Re: 치매의 원인들 2-1. 비타민 b 부족(Vitamin b deficiency)

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J Alzheimers Dis. Author manuscript; available in PMC 2012 Aug 27.

Published in final edited form as:

J Alzheimers Dis. 2006 Aug; 9(4): 429–433.

doi: 10.3233/jad-2006-9409

PMCID: PMC3428233

NIHMSID: NIHMS398084

PMID: 16917152

Thoughts on B-vitamins and dementia

Martha Clare Morris,a,b,c,* Julie A. Schneider,d,e,f and Christine C. Tangneyg

Author information Copyright and License information Disclaimer

The publisher's final edited version of this article is available at J Alzheimers Dis

Abstract

The B-vitamins, including vitamins B12, B6, B1, B2, niacin (B3) and folate (B9), have been implicated as protective risk factors against cognitive decline and Alzheimer’s disease. This commentary reviews the evidence to support protective relations of these vitamins, including consideration of known vitamin deficiency syndromes, theories of underlying biologic mechanisms, and the epidemiologic evidence. We also comment on the potential benefits and harms of vitamin supplementation as well as make recommendations for the direction of future studies.

비타민 B12, B6, B1, B2, 니아신(B3), 엽산(B9)을 포함한 비타민 B군은 인지 기능 저하 및 알츠하이머병에 대한 보호 위험 요인으로 알려져 있습니다. 이 해설에서는 알려진 비타민 결핍 증후군, 근본적인 생물학적 메커니즘에 대한 이론, 역학적 증거를 포함하여 이러한 비타민의 보호 관계를 뒷받침하는 증거를 검토합니다. 또한 비타민 보충제의 잠재적 이점과 해로움에 대해 논평하고 향후 연구 방향에 대한 권장 사항을 제시합니다.

Dietary niacin and the risk of incident Alzheimer’s disease and of cognitive decline

 FREE

1. M C Morris1,2,3, 
2. D A Evans1,2,4, 
3. J L Bienias1,2, 
4. P A Scherr5, 
5. C C Tangney6, 
6. L E Hebert1,2, 
7. D A Bennett1,4,7, 
8. R S Wilson1,4,7,8, 
9. N Aggarwal1,4,7

1. Correspondence to: Dr M C Morris Rush Institute for Healthy Aging, 1645 W. Jackson, Ste. 675, Chicago, IL 60612; martha_c_morrisrush.edu

Abstract

Background: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer’s disease (AD) and cognitive decline in a large, prospective study.

Methods: This study was conducted in 1993–2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical eval‎uations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria.

Results: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (β = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (β = 0.023 SU/year; p = 0.02), or those with fewer than 12 years’ education (β = 0.035 SU/year; p = 0.002)

Conclusion: Dietary niacin may protect against AD and age related cognitive decline.

결과: 에너지 조정 니아신 섭취는 알츠하이머병 발병과 인지 기능 저하에 보호 효과가 있는 것으로 나타났습니다. 로지스틱 회귀 모델에서 총 니아신 섭취량의 최저 5분위수에서 최고 5분위수에 따른 알츠하이머병 발병의 상대 위험도(95% 신뢰 구간)는 다음과 같습니다: 1.0(참조) 0.3(0.1~0.6), 0.3(0.1~0.7), 0.6(0.3~1.3), 0.3(0.1~0.7)으로 연령, 성별, 인종, 교육 및 ApoE e4 상태에 따라 조정했습니다. 식품을 통한 니아신 섭취량도 AD와 반비례하는 것으로 나타났습니다(조정된 모델에서 선형 추세에 대한 p = 0.002). 조정된 무작위 효과 모델에서 식품을 통한 니아신 섭취량이 많을수록 연간 인지 기능 저하 속도가 느려지는 것으로 나타났습니다(자연 로그 섭취량(mg) 증가당 0.019 표준화 단위(SU)) (p = 0.05). 심혈관 질환 병력이 있거나(β = 0.028 SU/년; p = 0.008), 기준 인지 점수가 낮은 참가자(β = 0.023 SU/년; p = 0.02), 교육 기간이 12년 미만인 참가자(β = 0.035 SU/년; p = 0.002)를 제외한 분석에서 더 강력한 연관성이 관찰되었습니다.

결론 :  식이 니아신은 알츠하이머병과 노화와 관련된 인지 기능 저하를 예방할 수 있습니다.

BMJ. 2002 Jun 22; 324(7352): 1512–1515.

doi: 10.1136/bmj.324.7352.1512

PMCID: PMC1123448

PMID: 12077044

Folic acid, ageing, depression, and dementia

E H Reynolds, consultant neurologist

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It is becoming clear that folic acid affects mood and cognitive function, especially in older people. Edward Reynolds draws together the evidence

Folic acid is important for functioning of the nervous system at all ages.1–4 In the fetus the relation between maternal folate status and the risk of neural tube defects is well established: clinical trials have shown that periconceptual preventive treatment with 400 μg or higher of folic acid significantly reduces the risks of such defects.4

In neonates, infants, children, and adolescents, inborn errors of folate transport and metabolism are associated with a variety of overlapping syndromes which are influenced by age of clinical presentation. These include developmental delay, cognitive deterioration, motor and gait abnormalities, behavioural or psychiatric symptoms, seizures, signs of demyelination or failure of myelination, and vascular changes seen on magnetic resonance imaging or postmortem examination.4 Less commonly, subacute combined degeneration and peripheral neuropathy may also occur.

In adult patients presenting with megaloblastic anaemia due to folate deficiency, approximately two thirds have neuropsychiatric disorders which overlap considerably with those associated with anaemia due to vitamin B-12 deficiency.2,5 However, depression is commoner in patients with folate deficiency, and subacute combined degeneration with peripheral neuropathy is more frequent in those with vitamin B-12 deficiency. The degree of anaemia is poorly correlated with the presence of neuropsychiatric disorders, but if these anaemias were left untreated nearly all patients would eventually develop neuropsychiatric complications.2 Over the past 35 years numerous studies have shown a high incidence of folate deficiency correlated with mental symptoms, especially depression and cognitive decline in epileptic, neurological, psychiatric, geriatric, and psychogeriatric populations.3,4 Furthermore, recent studies in elderly people suggest a link between folic acid, homocysteine, ageing, depression, and dementia, including Alzheimer's disease and vascular disease.4,6–9

In this paper I review the evidence relating folate deficiency to depression and dementia, especially in the ageing nervous system.

엽산이 특히 노인의 기분과 인지 기능에 영향을 미친다는 사실이 밝혀지고 있습니다. 에드워드 레이놀즈는 다음과 같은 증거를 종합합니다.

엽산은 모든 연령대의 신경계 기능에 중요합니다.1-4 태아의 경우 산모의 엽산 상태와 신경관 결손 위험 사이의 관계는 잘 확립되어 있으며, 임상 시험에 따르면 400μg 이상의 엽산으로 지각 주변 예방 치료를 하면 이러한 결손의 위험이 크게 감소하는 것으로 나타났습니다.4

신생아, 유아, 어린이 및 청소년의 경우, 선천적인 엽산 수송 및 대사 장애는 임상 증상의 연령에 따라 영향을 받는 다양한 중첩 증후군과 관련이 있습니다. 여기에는 발달 지연, 인지 기능 저하, 운동 및 보행 이상, 행동 또는 정신 증상, 발작, 탈수초 또는 수초화 실패 징후, 자기공명영상이나 사후 검사에서 보이는 혈관 변화 등이 포함됩니다.4 드물게 아급성 복합 변성 및 말초 신경 병증도 발생할 수 있습니다.

엽산 결핍으로 인한 거대적아구성 빈혈을 보이는 성인 환자의 약 3분의 2는 신경정신과적 장애를 가지고 있으며, 이는 비타민 B-12 결핍으로 인한 빈혈과 상당히 겹칩니다.2,5 그러나 엽산 결핍 환자에서 우울증이 더 흔하고 말초 신경 병증을 동반한 아급성 복합 변성은 비타민 B-12 결핍 환자에서 더 빈번하게 발생합니다. 빈혈의 정도는 신경정신과적 장애의 유무와 상관관계가 낮지만, 빈혈을 치료하지 않고 방치하면 거의 모든 환자가 결국 신경정신과적 합병증을 앓게 됩니다.2 지난 35년 동안 수많은 연구에서 간질, 신경계, 정신과, 노인 및 정신 노인 인구에서 정신 증상, 특히 우울증 및 인지 기능 저하와 관련된 엽산 결핍의 높은 발생률을 보여주었습니다.3,4 또한 최근 노인을 대상으로 한 연구에서는 엽산, 호모시스테인, 노화, 우울증, 알츠하이머병 및 혈관 질환을 포함한 치매 사이의 연관성을 시사하고 있습니다.4,6-9

이 논문에서는 엽산 결핍과 우울증 및 치매, 특히 노화 신경계와 관련된 증거를 검토합니다.

Cureus. 2020 Feb; 12(2): e6976.

Published online 2020 Feb 13. doi: 10.7759/cureus.6976

PMCID: PMC7077099

PMID: 32206454

Low Vitamin B12 Levels: An Underestimated Cause Of Minimal Cognitive Impairment And Dementia

Monitoring Editor: Alexander Muacevic and John R Adler

Shazia Jatoi,1 Abdul Hafeez,2 Syeda Urooj Riaz,

3 Aijaz Ali,1 Muhammad Ishaq Ghauri,3 and Maham Zehra1

Author information Article notes Copyright and License information Disclaimer

Abstract

Background

Vitamin B12 deficiency is linked to impaired cognition and memory along with a sensation of tingling and numbness, an outcome of poor myelination. Elevated methylmalonic acid and serum homocysteine levels are markers of Vitamin B12 deficiency. Elevated homocysteine levels are also often associated with Alzheimer’s disease and stroke. We conducted this study to determine the effect of vitamin B12 replacement therapy on vitamin B12-deficient patients with noted cognitive impairment.

Methods

We conducted a cross-sectional, multicenter study of patients with minimal cognitive impairment (MCI) to assess for Vitamin B12 and homocysteine levels. All patients found to be deficient in vitamin B12 underwent replacement therapy and were assessed again after three months via the Mini-Mental State Examination (MMSE) and a review of symptoms.

Results

A total of 202 patients were included in the study. Of those, 171 (84%) patients reported marked symptomatic improvement after vitamin B12 replacement while MMSE scores improved in 158 (78%) patients. Of the remaining 44 patients who reported no symptomatic improvement, MMSE scores improved in 26 while 18 patients showed no MMSE score improvements.

총 202명의 환자가 연구에 참여했습니다. 이 중 171명(84%)의 환자가 비타민 B12 보충제 복용 후 뚜렷한 증상 개선을 보였으며, 158명(78%)의 환자는 MMSE 점수가 개선되었습니다. 증상이 개선되지 않았다고 보고한 나머지 44명의 환자 중 26명은 MMSE 점수가 개선되었고, 18명의 환자는 MMSE 점수가 개선되지 않았습니다.

Conclusions

Vitamin B12 deficiency is linked to cognition, and replacement therapy may be an option to improve patient cognition outcomes. Further studies are needed to confirm‎ and refine the observed associations over a larger scale and to determine whether these findings will translate to a reduction in cognitive decline.

비타민 B12 결핍은 인지와 관련이 있으며, 보충 요법은 환자의 인지 결과를 개선할 수 있는 옵션이 될 수 있습니다. 관찰된 연관성을 더 큰 규모로 확인 및 개선하고 이러한 결과가 인지 기능 저하 감소로 이어질지 여부를 결정하기 위해서는 추가 연구가 필요합니다.

Keywords: vitamin b12 deficiency, acetyl homocysteine, cognition, memory deficit, mental health