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Naoki Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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efficient prediction of <B>VitaminB> B deficiencies via machine learning using routine Blood test results in patients with intense psychiatric episode
Frontiers in Psychiatry, 2020Co-Authors: Hidetaka Tamune, Jumpei Ukita, Yu Hamamoto, Hiroko Tanaka, Kenji Narushima, Naoki YamamotoAbstract:Background <B>VitaminB> B Deficiency is common worldwide and may lead to psychiatric symptoms; however, <B>VitaminB> B Deficiency epidemiology in patients with intense psychiatric episode has rarely Been examined. Moreover, <B>VitaminB> Deficiency testing is costly and time-consuming, which has hampered effectively ruling out <B>VitaminB> Deficiency-induced intense psychiatric symptoms. In this study, we aimed to clarify the epidemiology of these deficiencies and efficiently predict them using machine-learning models from patient characteristics and routine Blood test results that can Be oBtained within one hour. Methods We reviewed 497 consecutive patients, who are deemed to Be at imminent risk of seriously harming themselves or others, over a period of 2 years in a single psychiatric tertiary-care center. Machine-learning models (k-nearest neighBors, logistic regression, support vector machine, and random forest) were trained to predict each Deficiency from age, sex, and 29 routine Blood test results gathered in the period from SeptemBer 2015 to DecemBer 2016. The models were validated using a dataset collected from January 2017 through August 2017. Results We found that 112 (22.5%), 80 (16.1%), and 72 (14.5%) patients had <B>VitaminB> B1, <B>VitaminB> B12, and folate (<B>VitaminB> B9) Deficiency, respectively. Further, the machine-learning models were well generalized to predict Deficiency in the future unseen data, especially using random forest; areas under the receiver operating characteristic curves for the validation dataset (i.e., the dataset not used for training the models) were 0.716, 0.599, and 0.796, respectively. The Gini importance of these <B>VitaminB>s provided further evidence of a relationship Between these <B>VitaminB>s and the complete Blood count, while also indicating a hitherto rarely considered, potential association Between these <B>VitaminB>s and alkaline phosphatase (ALP) or thyroid stimulating hormone (TSH). Discussion This study demonstrates that machine-learning can efficiently predict some <B>VitaminB> deficiencies in patients with active psychiatric symptoms, Based on the largest cohort to date with intense psychiatric episode. The prediction method may expedite risk stratification and clinical decision-making regarding whether replacement therapy should Be prescriBed. Further research includes validating its external generalizaBility in other clinical situations and clarify whether interventions Based on this method could improve patient care and cost-effectiveness.
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efficient prediction of <B>VitaminB> B deficiencies via machine learning using routine Blood test results in patients with intense psychiatric episode
medRxiv, 2019Co-Authors: Hidetaka Tamune, Jumpei Ukita, Yu Hamamoto, Hiroko Tanaka, Kenji Narushima, Naoki YamamotoAbstract:Background: <B>VitaminB> B Deficiency is common worldwide and may lead to psychiatric symptoms; however, <B>VitaminB> B Deficiency epidemiology in patients with intense psychiatric episode has rarely Been examined. Moreover, <B>VitaminB> Deficiency testing is costly and time-consuming. It hampered to effectively rule out <B>VitaminB> Deficiency-induced intense psychiatric symptoms. In this study, we aimed to clarify the epidemiology of these deficiencies and efficiently predict them using machine-learning models from patient characteristics and routine Blood test results that can Be oBtained within one hour. Methods: We reviewed 497 consecutive patients deemed to Be at imminent risk of seriously harming themselves or others over 2 years. Machine-learning models were trained to predict each Deficiency from age, sex, and 29 routine Blood test results. Results: We found that 112 (22.5%), 80 (16.1%), and 72 (14.5%) patients had <B>VitaminB> B1, <B>VitaminB> B12, and folate (<B>VitaminB> B9) Deficiency, respectively. Also, the machine-learning models well generalized to predict the Deficiency in the future unseen data; areas under the receiver operating characteristic curves for the validation dataset (i.e. dataset not used for training the models) were 0.716, 0.599, and 0.796, respectively. The Gini importance of these <B>VitaminB>s provided further evidence of a relationship Between these <B>VitaminB>s and the complete Blood count, while also indicating a hitherto rarely considered, potential association Between these <B>VitaminB>s and alkaline phosphatase (ALP) or thyroid stimulating hormone (TSH). Discussion: This study demonstrates that machine-learning can efficiently predict some <B>VitaminB> deficiencies in patients with active psychiatric symptoms, Based on the largest cohort to date with intense psychiatric episode. The prediction method may expedite risk stratification and clinical decision-making regarding whether replacement therapy should Be prescriBed. Further research includes validating its external generalizaBility in other clinical situations and clarify whether interventions Based on this method can improve patient care and cost-effectiveness.
Hidetaka Tamune - One of the best experts on this subject based on the ideXlab platform.
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efficient prediction of <B>VitaminB> B deficiencies via machine learning using routine Blood test results in patients with intense psychiatric episode
Frontiers in Psychiatry, 2020Co-Authors: Hidetaka Tamune, Jumpei Ukita, Yu Hamamoto, Hiroko Tanaka, Kenji Narushima, Naoki YamamotoAbstract:Background <B>VitaminB> B Deficiency is common worldwide and may lead to psychiatric symptoms; however, <B>VitaminB> B Deficiency epidemiology in patients with intense psychiatric episode has rarely Been examined. Moreover, <B>VitaminB> Deficiency testing is costly and time-consuming, which has hampered effectively ruling out <B>VitaminB> Deficiency-induced intense psychiatric symptoms. In this study, we aimed to clarify the epidemiology of these deficiencies and efficiently predict them using machine-learning models from patient characteristics and routine Blood test results that can Be oBtained within one hour. Methods We reviewed 497 consecutive patients, who are deemed to Be at imminent risk of seriously harming themselves or others, over a period of 2 years in a single psychiatric tertiary-care center. Machine-learning models (k-nearest neighBors, logistic regression, support vector machine, and random forest) were trained to predict each Deficiency from age, sex, and 29 routine Blood test results gathered in the period from SeptemBer 2015 to DecemBer 2016. The models were validated using a dataset collected from January 2017 through August 2017. Results We found that 112 (22.5%), 80 (16.1%), and 72 (14.5%) patients had <B>VitaminB> B1, <B>VitaminB> B12, and folate (<B>VitaminB> B9) Deficiency, respectively. Further, the machine-learning models were well generalized to predict Deficiency in the future unseen data, especially using random forest; areas under the receiver operating characteristic curves for the validation dataset (i.e., the dataset not used for training the models) were 0.716, 0.599, and 0.796, respectively. The Gini importance of these <B>VitaminB>s provided further evidence of a relationship Between these <B>VitaminB>s and the complete Blood count, while also indicating a hitherto rarely considered, potential association Between these <B>VitaminB>s and alkaline phosphatase (ALP) or thyroid stimulating hormone (TSH). Discussion This study demonstrates that machine-learning can efficiently predict some <B>VitaminB> deficiencies in patients with active psychiatric symptoms, Based on the largest cohort to date with intense psychiatric episode. The prediction method may expedite risk stratification and clinical decision-making regarding whether replacement therapy should Be prescriBed. Further research includes validating its external generalizaBility in other clinical situations and clarify whether interventions Based on this method could improve patient care and cost-effectiveness.
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efficient prediction of <B>VitaminB> B deficiencies via machine learning using routine Blood test results in patients with intense psychiatric episode
medRxiv, 2019Co-Authors: Hidetaka Tamune, Jumpei Ukita, Yu Hamamoto, Hiroko Tanaka, Kenji Narushima, Naoki YamamotoAbstract:Background: <B>VitaminB> B Deficiency is common worldwide and may lead to psychiatric symptoms; however, <B>VitaminB> B Deficiency epidemiology in patients with intense psychiatric episode has rarely Been examined. Moreover, <B>VitaminB> Deficiency testing is costly and time-consuming. It hampered to effectively rule out <B>VitaminB> Deficiency-induced intense psychiatric symptoms. In this study, we aimed to clarify the epidemiology of these deficiencies and efficiently predict them using machine-learning models from patient characteristics and routine Blood test results that can Be oBtained within one hour. Methods: We reviewed 497 consecutive patients deemed to Be at imminent risk of seriously harming themselves or others over 2 years. Machine-learning models were trained to predict each Deficiency from age, sex, and 29 routine Blood test results. Results: We found that 112 (22.5%), 80 (16.1%), and 72 (14.5%) patients had <B>VitaminB> B1, <B>VitaminB> B12, and folate (<B>VitaminB> B9) Deficiency, respectively. Also, the machine-learning models well generalized to predict the Deficiency in the future unseen data; areas under the receiver operating characteristic curves for the validation dataset (i.e. dataset not used for training the models) were 0.716, 0.599, and 0.796, respectively. The Gini importance of these <B>VitaminB>s provided further evidence of a relationship Between these <B>VitaminB>s and the complete Blood count, while also indicating a hitherto rarely considered, potential association Between these <B>VitaminB>s and alkaline phosphatase (ALP) or thyroid stimulating hormone (TSH). Discussion: This study demonstrates that machine-learning can efficiently predict some <B>VitaminB> deficiencies in patients with active psychiatric symptoms, Based on the largest cohort to date with intense psychiatric episode. The prediction method may expedite risk stratification and clinical decision-making regarding whether replacement therapy should Be prescriBed. Further research includes validating its external generalizaBility in other clinical situations and clarify whether interventions Based on this method can improve patient care and cost-effectiveness.
Jeanluc Daval - One of the best experts on this subject based on the ideXlab platform.
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<B>VitaminB> B Deficiency causes neural cell loss and cognitive impairment in the developing rat
Proceedings of the National Academy of Sciences of the United States of America, 2009Co-Authors: Jeanluc Daval, Sebastien Blaise, Jeanlouis GueantAbstract:The article By Troen et al. (1) adds interesting evidence that <B>VitaminB>-B Deficiency is associated with selective Brain damage and cognitive decline. It reports a rarefaction of hippocampal microvasculature without neurodegeneration or gliosis in male C57BL6/J mice fed a B-<B>VitaminB>-deficient diet. Cognitive impairment was shown By using a Morris water maze. According to the authors, this may result from the microvascular rarefaction. In a recent article (2) we showed that rat pups from dams fed …
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Gestational <B>VitaminB> B Deficiency leads to homocysteine-associated Brain apoptosis and alters neuroBehavioral development in rats
American Journal of Pathology, 2007Co-Authors: Sebastien Blaise, Jeanlouis Gueant, Emmanuelle Nédélec, Henri Schroeder, Jean-marc Alberto, Carine Bossenmeyer-pourié, Jeanluc DavalAbstract:Hyperhomocysteinemia has Been identified as a risk factor for neurological disorders. To study the influence of early Deficiency in nutritional determinants of hyperhomocysteinemia on the developing rat Brain, dams were fed a standard diet or a diet lacking methyl groups during gestation and lactation. Homocysteinemia progressively increased in the offspring of the deficient group and at 21 days reached 13.3+/-3.7 micromol/L versus 6.8+/-0.3 micromol/L in controls. Homocysteine accumulated in Both neurons and astrocytes of selective Brain structures including the hippocampus, the cereBellum, the striatum, and the neurogenic suBventricular zone. Most homocysteine-positive cells expressed p53 and displayed fragmented DNA indicative of apoptosis. Righting reflex and negative geotaxis revealed a delay in the onset of integration capacities in the deficient group. Between 19 and 21 days, a poorer success score was recorded in deficient animals in a locomotor coordination test. A switch to normal food after weaning allowed restoration of normal homocysteinemia. Nevertheless, at 80 days of age, the exploratory Behavior in the elevated-plus maze and the learning and memory Behavior in the eight-arm maze revealed that early <B>VitaminB> B deprivation is associated with persistent functional disaBilities, possiBly resulting from the ensuing neurotoxic effects of homocysteine.
Jeanlouis Gueant - One of the best experts on this subject based on the ideXlab platform.
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<B>VitaminB> B Deficiency causes neural cell loss and cognitive impairment in the developing rat
Proceedings of the National Academy of Sciences of the United States of America, 2009Co-Authors: Jeanluc Daval, Sebastien Blaise, Jeanlouis GueantAbstract:The article By Troen et al. (1) adds interesting evidence that <B>VitaminB>-B Deficiency is associated with selective Brain damage and cognitive decline. It reports a rarefaction of hippocampal microvasculature without neurodegeneration or gliosis in male C57BL6/J mice fed a B-<B>VitaminB>-deficient diet. Cognitive impairment was shown By using a Morris water maze. According to the authors, this may result from the microvascular rarefaction. In a recent article (2) we showed that rat pups from dams fed …
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Gestational <B>VitaminB> B Deficiency leads to homocysteine-associated Brain apoptosis and alters neuroBehavioral development in rats
American Journal of Pathology, 2007Co-Authors: Sebastien Blaise, Jeanlouis Gueant, Emmanuelle Nédélec, Henri Schroeder, Jean-marc Alberto, Carine Bossenmeyer-pourié, Jeanluc DavalAbstract:Hyperhomocysteinemia has Been identified as a risk factor for neurological disorders. To study the influence of early Deficiency in nutritional determinants of hyperhomocysteinemia on the developing rat Brain, dams were fed a standard diet or a diet lacking methyl groups during gestation and lactation. Homocysteinemia progressively increased in the offspring of the deficient group and at 21 days reached 13.3+/-3.7 micromol/L versus 6.8+/-0.3 micromol/L in controls. Homocysteine accumulated in Both neurons and astrocytes of selective Brain structures including the hippocampus, the cereBellum, the striatum, and the neurogenic suBventricular zone. Most homocysteine-positive cells expressed p53 and displayed fragmented DNA indicative of apoptosis. Righting reflex and negative geotaxis revealed a delay in the onset of integration capacities in the deficient group. Between 19 and 21 days, a poorer success score was recorded in deficient animals in a locomotor coordination test. A switch to normal food after weaning allowed restoration of normal homocysteinemia. Nevertheless, at 80 days of age, the exploratory Behavior in the elevated-plus maze and the learning and memory Behavior in the eight-arm maze revealed that early <B>VitaminB> B deprivation is associated with persistent functional disaBilities, possiBly resulting from the ensuing neurotoxic effects of homocysteine.
Rajaprabhakaran Rajarethinam - One of the best experts on this subject based on the ideXlab platform.
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<B>VitaminB> B Deficiency and depression in the elderly review and case report
The Primary Care Companion To The Journal of Clinical Psychiatry, 2009Co-Authors: Susan Hanna, Leonard Lachover, Rajaprabhakaran RajarethinamAbstract:To the Editor: <B>VitaminB> B12 is a water-soluBle essential <B>VitaminB>. A memBer of <B>VitaminB> B complex, <B>VitaminB> B12 is also called coBalamin Because it contains the metal coBalt. <B>VitaminB> B12 is synthesized By Bacteria and is found mainly in meat, egg, and dairy products But lacks a reliaBle plant source.1 It is essential for the formation of red Blood cells and maintenance of a healthy nervous system as well as for the rapid synthesis of DNA during cell division. It is Believed that B12 along with folic acid may help prevent disorders of central nervous system development, mood disorders, and dementias. MegaloBlastic anemia is the common and serious illness associated with B12 Deficiency, But it is Believed that a mild decrease in the B12 level is associated with neurologic and psychiatric proBlems such as ataxia or mood disturBances.1 A common cause of <B>VitaminB> B12 Deficiency is poor intake or aBsorption.2 The protein-Bound <B>VitaminB> B12 is released By hydrochloric acid in the stomach during digestion. Once released, B12 comBines with the gastric intrinsic factor, and this complex is aBsorBed in the intestinal tract. Although <B>VitaminB> deficiencies are relatively uncommon in the Western world, it is estimated that 10% to 15% of individuals over the age of 60 years may suffer from B12 Deficiency and it is Believed that atrophic gastritis type B, which may afflict 20% to 50% of the elderly, may lead to poor aBsorption of B12 and folate.2–4 As the population ages, nutrition and its impact on the health of the elderly Become increasingly important in health maintenance of the elderly. In this report, we descriBe an elderly woman who suffered from severe psychotic depression who did not improve with conventional treatment But recovered significantly following administration of <B>VitaminB> B12, illustrating the possiBility that <B>VitaminB> B12 Deficiency may play a role in the development of mood disorder. Case report. Ms A, a 66-year-old married, African American retired teacher, was living with her daughter and granddaughter. She was seen in 2004 By one of the authors (S.H.) in the outpatient clinic following a psychiatric hospitalization for DSM-IV major depressive disorder with psychosis. The patient and the family reported a 6-month history of sad mood and lack of energy, interest, and motivation along with sleep disturBances following the loss of Ms A's foster children. She had no family history or past history of mental illness or suBstance aBuse. During those 6 months, she stayed in her Bed most of the time, was sad and withdrawn, and cried often. She neglected self-care and hygiene and lost aBout 30 pounds of Body weight. In August 2004, she was hospitalized (as noted in the previous paragraph) following worsening of her condition that included agitation, sleeplessness, and a fear that something Bad was going to happen to her. She reported no hallucinations or suicidal ideas. She was treated with sertraline 150 mg/d and risperidone 2 mg/d and stayed in the hospital for 10 days. At the time she was seen in the clinic for follow-up (less than a month after discharge from the hospital), she had a noticeaBle stiffness in her gait But otherwise was healthy physically. She was well dressed and groomed But exhiBited slow psychomotor activity. She appeared withdrawn and was slow in her speech. She denied feeling sad But was tearful and depressed during the interview. She did not exhiBit any overt psychotic symptoms But continued to have a vague fear that something Bad might happen to her. She had no suicidal thoughts But was generally hopeless aBout herself and her future. She did not exhiBit any evidence for intellectual decline (score of 25 out of 30 on the Mini-Mental State Examination5) or neurologic deficits. The patient was maintained on treatment with sertraline and risperidone and had a working diagnosis of major depressive disorder with psychotic features, in partial remission. As part of the initial workup, Blood tests were ordered, including thyroid-stimulating hormone, <B>VitaminB> B12, and folate levels. All laBoratory results were within normal limits except <B>VitaminB> B12, which was extremely low: the patient had a serum level of < 100 pg/mL (normal range: 200 to 900 pg/mL). At this point, the patient was referred to her primary care physician to follow up on her low <B>VitaminB> B12 level. She was treated with a series of <B>VitaminB> B12 injections, after which the serum B12 level increased to within normal limits (500 pg/mL). Following this, she showed significant improvement with her mood. Along with her mood, other symptoms and activities such as sleep, hygiene, self-care, and activity level improved. The treating psychiatrist (S.H.) discontinued the risperidone and reduced the dose of sertraline to 100 mg/d, and the patient recovered to her Baseline levels of mood and functioning soon thereafter. She continues to take sertraline. A serum <B>VitaminB> B12 level Between 200 pg/mL and 900 pg/mL is considered normal, But a threshold of 300 to 350 pg/mL is recognized as a marker for a desiraBle status in the elderly. The laBoratory diagnosis is usually Based on low serum <B>VitaminB> B12 levels or elevated serum methylmalonic acid and homocysteine levels. Elevated homocysteine is an important marker for <B>VitaminB> B12 and/or folate Deficiency. Classic Deficiency symptoms such as megaloBlastic anemia often fail to appear with suBtle deficiencies, as they are usually late clinical signs of severe Deficiency.3,4 Symptoms of <B>VitaminB> B12 Deficiency include anemia, neuropathy, and neuropsychiatric disorders.6 Depression, dementia, and mental impairment are often associated with <B>VitaminB> B12 and folate Deficiency, especially in the elderly.1 <B>VitaminB> B12 and folic acid are crucial for the transmethylation of neuroactive suBstances such as myelin and neurotransmitters (hypomethylation hypothesis). There are several theories concerning potential associations Between depression and levels of <B>VitaminB> B12 and folate. <B>VitaminB> 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.7 <B>VitaminB> B12 is also required for the synthesis of S-adenosylmethionine (SAM), which is needed as a methyl donor in many methylation reactions in the Brain. Since SAM has antidepressant properties, it is conceivaBle that an inhiBited synthesis may cause a reduction in SAM and may result in depression. This view is supported By a study8 which found that depressed suBjects had significantly higher methylmalonic acid levels than nondepressed suBjects. Detrimental effects on mood due to actions in the methylmalonic acid metaBolism pathway have not Been extensively studied and need further investigation. Psychiatric manifestations can occur in the presence of low serum B12 levels But in the aBsence of the other well-recognized neurologic and hematologic aBnormalities of pernicious anemia.1 Such symptoms may precede hematologic symptoms By months or years and may present as the only symptoms related to Deficiency. Durand and colleagues9 reported a similar case in 2003, in which a 64-year-old woman with no prior history of mental illness was hospitalized for confusion and a 2-month history of severe depression with delusions and Capgras' syndrome. She also had delusions with laBility of mood and hypomania prior to the hospitalization. She was found to have severe <B>VitaminB> B12 Deficiency, with a serum <B>VitaminB> B12 level of 52 pmol/L and a folate level within normal limits. AntiBodies to parietal cells were positive in the serum and antiBodies to intrinsic factor were negative. Her mental state improved dramatically within a few days following <B>VitaminB> B12 replacement therapy (hydroxycoBalamin 1000 ng/d IM for 10 days) and iron replacement therapy, and all her symptoms disappeared within 9 days of treatment. Evidence for neuropsychiatric symptoms related to <B>VitaminB> Deficiency is sparse, But when there is such a causal relationship the treatment response is dramatic and at times life saving. In view of the high prevalence of mild, preclinical B12 Deficiency, routine coBalamin supplementation in the general population, especially the elderly, may Be advisaBle.10 Supplementation with high doses of oral coBalamin is as effective as coBalmin administered By intramuscular injection to correct plasma markers of <B>VitaminB> B12 Deficiency, But the effects of lower oral doses of coBalamin on such markers are uncertain. However, a routine intake of 100 to 250 μg/d in the aBsence of malaBsorption may Be adequate to prevent deficiencies. Such an intervention may prevent major suffering in many elderly individuals. In conclusion, our patient illustrates the importance of considering the possiBility of B12 Deficiency and serum B12 determinations in patients for whom nutritional Deficiency is suspected, especially among the elderly. It may also Be prudent to consider this possiBility in all patients with organic mental disorders, atypical psychiatric symptoms, poor response to conventional treatment, and fluctuating symptomatology. Assessment of B12 levels should Be included as a standard evaluation with treatment-resistant depressive disorders, dementia, psychosis, or risk factors for malnutrition or among individuals with history of poor nourishment as well as patients who are aBove age 50. It is, however, encouraging to know that replacement of <B>VitaminB> B12 in the presence of a Deficiency is Beneficial therapeutically. Large-scale controlled studies and surveys of <B>VitaminB> status among the elderly and mentally ill may shed more light on this topic and may help improve the care of the mentally ill.
