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Biomedical subjects

A Beiser

Publications and source records attributed to A Beiser.

At least 19 recordsLinked to original sources
PubMed2004

Stroke risk profile, brain volume, and cognitive function: the Framingham Offspring Study.

BACKGROUND: Mid-life stroke risk factors have been related to late-life cognitive impairment. This association may result not only from clinical strokes but also from subclinical brain injury, such as a global atrophy demonstrable on quantitative brain MRI. METHODS: The authors evaluated the community-based cohort of Framingham Offspring Study participants. A total of 1,841 subjects (mean age, 62 years; 857 men, 984 women) who underwent quantitative MRI and cognitive testing between 1999 and 2001 and were free of clinical stroke and dementia constituted our study sample. The authors used age- and sex-adjusted linear regression models to relate previous (1991 to 1995) and recent (1998 to 2001) Framingham Stroke Risk Profile (FSRP) scores to the total cerebral brain volume ratio (TCBVr) on follow-up MRI, and further to relate the TCBVr with education-adjusted scores on neuropsychological tests administered at the time of imaging. RESULTS: There was an inverse association between FSRP scores and TCBVr. The TCBVr also showed a significant positive association with performance on tests of attention (Trails A), executive function (Trails B), and visuospatial function (visual reproduction, Hooper visual organization), but not with performance on tests of verbal memory or naming. CONCLUSIONS: The Framingham Stroke Risk Profile may identify subjects with smaller brains and poorer cognitive function among stroke- and dementia-free subjects, reinforcing the importance of managing stroke risk factors.

Adult↗
PubMed2001

Elevated midlife blood pressure increases stroke risk in elderly persons: the Framingham Study.

BACKGROUND: Stroke risk predictions are traditionally based on current blood pressure (BP). The potential impact of a subject's past BP experience (antecedent BP) is unknown. We assessed the incremental impact of antecedent BP on the risk of ischemic stroke. METHODS: A total of 5197 stroke-free subjects (2330 men) in the community-based Framingham Study cohort were enrolled from September 29, 1948, to April 25, 1953, and followed up to December 31, 1998. We determined the 10-year risk of completed initial ischemic stroke for 60-, 70-, and 80-year-old subjects as a function of their current BP (at baseline), recent antecedent BP (average of readings at biennial examinations 1-9 years before baseline), and remote antecedent BP (average at biennial examinations 10-19 years earlier), with adjustment for smoking and diabetes mellitus. Models incorporating antecedent BP were also adjusted for baseline BP. The effect of each BP component (systolic BP, diastolic BP, and pulse pressure) was assessed separately. RESULTS: Four hundred ninety-one ischemic strokes (209 in men) were observed in eligible subjects. The antecedent BP influenced the 10-year stroke risk at the age of 60 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.68 [95% confidence interval, 1.25-2.25]; and men, 1.92 [95% confidence interval, 1.39-2.66]) and at the age of 70 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.66 [95% confidence interval, 1.28-2.14]; and men, 1.30 [95% confidence interval, 0.97-1.75]). This effect was evident for recent and remote antecedent BP, consistent in hypertensive and nonhypertensive subjects, and demonstrable for all BP components. CONCLUSIONS: Antecedent BP contributes to the future risk of ischemic stroke. Optimal prevention of late-life stroke will likely require control of midlife BP.

Adult↗
PubMed2000

The preclinical phase of alzheimer disease: A 22-year prospective study of the Framingham Cohort.

OBJECTIVES: To relate performance on tests of cognitive ability to the subsequent development of probable Alzheimer disease (pAD) and to identify the pattern of earliest changes in cognitive functioning associated with a diagnosis of pAD. DESIGN: From May 1975 to November 1979, a screening neuropsychological battery was administered to Framingham Study participants. They were followed up prospectively for 22 years and examined at least every 2 years for the development of pAD. SETTING: A community-based center for epidemiological research. PARTICIPANTS: Subjects were 1076 participants of the Framingham Study aged 65 to 94 years who were free of dementia and stroke at baseline (initial) neuropsychological testing. MAIN OUTCOME MEASURE: Presence or absence of pAD during a 22-year surveillance period was related to test performance at initial neuropsychological testing. RESULTS: Lower scores for measures of new learning, recall, retention, and abstract reasoning obtained during a dementia-free period were associated with the development of pAD. Lower scores for measures of abstract reasoning and retention predicted pAD after a dementia-free period of 10 years. CONCLUSIONS: The "preclinical phase" of detectable lowering of cognitive functioning precedes the appearance of pAD by many years. Measures of retention of information and abstract reasoning are among the strongest predictors of pAD when the interval between initial assessment and the development of pAD is long. Arch Neurol. 2000.

Aged↗
PubMed2000

Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate.

BACKGROUND: The frequency of reactions reported to occur after the consumption of monosodium glutamate (MSG) is the subject of controversy. OBJECTIVE: We conducted a multicenter, multiphase, double-blind, placebo-controlled study with a crossover design to evaluate reactions reportedly caused by MSG. METHODS: In 3 of 4 protocols (A, B, and C), MSG was administered without food. A positive response was scored if the subject reported 2 or more symptoms from a list of 10 symptoms reported to occur after ingestion of MSG-containing foods within 2 hours. In protocol A 130 self-selected reportedly MSG-reactive volunteers were challenged with 5 g of MSG and with placebo on separate days (days 1 and 2). Of the 86 subjects who reacted to MSG, placebo, or both in protocol A, 69 completed protocol B to determine whether the response was consistent and dose dependent. To further examine the consistency and reproducibility of reactions to MSG, 12 of the 19 subjects who responded to 5 g of MSG but not to placebo in both protocols A and B were given, in protocol C, 2 challenges, each consisting of 5 g of MSG versus placebo. RESULTS: Of 130 subjects in protocol A, 50 (38. 5%) responded to MSG only, 17 (13.1%) responded to placebo only (P <. 05), and 19 (14.6%) responded to both. Challenge with increasing doses of MSG in protocol B was associated with increased response rates. Only half (n = 19) of 37 subjects who reacted to 5 g of MSG but not placebo in protocol A reacted similarly in protocol B, suggesting inconsistency in the response. Two of the 19 subjects responded in both challenges to MSG but not placebo in protocol C; however, their symptoms were not reproducible in protocols A through C. These 2 subjects were challenged in protocol D 3 times with placebo and 3 times with 5 g of MSG in the presence of food. Both responded to only one of the MSG challenges in protocol D. CONCLUSION: The results suggest that large doses of MSG given without food may elicit more symptoms than a placebo in individuals who believe that they react adversely to MSG. However, neither persistent nor serious effects from MSG ingestion are observed, and the responses were not consistent on retesting.

Adult↗
PubMed2000

Review of alleged reaction to monosodium glutamate and outcome of a multicenter double-blind placebo-controlled study.

Monosodium glutamate (MSG) has a long history of use in foods as a flavor enhancer. In the United States, the Food and Drug Administration has classified MSG as generally recognized as safe (GRAS). Nevertheless, there is an ongoing debate exists concerning whether MSG causes any of the alleged reactions. A complex of symptoms after ingestion of a Chinese meal was first described in 1968. MSG was suggested to trigger these symptoms, which were referred to collectively as Chinese Restaurant Syndrome. Numerous reports, most of them anecdotal, were published after the original observation. Since then, clinical studies have been performed by many groups, with varying degrees of rigor in experimental design ranging from uncontrolled open challenges to double-blind, placebo controlled (DBPC) studies. Challenges in subjects who reported adverse reactions to MSG have included relatively few subjects and have failed to show significant reactions to MSG. Results of surveys and of clinical challenges with MSG in the general population reveal no evidence of untoward effects. We recently conducted a multicenter DBPC challenge study in 130 subjects (the largest to date) to analyze the response of subjects who report symptoms from ingesting MSG. The results suggest that large doses of MSG given without food may elicit more symptoms than a placebo in individuals who believe that they react adversely to MSG. However, the frequency of the responses was low and the responses reported were inconsistent and were not reproducible. The responses were not observed when MSG was given with food.

Animals↗
PubMed2000

The impact of managed care insurance on use of lower-mortality hospitals by children undergoing cardiac surgery in California.

CONTEXT: Managed care plans aggressively seek to contain costs, but few data are available regarding their impact on access to high quality care for their members. OBJECTIVE: To assess the impact of managed care health insurance on use of lower-mortality hospitals for children undergoing heart surgery in California. DESIGN: Retrospective cohort study using state-mandated hospital discharge datasets. SETTING: Pediatric cardiovascular surgical centers in California. PATIENTS: Five thousand seventy-one children admitted for open cardiac surgical procedures during 1992-1994. RESULTS: Hospitals were divided into lower- and higher-mortality groups according to adjusted surgical mortality. Using multivariate logistic regression analysis to control for medical, socioeconomic, demographic, and distance factors, children with managed care insurance were less likely to be admitted to a lower-mortality hospital for surgery relative to children with indemnity insurance (odds ratio:.53; 95% confidence interval:.45,.63). Similar findings resulted when the analysis was stratified by race/ethnicity. In addition, length of stay, a correlate of health care costs, was no longer for children admitted to lower-mortality centers than for those at higher-mortality centers (adjusted difference:.54 days shorter at lower-mortality centers; 95% confidence interval: -1.50,. 41). CONCLUSIONS: During this study, children with managed care insurance had significantly reduced use of lower-mortality hospitals for pediatric heart surgery in California compared with children with indemnity insurance. Further study is necessary to determine the mechanisms of this apparent insurance-specific inequity.

California↗
PubMed1999

Lifetime risk of developing coronary heart disease.

BACKGROUND: The lifetime risk of developing coronary heart disease has not been estimated in a general population. We investigated the lifetime risks of initial coronary events at different ages. METHODS: We assessed data for 7733 participants in the Framingham Heart Study, who had been examined at least once at age 40-94 years between 1971 and 1975, found to be free of coronary heart disease, and then followed up. We estimated the lifetime risks of coronary heart disease (angina pectoris, coronary insufficiency, myocardial infarction, or death from coronary heart disease) by multiple-decrement life-table methods. FINDINGS: The 7733 patients were followed up for a total of 109,948 person-years. Overall, 1157 participants developed coronary heart disease. 1312 died from non-coronary heart disease causes. Lifetime risk of coronary heart disease at age 40 years was 48.6% (95% CI 45.8-51.3) for men and 31.7% (29.2-34.2) for women. At age 70 years, lifetime risk was 34.9% (31.2-38.7) for men and 24.2% (21.4-27.0) for women. After we excluded isolated angina pectoris as an initial event, the lifetime risk of coronary artery disease events at age 40 years was 42.4% for men and 24.9% for women. INTERPRETATION: Lifetime risk at age 40 years is one in two for men and one in three for women. Even at age 70 years it is one in three for men and one in four for women. This knowledge may promote efforts in education, screening, and treatment for prevention of coronary heart disease in younger and older patients.

Adult↗
PubMed1999

Low cholesterol as a risk factor for primary intracerebral hemorrhage: A case-control study.

We performed a case-control study to assess the relationship between primary intracerebral hemorrhage (ICH) and low serum cholesterol. Prospectively recruited, fully evaluated patients with ICH were compared to two independent control groups, one based in a primary care practice and one population-based. Low cholesterol was defined by the sex-specific lowest quintile of the primary care controls. The proportion of ICH cases with low cholesterol >3 months posthemorrhage was significantly greater than in controls (42 vs. 20% in either control group, p < 0.01). Subgroup analysis showed an overrepresentation of low cholesterols in probable hypertensive hemorrhage (47%, p < 0.05) but not in probable cerebral amyloid angiopathy (27%, p = 0.5). Low cholesterol increased the odds for hemorrhage 2.25-fold (1.12-4.50) after adjustment for age and apolipoprotein E genotype. These data confirm an increased risk for primary ICH associated with low cholesterol, a relationship that may apply specifically to hemorrhages from hypertensive vasculopathy.

Aged↗
PubMed1998

Intellectual decline after stroke: the Framingham Study.

BACKGROUND AND PURPOSE: The causes and characteristics of cognitive decline after stroke are poorly defined, because most studies have relied on the diagnosis of dementia after stroke, without measurement of prestroke cognitive function. METHODS: The Mini-Mental State Examination (MMSE) was used to assess the cognitive performance of 74 subjects from the Framingham Study cohort who had suffered a stroke during a 13-year period. We compared their poststroke cognitive performance with the prestroke MMSE scores collected during their biennial examinations, and their prestroke/poststroke changes in MMSE score were then compared with those of 74 control subjects matched for age and sex. Cases and controls underwent testing for symptoms of depression using the Center for Epidemiologic Studies of Depression (CES-D) scale, and these findings were correlated with their cognitive performance. Changes in cognitive performance in the cases were correlated with the CT-documented characteristics of the stroke. RESULTS: The cases had a significantly lower mean+/-SE MMSE score at prestroke baseline (27.28+/-0.34) than did the control subjects (28.08+/-0.21), a difference that became more pronounced (23.57+/-0.92 versus 28.31+/-0.25; P<.001) after stroke. The poststroke decline in cognitive function in the cases was correlated only with a large, left-sided stroke on CT. The CES-D scores were significantly higher in the cases, but nondepressed cases had significantly lower MMSE scores than nondepressed controls. CONCLUSIONS: Stroke is followed by a significant decline in cognitive performance when prestroke and poststroke measurements are compared. Although depression is more frequent in the stroke patients, their intellectual decline appears to be independent from the presence of depression.

Aged↗
PubMed1998

Circadian variation of urinary excretion of elastin and collagen crosslinks.

Urinary levels of collagen- and elastin-crosslink amino acids have been used as biologic markers for degradation of collagen and elastin in the body. Circadian variation of collagen-crosslink amino acids is well known. The current study was undertaken to determine whether there is also circadian variation in excretion of elastin-crosslink amino acids. We used an isotope dilution-HPLC assay to measure the elastin-crosslink amino acids, desmosine (DES) and isodesmosine (IDES), and the collagen-crosslink amino acids, hydroxylysyl pyridinoline (HP) and lysyl pyridinoline (LP), in urine. Sixteen apparently healthy subjects collected urine from 5:00 to 7:00 AM, and from 5:00 to 7:00 PM. Mean urinary excretion of DES and IDES in women was 56% and 41% higher (P < 0.001), respectively, in AM versus PM specimens when normalized by the creatinine content of the urine specimen. For men, the corresponding values were 11% and 13% higher (not statistically significant). Mean urinary excretion of HP and LP in women was 61% and 71% higher (P < 0.001), respectively, in AM versus PM specimens. For men, the corresponding values were 11% and 19% higher (not statistically significant). Differences were not found in the AM versus PM rates of excretion of creatinine in men or women. These findings demonstrate the occurrence of circadian variation in HP, LP, DES and IDES in women but not in men. We conclude that the time of collection of urine specimens, especially from women, must be taken into consideration in using the urinary levels of these crosslink amino acids as biologic markers for collagen or elastin degradation.

Adult↗
PubMed1997

Lifetime risk of dementia and Alzheimer's disease. The impact of mortality on risk estimates in the Framingham Study.

We estimated the remaining lifetime risks of developing Alzheimer's disease (AD) and dementia from all causes, based on data from longitudinal population studies. The risk of developing AD during one's lifetime depends on both disease incidence and life expectancy. Conventional estimates of cumulative incidence overestimate the risk when there is a substantial probability of mortality due to competing causes. A total of 2,611 cognitively intact subjects (1,061 men, 1,550 women; mean age, 66 +/- 7 years) were prospectively evaluated for the development of AD or other dementia. A modified survival analysis was used to estimate both cumulative incidence and the sex-specific remaining lifetime risk estimates for quinquennial age groups above age 65 years. Over a 20-year follow-up period, 198 subjects developed dementia (120 with AD). The remaining lifetime risk of AD or other dementia depended on sex, being higher in women, but varied little with age between 65 and 80 years. In a 65-year-old man, the remaining lifetime risk of AD was 6.3% (95% CI, 3.9 to 8.7) and the remaining lifetime risk of developing any dementing illness was 10.9% (95% CI, 8.0 to 13.8); corresponding risks for a 65-year-old woman were 12% (95% CI, 9.2 to 14.8) and 19% (95% CI, 17.2 to 22.5). The cumulative incidence between age 65 and 100 years was much higher: for AD, 25.5% in men and 28.1% in women; for dementia, 32.8% in men and 45% in women. The actual remaining lifetime risk of AD or dementia varies with age, sex, and life expectancy and is lower than the hypothetical risk estimated by a cumulative incidence in the same population.

Aged↗
PubMed1997

Residential lead-based-paint hazard remediation and soil lead abatement: their impact among children with mildly elevated blood lead levels.

OBJECTIVES: This prospective study describes the impact of residential lead-based-paint hazard remediations on children with mildly elevated blood lead levels. METHODS: Changes in blood lead levels were observed following paint hazard remediation alone and in combination with soil abatement. RESULTS: After adjustment for the confounding variables paint hazard remediation alone was associated with a blood lead increase of 6.5 micrograms/dL (P = 0.5), and paint hazard remediation combined with soil abatement was associated with an increase of 0.9 microgram/dL (P = 36). CONCLUSIONS: Lead-based-paint hazard remediation as performed in this study, is not an effective secondary prevention strategy among children with mildly elevated blood lead levels.

Boston↗
PubMed1996

Apolipoprotein E epsilon4 association with dementia in a population-based study: The Framingham study.

Apolipoprotein E type 4 allele (apoE epsilon4) is associated with Alzheimer's disease (AD) in the late-onset familial form and in sporadic cases, but the age-associated risk in a randomly sampled elderly population is not established. We examined the association of apoE epsilon4 with AD and other dementias (mainly multi-infarct or dementia following stroke) in 1,030 persons aged 71 to 100 years in the population-based Framingham Study cohort. Kaplan-Meier survival analysis revealed that 55% of the apoE epsilon4/epsilon4 homozygotes developed AD by age 80, whereas 27% of apoE epsilon3/epsilon4 heterozygotes developed AD by age 85, and 9% of those without a 4 allele developed AD by age 85 years. In comparison with persons without a 4 allele, the risk ration for AD was 3.7 (95% CI = 1.9 to 7.5) for apoE epsilon3/epsilon4 heterozygotes and 30.1 (95% CI = 10.7 to 84.4) for apoE epsilon4 homozygotes. ApoE epsilon2 (2/2, 2/3, or 2/4 genotypes) was associated with an absence of AD. One-half (n=21) of the 43 AD patients were either homozygous or heterozygous for apoE epsilon4. We found evidence for an association of apoE epsilon4 with other dementia, primarily multi-infarct dementia and stroke. The risk ratio was 2.3 (95% CI = 0.9 to 6.1) for non-AD dementias among persons with apoE epsilon3/epsilon4. Although the apoE epsilon4 allele is a potent risk factor for AD and may be associated with other forms of dementia, most apoE epsilon4 carriers do not develop dementia, and about one-half of AD is not apoE epsilon4 associated. The low positive predictive value of this marker (0.10) suggest that use of apoE genotyping as a screening test for AD is not supported.

Adult↗
PubMed1994

The impact of soil lead abatement on urban children's blood lead levels: phase II results from the Boston Lead-In-Soil Demonstration Project.

The Boston Lead-In-Soil Demonstration Project was a randomized environmental intervention study of the impact of urban soil lead abatement on children's blood lead levels. Lead-contaminated soil abatement was associated with a modest reduction in children's blood lead levels in both phases of the project; however, the reduction in Phase II was somewhat greater than that in Phase I. The combined results from both phases suggest that a soil lead reduction of 2060 ppm is associated with a 2.25 to 2.70 micrograms/dl decline in blood lead levels. Low levels of soil recontamination 1 to 2 years following abatement indicate that the intervention is persistent, at least over the short-term. Furthermore, the intervention appears to benefit most children since no measurable differences in efficacy were observed for starting blood and soil lead level, race, neighborhood, gender, and many other characteristics. However, soil abatement did appear to be more beneficial to children in the higher socioeconomic classes, with low baseline ferritin levels, and who spent time away from home on a regular basis and lived in nonowner occupied housing, and with adults who had lead-related hobbies and almost always washed their hands before meals. Children who lived in apartments with consistently elevated floor dust lead loading levels derived almost no benefit from the soil abatement. It was not possible to separate the effects of the variables that had a beneficial impact on efficacy because they were closely correlated and the number of subjects was small. We recommend that further research be conducted to identify subgroups of children to whom soil lead abatement might be targeted.

Boston↗
PubMed1993

Lead-contaminated soil abatement and urban children's blood lead levels.

OBJECTIVE: To test the hypothesis that a reduction of 1000 ppm or more of lead in soil accessible to children would result in a decrease of at least 0.14 mumol/L (3 micrograms/dL) in blood lead levels. SETTING: Urban neighborhoods with a high incidence of childhood lead poisoning and high soil lead levels. DESIGN: Randomized controlled trial of the effects of lead-contaminated soil abatement on blood lead levels of children followed up for approximately 1 year after the intervention. PATIENTS: A total of 152 children less than 4 years of age with venous blood lead levels of 0.34 to 1.16 mumol/L (7 to 24 micrograms/dL). Children were largely poor and had a mean age at baseline of 32 months, a mean blood lead level of 0.60 mumol/L (12.5 micrograms/dL), and a median surface soil lead level of 2075 ppm. INTERVENTIONS: Children were randomized to one of three groups: the study group, whose homes received soil and interior dust abatement and loose paint removal; comparison group A, whose homes received interior dust abatement and loose paint removal; and comparison group B, whose homes received only interior loose paint removal. MAIN OUTCOME MEASURES: Change in children's blood lead levels from preabatement levels to levels approximately 6 and 11 months after abatement. RESULTS: The mean decline in blood lead level between preabatement and 11 months after abatement was 0.12 mumol/L (2.44 micrograms/dL) in the study group (P = .001), 0.04 mumol/L (0.91 microgram/dL) in group A (P = .04), and 0.02 mumol/L (0.52 microgram/mL) in group B (P = .31). The mean blood lead level of the study group declined 0.07 mumol/L (1.53 micrograms/dL) more than that of group A (95% confidence interval [CI], -0.14 to -0.01 mumol/L [-2.87 to -0.19 micrograms/dL]) and 0.09 mumol/L (1.92 micrograms/dL) more than group B (95% CI, -0.16 to -0.03 mumol/L [-3.28 to -0.56 micrograms/dL]). When adjusted for preabatement lead level, the 11-month mean blood lead level was 0.06 mumol/L (1.28 micrograms/dL) lower in the study group as compared with group A (P = .02) and 0.07 mumol/L (1.49 micrograms/dL) lower than in group B (P = .01). The magnitude of the decline independently associated with soil abatement ranged from 0.04 to 0.08 mumol/L (0.8 to 1.6 micrograms/dL) when the impact of potential confounders, such as water, dust, and paint lead levels, children's mouthing behaviors, and other characteristics, was controlled for. CONCLUSIONS: These results demonstrate that lead-contaminated soil contributes to the lead burden of urban children and that abatement of lead-contaminated soil around homes results in a modest decline in blood lead levels. The magnitude of reduction in blood lead level observed, however, suggests that lead-contaminated soil abatement is not likely to be a useful clinical intervention for the majority of urban children in the United States with low-level lead exposure.

Child, Preschool↗
PubMed1993

Sputum eosinophilia negates need to perform sputum Gram's stain.

A total of 1878 sputum specimens were evaluated to assess the potential of encountering a sputum Gram's stain with clinically useful positive data in the presence of sputum eosinophilia. Wet preparations were used to assess the adequacy of the specimen and to quantitate eosinophils. Quantitative sputum Gram's stains were performed. When more than 50% of the cells observed on sputum wet preparation were eosinophils, there were no positive Gram's stains. When more than 20% of the cells were eosinophils, there was a 1% prevalence of potentially clinically useful positive Gram's stains. The data strongly suggest that sputum eosinophilia obviates the need to perform a sputum Gram's stain since it is extremely unlikely that it would be useful in diagnosing a bacterial infection of the lower respiratory tract.

Bacterial Infections↗
PubMed1991

Choline, an essential nutrient for humans.

Choline is required to make essential membrane phospholipids. It is a precursor for the biosynthesis of the neurotransmitter acetylcholine and also is an important source of labile methyl groups. Mammals fed a choline-deficient diet develop liver dysfunction; however, choline is not considered an essential nutrient in humans. Healthy male volunteers were hospitalized and fed a semisynthetic diet devoid of choline supplemented with 500 mg/day choline for 1 wk. Subjects were randomly divided into two groups, one that continued to receive choline (control), and the other that received no choline (deficient) for three additional wk. During the 5th wk of the study all subjects received choline. The semisynthetic diet contained adequate, but no excess, methionine. In the choline-deficient group, plasma choline and phosphatidylcholine concentrations decreased an average of 30% during the 3-wk period when a choline-deficient diet was ingested; plasma and erthrocyte phosphatidylcholine decreased 15%; no such changes occurred in the control group. In the choline-deficient group, serum alanine aminotransferase activity increased steadily from a mean of 0.42 mukat/liter to a mean of 0.62 mukat/liter during the 3-wk period when a choline-deficient diet was ingested; no such change occurred in the control group. Other tests of liver and renal function were unchanged in both groups during the study. Serum cholesterol decreased an average of 15% in the deficient group and did not change in the control group. Healthy humans consuming a choline-deficient diet for 3 wk had depleted stores of choline in tissues and developed signs of incipient liver dysfunction. Our observations support the conclusion and choline is an essential nutrient for humans when excess methionine and folate are not available in the diet.

Choline↗