• Remarkable Reversal of Aging in Mice
• The Numbers: Diabetes in America
• Does Maternal DHA Supplementation During Early Breast-Feeding Have Long-Term Benefits?
• State of the Union Speech Hints at Direction of Continuing Health Care Debate
• Vitamin of the Year?
• Doxylamine and Pyridoxine for Nausea and Vomiting of Pregnancy:
Together Again at Last
• Thyroid-Stimulating Hormone Levels During Pregnancy:
Should "Normal" Be Redefined?
• Does Polycystic Ovary Syndrome Raise Risk for Cardiovascular Disease?
• Behavioral Therapy Prevents Recurrences of Cardiovascular Events in Trial
• Pregnancy-Associated Restless Legs Syndrome Can Become Chronic
• Restless Legs Syndrome: Creeping Out of the Closet
• Brain Aging Delayed by Mediterranean Diet
• Early Cigarette Smoking Associated with Breast Cancer
• Update on Multiple Sclerosis Diagnostic Criteria
Nature 2010 Nov 28
Remarkable Reversal of Aging in Mice
Restoring telomerase function in mutant mice reversed signs of aging.
Is aging of cells and organisms an inevitable process? Some research suggests that aging can be retarded (JW Gen Med Dec 28 2006) A new report suggests that it might even be reversible.
One reason cells age is that telomeres — the tips of the chromosomes — become shorter with each cell division, a process that can be stopped by turning on the enzyme telomerase. A team from Boston created mice in which telomerase was not produced but could be turned on at the investigators' discretion. In mice with no telomerase, tissues atrophied, stem cells were depleted, tissue injury repair was compromised, and organs began to fail. Although chronologically young, they were physiologically very old and close to death.
One month after the investigators turned on production of the telomerase enzyme in these mice, telomeres had lengthened, new neurons had formed, and brain size had begun to enlarge. So had the sizes of spleen and testes, with marked increases in sperm production and litter size. Very soon, the mice were physiologically like the young adults that they were, chronologically. No evidence of tumor formation was noted.
Comment: This experiment was conducted in mice, not humans, and these mice were genetically engineered to age rapidly. Whether turning on telomerase can reverse aging in normal mice, let alone in humans, remains to be shown. Because telomerase is activated in many tumors, we also need to verify that turning on telomerase doesn't result in excess risk for cancer. Still, this is an exciting result in a mammal.
— Anthony L. Komaroff, MD Published in Journal Watch General Medicine January 4, 2011
Citation(s): Jaskelioff M et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2010 Nov 28; [e-pub ahead of print]. (http://dx.doi.org/10.1038/nature09603)
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http://www.cdc.gov/media/releases/2011/p0126_diabetes.html
The Numbers: Diabetes in America
Nearly 26 million Americans (11.3% of adults) now have diabetes, according to new CDC estimates of diagnosed and undiagnosed diabetes.
Nearly 80 million (35% of adults) qualify as having prediabetes. If the trend continues, one in three American adults could have diabetes by 2050.
The prevalence increases with increasing age — roughly 27% of seniors are estimated to have diabetes.
The CDC says the national prevalence of diabetes has increased 9% since 2008 for several reasons besides an increased incidence of the disease, namely:
• People with diabetes are living longer.
• The hemoglobin A1c test was recently incorporated into prevalence estimates. Earlier data relied on fasting glucose to derive estimates.
National Diabetes Fact Sheet, 2011 http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf
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J Pediatr 2010 Dec; 157:900
Does Maternal DHA Supplementation During Early Breast-Feeding
Have Long-Term Benefits?
Children whose mothers received DHA supplementation during the first 4 months of breast-feeding had enhanced sustained attention at age 5 years.
The omega-3 fatty acid docosahexaenoic acid (DHA; 22:6n-3) is a major component of developing retinal and neural membranes. The authors of the current study previously reported that full-term infants whose mothers received DHA supplementation during the first 4 months of lactation had significantly improved psychomotor development at age 30 months, compared with infants whose mothers did not receive DHA (Am J Clin Nutr 2005; 82:125). Now, they report visual and neuropsychological development in the same children at age 5 years.
The initial 230 pregnant women were randomized to receive DHA (about 200 mg/day) or an identical capsule with vegetable oil (without DHA) for the first 4 months of breast-feeding. Infants in the two groups had similar Apgar scores and head circumferences at birth. At age 5 years, measures of visual acuity and visual evoked potential tests did not differ between groups. However, children whose mothers received DHA while nursing had significantly better scores on the Sustained Attention Subscale of the Leiter Performance Scale (46.5±8.9 vs. 41.9±9.3). No differences were found in motor development, language skills, or executive function. Adjustment for maternal IQ and age did not alter the results.
Comment: The omega-3 fatty acid DHA has received substantial attention in both the adult and pediatric literature. This study showed that maternal DHA supplementation during the first 4 months of lactation significantly enhanced sustained attention at age 5 years. The authors of the study wrote: "The biologic or ‘real-life' significance of an improvement in sustained attention of the magnitude observed in this study at 5 years of age is difficult to ascertain, particularly because scores of both groups were within the normal range for age. Nonetheless, this finding underscores the importance of longer-term follow-up studies of early DHA supplementation." I support the authors' perspective in that sustained attention is an important component of academic achievement and social development throughout latency and adolescent development.
— Martin T. Stein, MD Published in Journal Watch Pediatrics and Adolescent Medicine
January 26, 2011
Citation(s): Jensen CL et al. Effects of early maternal docosahexaenoic acid intake on neuropsychological status and visual acuity at five years of age of breast-fed term infants. J Pediatr 2010 Dec; 157:900.PMID: 20655543
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http://s3.documentcloud.org/documents/29615/state-of-the-union-speech-2011.pdf
State of the Union Speech Hints at Direction of Continuing Health Care Debate
President Barack Obama's State of the Union message to the 112th Congress didn't spend much time on health care, but hinted that the debate — and its consequences for clinicians — will continue.
Here, from a transcript supplied by the Washington Post, is what the President had to say on the subject:
Now, I’ve heard rumors that a few of you have some concerns about the new health care law. So let me be the first to say that anything can be improved. If you have ideas about how to improve this law by making care better or more affordable, I am eager to work with you. We can start right now by correcting a flaw in the legislation that has placed an unnecessary bookkeeping burden on small businesses.
What I’m not willing to do is go back to the days when insurance companies could deny someone coverage because of a pre-existing condition. I’m not willing to tell James Howard, a brain cancer patient from Texas, that his treatment might not be covered. I’m not willing to tell Jim Houser, a small business owner from Oregon, that he has to go back to paying $5,000 more to cover his employees. As we speak, this law is making prescription drugs cheaper for seniors and giving uninsured students a chance to stay on their parents’ coverage. So instead of re-fighting the battles of the last two years, let’s fix what needs fixing and move forward.
And, a bit later on:
And their [the bipartisan Fiscal Commission's] conclusion is that the only way to tackle our deficit is to cut excessive spending wherever we find it — in domestic spending, defense spending, health care spending, and spending through tax breaks and loopholes.
This means further reducing health care costs, including programs like Medicare and Medicaid, which are the single biggest contributor to our long-term deficit. Health insurance reform will slow these rising costs, which is part of why nonpartisan economists have said that repealing the health care law would add a quarter of a trillion dollars to our deficit. Still, I’m willing to look at other ideas to bring down costs, including one that Republicans suggested last year: medical malpractice reform to rein in frivolous lawsuits.
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Vitamin of the Year?
Let the sunshine in: Vitamin D deficiency has neuropsychiatric implications.
The number of patients undergoing tests for vitamin D deficiency or taking vitamin D3 supplements seems to be increasing exponentially, and low vitamin D levels in dermatologic (JW Dermatol May 22 2009) and general medical disorders (JW Gen Med Dec 31 2009) have received attention. Although a recent report from the Institute of Medicine concluded that no current evidence supported a role for vitamin D in conditions other than bone health, new studies have focused on its potential role in neuropsychiatric disorders, including depression, cognitive dysfunction, schizophrenia, and multiple sclerosis (MS).
Some basic information about vitamin D might improve our understanding of the research. Vitamin D (also called calciferol) comprises a group of fat-soluble vitamins with a cholesterol backbone. Vitamin D3 (cholecalciferol) is formed in the skin after exposure to sunlight, binds to a protein for transportation in the blood, and is converted to its active form (1,25 dihydroxyvitamin D) through metabolism in the liver and then the kidney. Dietary sources include fortified milk or cereals, eggs, and fatty fish. Deficiency can result from inadequate intake, lack of sun exposure, fat malabsorption (such as in celiac and Crohn diseases), and liver and renal disorders.
A neurosteroid hormone, vitamin D binds to receptors in the brain and has multiple actions. The vitamin is neuroprotective (through its neurotropic, anti-inflammatory, antioxidative, and anti-ischemic properties), regulates the metabolism of multiple neurotransmitters and growth factors, and suppresses the expression of inflammatory cytokines. These may be reasonable mechanisms for how low serum levels of vitamin D (25 hydroxyvitamin D [25(OH)D]) could result in or exacerbate cognitive problems and depression and otherwise influence neuropsychiatric disorders.
One 2010 study examined the link between vitamin D and depression in 2070 elders (mean age, 74) in the community. Of those with deficient 25(OH)D levels (<10 mg/mL), 35% had depressive symptoms (JW Psychiatry Aug 9). Two research groups (JW Neurol Jul 27) focused on vitamin D and MS, which is more common at latitudes with less sunlight. Handunnetthi and colleagues hypothesized that living at such latitudes combined with a polymorphism sensitive to D3 may predispose individuals to MS. Burton and colleagues gave high-dose vitamin D (with calcium) to MS patients. After 1 year, it was well tolerated, produced very high plasma 25(OH)D levels, and was possibly linked to fewer relapses.
Several research groups examined 25(OH)D levels and cognition. In a study of 752 women (mean age, 80), the low-level group (<10 ng/mL) had significantly lower mean cognitive scores and a higher prevalence of scores indicating global cognitive impairment (JW Psychiatry Nov 23 2009). Other researchers have also examined this possible link (JW Neurol Mar 30). In a cross-sectional study of 318 elders, dementia was more common with 25(OH)D levels below 20 ng/mL. In a longitudinal study following 1604 men, researchers found a nonsignificant trend toward increasing global cognitive impairment with decreasing 25(OH)D levels.
In a study of bone health in patients with various psychiatric disorders, low vitamin D status was found in patients with schizophrenia. Use of antipsychotics and mood stabilizers was associated with lower D levels (JW Psychiatry Oct 18).
Few studies, however, have examined dietary intake. In a just-published study of 5596 community-dwelling women (mean age, 80), researchers assessed weekly vitamin D intake via a food frequency questionnaire (Neurology 75:1810). The "inadequate intake" group was older, reported disability more often, and had a lower mean cognitive score and greater frequency of impaired scores than the "recommended intake" group. After adjustment for all confounders (e.g., chronic disease, hypertension, depression, psychoactive drug use), cognitive impairment remained associated with inadequate intake — and with older age, disability, and depression. Explanations other than cause and effect might exist for the association of low dietary vitamin D with cognitive impairment. Poor vitamin D intake may be a marker for other dietary or nutritional deficiencies. Although body-mass index was the same in the disabled and nondisabled group, disabled women with poor cognition might eat poorly.
A large controlled study of vitamin D3 supplementation now seems justified to ascertain its potential effects on neuropsychiatric status, including mood and cognition. But what steps should we clinicians take? The clinical rationale for measuring 25(OH)D levels in our patients is substantial. Levels below 10 ng/mL are "deficient," but intervention for borderline levels (<30 ng/mL) is probably reasonable. According to the IOM report, insufficient 25(OH)D levels have not been systematically evaluated. A level below 20 ng/mL appears to place an individual at risk, and levels above 30 ng/mL are not consistently associated with increased benefit. Because of the risk for melanoma, we should be hesitant to tell our patients to expose themselves to more sunlight. Supplementation (with D3) can be prescribed, with follow-up testing; if levels do not increase with 2000 IU/day, the clinician should consider an evaluation for absorption problems (e.g., celiac disease). Adverse effects with long-term, very large doses of vitamin D can include nausea, vomiting, poor appetite, constipation, weakness, and weight loss. As with other vitamins, the benefit and long-term safety of supplementation have not been demonstrated.
— Jonathan Silver, MD Published in Journal Watch Psychiatry January 3, 2011
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Am J Obstet Gynecol 2010 Dec; 203:571.e1
Doxylamine and Pyridoxine for Nausea and Vomiting of Pregnancy:
Together Again at Last
New combined formulation is effective and well-tolerated
Nausea and vomiting of pregnancy (NVP) is common and can be debilitating. The combination of doxylamine succinate and pyridoxine hydrochloride (Bendectin) was voluntarily discontinued in 1983 by the manufacturer because of alleged birth defects in offspring of users. These claims were subsequently shown to be unfounded and the litigations were rejected, but no product has since been FDA-approved for NVP. Now, investigators have conducted a randomized controlled trial, sponsored by a different manufacturer, to assess efficacy of a new delayed-release formulation of the same two agents (Diclectin). Two hundred and eighty women with pregnancies of 7 to 14 weeks' gestation and NVP that was resistant to dietary and lifestyle management were randomized to receive placebo or Diclectin (10 mg of each agent; dosages were escalated as needed). The primary outcome was improvement as measured with a 15-point pregnancy emesis scale to assess symptoms and quality of life.
Diclectin, compared with placebo, was associated with greater improvements in emesis scores (change from baseline, –4.8 vs. –3.9; P=0.006) and quality of life, with a trend toward fewer missed days of work in the Diclectin group. Substantially more women in the Diclectin group (49% vs. 33%, P=0.009) asked to continue using their assigned treatment at the end of the 15-day trial period. Adverse events did not differ between groups.
Comment: The discontinuation (which was not based on definitive safety concerns) of an effective tool in the battle against nausea and vomiting of pregnancy was followed by a marked rise in hospitalizations for this condition. Taken together with previous findings supporting Diclectin's safety, these data, which offer compelling evidence of the efficacy and tolerability of a new formulation of an old pair of agents, should reassure patients, providers, epidemiologists, litigators, and regulatory agencies alike.
— Allison Bryant, MD, MPH Published in Journal Watch Women's Health January 6, 2011
Citation(s): Koren G et al. Effectiveness of delayed-release doxylamine and pyridoxine for nausea and vomiting of pregnancy: A randomized placebo controlled trial. Am J Obstet Gynecol 2010 Dec; 203:571.e1. PMID: 20843504
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J Clin Endocrinol Metab 2010 Sep; 95:E44
Thyroid-Stimulating Hormone Levels During Pregnancy:
Should "Normal" Be Redefined?
Rates of pregnancy loss were substantially higher in women with first-trimester TSH levels of 2.5 to 5.0 mIU/L than in those with lower levels.
Consensus about what constitutes normal levels of thyroid-stimulating hormone (TSH) during pregnancy is shifting; moreover, the effects of subclinical hypothyroidism on maternal or neonatal health remain largely unknown. In a prospective study, researchers assessed pregnancy outcomes in women who were screened during the first trimester for TSH and thyroid-peroxidase antibody. All participants were negative for thyroid-peroxidase antibody; 3481 had TSH levels <2.5 mIU/L and 642 had TSH levels 2.5 to 5.0 mIU/L.
Women with TSH levels <2.5 mIU/L had lower rates of spontaneous pregnancy loss than did those with TSH levels 2.5 to 5.0 mIU/L (3.6% vs. 6.1%; P=0.006); rates of preterm delivery were similar between groups. In adjusted analysis, likelihood of miscarriage rose incrementally with TSH levels (odds ratio, 1.2; P=0.047), suggesting that the relation between TSH levels and miscarriage risk is continuous.
Comment: Subclinical hypothyroidism is diagnosed in asymptomatic women when TSH levels are elevated but thyroxine (T4) levels are normal. The American College of Obstetricians and Gynecologists recommends evaluating TSH levels in women who are symptomatic, have thyroid disease, or have medical conditions associated with thyroid disease (e.g., diabetes); however, routine screening for subclinical hypothyroidism is not recommended (Obstet Gynecol 2007; 110:959). These results suggest that maternal TSH levels (even those within the range considered to be normal) can influence pregnancy outcomes. Until a prospective randomized trial of new screening strategies is performed, we await experts' opinions about TSH screening in asymptomatic pregnant women.
— Wendy S. Biggs, MD Published in Journal Watch Women's Health January 6, 2011
Citation(s): Negro R et al. Increased pregnancy loss rate in thyroid antibody negative women with TSH levels between 2.5 and 5.0 in the first trimester of pregnancy. J Clin Endocrinol Metab 2010 Sep; 95:E44. (http://dx.doi.org/10.1210/jc.2010-0340)
PMID: 20534758
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Obstet Gynecol 2011 Jan; 117:6
Does Polycystic Ovary Syndrome Raise Risk for Cardiovascular Disease?
PCOS was associated with excess risk for incident diabetes and dyslipidemia during nearly 2 decades of follow-up.
Polycystic ovary syndrome (PCOS) is associated with an adverse cardiovascular risk profile, but is long-term prevalence of such risk factors actually higher? To address this question, investigators evaluated data from a cohort of 1127 women (age range at enrollment, 20–32) who were followed for 20 years in a study on coronary artery risk development. PCOS (identified based on self-report of clinical symptoms and measurement of serum androgens) was present in 53 women (4.7%) at baseline.
White race, nulliparity, and higher mean fasting insulin levels were more common among women with PCOS at baseline than among those without PCOS. Baseline prevalences of hypertension, diabetes, and dyslipidemia were similar in both groups; however, adjusted analysis showed that women with PCOS at baseline were twice as likely to develop diabetes and dyslipidemia within 18 to 20 years. Notably, normal-weight women with PCOS had threefold higher odds of developing diabetes than did normal-weight women without PCOS. Fully 63% of women who were classified with PCOS at baseline experienced resolution of their symptoms during follow-up; women with persistent PCOS were at highest risk for developing diabetes.
Comment: These data bolster the conclusion that PCOS should not be regarded as an ovarian disease, but rather as a metabolic disease with diverse effects. Clinicians should counsel women with PCOS about its long-term consequences and should monitor them carefully over time for development of cardiovascular disease, dyslipidemia, and diabetes.
— Robert W. Rebar, MD Published in Journal Watch Women's Health January 27, 2011
Citation(s): Wang ET et al. Polycystic ovary syndrome and risk for long-term diabetes and dyslipidemia. Obstet Gynecol 2011 Jan; 117:6.PMID: 21173640
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http://archinte.ama-assn.org/cgi/content/short/171/2/134
Behavioral Therapy Prevents Recurrences of Cardiovascular Events in Trial
Cognitive-behavioral therapy, with a focus on stress management, is associated with fewer recurrent cardiovascular events in patients with coronary heart disease, according to an Archives of Internal Medicine study.
Some 350 adults who had recently had a coronary heart disease event were randomized to either usual care alone or usual care plus cognitive-behavioral therapy. Psychologists and nurses led 20 2-hour group sessions over 1 year. The therapy emphasized ways to reduce daily stress, time urgency, and hostility.
Over 8 years' follow-up, the intervention group experienced 41% fewer first recurrent cardiovascular events and 45% fewer recurrent myocardial infarctions, compared with the control group. All-cause mortality did not differ significantly between groups.
The authors speculate that the CBT group may have reduced their behavioral and emotional reactivity, "which would lead to less psychophysiologic burden on the cardiovascular system." They estimate that roughly 10 people would need to be treated in order to prevent one cardiovascular event.
Randomized Controlled Trial of Cognitive Behavioral Therapy vs Standard Treatment to Prevent Recurrent Cardiovascular Events in Patients With Coronary Heart Disease. Secondary Prevention in Uppsala Primary Health Care Project (SUPRIM).Mats Gulliksson, MD, PhD; Gunilla Burell, PhD; Bengt Vessby, MD, PhD; Lennart Lundin, MD, PhD; Henrik Toss, MD, PhD; Kurt Svärdsudd, MD, PhD.Arch Intern Med. 2011;171(2):134-140. doi:10.1001/archinternmed.2010.510
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Neurology 2010 Dec 7; 75:2117
Pregnancy-Associated Restless Legs Syndrome Can Become Chronic
Pregnancy-associated RLS raised risk for RLS during subsequent pregnancies and beyond.
The neurological disorder restless legs syndrome (RLS) is characterized by creeping, crawling sensations (primarily nocturnal) in the lower extremities that are relieved by movement. Pregnancy-associated RLS is clinically similar to nonpregnancy RLS, occurs during as many as 30% of pregnancies (most often during the third trimester), and usually resolves shortly after delivery. Decisions about possible treatment are challenging; if symptoms are severe, clonazepam or gabapentin at bedtime can be considered after evaluating potential risks to the fetus. Risk factors include family history and multiparity. In an epidemiological study of RLS in Italy, researchers sought to determine if women with RLS during pregnancy were at excess risk for developing chronic RLS.
A total of 74 participants who had experienced new-onset RLS during previous pregnancies and 133 who had never experienced RLS (non-RLS comparison group) were followed for a mean of 77 months to determine if they met diagnostic criteria for RLS. Prevalence of RLS at follow-up was 24% in the new-onset RLS group and 8% in the comparison group. Of 24 women in the new-onset RLS group and 33 women in the comparison group who had another pregnancy during follow-up, 58% and 3%, respectively, experienced RLS during their second pregnancies.
Comment: Women who experience RLS during pregnancy should be advised that symptoms might recur and become chronic. In that sense, pregnancy-associated RLS is similar to gestational diabetes and hypertension. This was a large study with a long follow-up and prevalences similar to those observed in other studies of RLS. Thus, these findings are likely to apply to the U.S. population.
— Autumn Klein, MD, PhD Dr. Klein is an Instructor in Neurology at Harvard Medical School and Director of the Program in Women's Neurology, Brigham and Women's Hospital, Boston.
Published in Journal Watch Women's Health January 27, 2011
Citation(s): Cesnik E et al. Transient RLS during pregnancy is a risk factor for the chronic idiopathic form. Neurology 2010 Dec 7; 75:2117PMID: 21135386
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Dev Med Child Neurol 2011 Jan; 53:40
Restless Legs Syndrome: Creeping Out of the Closet
RLS was associated with bed-wetting, sleep difficulty, and hyperactivity/inattention.
Restless legs syndrome (RLS) is a sensory-motor disorder with four essential characteristics: (1) having an irresistible urge to move the legs (i.e., a "creepy-crawly" tingling sensation), (2) begins or worsens during periods of rest, (3) is relieved by movement, and (4) occurs or worsens at night. Although the incidence of RLS in the pediatric population is unknown, retrospective reports by adults with RLS suggest that symptoms frequently appear in childhood.
In this study, 3304 adolescents (age range, 15–18 years; 49% male) at nine high schools in Turkey completed an RLS sleep questionnaire followed by a face-to-face or telephone interview to confirm the diagnosis of RLS. RLS had been present for at least 1 year in 3.6% of participants; 2.0% reported symptoms more than once weekly. Compared with adolescents without RLS, those with RLS reported significantly more nocturnal bed-wetting (0.8% vs. 4.2%), sleeping difficulty (32% vs. 47%), hyperactivity/inattention (14% vs. 25%), and limb movements during sleep (9% vs. 18%).
Comment: Although most pediatricians are familiar with RLS, I suspect that few have made this diagnosis in their patients. That certainly is my experience. The risk for coexisting conditions (e.g., enuresis, sleep dysregulation, and attention-deficit/hyperactivity disorder) informs us of the effect of RLS on quality of life in adolescents. In addition, iron-deficiency anemia and caffeine intake have been associated with RLS.
— Martin T. Stein, MD Published in Journal Watch Pediatrics and Adolescent Medicine January 26, 2011
Citation(s):Yilmaz K et al. Prevalence and correlates of restless legs syndrome in adolescents. Dev Med Child Neurol 2011 Jan; 53:40.PMID: 20875044
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Vital Choices Newsletter (http://newsletter.vitalchoice.com/e_article001998945.cfm?x=bj268QN,b1h1R7NC)
Brain Aging Delayed by Mediterranean Diet
Chicago study links diets rich in vegetables, fish, beans, and olive oil to slower mental decline; Adherence to U.S. guidelines, which give fish less weight, showed no benefits
by Craig Weatherby
A pretty clear scientific consensus holds that the so-called “Mediterranean” diet helps protect heart health.
For an overview, see “Mediterranean Myths: Region's Actual Diets Differ from Ideal”, which links to related reports.
And research showing potential brain health benefits from Mediterranean-style diets keeps growing as well.This isn’t surprising, since cardiovascular disease and dementia share degenerative pathways and appear influenced by similar dietary factors.
We covered some of the relevant research in three articles: “Mediterranean-Style Diets May Prevent Brain and Vein Problems, “Med Diet and Low Blood Pressure May Deter Dementia”, and Antioxidant Unique to Extra Virgin Olive Oil Protects Mouse Brain Cells”.
And in 2005, researchers at Chicago’s Rush University Medical Center found that participants in the Chicago Healthy Aging Project who ate fish twice a week slowed their age-associated loss of mental function by 13 percent per year. As the authors put it, “The rate reduction is the equivalent of being 3 to 4 years younger in age.” (For the full story, see “New Findings Boost Brain-Protecting Power of Fish”.)
Now a Rush Center team reports on their analysis of six years’ worth of diet and health data collected from 3,759 people in the same Chicago Healthy Aging Project, all aged over 65. Chicago study associates Mediterranean diet with slower brain decline
Every three years, the volunteers filled out a diet survey, and took tests of their memory and basic thinking skills. After six years, the researchers analyzed how closely each of the participants adhered to an idealized Mediterranean diet … one defined as favoring vegetables, beans, fish, fruit, nuts, whole grains, olive oil (especially extra virgin), and moderate wine drinking.
Out of a maximum score of 55, meaning closest adherence to the defined Mediterranean diet, the average study participant scored 28. The highest-scoring people were also those whose cognitive tests showed a slower rate of mental decline … after accounting for protective factors such as levels of activity, education, and mental exercise.The researchers also analyzed how closely study participants adhered to the recommendations from the 2005 Dietary Guidelines for Americans. In contrast, closest adherence to the 2005 U.S. diet guidelines – which gave less weight to fish, beans, and moderate drinking – did not correspond with differences in rates of cognitive decline.
Christy Tangney, Ph.D., who led the study, said that the results support other studies showing that eating close to the ideal Mediterranean diet pattern reduces the risk of heart disease, certain cancers, and diabetes. “The more we can incorporate vegetables, olive oil, and fish into our diets and moderate wine consumption, the better for our aging brains and bodies,” Tangney said.
The study was supported by a grant from the National Institute on Aging.
Sources Rush University Medical Center (RUMC). Mediterranean Diet Associated With Slower Rate of Cognitive Decline. January 03, 2011. Accessed at http://www.rush.edu/webapps/MEDREL/servlet/NewsRelease?ID=1455. Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. Am J Clin Nutr. 2010 Dec 22. [Epub ahead of print]
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http://archinte.ama-assn.org/cgi/content/short/171/2/125
Early Cigarette Smoking Associated with Breast Cancer
Young female patients who smoke may benefit from knowing that early smoking is associated with a modest increase in breast cancer risk, according to an Archives of Internal Medicine study.
Researchers analyzing updated data from the Nurses' Health Study report that they have confirmed their 2002 finding of a slight elevation in breast cancer risk associated with smoking. During some 3 million person-years of follow-up between 1976 and 2006, women who smoked more than 25 cigarettes per day for more than 35 years and began smoking before age 18 had a hazard ratio for invasive breast cancer of 1.25, compared with never-smokers.
The effect was stronger when smoking began before the woman's first birth and before menopause. Postmenopausal smoking was associated with a slightly decreased risk. There was no apparent increased risk from exposure to secondhand smoke.
Cigarette Smoking and the Incidence of Breast Cancer:Fei Xue, MD, ScD; Walter C. Willett, MD, DrPH; Bernard A. Rosner, PhD; Susan E. Hankinson, ScD; Karin B. Michels, ScD, PhD
Arch Intern Med. 2011;171(2):125-133. doi:10.1001/archinternmed.2010.503. http://archinte.ama-assn.org/cgi/content/short/171/2/125
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Ann Neurol 2011 Jan 11
Update on Multiple Sclerosis Diagnostic Criteria
New criteria are aimed at simplifying magnetic resonance imaging requirements in assessment of clinically isolated syndromes.
This update of the 2005 McDonald criteria for diagnosing multiple sclerosis (MS) is an effort to simplify and improve on the previous criteria (Ann Neurol 2005; 58:840) in light of recent investigations. The authoring panel stresses that these criteria should be used only for assessing a classic demyelinating event. The new criteria are as follows:
• Magnetic resonance imaging (MRI) can now demonstrate dissemination in space (DIS) by as few as two lesions, with 1 T2 lesions in 2 typical MS locations (juxtacortical, periventricular, infratentorial, spinal cord) — a simpler algorithm than was previously used.
• Dissemination in time (DIT) can now be satisfied by one of the following two criteria:
— A new T2 lesion on a second MRI scan obtained at least 30 days after a first scan (simplified from the prior need to reestablish baseline with a new MRI scan 30 days after the clinical event, which would amount to three scans to document a new lesion).
— Co-occurrence of 2 asymptomatic T2 lesions on the very first MRI scan, at least one of which enhances with gadolinium (Gd) and at least one of which does not enhance.
• A diagnosis of primary progressive MS (PPMS) requires 1 year of disease progression plus two of the following: a positive brain MRI, 2 T2 spinal cord lesions, oligoclonal bands and/or elevated immunoglobulin G index in the cerebrospinal fluid.
• Neuromyelitis optica should be considered with transverse myelitis extending beyond three spinal segments, bilateral or severe optic neuritis, or intractable hiccups or nausea/vomiting accompanied by a medullary lesion on MRI.
Comment: This updated set of evidence-based criteria will simplify entry of patients into MS clinical studies. Several caveats about the underlying evidence must be stressed. These criteria were derived in patients who presented with very typical demyelinating syndromes (e.g., optic nerve, brainstem, and spinal cord localizations), had a mean age of 31 to 32, were Western European, and were scanned with MRI magnetic field strengths 1.5 T. The dating of lesions on a single scan with Gd for DIT is an interesting development, as Gd sensitivity can be influenced by several variables (e.g., dose, timing, agent, field strength, T1 sequence).
In clinical practice, these criteria are not appropriate for patients with nonspecific neurological symptoms and signs and an abnormal MRI scan. Caution is also advisable for patients older than 50 or younger than 20. As always, other diseases must be excluded; careful history and exam are needed to identify "red flags" against MS diagnosis. In clinical practice, for young adults who present with very clear demyelinating syndromes, these criteria will aid initial and follow-up assessments for MS risk stratification, diagnosis, and treatment discussions.
— Robert T. Naismith, MD Published in Journal Watch Neurology January 25, 2011
Citation(s): Polman CH et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the "McDonald criteria." Ann Neurol 2011 Jan 11; [e-pub ahead of print]. (http://dx.doi.org/10.1002/ana.22366)
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