nutritional deficiency - alternative mental health · exacerbate niacin deficiency and can on its...

Directory of Medical Conditions and Procedures Associated with Psychiatric Illness

1 Citation * Copyright Dion Zessin, March 29, 2014

Researched by Dion Zessin

1.1 Thiamine (vitamin B₁) deficiency Thiamine is a water-soluble vitamin that is required as a cofactor by several enzymes involved in carbohydrate metabolism. It is present in all

vegetables and the out layers of grains. Body stores are small lasting a total of approximately one month, and healthy individuals usually develop

thiamine deficiency within a week of no thiamine intake, with resting tachycardia, weakness, decreased deep tendon reflexes, and sometimes

peripheral neuropathy. Thiamine deficiency commonly presents subacutely and can lead to metabolic coma and death. A lack of thiamine can be

caused by malnutrition, and/or foods high in anti-thiamine factors (tea, coffee, betel nuts) and by grossly impaired nutritional status associated

with chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS, and persistent vomiting. It is thought that many people with

diabetes have a deficiency of thiamine and that this may be linked to some of the complications that can occur.

Medical Condition Titled on

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Postpartum Depression

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Anxiety Panic /OCD

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Schizophrenia-like Psychosis/ Psychosis

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Wernicke-Korsakoff Syndrome 22134191 22334191 Schizophrenia, Bipolar Disorder

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Nutritional Deficiency




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Wernicke’s Disease 8976472 Schizophrenia

Wernicke’s Encephalopathy 8135689 16925799 18354948

Schizophrenia

Wernicke-Korsakoff Syndrome 19950117 Anorexia Nervosa and Psychosis

Wernicke Encephalopathy 2204786 Autism

Korsakoff Psychosis 14253685* Korsakoff Psychosis

Wernicke-Korsakoff Asnemic Syndrome

9845417 Schizoaffecive Disorder

Starvation-induced Wernicke’s Encephalopathy

15149304 Schizophrenia

Thiamine Deficiency 18785108 Depression

Low Plasma Thiamine Levels 20121971* Behavioral Disturbance

Thiamine Deficiency 20384190 Psychotic Symptoms

Thiamine Nutritional Status 23173173 Depression

Thiamine Deficiency 2369956 Delirium

Notes: PMID# 19950117 Anorexia Nervosia was the cause of Wernicke-Korsakoff Syndrome and psychosis. Most of the rest

of the documents are psychiatric patients that are malnourished that get Wernicke-Korsakoff Syndrome.



1.2 Niacin (vitamin B₃, nicotinic acid) deficiency

Niacin is a B-group vitamin found as nicotinic acid, as NAD or NAPD, and as nicotinamide. It is in meat, poultry, fish, wholemeal cereals, pulses,

and coffee. It also occurs in maize as niacytin, though this is only absorbed if it is hydrolysed externally; humans eating diets based on maize are

prone to niacin deficiency. There are no substantial body stores of niacin, and it takes 1-2 months’ dietary deficiency leads to pellagra.

Alcoholics are predisposed to niacin deficiency, known in its neuropsychiatric form as alcoholic pellagra encephalopathy or acute nicotinic acid

deficiency encephalopathy, though is much less common than Wernicke-Korsakoff syndrome. Symptoms of niacin deficiency are; thick scaly

pigmented rash on skin exposed to sunlight, swollen mouth and bright red tongue, vomiting and diarrhea, headache, apathy, fatigue,

depression, disorientation, and memory loss.


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Pellagra 14817187* 14817187* Psychiatric Problems and Psychosis

Pellagra 14921752* 13132980*

Psychosis

Pellagra 4256434* Psycho- pathology

Pellagra 14371242* 13271980*

Psychosis

Pellagra 4680826* Psychiatric Manifestations

Pellagra Encephalopathy 23926211 Delusions & Visual Hallucinations

Pellagra 19061687 Delusional Parasitosis

Alcohol Pellagra 11470038 Psychosis

Alcohol Pellagra 9719389 Neuropsychiatric




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Encephalopathy Symptoms

Notes: Niacin deficiency in industrialized countries is mostly associated with alcoholism—which manifests as depression,

delusional parasitosis, or psychosis. Many of these documents are listed as citations—which several are not in English.

1.3 Pyridoxine (vitamin B₆) deficiency Isolated pyridoxine deficiency is very rare as pyridoxine is widespread in foods, though mal-nutrition or a diet restricted to unenriched grains

increases the risk. Acquired deficiency is usually associated with one or more of: inflammatory disorders and catabolic states, malnutrition,

coeliac disease, hepatitis and biliary obstruction, chronic renal failure, dialysis, alcoholism, and a number of drugs. Deficiency of pyridoxine can

exacerbate niacin deficiency and can on its own cause a syndrome identical to pellagra. Pyridoxine deficiency can also impair homocysteine

metabolism, causing homocystinaemia and homocystinuria. Symptoms of serious deficiency include muscle weakness, nervousness, irritability,

depression, difficulty concentrating, and short-term memory loss.


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Homocystinuria due to Cystathionine beta-synthase Deficiency

3591841 3591841 3591841 Depression, OCD, Personality Disorders and Aggressive Behaviors

Multiple Marginal Nutrient 23124011 Depression




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Deficiencies

Vitamin B6 and Plasma P5P Concentrations

18838531 15479988

Depression

Pyridoxine Deficiency 9625217 Psychological Distress

Pyridoxine Deficiency 6733177 Depression

Pyridoxine Deficiency in Coeliac Disease

6369511 Depression

Pyridoxine Deficiency in Coeliac Disease

5366274* Neuropsychiatric Disorder

Notes: Marginal pyridoxine deficiency mostly causes depression can contribute to homocystinuria and more severe

neuropsychopathology.

1.4 Cobalamin (vitamin B₁₂) deficiency and methymalonic aciduria Cobalamin consists of corrinoid structure with cobalt in the center of the molecule. Neither humans or animals are able to synthesize this

vitamin. Food of the animal source are the only natural source of cobalamin in the human diet. There are only two enzymatic reactions in

mammalian cells that require cobalamin as a cofactor. Methylcobalamin is a cofactor for methionine synthase. The enzyme methylmalonyl-

CoA-mutase requires adenosylcobalamin as a cofactor. Therefore, serum concentrations of homocysteine and methylmalonic acid will increase

cobalamin deficiency. Body stores are only 2-5mg, mostly in liver and bone marrow, and there is recycling via entrohepatic circulation, keeping

the daily requirement down to about 2ug/day (more in pregnancy and lactation). Deficiency after malabsorption therefore occurs in 2-5 years,

and deficiency in vegetarians usually after 10-20 years assuming normal initial stores. There are also inherited disorders of B12 usage that can

present with psychosis, such as cobalamin C disease. This causes methylmalonic aciduria with homocystinuria. It usually presents in infancy but

can present in adults with a clinical picture resembling B12 deficiency and including psychosis. A rare disorder called cobalamin G disease is also

an inherted disorder that can cause neuropsychiatric complications. Cobalamin deficiency is associated with hematologic, neurologic, and



psychiatric manifestations. In addition to hematologic, and neuropsychiatric manifestations of cobalamin deficiency, it may exert indirect

cardiovascular effects.


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Cobalamin Deficiency 19892219 Schizophrenia-like Psychosis

Vitamin B₁₂ Deficiency 3057051 3057051 3057051 3057051 3057051 Delirium, Hallucinations, Depression, Psychotic States, Mania, Schizophreniform States

Cobalamin Deficiency 3374544 Neuropsychiatric Abnormalities

Vitamin B₁₂ Deficiency 18472513 Psychosis

Vitamin B₁₂ Deficiency 22345852 22227032

OCD

Vitamin B₁₂ Deficiency 17632664* Mania

Vitamin B₁₂ Deficiency 6691503 Mania

Vitamin B₁₂ Deficiency 5434402 Parasitophobia

Vitamin B₁₂ Deficiency 18291301 Depression

Cobalamin Deficiency 2329255 Mania

Cobalamin C Disease 14568819 Psychosis

Cobalamin G Disease 15204806* Neuropsychiatric Illness

Vitamin B₁₂ Deficiency 21777723 Psychotic Depression

Vitamin B₁₂ Deficiency 19095695 22027500

Psychotic Disorder




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Vitamin B₁₂ Deficiency 22726236 Psychotic Features, Mood Disorder Mixed

Cobalamin Deficiency 23697293 Psychotic Features, Mood Oscillations, Reversible Dementia

Vitamin B₁₂ Deficiency 22032226 Delirium

Late On-set Cobalamin C Disease

17853453 Neuropsychiatric Disturbance

Notes: Cobalamin C Disease, and Cobalamin G Disease are two inherent disorders that are listed in this section under

Cobalamin Deficiency.

1.5 Folate (vitamin B₉) deficiency

Folates are synthesized by plants and microorganisms and there are a variety of dietary sources for humans, amongst which the most significant

are green vegetables, citrus fruits, and animal products. In a healthy state , body stores are 5-20 mg and the daily requirement is 50-100 ug, so

deficiency can manifest after a few months. High homocysteine levels are also a good marker of folate deficiency. Aside from inadequate intake,

deficiency may arise from malabsorption (e.g. widespread jejunal disease, intestinal bacterial overgrowth, zinc deficiency), increased demands

(pregnancy, infancy, diseases associated with rapid cellular proliferation), or be drug-induced. Symptoms of folate deficiency include glossitis

and angular stomatitis, other gastrointestinal symptoms (anorexia, nausea, vomiting, abdominal pain, and diarrhea), fever, hyperpigmentation

of mucous membranes and skin (particularly on dorsal aspects of fingers, the toes, and creases of palms and soles). Cognitive impairment may

be present, with irritability and sleep disruption. There may be macrocytic anemia with neutrophil hypersegmentaltion, as for B12 deficiency.

One other mechanism of neurological folate deficiency is the cerebral folate deficiency syndrome. This is a term applied to any

neuropsychiatric condtion where there are low levels in the CSF of 5-MTHF, the active CSF folate metabolite, with normal folate metabolism



outside the central nervous system (indicated by normal hematological values, normal serum homocysteine levels, and normal serum and red

cell folate).


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Cerebral Folate Deficiency 20445197 Catatonic Schizophrenia

MTHFR Deficiency 24461181 Schizophrenia

Folate Deficiency 15643093 Schizophrenia-like Psychosis

Folic Acid Deficiency 9885631 Psychotic Symptoms

Folic Acid Deficiency 2676810 Psychological Disorders

Dietary Folate Intake 22251911 18062830

Depression

MTHFR C677T Polymorphism 23831680 21125200

Depression

MTHFR C677T Mutation 94551725 Schizophrenia-like Psychosis

MTHFR C677T Polymorphisms 23586533 Psychotic and Mood Disorders

Dihydrofolate Reductase Deficiency (DHFR)

21310276 Depression

Folate Hydrolase 1561C>T Polymorphism

21597034 Depression

MTHFR Deficiency 18356252 Psychosis

Notes: The MTHFR gene polymorphisms and the DHFR gene polymorphisms are included in this section.



1.6 Zinc deficiency

Much of what is known about severe zinc deficiency was derived from the study of individuals born with acrodermatitis enteropathica, a genetic

disorder resulting from the impaired uptake and transport of zinc. The symptoms of severe zinc deficiency include the slowing or cessation of

growth and development, delayed sexual maturation, characteristic skin rashes, chronic and severe diarrhea, immune system deficiencies,

impaired wound healing, diminished appetite, impaired taste sensation, night blindness, swelling and clouding of the corneas, and behavioral

disturbances. Before the cause of acrodermatitis enteropathica was known, patients typically died at infancy. Oral zinc therapy results in

complete remission of symptoms, though it must be maintained indefinitely in individuals with a genetic disorder. Although dietary zinc

deficiency is unlikely to cause severe zinc deficiency in individuals without a genetic disorder, zinc malabsorption or conditions of increased zinc

loss, such as severe burn or prolonged diarrhea, may also result in severe zinc deficiency. Severe zinc deficiency has also been reported in

individuals undergoing total parental nutrition without zinc, in those who abuse alcohol, and in those who are taking certain medications like

penicillamine. It is now recognized that milder zinc deficiency contributes to a number of health problems, especially common in children who

live in developing countries.


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Hypozincemia 20156515 Depression

Hypozincemia 8071476 Depression

Gestational Zinc Deficiency 2182985 1491625

Schizophrenia

Zinc Deficiency 3312133 8477292

Anorexia Nervosa

Zinc Deficiency 21093288 Depression

Dietary Intake of Zinc 21932045 Depression

Zinc Deficiency 24367556 Wide Range of Psychiatric Disorders



1.7 Omega-3 Fatty Acids The three types of omega-3 fatty acids involved in human physiology are ALA (ᾳ-linolenic acid found in plant oils), EPA (eicosapentaenoic

acid)and DHA (docosahexaenoic acid), (both commonly found in marine oils). Omega-3 fatty acids are vital for metabolism and are considered

essential fatty acids meaning they cannot be synthesized by the human body—except mammals have a limited ability when the diet includes

shorter-chain omega-3 fatty acid ALA , to form the long chain important omega-3 fatty acids EPA, and then from EPA, DHA with even greater

inefficiency. Various physical signs are associated with deficiencies of these essential fatty acids. These include excessive thirst , frequent

urination, rough dry or scaly skin, dry or dull or ‘lifeless’ hair, dandruff, and soft or brittle nails. Raised bumps on the skin are particularly

characteristic. (This is called ‘follicular keratosis’ as it results from a build-up of hard, dry skin around the hair follicles).


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Omega-3 Deficiency 23890734 Affective Functioning

Polysaturated Fatty Acid Deficits

20667702 Psychotic State and Schizophrenia

Abnormal Phospholipid Metabolism


Essential Fatty Acid Deficiency 8888126 Schizophrenia

Omega-3 Fatty Acid Deficiency 21838665 21838665 Major Depression, Bipolar Disorder

DHA Deficiency 20147466 20147466 Affective Disorders, Unipolar Depression, Bipolar Disorder

Omega-3 Deficiency 19268372 Perinatal Depression




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Omega-3 DHA Deficits 17188654 Major Depression

1.8 Selenium deficiency The following are signs of selenium deficiency: Keshan’s disease, which is fatal may be a sign of selenium deficiency. The disease is caused due to

a dietary deficiency of selenium and is often fatal as it affects children as well as women of child bearing age. The disease has a number of

symptoms such as heart failure and pulmonary edema. Keshan’s disease also makes the body prone to illness. Another major result of selenium

deficiency is Kashin-Beck disease which occurs in the body when both selenium as well as iodine are deficient. This disease has a number of

symptoms such as degeneration, necrosis, or atrophy in the cartridge tissue causing disproportionate or stunted growth. A selenium deficiency

could also induce hypothyroidism. This could manifest itself in a countless number of other disorders and symptoms such as excessive fatigue,

goiter, cretinism, as well as recurrent miscarriages. Other important selenium deficiency symptoms include those that are mostly related to the

slow functioning of the immune system. These could include gastrointestinal problems, hair loss, diarrhea, and fatigue,. It may also include

neurological symptoms such as mood swings and depression.


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Sub-clinical Selenium Deficiency

2096413 1873372

Mood

Selenium Status 11601874 11987485* 12169160*

Mood, Behavior

Selenium Depletion 12160688 Mood & Behavior in Dialysis




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Selenium Depletion 12208163 Mood & Behavior in Alcoholism

Selenium Intake 12509066 Mood & Psychological Functioning

Selenium Deficiency 17980499* Suicide

Selenium Deficiency 18449137 18449137 Depression and Suicidal Behavior

Selenium Deficiency 22853878 Postpartum Depression

Selenium Deficiency 19699836 Perinatal Depression

1.9 Iron Deficiency

Iron deficiency is one of the most common nutritional deficiencies. Iron is present in all cells in the human body, and has several functions.

Examples include as a carrier of oxygen to the tissues from the lungs in the form of hemoglobin , as a transport medium for electrons within the

cells in the form of cytochromes, as an internal part of an enzyme reactions in various tissues. Too little iron can interfere with these vital

functions and lead to morbidity and death. The eventual consequence of iron deficiency is iron deficiency anemia where the body stores have

been depleted and the body is unable to maintain levels of hemoglobin in the blood. Children and premenopausal women are the groups most

prone to the disease. Symptoms of iron deficiency can occur before the condition has progressed to iron deficiency anemia. Symptoms of iron

deficiency may include: fatigue, dizziness, pallor, hair loss, twitches, irritability, weakness, pica, brittle or grooved nails, restless leg syndrome

and impaired immune function.




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Iron Deficiency 23582950 ADHD

Iron Deficiency 23480325 ADHD and other Psychiatric Disorders

Iron Status 23082739 ADHD

Iron Deficiency Anemia 22286844 Depression

Iron Deficiency Anemia 21856970 Depression

Iron Deficiency Anemia 16243877 Hallucinations

Low Hemoglobin 14652362 Postpartum Depression

Iron Deficiency 22872286 Behavioral Impairment

Perinatal Iron Deficiency 24065908 Neurocognitve Development and Psychiatric Illness

Iron Deficiency 23735056 Mood Disorders, Autism, ADHD, Developmental Disorders

Maternal Iron Deficiency 20093425 18838630

Risk of Schizophrenia

Prenatal Nutritional Deficiency 18682377 Risk of Schizophrenia

Low Serum Ferritin 17984624 ADHD

Iron Deficiency 17692449 Suicide Behaviors

Low Ferritin Levels 17063146 Depression

Iron Deficiency and Hypoceruloplasminemia

11889836 Schizophrenia-like Psychosis

Co-occurrence of Anemia, Marginal Vitamin B6, and

23124011 Depression




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Folate Status

Serum Ferritin Concentrations 21470691 Depression

Plasma Ferritin Concentrations 21130499 Postpartum Depression

1.10 Ascorbic Acid (vitamin C) deficiency Scurvy is caused by prolonged dietary deficiency of vitamin C, the plasma concentration of which appears inversely related to mortality from all

causes. Its clinical importance relates principally to its role as a cofactor in a number of enzyme reactions involved in collagen synthesis,

dysfunction of which disrupts connective tissue integrity, resulting in impaired wound healing and capillary bleeding. In the UK, overt scurvy is

diagnosed only rarely. However, subclinical vitamin C deficiency appears quite common, one study estimated that 25% of men and 16% of

women in the low income/materially deprived population had vitamin C deficiency, with smoking as a strong predictor. Because many of the

early symptoms of vitamin C deficiency (fatigue, malaise, depression, and irritably) are non-specific, the diagnostic possibility of scurvy is usually

delayed until hemorrhagic manifestations occur. The classical cutaneous features consist of perifollcullar purpura, contorted (corkscrew) hairs

and follicular hyperkeratosis, particularly affecting the legs. Large areas of purpura or ecchymosis may occur. Swelling and bleeding of the gums

is an early mucosal symptom, and progressively severe gum disease causes tooth loss. Subperiosteal hemorrhage, particularly in the femur and

tibia, can present as pain, pseudoparalysis, swelling and discoloration of the legs. Hemorrhage into joints and muscle is very uncomfortable.

Diagnosis is generally made on the basis of clinical features, corroborated by a history of dietary inadequacy, and subsequent rapid resolution of

symptoms with the restoration of adequate vitamin C intake.


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Ascorbic Acid Deficiency 4397430* 4397430* Depression,




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Hypochondriasis

Scurvy 23214273 Depression

Scurvy 17637387 Psychosis

Scurvy 16729566 16121659

Schizophrenia

Scurvy 17372835 Depression

Plasma Vitamin C Concentrations

6668228 N/A

Notes: PMID# 4397430 lists ascorbic acid deficiency as the cause of depression and hypochondriasis. The rest of the

abstracts are mental patients who were malnourished and contracted scurvy.

1.11 Magnesium deficiency Magnesium is a cofactor in more than 300 enzyme systems that regulate diverse biochemical reactions in the body, including glucose control,

and blood pressure regulation. Magnesium is required for energy production, oxidative phosphorylation, and glycolysis. It contributes to the

structural development of bone and is required for the synthesis of DNA, RNA and antioxidant glutathione. Magnesium also plays a role in the

active transport of calcium and potassium ions across cell membranes, a process that is important to nerve impulse conduction, muscle

contraction, and normal heart rhythm. An adult body contains approximately 25g magnesium, with 50% to 60% present in the bones and most

of the rest in soft tissues. Less than 1% of total magnesium is in blood serum. Early signs of magnesium deficiency include loss of appetite,

nausea, vomiting, fatigue, and weakness. As magnesium deficiency worsens, numbness, tingling, muscle contractions and cramps, seizures,

personality changes, abnormal hear rhythms, and coronary spasms can occur. Severe magnesium deficiency can result in hypocalcaemia or

hypokalemia because mineral homeostasis is disrupted.




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Magnesium Deficiency 16846100 9368236 9368235

ADHD

Magnesium Deficiency 1809739* Schizophrenia

Magnesium Deficiency 5384711* 5382113*

Postoperative Psychosis

Magnesium Deficiency 19944540 Depression

Magnesium Deficiency 21835188 Anxiety

Hypomagnesemia 17845894 Depression

Magnesium Deficit 1164868 Anxiety

Plasma Magnesium Levels 22564338 Depression

Dietary Intake of Magnesium 19085527 Depression

Hypomagnesemia 15656021 Anorexia Nervosa

Plasma Magnesium Levels 7800167 N/A

Magnesium Deficiency 2722406 Depression

Magnesium Deficiency 4039951 Psychosis

Magnesium Deficiency 23289218 Anxiety-Depressive Syndrome

Magnesium Intake 22695027 Depression

1.12 Vitamin D deficiency

Vitamin D deficiency can result from inadequate exposure to sunlight; malabsorption; accelerated catabolism from certain medications; and, in

infants, from the minimal amount of vitamin D found in breast milk. Vitamin D deficiency is often a silent disease. By definition, rickets occurs in

children whose growth plates have not fused. These children are often found to have started walking late or prefer to sit down for prolonged

periods. In adults, vitamin D deficiency results in osteomalacia, which presents as a poorly mineralized skeletal matrix. Adults in thses cases can



experience chronic muscle aches and pains. Vitamin D deficiency is the most common cause of nutritional rickets. Rare genetic forms of rickets

occur because of defects in vitamin D metabolism. Vitamin D-dependent rickets typeI occurs because of a defect in the renal 25-hydroxyvitamin

D-1 alpha-hydroxylase that results in decreased 1,25(OH)₂ D production. Vitamin D-dependent rickets type II occurs when a mutation exists in

the VDR.


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Vitamin D Deficiency 24060571 First Episode Psychosis

Serum 25-hydroxyvitamin D3 and D2 Concentrations

22848531 Non-clinical Psychotic Experiences

Vitamin D Deficiency 22571731 Psychotic Features

Vitamin D Deficiency 22191178 Suicide Risk

Vitamin D Deficiency 20441728 Psychosis

Vitamin D-dependent Rickets Type IIA

14751420 Psychosis and Schizophrenia

Low Maternal Vitamin D 12892860 Schizophrenia

Vitamin D Deficiency 23609390 23377209 23636546 22372707 22790678 20823081 18458202

Depression

Vitamin D Deficiency 22879429 Maternal Depression

Developmental Vitamin D Deficiency





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Vitamin D Deficiency 24610453 ADHD

Rickets 22445669* Association with Nonaffective Psychosis

1.13 Riboflavin (vitamin B₂) deficiency

Vitamin B2, also called riboflavin, is a water-soluble vitamin present in most animal and plant tissues. It is one of the essential B vitamins, known to help support adrenal function, help calm and maintain a healthy nervous system, and facilitate key metabolic processes, including helping to turn food into energy. Riboflavin deficiency (called ariboflavinosis) can appear at intakes of less than 0.5-0.6 mg/day. Too little riboflavin can cause weakness, throat swelling/soreness, a swollen tongue, skin cracking (including the corners of mouth), dermatitis, and anemia. Riboflavin deficiency can also affect vision, including blurred vision and itching, watering, sore, or bloodshot eyes, as well as becoming light sensitive and easily fatigued. Particular groups may be especially susceptible to riboflavin deficiency, including the elderly, the chronically ill, and alcoholics.


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Riboflavin Deficiency 1605056 7139210

Psychiatric Inpatients

acyl-CoA dehydrogenation Disorder

1564483 Psychiatric Illness

acyl-CoA dehydrogenase Deficiency

19783111 Depressive State

Riboflavin Status 22081620 Depression



1.14 Starvation


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Starvation 3370268 15139247 16314020

Depression and Anorexia Nervosa and Bulimia

Body Weight 2797333 Depression and Anorexia Nervosa

Starvation Diet 5140791* Mental Disorders

Crash Diet Weight Loss 4594088* Psychotic Disturbances

Starvation 20531059 Psychosis

Starvation 9739179 Schizophrenia, Schizophrenia-like Disorders

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