Year : 2021 | Volume
: 9 | Issue : 2 | Page : 59--66
Pitru grahonmada: Vitamin B12 deficiency-induced neuropsychiatric manifestations?
Kshama Gupta, Prasad Mamidi
Department of Kayachikitsa, R.B. Ayurvedic Medical College and Hospital, Agra, Uttar Pradesh, India
Dr. Kshama Gupta
Department of Kayachikitsa, R.B. Ayurvedic Medical College and Hospital, Agra, Uttar Pradesh
“Unmada” is a broad psychopathological entity of Ayurveda that includes various psychiatric and neuropsychiatric conditions. Pitru grahonmada (PG) is one among 18 types of bhutonmada or grahonmada, and it is caused by affliction of “pitru graha” (an evil spirit or super natural power or extraterrestrial force or an idiopathic factor). Previous studies have established the similarity between grahonmadas and different psychiatric and neuropsychiatric conditions. No studies have been conducted on PG till date. The aim and objective of the present study is to explore PG with the help of contemporary psychiatric literature. Ayurvedic literature related to PG has been collected from major classical Ayurvedic texts and from their commentaries. PG is characterized by features such as “Aprasanna drishtim and Apashyantam” (vision loss or abnormalities), “Chala netra pakshmaanaam” (abnormal eye movements), “Shankitekshanam” (suspicious looks), “Apasavya vastram” (confusion or memory loss or disorientation), “Deena vadanam” (depression), “Anannabhilasha or Arochaka or Avipaaka or Alpaagni or Manda paavaka” (various gastrointestinal tract abnormalities), “Pratihata vaacham or Skhalat vaacham” (speech abnormalities), “Nidraalu” (excessive sleepiness), “Samsushka taalukam” (oral manifestations of Vitamin B12 deficiency), “Shaantaatma” (catatonia or depression or reduced psycho-motor activity) and “Tila, guda, maamsa, and paayasa priyam” (cravings for sugar and meat). These features of PG have shown striking similarity with Vitamin B12 deficiency-induced neuropsychiatric conditions. PG has shown similarity with various neuropsychiatric manifestations induced by Vitamin B12 deficiency which needs to be established by further studies.
|How to cite this article:|
Gupta K, Mamidi P. Pitru grahonmada: Vitamin B12 deficiency-induced neuropsychiatric manifestations?.Int J Yoga - Philosop Psychol Parapsychol 2021;9:59-66
|How to cite this URL:|
Gupta K, Mamidi P. Pitru grahonmada: Vitamin B12 deficiency-induced neuropsychiatric manifestations?. Int J Yoga - Philosop Psychol Parapsychol [serial online] 2021 [cited 2022 May 19 ];9:59-66
Available from: https://www.ijoyppp.org/text.asp?2021/9/2/59/329694
“Unmada” is characterized by the deviation of various mental faculties such as manas (mind), buddhi (decision), smriti (memory), sangya gyanam (orientation and responsiveness), bhakti (desire), sheela (habit), cheshta (activity), and achaara (conduct). Unmada is classified into two groups based on etiopathology and treatment, doshaja unmada (occurs due to vitiation of three doshas inside the body) and bhutonmada or grahonmada (occurs without the involvement of doshas). Bhutonmada is characterized by various patterns of abnormal behavior and psychomotor activity such as abnormalities of speech, valor, potency, activities, intelligence, knowledge, and strength. The behavioral abnormalities seen in bhutonmada occur abruptly without any known cause (idiopathic?) Acharya Vagbhata has described 18 types of grahonmadas (deva, asura, rushi, guru, vruddha, siddha, pitru, gandharva, yaksha, rakshasa, sarpa, brahma rakshasa, pishacha, kushmanda, nishada, preta, maukirana, and vetala). Pitru grahonmada (PG) is one among these 18 types of grahonmada.
According to “Acharya Charaka,” PG is characterized by the features such as aprasanna drishtim (abnormalities of vision), apashyantam (loss of vision), nidraalu (excessive sleepiness or fatigue), pratihata vaacham (obstructed speech or reduced speech), anannaabhilaasha (anorexia), arochakam (loss of appetite) and avipaakam (indigestion). According to “Acharya Sushruta,” pretebhyo visrujati pindaan (doing rituals), shaantaatma (reduced psycho-motor activity), apasavya vastra (performing rituals in a disorganized manner which denotes confusion or disorientation or memory loss) and maamsa, tila, guda and paayasa abhikaama (craving for meat, sesame, sugar, and sweets) are the features of PG. In Ashtanga samgraha (written by vriddha Vagbhata) along with the above features, chala netra pakshmaanaam (abnormal eye movements), shankitekshanam (suspicious looks/paranoid), deena vadanam (depression), and samsushka taalum (dry palate or oral manifestations) are also mentioned. The description of PG in “Ashtanga hridaya” and in “Madhava nidaana” is almost similar to the above texts. Various grahonmadas have shown similarity with different psychiatric and/or neuropsychiatric conditions according to the previous works, but studies on PG have been lacking.,,,,,,,,,,,, Till date, no studies have been conducted on PG and it is an unexplored concept in the field of Ayurvedic psychiatry. The aim and objective of the present study is to explore the condition of PG with the help of contemporary psychiatric literature.
Ayurvedic literature regarding “unmade,” “bhutonmada,” “grahonmada” and “PG” has been collected from major Ayurvedic texts such as Charaka samhita, Sushruta samhita, Ashtanga sangraha, Ashtanga hridaya, and Madhava nidaana including their commentaries. Electronic databases “Google” and “Google scholar” have been searched to find out the relevant studies and reviews published on “unmade,” “bhutonmada,” “grahonmada,” and various psychiatric and neuropsychiatric conditions caused by Vitamin B12 deficiency till August 2020, irrespective of their appearance/publication year. The keywords used for search were “Unmada,” “Bhutonmada,” “Grahonmada,” “Dementia,” “Depression,” “Schizophrenia,” “Vitamin B12 deficiency,” “Neuropsychiatric symptoms,” “Optic atrophy,” “Optic neuropathy,” “Hyperphagia,” “Blepharospasm,” “Delusions,” “Suspiciousness,” “Memory impairment,” “Atrophic gastritis,” “Malasborption,” “Chronic fatigue syndrome,” “Hypersomnia,” “Megaloblastic anemia,” “Catatonia,” “Psychomotor activity,” “Food cravings,” and other relevant terms. Abstracts, full texts that are open access and published in English language were only considered.
Vitamin B12 and Its Deficiency
B12 deficiency often goes undetected, with manifestations that range from asymptomatic to a wide spectrum of hematologic and/or neuropsychiatric features. The most common etiology of Vitamin B12 deficiency is food-cobalamin malabsorption resulting from gastric dysfunction. Vitamin B12 deﬁciency has been associated with neurologic, cognitive, psychotic, mood symptoms as well as treatment resistance. It is estimated that up to 40% of older adults have Vitamin B12 (cobalamin) deﬁciencies. Cobalamin is a family of complex molecule which is synthesized by anaerobic bacteria and is found in foods of animal origin (e.g., ﬁsh, meat, dairy products, and eggs) as well as fortiﬁed cereals. Defects at any step of the absorption process can cause cobalamin deﬁciencies of varying degrees. Food-cobalamin malabsorption, autoimmune factors, decreased intake or malnutrition, genetic factors and intestinal malabsorption (chronic pancreatitis), Crohn's disease, Whipple's disease, celiac disease, amyloidosis, scleroderma, intestinal lymphomas or tuberculosis, tapeworm infestation, bacterial overgrowth, etc., are the causes for Vitamin B12 deficiency.
Neuropsychiatric symptoms due to Vitamin B12 deﬁciency have been described since the early 1900s. Commonly described neuropsychiatric manifestations associated with Vitamin B12 deﬁciency include motor, sensory and autonomic symptoms; cognitive impairment, mood and psychotic symptoms. Some of these symptoms include paresthesias, ataxia, proprioception and vibration loss, memory loss, delirium, dementia, depression, mania, hallucinations, delusions, personality changes, and abnormal behavior. Neurologic symptoms have been the hallmark of Vitamin B12 deﬁciency, which include paresthesias, ataxia, proprioception and vibration loss, abnormal reﬂexes, bowel/bladder incontinence, optic atrophy, orthostatic hypotension, and autonomic disturbances. Psychosis can be the presenting symptom in Vitamin B12 deﬁciency. Reported psychiatric symptoms include suspiciousness, persecutory or religious delusions, auditory and visual hallucinations, tangential or incoherent speech, and disorganized thought-process. An association of Vitamin B12 deﬁciency and depressive symptoms in elderly patients has been established.
Etiology, Pathogenesis, Clinical Course and Prognosis of Pitru grahonmada and Vitamin B12 Deficiency
There is no specific etiology, pathogenesis, and prognosis explained for PG in Ayurvedic texts. The samaanya nidaana, sampraapti, and saadhyaasaadhyata (common etiology, pathogenesis, and prognosis) explained for bhutonmada is also applicable for PG. Grahavesha (affliction by supernatural power), prgnaaparaadha or karma (deeds of present life or past life) are explained as causative factors for bhutonmada. In bhutonmada, the symptoms occur suddenly without any known reason or triggered by chidra kaala (various predisposing factors). The course and prognosis of bhutonmada are unpredictable in nature.
The clinical picture of Vitamin B12 deﬁciency is highly polymorphic and of varying severity, ranging from asymptomatic to rare and severe disorders. The prognosis of neuropsychiatric conditions induced by Vitamin B12 deficiency depends on symptom severity, duration, and clinical diagnosis. It has been proposed that treating deficiencies in the early stages yield better results, as structural and irreversible changes in the brain may also occur if left untreated. It seems that the clinical picture, course, and prognosis of Vitamin B12 deficiency-induced neuropsychiatric conditions are highly polymorphic and variable as seen in grahonmada.
There is striking similarity between the signs and symptoms of PG and various neuropsychiatric conditions caused by Vitamin B12 deficiency. This similarity has been explored in the following sections.
Aprasanna drishtim and Apashyantam (vision abnormalities or vision loss)
The term of optic neuropathy actually regroups a broad spectrum of ophthalmological or systemic conditions that can affect the optic nerve. The pathophysiological mechanisms of optic neuropathies vary widely including inflammatory, traumatic, ischemic, autoimmune, genetic, or toxic mechanisms. In case of bilateral, symmetric, slowly progressive optic neuropathies, the three main causes to be investigated are hereditary, metabolic, and toxic. A dosage of B1, B6, B12 and folate vitamins are useful if a vitamin deficiency is suspected. Optic atrophy is one of the neurological manifestations of Vitamin B12 deficiency., Neuro-ophthalmological presentations, including optic neuropathy and optic atrophy are rare in Vitamin B12 deficiency. The typical clinical picture of Vitamin B12 deficiency-induced optic neuropathy includes bilateral, progressive and painless visual loss, central or ceco-central scotoma, color vision defects, and inappropriate visual-evoked responses. Optic neuropathy is a rare, but important, manifestation of Vitamin B12 deficiency that should be suspected in patients with risk factors for malnutrition. Vitamin B12 optic neuropathy is a reversible, treatable cause of vision loss and may be a harbinger for other manifestations of the disease. Aprasanna drishtim and Apashyantam of PG denotes vision loss or vision abnormalities caused by underlying optic atrophy or optic neuropathy induced by Vitamin B12 deficiency.
Chala netra pakshmaanaam (abnormal eye movements)
Eye movement disorders are rarely reported in Vitamin B12 deficiency. There is a case report which has described two cases, one with bilateral inter nuclear ophthalmoplegia and the other with downbeat nystagmus. In contrast to frequent optic nerve involvement, eye movement disorders in Vitamin B12 deficiency, which is extremely rare, has only been reported 11 times in the literature. Serum Vitamin B12 should be measured in any patient with unexplained eye movement disorder. Blepharospasm is a form of focal dystonia characterized by involuntary contractions of the orbicularis oculi muscles resulting in bilateral closure of the eyes. According to a study, a patient with severe blepharospasm in whom investigations revealed low Vitamin B12 levels, elevated homocysteine levels as well as other laboratory features which have supported B12 deficiency. Blepharospasm can be a rare manifestation of Vitamin B12 deficiency, which is reversible with therapy. Vitamin B12 levels and homocysteine levels should be tested in patients with blepharospasm in whom there is no obvious cause for blepharospasm. Isolated paralysis of upward gaze may be a feature of Vitamin B12 deficiency. “Wandering eyes” has been reported in Vitamin B12 deficiency. Thus, conditions such as ophthalmoplegia, nystagmus, other abnormal eye movements, and blepharospasm induced by Vitamin B12 deficiency are similar to “chala netra pakshmaanaam” of PG.
Shankitekshanam (suspicious looks/paranoid)
Vitamin B12 deficiency has been highly linked to several psychiatric disorders such as impaired memory, irritability, depression, dementia, delirium, schizophrenia, and psychosis. Published studies on Vitamin B12 deficiency have documented the prevalence of 29%, 44%, and 70.8% among patients with primary dementia and schizophrenia, depression, respectively. Neurocognitive impairment resulting from Vitamin B12 deﬁciency is usually accompanied by other neurologic abnormalities and may present as paranoia, irritability, dementia, hallucinations, psychosis, depression, or disorientation. The common psychiatric manifestations of Vitamin B12 deficiency include depression, agitation or violence, delirium with or without delusions, and hallucinations and acute paranoid states. A growing body of evidence suggests a role of Vitamin B12 deficiency in mood and psychotic disorders. Delusions, hallucinations, personality changes, and abnormal behavior are the neuropsychiatric symptoms of Vitamin B12 deficiency. Suspiciousness, persecutory or religious delusions, auditory and visual hallucinations, and disorganized thought process are seen in Vitamin B12 deficiency-induced psychotic conditions. Low serum Vitamin B12 is prevalent among patients admitted with psychiatric illnesses, especially those with schizophrenia. Schizophrenia, a long duration of psychiatric illness, and acute hospitalization were independently associated with low serum B12 levels among admitted psychiatric patients. Thus “shankitekshanam” described in PG denotes “suspiciousness” or “persecutory delusions” or “schizophrenia” induced by Vitamin B12 deficiency.
Apasavya vastram (confusion or disorientation or cognitive impairment)
“Apasavya vastram” means wearing towel on right shoulder instead of left while performing rituals. It signifies that the person suffering with PG performs rituals in disorganized way or improper manner. This may due to confusion, disorientation, forgetfulness (memory impairment), or cognitive impairment. Vitamin B12 deficiency has been linked to memory impairment, dementia, delirium, schizophrenia, psychosis, and depression. A case report has revealed that, a patient with spinal cord injury associated with Vitamin B12 deficiency had clinical features of delirium such as alteration in consciousness, disorientation, memory impairment, disorganized thinking, visual hallucinations and disturbances in concentration, attention, and thinking. Psychiatric disturbances caused by Vitamin B12 deficiency also include delirium, dementia, and hallucinations. The association of Vitamin B12 deﬁciency and cognitive dysfunction has been extensively documented, and some authors state that it can be linked credibly to mental decline. Symptoms described include slow mentation, memory impairment, attention deﬁcits, and dementia. Vitamin B12 deﬁciency has been associated with attention deﬁcits, acute mental-status changes, and acute cognitive changes with electroencephalography abnormalities. Psychiatric symptoms attributable to Vitamin B12 deficiency fall into several clinically separate categories such as slow cerebration, confusion, memory changes, delirium with or without hallucinations and/or delusions, depression, acute psychotic states, manic, and schizophreniform states. Irrational behavior, confusion, forgetfulness or memory impairment, and other psychotic features were observed in Vitamin B12 deficiency patients. Based on these observations, it seems that “Apasavya vastram” mentioned in PG denotes an underlying acute confusion or disorientation or memory, cognition, attention, and concentration impairment caused by Vitamin B12 deﬁciency.
Deena vadanam (depression)
Deficiencies in Vitamin B12 can lead to various neurological and psychiatric disorders such as depression, dementia, and brain atrophy. Depression, dementia, and mental impairment are often associated with Vitamin B12 and folate deficiency, especially in the elderly. Vitamin B12 and folic acid are crucial for the transmethylation of neuroactive substances such as myelin and neurotransmitters. There are several theories concerning potential associations between depression and levels of Vitamin B12 and folate. Vitamin B12 and folate are connected with the synthesis of monoamines such as dopamine and serotonin and are involved in single carbon transfer methylation reactions connected with the production of these monoamine neurotransmitters that are implicated in the pathophysiology of neuropsychiatric disorders such as depression and psychosis. Assessment of B12 levels should be included as a standard evaluation with treatment-resistant depressive disorders, dementia, psychosis, or among individuals with history of poor nourishment. As there is growing evidence that B12 deficiency is associated with depression and organic psychosis lends credence to consideration of obtaining B12 levels in patients who presents with these problems.
As there is an important association between Vitamin B12 levels and depressive symptoms, supporting the approach of measurement and replacement of Vitamin B12 in the treatment of depression in clinical practice is strongly recommended. Adequate Vitamin B12 levels may also play a role in depression treatment response. Depression often accompanies a medical condition. It may also happen that the presence of a chronic disease changes the social situation of a patient, who then responds to the change by developing depression. Among the various systemic diseases, Vitamin B12 deﬁciency and folic acid deﬁciency are particularly likely to cause depression. “Deena vadanam” mentioned in PG denotes depression induced by an underlying Vitamin B12 deficiency.
Anannaabhilaasha, Arochaka, Avipaaka, Alpaagni, and Manda paavaka (various gastrointestinal tract abnormalities such as anorexia, indigestion, and malabsorption)
According to a study, chronic atrophic gastritis leads to Vitamin B12 deficiency and increasing weakness, loss of memory, and mental depression were common symptoms. Flatulent dyspepsia and epigastric pain were also reported in the same study. Since it is known that malabsorption of Vitamin B12 may persist in clinically asymptomatic patients with tropical sprue, it is likely that such asymptomatic cases may develop Vitamin B12 deficiency and present clinically as cases of neuropathy. Malabsorption of Vitamin B12 was present in all patients who had deficiency of this Vitamin. The most common etiology of Vitamin B12 deficiency is food-cobalamin malabsorption resulting from gastric dysfunction. Histomorphologically, pernicious anemia is characterized by fundic atrophic gastritis (Type A) leading to atrophy of the fundus and achlorhydria. Abnormal gastric endoscopic findings appear to be correlated with B12 levels. Helicobacter pylori infection is associated with cobalamin deficiency, implicating H. pylori as an etiological factor for B12 deficiency.
Absorption of Vitamin B12 is complex, and the stomach plays an important role. Gastric dysfunction, such as gastritis and gastric atrophy may lead to an increase in intrinsic factor secretion and malabsorption, eventually resulting in Vitamin B12 deficiency. Atrophic gastritis is one of the important causes of Vitamin B12 deficiency. It has been reported that H. pylori infection resulting in chronic gastritis, plays a role in the development of gastric atrophy and intestinal metaplasia. The degree of chronic gastritis and gastric atrophy depends upon the severity of infection. Deficiency of Vitamin B12 can be seen in conditions of inadequate dietary intake, disorders related to secretion of gastric pepsin, disorders of pancreatic secretion and intrinsic factor secretion from gastric parietal cells, and ileum disease in which absorption is disrupted. H. pylori seem to be a causative agent in the development of adult Vitamin B12 deficiency. Eradication of H. pylori infection alone may correct Vitamin B12 levels and improve anaemia. Anannaabhilaasha, Arochaka, Avipaaka, Alpaagni, and Manda paavaka of PG denotes various factors such as malabsorption, atrophic gastritis, H. pylori infection, and other gastrointestinal tract abnormalities commonly seen in Vitamin B12 deficiency.
Pratihata vaacham and Skhalat vaacham (speech abnormalities)
Abnormal speech has been reported in patients with Vitamin B12 deficiency. Hoarseness of voice and vocal cord palsy have been documented in cases of Vitamin B12 deficiency. Tangential speech or incoherent speech is also seen in Vitamin B12 deficiency-induced psychotic conditions. Pratihata vaacham and Skhalat vaacham of PG denotes vocal cord palsy or incoherent speech or mutism, etc., conditions induced by Vitamin B12 deficiency.
Nidraalu (excessive sleepiness or fatigue)
Sleepiness is the impairment of normal arousal mechanism and is characterized by a tendency to fall asleep. Persons who are sleepy are temporarily aroused by activity, whereas fatigue is intensified by activity, at least in the short term. Patients with sleepiness feels better aft a nap, but patients with fatigue report a lack of energy, mental exhaustion, poor muscle endurance, delayed recovery after physical exertion, and nonrestorative sleep. Malaise and lethargy are the depressive symptoms induced by Vitamin B12 deficiency. Damage to peripheral nerves due to Vitamin B12 deficiency, results in sleepiness, altered taste and smell, and optic atrophy. A study of 12 women who fulfilled the criteria of both chronic fatigue syndrome (CFS) and fibromyalgia found the levels of Vitamin B12 in the cerebrospinal fluid were significantly correlated with measures of fatigability and neurasthenia. Is a B12 deficiency consistent with the presentation of CFS? As in the case of folic acid, fatigue and depression are the features common to both disorders, suggesting inadequate B12 could contribute to the clinical picture in a subset of patients. A substantial amount of Vitamin B12 appears to be necessary to relieve the symptoms of CFS, compared to the amount needed to correct a B12 deficiency; thus, the vitamin appears to exert a pharmacologic effect. Vitamin B12 administration may relieve CFS symptoms by reversing the erythrocyte abnormalities leading to improved tissue oxygenation. Vitamin B12 deficiency was found to be associated with fatigue and depressive symptoms. Depression and fatigue are known to be strongly correlated. Besides, fatigue is a common symptom of depression. Vitamin B12-induced anemia, on the other hand, could be a mediating factor, since this may also induce fatigue. There is a relationship between Vitamin B12 deficiency and increased levels of fatigue and depression in lacunar stroke patients. “Nidraalu” of PG denotes fatigue or excessive sleepiness induced by Vitamin B12 deficiency.
Samsushka taalukam (dry palate or oral manifestations)
The most common causes of megaloblastic anemias are cobalamin (Vitamin B12) and folate (Vitamin B9) deficiency. Clinically, megaloblastic anemia progresses slowly, and symptoms include weakness, fatigue, shortness of breath, and neurologic abnormalities. Oral signs and symptoms, including glossitis, angular cheilitis, recurrent oral ulcer, oral candidiasis, diffuse erythematous mucositis, and pale oral mucosa. A wide range of oral signs and symptoms may appear in anemic patients as a result of basic changes in the metabolism of oral epithelial cells. These changes give rise to abnormalities in cell structure and the keratinization pattern of the oral epithelium leading to a “beefy” red and inflamed tongue with erythematous macular lesions on the dorsal and border surfaces because of marked epithelial atrophy and reduced thickness of the epithelial layer. Erythematous macules may occur on the surface of the patient's cheek mucosa and tongue. In addition, soreness of the tongue and generalized ulceration, as well as reduced taste sensitivity, generalized sore mouth, or burning mouth are usually reported in the literature. Candidiasis and angular cheilitis are common oral complaints of patients with megaloblastic anemia. Megaloblastic anemia has a complex pathogenesis. Oral lesions are among the most common initial symptoms. The oral manifestations of glossitis, stomatitis, and mucosal ulceration in Vitamin B12 deficiency have long been recognized. These oral changes may occur in the absence of symptomatic anaemia. “Samsushka taalukam” of PG denotes various oral manifestations as explained above due to Vitamin B12 deficiency induced megaloblastic anaemia.
Shaantaatma (reduced psycho-motor activity/catatonia/depression)
Catatonia has been associated with extreme Vitamin B12 deficiency. Catatonia is a condition that includes symptoms such as catalepsy, stupor, rigidity, posturing, and waxy ﬂexibility. Negativism, mutism, and catatonic excitement are other common symptoms. Catatonia can be a subtype of schizophrenia, a symptom of the mood disorders, or an entity caused by a medical condition or substance. Vitamin B12 deﬁciency has been linked to many psychiatric entities, and there is a case report according to which a patient has developed catatonia secondary to a low Vitamin B12 level, which improved after supplementation. Vitamin B12 deficiency-induced catatonia patient has shown many symptoms of catatonia, including stupor, mutism, rigidity, posturing, and waxy ﬂexibility. Low or reduced psycho-motor activity is also seen in depression, dementia, and also in catatonia. “Shaantaatma” of PG denotes depression or catatonia or reduced psychomotor activity induced by Vitamin B12 deficiency.
Tila, guda, maamsa, and paayasa priyam (cravings for sesame, meat, sugar, and sweets)
Literature consistently demonstrates that individuals experiencing emotional distress, especially depression, report a craving and preference for sweet carbohydrate/fat rich foods. Unipolar depressed individuals increase their preference for sweet carbohydrate/fat rich foods as they become depressed. They also increase their consumption of carbohydrates from sucrose. Several studies indicate that sweet carbohydrate/fat rich foods are consumed because of the resulting mood enhancement. The cravings and preference which some depressed individuals have for sweet carbohydrate/fat rich foods seems to result from the enhancement in mood following consumption. Depression is strongly and consistently associated with obesity, lower physical activity and (among the obese) higher caloric intake. Depression was associated with significantly higher daily caloric intake among those with BMI over 30. Patients with Alzheimer's disease had a greater preference than normal controls for relatively high-fat, sweet foods and for high-sugar, low-fat foods, but did not significantly differ in preference for other foods, including those high in complex carbohydrates and protein. Vascular dementia patients showed a similar pattern, not significantly different from that for Alzheimer's patients. Craving for sweet food may be a significant part of the clinical syndrome of dementia. Depression and variation in dopamine-related genes have both independently been associated with food consumption. Depressive symptoms could synergistically interact with genetic variation to influence food intake. Relationship between depression and food intake may vary as a function of genetic polymorphism.
Many of the easily noticeable food patterns that precede depression are the same as those that occur during depression. These may include poor appetite, skipping meals, and a dominant desire for sweet foods. The consumption of diets low in carbohydrate tends to precipitate depression, since the production of brain chemicals serotonin and tryptophan that promote the feeling of well-being, is triggered by carbohydrate-rich foods. A high quality protein diet contains all essential amino acids. Foods rich in high quality protein include meats, milk and other dairy products, and eggs. Many of the neurotransmitters in the brain are made from amino acids. The neurotransmitter dopamine is made from the amino acid tyrosine, and the neurotransmitter serotonin is made from the tryptophan. If there is a lack of any of these two amino acids, there will not be enough synthesis of the respective neurotransmitters, which is associated with low mood and aggression in the patients. It is not clear yet whether poor nutrition, as a symptom of depression, causes folate deficiency or primary folate deficiency produces depression and its symptoms. These indicate the possible importance of iron in the etiology of depression since its deficiency is known to cause fatigue and depression. Iron-deficiency anemia is associated, for instance, with apathy, depression, and rapid fatigue when exercising. Tila, guda, maamsa, and paayasa priyam (fond of sesame, meat, sugar, and sweet foods) of PG indicate cravings toward food rich in iron, calcium, aminoacids, proteins, sugars, etc. Such type of cravings may denote deficiency of essential vitamins or minerals inside the body. These cravings denote anemia, nutritional deficiencies (due to malabsorption), depression, etc., conditions induced by Vitamin B12 and other deficiencies.
“PG” is one among 18 types of grahonmada. The signs and symptoms of PG such as aprasanna drishtim, apashyantam, chala netra pakshmaanaam, shankitekshanam, apasavya vastram, deena vadanam, anannabhilasha, arochaka, avipaaka, alpaagni, manda paavaka, pratihata vaacham, skhalat vaacham, nidraalu, samsushka taalukam, shaantaatma and tila, guda, maamsa, and paayasa priyam have shown similarity with conditions such as Vitamin B12 deficiency-induced optic atrophy, optic neuropathy, ophthalmoplegia, nystagmus, abnormal eye movements, paranoia, disorientation, memory impairment, depression, atrophic gastritis, malabsorption, H. pylori infection, speech abnormalities, glossitis or various oral manifestations, catatonia, fatigue, and food cravings. PG has shown similarity with various neuropsychiatric conditions caused by Vitamin B12 deficiency. Although further research is still required to substantiate the claims, the descriptive results of the present study provide fundamental understanding on potential ideas pertaining to “PG” and pave the path for future research directions.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
|1||Gupta K, Mamidi P. Kaphaja unmada: Myxedema psychosis? Int J Yoga Philosop Psychol Parapsychol 2015;3:31-9.|
|2||Mamidi P, Gupta K. Guru, vriddha, rishi and siddha grahonmaada: Geschwind syndrome? Int J Yoga Philosop Psychol Parapsychol 2015;3:40-5.|
|3||Mamidi P, Gupta K. Obsessive compulsive disorder – “Sangama graha”: An Ayurvedic view. J Pharm Sci Innov 2015;4:156-64.|
|4||Agnivesha, Elaborated by Charaka and Dridhabala Commentary by Chakrapani. Charaka Samhita, Chikitsa Sthana, Unmada Chikitsitam Adhyaya, 9/20, Edited by Vaidya Jadavji Trikamji Acharya. Varanasi: Chaukhamba Surbharati Prakashan; 2008. p. 469.|
|5||Sushruta. Sushruta Samhita, Commentary by Dalhana. Uttara Tantra, Amanusha Upasarga Pratishedha Adhyaya, 60/12, Edited by Vaidya Jadavji Trikamji Acharya and Narayana Ram Acharya. Varanasi: Chaukhamba Orientalia; 2009. p. 795.|
|6||Vriddha Vagbhata. Ashtanga Sangraha, Commentary by Indu, Uttara Tantra, Bhoota Vigyaneeyam Adhyaya, 7/24, Edited by Shivprasad Sharma. 3rd ed. Varanasi: Chowkhamba Sanskrit Series Office; 2012. p. 670.|
|7||Vagbhata. Ashtanga Hridaya, Commentary by Arunadatta and Hemadri, Uttara Tantra, Bhoota Vigyaneeyam Adhyaya, 4/41-42, Edited by Bhishagacharya Harishastri Paradkara Vaidya. 9th ed. Varanasi: Chowkhamba Sanskrit Series Office; 2005. p. 792.|
|8||Madhavakara. Rogavinischaya/Madhava Nidana, Unmada Nidana, 20/22, Commentary “Madhukosha” by Vijayarakshita & Shrikanthadatta, Edited by Brahmananda Tripathi. 1st ed. Varanasi: Chaukhamba Surbharati Prakashan; 2012. p. 489-90.|
|9||Gupta K, Mamidi P. Gandharva grahonmada: Bipolar disorder with obsessive-compulsive disorder/mania? Int J Yoga Philosop Psychol Parapsychol 2017;5:6-13.|
|10||Mamidi P, Gupta K. Vetaala Grahonmada: Parkinson”s disease with obsessive-compulsive disorder?/Autoimmune neuropsychiatric disorder? Int J Yoga Philosop Psychol Parapsychol 2017;5:35-41.|
|11||Gupta K, Mamidi P. Deva shatru/Daitya/Asura grahonmada: Antisocial/Narcissistic/Borderline personality disorder? Int J Yoga Philosop Psychol Parapsychol 2018;6:10-5.|
|12||Gupta K, Mamidi P. Yaksha grahonmada: Bipolar disorder with obsessive-compulsive disorder? Int J Yoga Philosop Psychol Parapsychol 2018;6:16-23.|
|13||Gupta K, Mamidi P. Deva grahonmada: Interictal behavior syndrome of temporal lobe epilepsy?/Obsessive-compulsive disorder with mania? Int J Yoga Philosop Psychol Parapsychol 2018;6:41-50.|
|14||Mamidi P, Gupta K. Rakshasa grahonmada: Antisocial personality disorder with psychotic mania? Int J Yoga Philosop Psychol Parapsychol 2018;6:24-31.|
|15||Mamidi P, Gupta K. Brahma rakshasa grahonmada: Borderline personality disorder?/tourette syndrome – Plus? Int J Yoga Philosop Psychol Parapsychol 2018;6:32-40.|
|16||Gupta K, Mamidi P. Nishaada grahonmada: Behavioral and Pscyhological symptoms of dementia?/Frontotemporal dementia?/Hebephrenia? J Neurobehav Sci 2018;5:97-101.|
|17||Mamidi P, Gupta K. Uraga grahonmada: Extrapyramidal movement disorder?/Tourette syndrome – PLUS? Indian J Health Sci Biomed Res 2018;11:215-21.|
|18||Gupta K, Mamidi P. Preta grahonmada – Catatonia? Med J DY Patil Vidyapeeth 2018;11:461-5.|
|19||Mamidi P, Gupta K. Maukirana grahonmada – Psychiatric manifestations of Graves” hyperthyroidism and ophthalmopathy? Med J DY Patil Vidyapeeth 2018;11:466-70.|
|20||Gupta K, Mamidi P. Kushmanda grahonmada – Paraneoplastic neurological syndrome with testicular cancer? J Neurobehav Sci 2018;5:172-6.|
|21||Gupta K, Mamidi P. Bhutonmada”s of Harita samhita – An explorative study. Int J Yoga Philosop Psychol Parapsychol 2020;8:3-12.|
|22||Dholakia KR, Dharmarajan TS, Yadav D, Oiseth S, Norkus EP, Pitchumoni CS. Vitamin B12 deficiency and gastric histopathology in older patients. World J Gastroenterol 2005;11:7078-83.|
|23||Lachner C, Steinle NI, Regenold WT. The neuropsychiatry of Vitamin B12 deficiency in elderly patients. J Neuropsychiatry Clin Neurosci 2012;24:5-15.|
|24||Grzybowski A. Problems related to the diagnosis of Vitamin B12 deficiency optic neuropathy. Acta Ophthalmol 2014;92:e74-5.|
|25||Touitou V, LeHoang P. Diagnostic approach in optic neuropathy. Rev Neurol (Paris) 2012;168:691-6.|
|26||Kumar S. Vitamin B12 deficiency presenting with an acute reversible extrapyramidal syndrome. Neurol India 2004;52:507-9.|
|27||Ralapanawa DM, Jayawickreme KP, Ekanayake EM, Jayalath WA. B12 deficiency with neurological manifestations in the absence of anaemia. BMC Res Notes 2015;8:458.|
|28||Chavala SH, Kosmorsky GS, Lee MK, Lee MS. Optic neuropathy in Vitamin B 12 deficiency. Eur J Intern Med 2005;16:447-8.|
|29||Akdal G, Yener GG, Ada E, Halmagyi GM. Eye movement disorders in Vitamin B12 deficiency: Two new cases and a review of the literature. Eur J Neurol 2007;14:1170-2.|
|30||Kosker M, Tanriverdio C, Dostbil A, Tomcuk T, Kalabak AA. Vitamin B12 deficiency as a first sign of acquired horizontal pendular nystagmus. J Neuroinfect Dis 2015;1:6.|
|31||Edvardsson B, Persson S. Blepharospasm and Vitamin B12 deficiency. Neurol India 2010;58:320-1.|
|32||Sandyk R. Paralysis of upward gaze as a presenting symptom of Vitamin B12 deficiency. Eur Neurol 1984;23:198-200.|
|33||Zanus C, Alberini E, Costa P, Colonna F, Zennaro F, Carrozzi M. Involuntary movements after correction of Vitamin B12 deficiency: A video-case report. Epileptic Disord 2012;14:174-80.|
|34||Kibirige D, Wekesa C, Kaddu-Mukasa M, Waiswa M. Vitamin B12 deficiency presenting as an acute confusional state: A case report and review of literature. Afr Health Sci 2013;13:850-2.|
|35||Harrington AL, Dixon TM, Ho CH. Vitamin B(12) deficiency as a cause of delirium in a patient with spinal cord injury. Arch Phys Med Rehabil 2011;92:1917-20.|
|36||Berry N, Sagar R, Tripathi BM. Catatonia and other psychiatric symptoms with Vitamin B12 deficiency. Acta Psychiatr Scand 2003;108:156-9.|
|37||Ssonko M, Ddungu H, Musisi S. Low serum Vitamin B12 levels among psychiatric patients admitted in Butabika mental hospital in Uganda. BMC Res Notes 2014;7:90.|
|38||Hector M, Burton JR. What are the psychiatric manifestations of Vitamin B12 deficiency? J Am Geriatr Soc 1988;36:1105-12.|
|39||Rusher DR, Pawlak R. A review of 89 published case studies of Vitamin B12 deficiency. J Hum Nutr Food Sci 2013;1:1008.|
|40||Hanna S, Lachover L, Rajarethinam RP. Vitamin B12 deficiency and depression in the elderly: Review and case report. Prim Care Companion J Clin Psychiatry 2009;11:269-70.|
|41||Metzler MS, Miller MD, William H, Edwards MD, Stephen C. Psychiatric manifestation of Vitamin B-12 deficiency: An update. Jeff J Psychiatry 1991;9:43-8.|
|42||Miyoshi K. Depression associated with physical illness. Japan Med Assoc J 2001;44:279-82.|
|43||Wood IJ, Ralston M, Ungar B, Cowling DC. Vitamin B12 deficiency in chronic gastritis. Gut 1964;5:27-37.|
|44||Jeejeebhoy KN, Wadia ND, Desai HG. Role of Vitamin B12 deficiency in tropical nutritional neuromyelopathy. J Neurol Neurosurg Psychiat 1967;30:7-12.|
|45||Korkut E, Kandis H, Korkut S, Baltaci D, Kara IH, Saritas A. The association of Vitamin B12 levels with gastroscopy findings and H. pylori status in adults attending an out-patient gastroenterology clinic. Arch Hell Med 2012;29:85-90.|
|46||Kaptan K, Beyan C, Ural AU, Çetin T, Avcu F, Gülşen M, et al. Helicobacter pylori – Is it a novel causative agent in Vitamin B12 deficiency? Arch Intern Med 2000;160:1349-53.|
|47||Chakrabarty B, Dubey R, Gulati S, Yoganathan S, Kumar A, Kumar A. Isolated cerebellar involvement in Vitamin B12 deficiency: A case report. J Child Neurol 2014;29:P161-3.|
|48||Rosenthal TC, Majeroni BA, Pretorius R, Malik K. Fatigue: An overview. Am Fam Physician 2008;78:1173-9.|
|49||Hunt A, Harrington D, Robinson S. Vitamin B12 deficiency. BMJ 2014;349:g5226.|
|50||Werbach MR. Nutritional strategies for treating chronic fatigue syndrome. Altern Med Rev 2000;5:93-108.|
|51||Huijts M, Duits A, Staals J, van Oostenbrugge RJ. Association of Vitamin B12 deficiency with fatigue and depression after lacunar stroke. PLoS One 2012;7:e30519.|
|52||Pontes HA, Neto NC, Ferreira KB, Fonseca FP, Vallinoto GM, Pontes FS, et al. Oral manifestations of Vitamin B12 deficiency: A case report. J Can Dent Assoc 2009;75:533-7.|
|53||Field EA, Speechley JA, Rugman FR, Varga E, Tyldesley WR. Oral signs and symptoms in patients with undiagnosed Vitamin B12 deficiency. J Oral Pathol Med 1995;24:468-70.|
|54||Catalano G, Catalano MC, Rosenberg EI, Embi PJ, Embi CS. Catatonia. Another neuropsychiatric presentation of Vitamin B12 deficiency? Psychosomatics 1998;39:456-60.|
|55||Christensen L. The effect of food intake on mood. Clin Nutr 2001;20:161-6.|
|56||Simon GE, Ludman EJ, Linde JA, Operskalski BH, Ichikawa L, Rohde P, et al. Association between obesity and depression in middle-aged women. Gen Hosp Psychiatry 2008;30:32-9.|
|57||Mungas D, Cooper JK, Weiler PG, Gietzen D, Franzi C, Bernick C. Dietary preference for sweet foods in patients with dementia. J Am Geriatr Soc 1990;38:999-1007.|
|58||Agurs-Collins T, Fuemmeler BF. Dopamine polymorphisms and depressive symptoms predict foods intake. Results from a nationally representative sample. Appetite 2011;57:339-48.|
|59||Rao TS, Asha MR, Ramesh BN, Rao KS. Understanding nutrition, depression and mental illnesses. Indian J Psychiatry 2008;50:77-82.|