Nonglycemic Effects of Incretins

In addition to their beneficial effects on blood glucose, particularly postprandial glucose, as well as body weight and pancreatic beta cell function, the glucagon-like peptide-1 (GLP-1) receptor agonists (Exenatide, Liraglutide) and dipeptidyl peptidase-4 (DPP-4) inhibitors (Sitagliptin, Vildagliptin) have other beneficial effects. These effects on blood pressure and blood lipids, although not making incretins suitable as primary therapy, may be important benefits to consider in selecting diabetes therapy, because patients with type 2 diabetes mellitus (T2DM) are at increased risk for cardiovascular disease.

Blood Pressure

GLP-1 receptor agonists and DPP-4 inhibitors produce modest reductions in systolic blood pressure and, in some cases, diastolic blood pressure. The importance of hypertension as a cardiovascular risk factor is well established. As concluded by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, each increment of 20/10 mm Hg above 115/75 mm Hg doubles the risk of cardiovascular disease.

Lipid Profile

the GLP-1 receptor agonists and DPP-4 inhibitors produce significant reductions in the triglyceride level. Exenatide and vildagliptin also produce significant improvements in total, LDL-, and HDL-cholesterol. The benefits on reducing cardiovascular risk by lowering total and LDL-cholesterol and raising HDL-cholesterol are well established. As such, they are important targets for treatment as recommended by the National Cholesterol Education Program Expert Panel - Adult Treatment Panel III

Conclusion

The GLP-1 receptor agonists and DPP-4 inhibitors lower blood pressure and improve the lipid profile, which, although not appropriate as primary therapy, makes them especially valuable treatment options for patients with T2DM. These improvements may help to reduce the risk of cardiovascular events. Various approaches can be taken to initiate and modify GLP-1 receptor agonist and DPP-4 inhibitor therapy to improve efficacy and tolerability based on patient characteristics and concomitant therapies.

References

1. Boschmann M, Engeli S, Dobberstein K, et al. Dipeptidyl-peptidase-IV inhibition augments postprandial lipid mobilization and oxidation in type 2 diabetic patients. J Clin Endocrinol Metab. 2008. In press.
2. Viswanathan P, Chaudhuri A, Bhatia R, et al. Exenatide therapy in obese patients with type 2 diabetes mellitus treated with insulin. Endocr Pract. 2007;13:444-450.
3. Ratner RE, Maggs D, Nielsen LL, et al. Long-term effects of exenatide therapy over 82 weeks on glycaemic control and weight in over-weight metformin-treated patients with type 2 diabetes mellitus. Diabetes Obes Metab. 2006;8:419-428.
4. Vilsboll T, Zdravkovic M, Le Thi T, et al. Liraglutide, a long-acting human glucagon-like peptide-1 analog, given as monotherapy significantly improves glycemic control and lowers body weight without risk of hypoglycemia in patients with type 2 diabetes. Diabetes Care. 2007;30:1608-1610.
5. Colagiuri S, Frid A, Zdravkovic M, et al. The once-daily human GLP-1 analog liraglutide reduces systolic blood pressure in patients with type 2 diabetes. Paper presented at: American Diabetes Association 68th Scientific Session; June 6-10, 2008; San Francisco, CA.
6. Mistry GC, Maes AL, Lasseter KC, et al. Effect of sitagliptin, a dipeptidyl peptidase-4 inhibitor, on blood pressure in nondiabetic patients with mild to moderate hypertension. J Clin Pharmacol. 2008;48:592-598.
7. Chobanian AV, Bakris GL, Black HR, et al; for the National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension. 2003;42:1206-1252.
8. Blonde L, Rosenstock J, Sesti G, et al. Liraglutide: superior glycemia control vs exenatide when added to metformin and/or SU in type 2 diabetes. Paper presented at: Canadian Diabetes Association/Canadian Society of Endocrinology and Metabolism Annual Meeting; October 15-18, 2008; Montreal, Quebec, Canada.
9. Scott R, Wu M, Sanchez M, et al. Efficacy and tolerability of the dipeptidyl peptidase-4 inhibitor sitagliptin as monotherapy over 12 weeks in patients with type 2 diabetes. Int J Clin Pract. 2007;61:171-180.
10. Rosenstock J, Brazg R, Andryuk PJ, Lu K, Stein P; for the Sitagliptin Study 019 Group. Efficacy and safety of the dipeptidyl peptidase-4 inhibitor sitagliptin added to ongoing pioglitazone therapy in patients with type 2 diabetes: a 24-week, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Clin Ther. 2006;28:1556-1568.
11. Bolli G, Dotta F, Rochotte E, et al. Efficacy and tolerability of vildagliptin vs. pioglitazone when added to metformin: a 24-week, randomized, double-blind study. Diabetes Obes Metab. 2008;10:82-90.
12. Rosenstock J, Baron MA, Dejager S, Mills D, Schweizer A. Comparison of vildagliptin and rosiglitazone monotherapy in patients with type 2 diabetes. Diabetes Care. 2007;30:217-223.
13. Grundy SM, Becker D, Clark LT, et al. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Final report. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf. Accessed January 20, 2009.
14. Daniel A. Nadeau, MD. Incretin Benefits Beyond Glycemic Control. From Primary Care Education Consortium, Medscape Internal Medicine. Posted 03/19/2009. Available at: http://www.medscape.com/viewarticle/588945?src=mp&spon=18&uac=82830HJ
    

Increased physical activity in middle age is followed by a reduction in mortality comparable with that associated with smoking cessation.

From British Medical Journal

Total Mortality After Changes in Leisure Time Physical Activity in 50 Year Old Men: 35 Year Follow-up of Population Based Cohort

Objective: To examine how change in level of physical activity after middle age influences mortality and to compare it with the effect of smoking cessation.
Design: Population based cohort study with follow-up over 35 years.
Setting: Municipality of Uppsala, Sweden.
Participants: 2205 men aged 50 in 1970-3 who were re-examined at ages 60, 70, 77, and 82 years.
Main Outcome Measure: Total (all cause) mortality.
Results: The absolute mortality rate was 27.1, 23.6, and 18.4 per 1000 person years in the groups with low, medium, and high physical activity, respectively. The relative rate reduction attributable to high physical activity was 32% for low and 22% for medium physical activity. Men who increased their physical activity level between the ages of 50 and 60 continued to have a higher mortality rate during the first five years of follow-up (adjusted hazard ratio 2.64, 95% confidence interval 1.32 to 5.27, compared with unchanged high physical activity). After 10 years of follow-up their increased physical activity was associated with reduced mortality to the level of men with unchanged high physical activity (1.10, 0.87 to 1.38). The reduction in mortality associated with increased physical activity (0.51, 0.26 to 0.97, compared with unchanged low physical activity) was similar to that associated with smoking cessation (0.64, 0.53 to 0.78, compared with continued smoking).
Conclusions: Increased physical activity in middle age is eventually followed by a reduction in mortality to the same level as seen among men with constantly high physical activity. This reduction is comparable with that associated with smoking cessation.

Physical inactivity is associated with increased incidence rates of obesity, diabetes, cardiovascular diseases, osteoporosis, and cancer. Short term randomised controlled trials in young to middle aged adults have shown a healthier risk profile with exercise. It is therefore recommended that adults engage in at least 30 minutes of moderate physical activity preferably on all days of the week. Adherence to these guidelines is associated with half the risk of mortality seen in sedentary people.

Principal findings of this study
Increased levels of physical activity in middle age have an effect on mortality. After a 10 year period of increased physical activity the excess mortality seen in inactive men was reduced to the same levels of mortality as seen in physically active men. There is, however, a period of at least 5 years before this risk reduction during which the risk is higher. The halved mortality rate after 10 years of follow-up after increased physical activity between the ages of 50 and 60 (compared with continued inactivity) was similar to that seen after smoking cessation (compared with continued smoking).

Full text article at BMJ

Blood pressure lowering efficacy of angiotensin converting enzyme (ACE) inhibitors for primary hypertension

With the popularity of ACE inhibitors in mind, investigators conducted a systematic review of published studies to determine how effective the drugs actually are in reducing blood pressure. They also examined dose effectiveness, adverse effects, and the role of co-occurring conditions.

The Study Findings

Researchers looked for double-blind studies comparing ACE inhibitors and placebo. All included studies were at least 3 weeks in duration and measured blood pressure as an endpoint at 3-12 weeks. Studies that featured a response-dependent titration of medications were included in the review. Only research that focused on patients with a blood pressure above 140/90 mm Hg was reviewed.

The review included 92 trials with a total of 12,954 participants (mean age, 54 years). Mean baseline blood pressure was 157/101 mm Hg and mean pulse pressure was 56 mm Hg. The majority (75%) of included studies was industry-sponsored, and 82% of the trials examined fixed-dose ACE inhibitors. The duration of trials was generally short, which limited data with regard to adverse events and study withdrawals.

The main potential source of bias in the research was a lack of information with regard to how the studies were blinded. In addition, the reviewers suggested that the researchers could have preferentially selected patients more likely to respond to ACE inhibitors. This selection bias could make ACE inhibitors appear more effective than they truly are.

The studies covered 14 ACE inhibitors. The degree of homogeneity with regard to their efficacy in reducing blood pressure was remarkable. No one medication appeared superior to others.

Overall, ACE inhibitors had a modest collective effect in reducing blood pressure. The mean reduction in systolic blood pressure ranged between 6 mm Hg and 9 mm Hg, and the mean reduction in diastolic blood pressure was 4-5 mm Hg. Less data were available with regard to the blood pressure effects of ACE inhibitors at 1-12 hours after dosing, but the average decrease in blood pressure with ACE inhibitors around their peak concentration was greater than their average efficacy (11.4/6.4 mm Hg).

Dose Effectiveness

The study provided some important information about the relationship between the dose of ACE inhibitors and their effect on blood pressure. Doses lower than the manufacturers' maximum recommended dosage had the same blood pressure-lowering effect as the maximum dose. For example, doses of one eighth to one quarter of the maximum achieved the blood pressure-lowering effect of the maximum dose in 60% to 70% of cases. Half of the maximum dose achieved it 90% of the time. There was no blood pressure-lowering effect at or below one sixteenth of the maximum suggested dose. These data suggest that use of the maximum dosage of ACE inhibitors to achieve greater blood pressure control is usually unnecessary.

The research also identified dosing information for individual ACE inhibitors and suggested that the manufacturers' recommended starting doses of benazepril, moexipril, and ramipril are higher than the minimum dose needed to reduce blood pressure. Conversely, captopril did not appear effective in reducing blood pressure at the manufacturers' recommended starting dose. Most of the maximum blood pressure-lowering effect of lisinopril was achieved at only one eighth of the recommended maximum dose.

ACE inhibitor dosing was also one of the biggest deficits in the current review. It was clear to the review authors that not all data in regard to the efficacy of different doses of ACE inhibitors were published. Instead, the data were supplied to regulators privately to determine the appropriate dosing range of ACE inhibitors.

Only half of trials provided data in regard to the rate of withdrawal due to adverse events. Collectively, there was no difference between ACE inhibitors and placebo in this critical outcome. ACE inhibitors did not significantly affect patients' heart rate.

Addressing Other Health Issues

Physicians might choose ACE inhibitors to treat hypertension for other possible health benefits associated with these medications, especially the potential to prevent type 2 diabetes. ACE inhibitors can have a positive effect on glucose metabolism through multiple mechanisms, and previous research suggested that they could prevent incident diabetes compared with other antihypertensive medications. Specifically, the Captopril Prevention Project demonstrated a 14% relative reduction in this outcome among participants receiving captopril vs a diuretic or beta-blocker. This benefit, associated with captopril, was evident regardless of the baseline risk for diabetes, although the incidence of diabetes was not a primary outcome of the study.

The Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) trial directly examined the effect of ramipril vs placebo on the incidence of diabetes. This study examined patients with impaired fasting glucose levels or reduced insulin sensitivity but no history of cardiovascular disease. After a median of 3 years of treatment, ramipril was not associated with a significantly lower incidence of diabetes compared with placebo. Median fasting plasma glucose levels were also similar at the end of the trial. However, ramipril was associated with a higher rate of return to normoglycemia.

Physicians might also consider using ACE inhibitors for hypertension in order to prevent incident heart failure. However, although ACE inhibitors are associated with numerous positive outcomes, including reduced mortality, among patients with known heart failure, little evidence exists that they provide special protection against new heart failure. In a study of quinapril and placebo initiated shortly after myocardial infarction, there was no difference between treatment groups in a composite outcome of cardiovascular death and significant cardiovascular events. Specifically, no difference was found in the risk for heart failure among those patients at high cardiovascular risk. Similarly, in the Antihypertensive and Lipid-Lowering Treatment to Prevent Hearth Attack Trial (ALLHAT), the incidence of heart failure was similar among patients receiving lisinopril and chlorthalidone.

Commentary

Although ACE inhibitors may not provide special protection against diabetes or heart failure among patients with hypertension, physicians should still consider these medications when managing hypertension. In fact, the nature of hypertension management dictates that they have to because most patients require more than 1 medication initially. In a recent study of men receiving care at a Veteran Affairs hospital, 60.4% of subjects with hypertension and significant cardiovascular risk were receiving multiple antihypertensive medications. Nevertheless, only 28% of these same patients had reached their goal blood pressure levels, indicating that they needed titration of their medications, if not the addition of other antihypertensive drugs.

Authors' conclusions

There are no clinically meaningful BP lowering differences between different ACE inhibitors. The BP lowering effect of ACE inhibitors is modest; the magnitude of trough BP lowering at one-half the manufacturers' maximum recommended dose and above is -8/-5 mm Hg. Furthermore, 60 to 70% of this trough BP lowering effect occurs with recommended starting doses. The review did not provide a good estimate of the incidence of harms associated with ACE inhibitors because of the short duration of the trials and the lack of reporting of adverse effects in many of the trials.

Clinical Pearls

• In the current review, ACE inhibitors were associated with an average reduction in systolic blood pressure between 6 mm Hg and 9 mm Hg and in diastolic blood pressure of 4-5 mm Hg;
  
  
• ACE inhibitors achieved most of their power in reducing blood pressure at half of the maximum recommended dose, or less;
  
  
• ARBs provide similar reductions in blood pressure compared with ACE inhibitors; and
  
  
• There is no strong evidence that ACE inhibitors can prevent incident diabetes mellitus or heart failure.

Sources: Medscape Family Medicine Best Evidence Review
Cochrane Database Syst Rev. 2008; (4):CD003823 (ISSN: 1469-493X)
Full text at Cochrane Library

Chronic Pain Linked to Low Vitamin D

Inadequate vitamin D may represent an underrecognized source of nociperception and impaired neuromuscular functioning, say researchers.

"Physicians who care for patients with chronic, diffuse pain that seems musculoskeletal — and involves many areas of tenderness to palpation — should strongly consider checking vitamin-D level," Michael Turner, MD, from the Mayo Clinic in Rochester, Minnesota, said in a news release issued Friday.

"For example," he added, "many patients who have been labeled with fibromyalgia are, in fact, suffering from symptomatic vitamin-D inadequacy. Vigilance is especially required when risk factors are present, such as obesity, darker pigmented skin, or limited exposure to sunlight."

Dr. Turner was lead investigator of a study published in the journal Pain Medicine in November 2008. The work suggests a correlation between inadequate vitamin-D levels and the amount of narcotic medication taken by chronic pain patients.

Required Nearly Twice As Much Pain Medication

The researchers found that patients who had inadequate vitamin-D levels and required narcotic pain medication were taking much higher doses — nearly twice as much — as those with adequate levels. These patients also reported worse physical function and worse overall health perception.

The investigators retrospectively studied 267 patients admitted to the Mayo Comprehensive Pain Rehabilitation Center. They compared serum 25-hydroxyvitamin-D levels at the time of admission with other parameters such as the amount and duration of narcotic pain medication used, self-reported levels of pain, emotional distress, physical functioning, health perception, and demographic information such as sex, age, diagnosis, and body-mass index.

Patients with vitamin-D levels below 20 ng/mL were considered to have inadequate amounts. The prevalence of low vitamin D was 26% (95% CI, 20.6% – 31.1%).

Among patients using opioids, the mean morphine-equivalent dose for the inadequate vitamin-D group was 133.5 mg/day compared with 70.0 mg/day for the adequate group (P = .001). The mean duration of opioid use for the inadequate and adequate groups was 71.1 months and 43.8 months, respectively (P = .023).

The researchers also observed a link between increasing body-mass index and decreasing levels of vitamin D.

Inadequate Vitamin D May Create or Sustain Pain

The preliminary results suggest that inadequate vitamin D may play a role in creating or sustaining chronic pain. During an interview, Dr. Turner suggested that patients with inadequate vitamin D may benefit from cholecalciferol 50,000 international units dosed according to the level of deficiency.

But he urged caution for patients with calcium- or phosphate-processing disorders. "Increasing vitamin-D levels could be problematic in patients with kidney failure or stones or primary hyperparathyroidism or sarcoidosis. This doesn't preclude increasing levels, but it might warrant discussion with an endocrinologist," he said.

For patients with adequate vitamin D looking to maintain levels, he recommends10 to 15 minutes of sun exposure with no sunscreen on the trunk and arms and legs 3 times a week.

Source: Pain Med. 2008;9:979-984. Abstract

Marked Decline in Breast Cancer Risk After Stopping Contraceptive pills

Following the release of the 2002 report of the Women's Health Initiative (WHI) trial of estrogen plus progestin (EPT), the use of menopausal hormone therapy in the United States decreased substantially. Subsequently, the incidence of breast cancer also dropped, suggesting a cause-and-effect relation between hormone treatment and breast cancer.

In a study published in N Engl J Med 2009, Leon Speroff, MD and Wendy Y. Chen, MD, MPH analyzed the results of the WHI randomized clinical trial—in which one study group received 0.625 mg of conjugated equine estrogens plus 2.5 mg of medroxyprogesterone acetate daily and another group received placebo—and examined temporal trends in breast-cancer diagnoses in the WHI observational-study cohort. Risk factors for breast cancer, frequency of mammography, and time-specific incidence of breast cancer were assessed in relation to combined hormone use.

RESULTS: In the clinical trial, there were fewer breast-cancer diagnoses in the group receiving estrogen plus progestin than in the placebo group in the initial 2 years of the study, but the number of diagnoses increased over the course of the 5.6-year intervention period. The elevated risk decreased rapidly after both groups stopped taking the study pills, despite a similar frequency of mammography. In the observational study, the incidence of breast cancer was initially about two times as high in the group receiving menopausal hormones as in the placebo group, but this difference in incidence decreased rapidly in about 2 years, coinciding with year-to-year reductions in combined hormone use. During this period, differences in the frequency of mammography between the two groups were unchanged.

The authors concluded that increased risk of breast cancer associated with the use of estrogen plus progestin declined markedly soon after discontinuation of combined hormone therapy and was unrelated to changes in frequency of mammography.

This report from the WHI is not the first about the change in breast cancer prevalence that occurred after the initial WHI publications in 2002, but it is of value because it documents that the change cannot be attributed solely to a decrease in the use of mammography.

The WHI recently updated results on breast cancer risk after discontinuation of the combination EPT arm. Overall results were published for the post-intervention phase in 2008. With mean follow-up of 2.4 years for this phase, a nonsignificant increased risk of breast cancer was still observed (HR, 1.27; 95% CI, 0.91-1.78), with a possible downward trend in cancer risk with follow-up.

This newest report is a more detailed analysis on breast cancer outcomes and also drew data from the observational cohort of the WHI. HRs for 6-month time intervals were calculated for both the intervention and nonintervention phase of the clinical trial. In an intention-to-treat analysis, there was no difference in the slopes of the HRs over time comparing the intervention and post-intervention phases (P = 0.28). However, after adjusting for adherence by censoring nonadherent subjects, there was a statistically significant difference in the slopes with HRs increasing over time for women using EPT, but declining after discontinuation (P = 0.005). Although breast cancer cases appeared to decline more in the intervention arm compared to placebo, mammography rates were similar in both arms. During the post-intervention phase, both breast biopsies and mammograms with abnormalities were more common in the EPT arm compared to placebo. Similar results for breast cancer incidence rates were seen using the observational data, although mammography rates were higher among women who used HT compared to those who did not.

After the WHI results were released in 2002, there was a large decline in HT use in the United States. Several investigators then reported a decline in US breast cancer rates correlating with reporting of the WHI trial results. Given the temporal association, it was speculated that this decrease in breast cancer incidence may have been due to the widespread discontinuation of HT, although other investigators noted that there was also a concomitant decline in mammography utilization, which may also have explained the changes. However, mammography rates were similar in the intervention arms of the WHI trial and were stable over time for women in the observational study, so it would seem unlikely that changes in mammography utilization alone can explain the recent decline in US breast cancer rates.

Anti-Obesity Drugs and the Neural Connection

Obesity is a curse, one that’s extremely difficult to shake off. It’s not just an aspect that’s socially unacceptable (if you’re fat, chances are that you’re not likely to be liked), it’s also dangerous for your health. Obese and overweight people are more susceptible to diseases like diabetes, strokes and cardiac arrests, illnesses that can cause lifelong disabilities and even death.

While a low calorie diet combined with a good exercise routine is the best way to combat obesity, not many people are willing to put themselves through the hardship that this entails. And some people are too morbidly obese to even attempt the mildest form of exercise. This is when they turn to drastic measures like surgery or anti-obesity drugs. While liposuction and stomach tucks come with their own set of complications, it’s the drugs that are used to lose weight that have the most dangerous side effects.

Anti-obesity drugs like taranabant, rimonabant and orlistat work in any one of the following ways:

· They suppress your appetite

· They increase your body’s metabolism

· They interfere with your body’s ability to absorb and break down fat

· They inhibit digestion

· They lower caloric absorption

The problem with these drugs is that they inhibit certain basic bodily functions in order to work, and it is because of this very fact that they’re dangerous. Drugs that suppress appetite, otherwise known as cannabinoid receptors, have been proven to cause brain damage in juvenile mice. They interfere with neural connectivity, and lead to depression, anxiety and suicidal tendencies. This tendency to inhibit neurological development in mice could be mirrored in human infants; and since infancy is a stage where the brain is plastic and keeps modifying at a rapid pace, these drugs could possible cause brains with stunted growths.

The study, undertaken by the Massachusetts Institute of Technology, cautioned that drugs like rimonabant and tarabant which are responsible for suppressing appetite, are liable to target certain psychological pathways that are extremely important for keeping our bodies and brains at an equilibrium.

Besides affecting your mood, anti-obesity drugs could also give you high blood pressure and increase your pulse rate. All these factors lead us to question the efficacy and value of anti-obesity drugs. While doctors prescribe them only in concert with a diet and exercise regime, there are many cases of abuse where people continue to take them without prescriptions. The danger in this is that they’re unaware of the drugs’ potential side effects.

Yes, obesity is socially unacceptable, but if there’s one thing that’s more taboo than the problem of being overweight, it’s insanity. So if you want to keep your brains intact, it’s best you steer clear of these drugs and try to lose weight the regular way. Yes, it’s hard, but you need to remember that the good things in life don’t come easily.

By-line:

This article is contributed by Sarah Scrafford. She invites your questions, comments and freelancing job inquiries at her email address: sarah.scrafford25@gmail.com.

Early detection of Alzheimer's disease

Researchers at the University Of Pennsylvania School Of Medicine have done a breakthrough study pioneering a biomarker test that can confirm or rule out Alzheimer's disease. The test measures cerebrospinal fluid (CSF) concentrations of two of the disease's biochemical hallmarks, amyloid beta42 peptide and tau protein.

With this information in hand, the scientists also predict whether a person's mild cognitive impairment would convert to Alzheimer's disease over time. The research team, led by Dr. Leslie M. Shaw, Co-Director of the Penn Alzheimer's Disease Neuroimaging Initiative (ADNI) Biomarker Core, could detect this devastating disease at the earliest stages, before dementia symptoms appeared and widespread irreversible damage occurred.
By improving upon a previously suggested pathological CSF biomarker signature, the researchers found evidence of neuron degeneration, marked by an increase in CSF concentration of tau proteins, and plaque deposition, indicated by a decrease in amyloid beta42 concentration. Also, people with two copies of the genetic risk factor for Alzheimer's disease, APOE e4 , had the lowest concentrations of amyloid beta42, compared to those with one or no copies.
"With this test, we can reliably detect and track the progression of Alzheimer's disease," said Shaw. He added: "Validated biomarker tests will improve the focus of Alzheimer's clinical trials enrolling patients at earlier stages of the disease to find treatments that can at least delay, and perhaps stop- neurodegeneration. In addition, prevention trials can test methods to delay or block mild cognitive impairment from converting to full-blown Alzheimer's."
The study appears in the online edition of the Annals of Neurology.
Source-ANI
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3000 Steps In 30 Minutes for a Meaningful Exercise Program

Researchers are now suggesting people to walk 150 minutes a week, which is equivalent to 30 minutes each day 5 times a week, though moderate physical activity is known to be beneficial to health. Researchers at the School of Exercise and Nutrition, San Diego State University, point out that pedometers widely used as a physical activity monitoring tool are unable to measure activity intensity.
They have determined that a rate of at least 100 steps per minute achieves moderate intensity activity. According to them, a simple pedometer-based recommendation of 3000 steps in 30 minutes can get people started on a meaningful exercise program.
The researchers monitored 58 woman and 39 men for oxygen uptake while walking on a treadmill. The subjects completed 46-minute sessions at different treadmill speeds between 65 and 110 meters per minute. All subjects wore pedometers, and their heart rates were recorded.
The research team used 3 METs, or metabolic equivalents, as the minimum level of oxygen demand which approximates moderate exercise, to monitor participants in order to determine whether they had reached the moderate-exercise level at a given treadmill speed. From these data, the researchers found that for men, step counts associated with walking at 3 METs were between 92 and 102 steps per minute. For women, according to them, the range was between 91 and 115 steps per minute.
The study been published in the American Journal of Preventive Medicine.
Source-ANI
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