normal TSH can reflect a selenium deficit: the deiodinases, selenoenzymes, convert inactive T4 into active T3. A picture of chronic fatigue with cold intolerance, moderate weight gain, mild bradycardia and dry skin should raise this deficit, even without a TSH abnormality.
Muscular and cardiovascular signs
Muscle weakness, diffuse myalgia and dilated cardiomyopathy (Keshan disease) characterise severe deficiencies, seen in regions with selenium-depleted soils. In everyday practice, muscle fatigue on exertion and prolonged recovery point to an insufficiency.
Immune and antioxidant signs
Increased susceptibility to viral infections, reduced NK activity and low-grade chronic inflammation can accompany the deficit. The neutralisation of membrane lipid peroxides, ensured by GPx4, is compromised: cells become more vulnerable to ferroptosis and membrane oxidation.
Iodine — Potassium iodide
Iodine is the building block of the thyroid hormones T3 and T4, which regulate the basal metabolic rate, thermogenesis, neurological development and cell differentiation.
Classic thyroid signs
The goitre (enlargement of the thyroid) is the reference anatomical sign of chronic iodine deficiency. The functional manifestations of hypothyroidism go with it: significant fatigue, cold intolerance, bradycardia, constipation, dry skin, unexplained weight gain and cognitive slowing.
Cognitive and neuropsychological signs
Intellectual slowness, a failing memory, difficulty maintaining concentration and a depressed mood can result from a functional hypothyroidism linked to an iodine deficit. Gestational deficiency, recognised by the WHO as the leading global cause of preventable intellectual disability, illustrates how critical this intake is.
Hair and skin signs
Hair loss, dry and thickened skin, brittle nails and pallor are signs associated with iodine-related hypothyroidism.
Manganese — Manganese citrate
Manganese is the cofactor of mitochondrial superoxide dismutase (MnSOD) and of arginase, as well as a key player in the synthesis of connective and bone tissue.
Osteoarticular signs
Bone fragility, joint pain and slow recovery after physical exertion can point to a manganese deficit. The glycosaminoglycans of the cartilage extracellular matrix depend on glycosyltransferases for which manganese is the cofactor.
Metabolic and neurological signs
Slight tremors, mood instability, muscle weakness and fine-coordination problems can accompany a marked deficiency.
Chromium — Chromium picolinate
Chromium is the functional cofactor of chromodulin, which amplifies the activity of insulin receptors and potentiates insulin signal transduction.
Metabolic signs
Compulsive sugar cravings, reactive postprandial hypoglycaemia, meal-correlated mood fluctuations and incipient insulin resistance are the most common manifestations of a chromium deficit. Glucose tolerance deteriorates, and fasting blood sugar can rise slightly without reaching the diabetic threshold.
Associated signs
Increased anxiety, cognitive fatigue after meals, progressive abdominal weight gain and a slightly elevated cholesterol level complete the metabolic picture.
Magnesium — Magnesium citrate
A cofactor of more than three hundred cellular biochemical reactions, magnesium is involved in ATP production, nerve transmission, muscle contraction and glutathione synthesis. Its deficiency is one of the most widespread in Western populations, and yet one of the least systematically investigated.
Neuromuscular signs
Night cramps (calves, toes), fasciculations (eyelid twitching, fine tremors), diffuse muscle tightness and hypersensitivity to sound or light stimuli are characteristic of a magnesium deficiency.
Neuropsychological signs
Irritability, underlying anxiety, sleep disturbances (difficulty falling asleep, frequent night waking) and persistent fatigue despite seemingly sufficient sleep are the most frequent manifestations. A magnesium deficit reduces GABA production and alters serotonergic signalling, two mechanisms directly involved in anxiety and depression.
Cardiovascular signs
Palpitations, a slightly elevated blood pressure without obvious cause, benign extrasystoles and increased susceptibility to arrhythmias can point to a magnesium deficiency, as magnesium is an essential regulator of cardiac excitability.
Cephalic signs
Migraines and recurrent tension headaches have been associated with a magnesium deficit in several clinical studies. Supplementation with magnesium citrate reduces the frequency of attacks in migraine sufferers with low erythrocyte levels.
Potassium — Potassium citrate
The majority intracellular electrolyte (98% of body potassium is intracellular), potassium governs the membrane potential of excitable cells, myocardial contraction and blood-pressure regulation through its natriuretic effect.
Neuromuscular signs
Muscle cramps, generalised weakness, paraesthesia and disproportionate physical fatigue are the first signs of incipient hypokalaemia. Constipation can accompany these, reflecting reduced intestinal peristalsis.
Cardiovascular signs
Palpitations, benign arrhythmias (extrasystoles) and mild arterial hypertension can result from a potassium deficit. Its insufficiency favours sodium retention and, through this, a rise in blood pressure.
THE AMINO ACIDS AND THE ORGANIC ACID
L-Glutamine — Free form
L-glutamine is the preferred fuel of enterocytes and lymphocytes, as well as the precursor of GABA and glutathione. Its deficit primarily affects the interfaces between the body and its environment: the intestinal mucosa and the immune system.
Intestinal signs
Increased intestinal permeability shows up as frequent bloating, diffuse abdominal pain, intermittent diarrhoea or constipation, progressive food intolerances and susceptibility to gastrointestinal infections. These reflect the disorganisation of the epithelial tight junctions whose structural maintenance L-glutamine ensures.
Immune and general signs
Chronic fatigue with no identified cause, susceptibility to recurrent infections, persistent low-grade inflammation and slow muscle recovery after exercise can indicate an L-glutamine insufficiency. Stress-induced muscle catabolism releases glutamine, but at the expense of muscle tissue and protein synthesis.
Neuropsychological signs
An L-glutamine deficit reduces the availability of GABA, the major inhibitory neurotransmitter, contributing to anxiety, sleep disturbances and underlying irritability.
Glycine — Free form
Glycine is the main constituent of collagen strands (one residue in three), an inhibitory spinal neurotransmitter and a cofactor of glutathione synthesis. Its deficiency, often part of a poly-deficient picture, affects collagen structures and hepatic detoxification.
Joint, skin and tendon signs
Skin that loses elasticity early, brittle nails, recurrent tendon pain (tendinitis, enthesopathies), slowed healing and joint fragility reflect insufficient renewal of type I collagen.
Neurological signs
Sleep disturbances, a prolonged sleep-onset latency and a subjectively mediocre sleep quality can result from a glycine deficit, which, via its glycine receptors in the brainstem, exerts an inhibitory action on the waking neurons.
Hepatic signs
A less effective phase II hepatic detoxification, showing up as increased sensitivity to xenobiotics, reduced alcohol tolerance and slow recovery after exposure to pollutants, can reflect a glycine deficit, the main amino acid of hepatic conjugation.
Malic acid — L-malic acid
Malic acid is an intermediate of the Krebs cycle, converted into oxaloacetate by malate dehydrogenase, a central step in aerobic ATP production. Its presence in base One serves a dual role: supporting mitochondrial energy flow and gently chelating aluminium that accumulates in the liver.
Energy and muscular signs
Persistent muscle fatigue on exertion, slow recovery and diffuse muscle pain with no clear cause (fibromyalgic profile) have been associated with insufficient malate levels. Magnesium malate is one of the best-documented forms for reducing chronic muscle pain and fatigue (Russell et al., 1995).
Signs of insufficient detoxification
Increased sensitivity to environmental exposures (aluminium, air pollutants), postprandial or post-chemical-exposure fatigue and slowed hepatic clearance can indicate insufficient support of the mitochondrial anaplerotic axis.
Reading note: the symptoms described in this article reflect data from the scientific and clinical literature of orthomolecular medicine and micronutrition. They do not, on their own, allow a diagnosis. Their recognition is an orientation tool, not a prescription. In case of doubt or persistent signs, a consultation with a practitioner qualified in micronutrition or orthomolecular medicine, together with an appropriate biological work-up, remains essential.