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Autoimmune Diseases Linked to Dementia

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Autoimmune Diseases

Researchers showed that compared with a control group admitted to the hospital for another reason, people hospitalized with an autoimmune disease were more likely to be later admitted with dementia.

“Fundamentally, this is an epidemiology study using the power of big numbers of patients to look at a hypothesis, namely that Alzheimer’s disease may have an autoimmune component, and our bottom line in epidemiological and population terms is that yes, the study supports that hypothesis,” study author Michael J. Goldacre, emeritus professor of public health, University of Oxford, United Kingdom.

The 25 diseases on the list for evaluation included those that are common and chronic and for which there’s an accepted autoimmune component. The list did not include type 1 diabetes because, as Dr Goldacre explained, he and his colleagues had already published a paper that linked diabetes with subsequent dementia.

The researchers also constructed a control cohort of patients hospitalized with various other medical and surgical conditions and injuries.

From April 1, 1998, to March 31, 2012, over 1.8 million people were admitted to the hospital with an autoimmune disease. The number in the different autoimmune groups ranged from 1019 for Goodpasture’s syndrome (where antibodies attack the lungs and kidneys), to 316,043 for rheumatoid arthritis (RA). About 7 million people were included in the control cohort.

The autoimmune disease cohort that eventually had the most dementia cases (48,146) was myxoedema (hypothyroidism). This condition “is quite common in elderly people, particularly women,” commented Dr Goldacre.

Overall, patients admitted to the hospital with an autoimmune disease were 20% more likely to have a subsequent admission for dementia than those without an admission for an autoimmune disease (adjusted rate ratio [RR], 1.20; 95% confidence interval [CI], 1.19 – 1.21).

Of the 25 diseases studied, 18 showed significant positive associations with dementia at P < .05 (with 14 significant at P < .001), including multiple sclerosis (RR, 1.97; 95% CI, 1.88 – 2.07), psoriasis (RR, 1.29; 95% CI, 1.25 – 1.34), and systemic lupus erythematosus (RR, 1.46; 95% CI, 1.32 – 1.61).

The authors noted that by chance alone, only one or two would be significant at P = .05.
However, although significant, effect sizes were small.

“As risks go, it’s a relatively small elevation,” said Dr Goldacre. “Risks start to seem important at the individual patient level when they are about two-fold or over, when the risk is something like doubled.”

Researchers found no notable differences in the RRs for dementia after excluding cases of dementia recorded within a year of the autoimmune disease admission. This suggests that the dementia diagnosis was not the result of being admitted soon after an autoimmune disease admission.

Different Dementias

Investigators subdivided patients admitted with a record of dementia into those having AD and those having vascular dementia.

Of the 81,502 people with an autoimmune disease and dementia, 20,032 had a record of AD and 22,536 a record of vascular dementia. The risk for vascular dementia after an admission with an autoimmune disease was higher (RR, 1.28; 95% CI, 1.26 – 1.31) than the risk for AD (RR, 1.06; 95% CI, 1.04 – 1.08).

“We think that’s probably because these autoimmune diseases are themselves conditions that predispose to atherosclerotic vascular disease,” said Dr Goldacre.

Some autoimmune diseases were associated with an elevated risk for future vascular dementia but not AD. This was the case for RA, where the RR for vascular dementia was 1.16 (95% CI, 1.12 – 1.20) but for AD, it was 0.89 (95% CI, 0.86 – 0.93).

“We might have been tempted to just dismiss the seemingly protective effect — the inverse relationship between RA and AD — were it not for the fact that others have reported on that before, so it’s not an entirely sort of eccentric finding,” said Dr. Goldacre.
The finding helps support the hypothesis that nonsteroidal anti-inflammatory drugs (NSAIDs) protect against AD. “People with rheumatoid arthritis generally take NSAIDs to manage their condition, so if rheumatoid arthritis is at least partially a proxy for NSAID use, the real association may be between NSAID use and a reduced risk of AD,” write the authors.

Since dementia subgroups were not well coded on hospital records, the authors cautioned that the separate analyses of AD and vascular dementia should be viewed with caution.

In analyzing the data separately for men and women, the researchers found that the adjusted RRs for dementia were broadly similar when they looked at individual diseases, but for all of them together, the RR was higher in men than women.

Dr Goldacre pointed out that autoimmune diseases are generally more common in women than men. “It’s often the case that the sex with the lower disease frequency has outcomes that are worse than the sex with the higher disease frequency.”

For example, he said, although women don’t develop myocardial infarction as often as men, they tend to have a slightly higher death rate from it, he said. “I am highly speculative, but that pattern might fit here.”

The researchers also analyzed the data according to time interval between the autoimmune disease and dementia admissions. Most associations remained significant for 5 or more years, although they were generally stronger with shorter time intervals.

Emerging Field

“We certainly are seeing more and more research on the link between AD and the immune system and neuroinflammation,” said Dr Hendrix. “This kind of paper helps show that there is something going on and we need to do more research to really understand it.”
An “emerging” field of research for the Alzheimer’s Association is developing anti-inflammatory agents targeted to the brain, said James A. Hendrix, PhD, director, Global Science Initiatives, Alzheimer’s Association.

“A possible strategy would be to develop a drug that has excellent brain penetration and has brain-specific targets, so it targets the microglia or other cells in the brain that are associated with the immune system and neuroinflammation.”

Another strategy might be to “repurpose” anti-inflammatory drugs and see whether they can affect neuroinflammation with limited side effects. “We will leave no stone unturned with this,” said Dr Hendrix.

Indeed, last summer, the Alzheimer’s Association announced a $7 million investment in clinical trials targeting brain inflammation (see Medscape Medical News’ coverage of the Part the Cloud Challenge on Neuroinflammation).

Dr Hendrix said the association between RA and vascular dementia uncovered by the study was news to him. “That says that we really don’t have a good understanding of the role of the immune system and inflammation when it comes to vascular dementia. For me, that was the one of the things that stood out in the paper generally.”

He outlined a number of “caveats” to the research. For one thing, the authors looked only at hospital records. “These were people who went into hospital complaining of an autoimmune disease or disorder, so it was probably pretty severe to force them to go to a hospital for care,” said Dr Hendrix.

Also, only about half of those who developed dementia were classified as having AD or vascular dementia. “It’s really challenging under the best of circumstances to do a differential diagnosis of dementia,” said Dr Hendrix.

The Unit of Health-Care Epidemiology was funded by the English National Institute for Health Research to build the linked data set. The authors have disclosed no relevant financial relationships.

J Epidemiol Community Health. Published online March 1, 2017. Abstract

Source: MedScape

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2nd Annual Infection Control, Sterilization and Decontamination in Healthcare Congress

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According to the European Centre for Disease Prevention and Control (ECDC), every year an estimated 4.1 million patients acquire Healthcare-Associated Infection (HAI) in European acute hospitals resulting approximately 37,000 deaths. In the UK, it is been found that at any given time 6.4% of all patients are affected by HAIs.

The main challenges restricting the control of HAIs are mainly lack of evidence based guidelines on the cost effectiveness of measures, feedback of surveillance data, and low availability of skilled workers. There are new guidelines released for handling medical devices which are seen as new opportunities for advancements of present technology in controlling infection and enhancing patient safety.

After the success of inaugural congress held on 25th-26th February 2016, MnM Conferences is organizing 2nd Annual Infection Control, Sterilization and Decontamination in Healthcare Congress, scheduled for 21st & 22nd March 2017 in London, UK aiming at providing platform to experts from hospitals, academia, and government institutions discussing the innovations, challenges, and future aspects of infection control, decontamination, and sterilization.

Key highlights:

  • Panel Discussion: Effective policies for staff training and management in hospitals
  • Effective ways for investigation and validation of infections
  • Protein residue detection in sterilization
  • Setting standards for training in manual handling of surgical instruments
  • Handling robotic surgery equipment such as Da Vinci Robot for cleaning and sterilization
  • Ways of improving and maintaining water quality standards

Conference registration form

Web Page

No more information is available on infobioquimica.org. For further requests, you can contact the organizers of the event.

What Clinical Laboratorians Should Do in Response to Extremely Low Hemoglobin A1c Results

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A case of extremely low HbA1c results was reported, in which liver cirrhosis, subacute hemorrhage and recent transfusion all contributed to the low result. This case illustrates when HbA1c should not be used as a clinically relevant diabetes marker. However, low or extremely low HbA1c (<5.0% or <4.0%) may occur in apparently healthy individuals. When this occurs, it is an independent risk factor associated with liver diseases, hospitalization, and all-cause mortality. From the clinical laboratory perspective, the clinical cause of extremely low HbA1c should be determined, and suggestions of different test utilization or increased health surveillance should be given to care providers.

Download PDF.

Ping Wang, PhD, DABCC, FACB; What Clinical Laboratorians Should Do in Response to Extremely Low Hemoglobin A1c Results. Lab Med 2017; 48 (1): 89-92. doi: 10.1093/labmed/lmw050

Source: Lab Medicine Oxford Academic

To Screen or Not to Screen?

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Catching chronic health conditions early—even before you have symptoms—seems like a great idea. That’s what screening tests are designed to do. Some screenings can reduce your risk of dying from the disease. But sometimes, experts say, a test may cause more harm than good. Before you get a test, talk with your doctor about the possible benefits and harms to help you decide what’s best for your health.

Screening tests are given to people who seem healthy to try to find unnoticed problems. They’re done before you have any signs or symptoms of the disease. They come in many forms. Your doctor might take your health history and perform a physical exam to look for signs of health or disease. They can also include lab tests of blood, tissue, or urine samples or imaging procedures that look inside your body.

“I wouldn’t say that all people should just simply get screening tests,” says Dr. Barnett S. Kramer, a cancer prevention expert at NIH. “Patients should be aware of both the potential benefits and the harms when they’re choosing what screening tests to have and how often.”

Teams of experts regularly look at all the evidence about the balance of benefits and harms of different screening tests. They develop guidelines for who should be screened and how often.

Choosing whether you should be screened for a health condition isn’t always easy. Screening suggestions are often based on your age, family health history, and other factors. You might be screened for many conditions, including diabetes, sexually transmitted infections, heart disease, osteoporosis, obesity, depression, pregnancy issues, and cancers.

Every screening test comes with its own risks. Some procedures can cause problems like bleeding or infection. A positive screening test can lead to further tests that come with their own risks.

“Most people who feel healthy are healthy,” says Kramer. “So a negative test to confirm that you’re healthy doesn’t add much new information.” But mistakenly being told that you do or don’t have a disease can be harmful. It’s called a misdiagnosis.

A false negative means that you’re told you don’t have the disease, but you do. This can cause problems if you don’t pay attention to symptoms that appear later on because you think you don’t have the disease. A false positive means that you’re told you may have the disease, but you don’t. This can lead to unnecessary worry and potentially harmful tests and treatments that you don’t need.

Even correctly finding a disease may not improve your health or help you live longer. You may learn you have an untreatable disease long before you would have. Or find a disease that never would have caused a problem. This is called overdiagnosis. Some cancers, for example, never cause symptoms or become life-threatening. But if found by a screening test, it’s likely to be treated. Cancer treatments can have harsh and long-lasting side effects. There’s no way to know if the treatment will help you live longer.

An effective screening test may decrease your chances of dying of the condition. Most have not been shown to lengthen your overall life expectancy, Kramer explains. Their usefulness varies and may depend on your risk factors, age, or treatment options.

If you’re at risk for certain health conditions—because of a family history or lifestyle exposures, like smoking—you may choose to have screenings more regularly. If you’re considering a screening, talk with your health care provider.

References

Population-based screening for cancer: Hope and hype. Shieh Y, Eklund M, Sawaya GF, et al. Nat Rev Clin Oncol. 2016 Sep;13(9):550-65. doi: 10.1038/nrclinonc.2016.50. Review. PMID: 27071351.

Source: NIH

A chemical found in tumors may help stop tumor growth, according to a new study

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LIGHT is an immune-stimulating chemical messenger previously found to have low levels of expression in patients with colon cancer metastases. The results are published in Cancer Research.

Colon cancer is the second-leading cause of cancer-related death in the U.S. and, despite advances in treatment, long-term survival of patients with liver metastases is rare.

“For most patients with colon cancer that has spread to the liver, current treatments are palliative and not curative,” says Dr. Ajay Maker, associate professor of surgery in the UIC College of Medicine and corresponding author on the paper. “And while studies have suggested that immunotherapy may be a promising approach for advanced cancers, the use of such treatments for advanced gastrointestinal metastases have not yet been very successful.”

Maker, a surgical oncologist, says that this study is exciting because it looks at an immunotherapy intervention for a previously unresponsive gastrointestinal cancer. The intervention, he says, essentially trains the immune system to recognize and attack the tumor, and to protect against additional tumor formation–a significant issue in colon cancer.

Maker and his colleagues established colon cancer tumors in a mouse model, in which the animals had an intact and unedited immune system. Once tumors were sizable, the mice were randomized into two groups–one group had the cytokine LIGHT turned on in the tumors, and the other served as a control group for comparison.

Tumors exposed to LIGHT showed an influx of T-cells that resulted in rapid and sustained diminishment in size, even after expression of the cytokine stopped. In mice with liver metastases, expression of LIGHT similarly provoked a potent immune response that resulted in a significant decrease in tumor burden.

“We demonstrated that delivery of a therapeutic immune-stimulating cytokine caused T-cells to traffic to tumors and to become activated tumor-killing cells,” Maker said. “This activity is especially exciting because it resulted in a profound anti-tumor immune response without any other chemotherapy or intervention. The treatment manipulates our natural defenses to fight off the tumor in the same way it has been trained to attack other foreign invaders in our body.”

“Not only did we find that LIGHT expression promoted tumor regression, upon further study we also identified the specific type of T-cell — CD8 — that was responsible for shrinking the tumor,” Maker said. “These findings are powerful and have great clinical potential.”

Source: Science Blog

Fat tissue can communicate with other organs

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Mammals, including people, have 2 main types of fat: white and brown. Most body fat is white fat, which stores extra energy that can then be used when needed—for example, when exercising. Whereas brown fat burns energy to help regulate body temperature.

Several cell types, including fat cells, make small pieces of genetic material, called microRNAs. The precise roles of microRNAs are currently under intense investigation. High levels of certain microRNAs have shown to correlate with the presence of several diseases, including cancer, diabetes, heart disease, and obesity.

The amount of microRNA in white fat tissue is known to decline with age. This is due to lower levels of an enzyme that processes microRNAs called Dicer. To better understand the relationship between fat cells, microRNA, and metabolism, a team led by Dr. C. Ronald Kahn of the Joslin Diabetes Center and Harvard Medical School looked at the effects of removing Dicer from both white and brown fat cells in mice. The study was supported in part by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared on February 23, 2017, in Nature.

Removing the Dicer gene from fat cells prevented the cells from making microRNAs. Animals missing the enzyme in their fat cells had less white fat than control mice. They also had brown fat with altered properties and were insulin resistant.

The researchers measured microRNA levels in blood samples taken from both normal and genetically altered mice. Most microRNAs are found in tiny, fluid-filled sacs called exosomes. Levels of hundreds of microRNAs were significantly lower in the exosomes of mice lacking Dicer in their fat. Of these, 88% were reduced by more than 4-fold. MicroRNAs circulating in the blood outside of exosomes were also lower in the mice lacking Dicer.

People with lipodystrophy—a condition characterized by a lack of fat tissue—had low levels of circulating exosomal microRNAs as well. These results suggest that fat tissue is the main source of circulating exosomal microRNAs in the body.

The researchers transplanted fat from normal mice into mice lacking Dicer in fat tissue. They found that most microRNAs were restored to at least half of their normal levels. Brown fat transplants, but not white fat transplants, also improved the animals’ glucose metabolism.

The scientists next investigated whether microRNAs released by fat tissue could affect other tissues. Through a series of experiments, they showed that circulating exosomal microRNAs from one mouse could regulate gene expression in the liver of another.

These findings suggest that microRNAs made in fat tissue can regulate metabolism and gene expression throughout the body. Because fat is easily accessible, it might offer a way to deliver microRNAs to regulate genes in other organs.

“This mechanism may offer the potential to develop an entirely new therapeutic approach,” Kahn says.

Author: Tianna Hicklin, Ph.D.

Source: NIH

WHO publishes list of bacteria for which new antibiotics are urgently needed

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WHO published its first ever list of antibiotic-resistant “priority pathogens” – a catalogue of 12 families of bacteria that pose the greatest threat to human health.

The list was drawn up in a bid to guide and promote research and development (R&D) of new antibiotics, as part of WHO’s efforts to address growing global resistance to antimicrobial medicines.

The list highlights in particular the threat of gram-negative bacteria that are resistant to multiple antibiotics. These bacteria have built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-resistant as well.

“This list is a new tool to ensure R&D responds to urgent public health needs,” says Dr Marie-Paule Kieny, WHO’s Assistant Director-General for Health Systems and Innovation. “Antibiotic resistance is growing, and we are fast running out of treatment options. If we leave it to market forces alone, the new antibiotics we most urgently need are not going to be developed in time.”

The WHO list is divided into three categories according to the urgency of need for new antibiotics: critical, high and medium priority.

The most critical group of all includes multidrug resistant bacteria that pose a particular threat in hospitals, nursing homes, and among patients whose care requires devices such as ventilators and blood catheters. They include Acinetobacter, Pseudomonas and various Enterobacteriaceae (including Klebsiella, E. coli, Serratia, and Proteus). They can cause severe and often deadly infections such as bloodstream infections and pneumonia.

These bacteria have become resistant to a large number of antibiotics, including carbapenems and third generation cephalosporins – the best available antibiotics for treating multi-drug resistant bacteria.

The second and third tiers in the list – the high and medium priority categories – contain other increasingly drug-resistant bacteria that cause more common diseases such as gonorrhoea and food poisoning caused by salmonella.

G20 health experts will meet this week in Berlin. Mr Hermann Gröhe, Federal Minister of Health, Germany says “We need effective antibiotics for our health systems. We have to take joint action today for a healthier tomorrow. Therefore, we will discuss and bring the attention of the G20 to the fight against antimicrobial resistance. WHO’s first global priority pathogen list is an important new tool to secure and guide research and development related to new antibiotics.”

The list is intended to spur governments to put in place policies that incentivize basic science and advanced R&D by both publicly funded agencies and the private sector investing in new antibiotic discovery. It will provide guidance to new R&D initiatives such as the WHO/Drugs for Neglected Diseases initiative (DNDi) Global Antibiotic R&D Partnership that is engaging in not-for-profit development of new antibiotics.

Tuberculosis – whose resistance to traditional treatment has been growing in recent years – was not included in the list because it is targeted by other, dedicated programmes. Other bacteria that were not included, such as streptococcus A and B and chlamydia, have low levels of resistance to existing treatments and do not currently pose a significant public health threat.

The list was developed in collaboration with the Division of Infectious Diseases at the University of Tübingen, Germany, using a multi-criteria decision analysis technique vetted by a group of international experts. The criteria for selecting pathogens on the list were: how deadly the infections they cause are; whether their treatment requires long hospital stays; how frequently they are resistant to existing antibiotics when people in communities catch them; how easily they spread between animals, from animals to humans, and from person to person; whether they can be prevented (e.g. through good hygiene and vaccination); how many treatment options remain; and whether new antibiotics to treat them are already in the R&D pipeline.

“New antibiotics targeting this priority list of pathogens will help to reduce deaths due to resistant infections around the world,” says Prof Evelina Tacconelli, Head of the Division of Infectious Diseases at the University of Tübingen and a major contributor to the development of the list. “Waiting any longer will cause further public health problems and dramatically impact on patient care.”

While more R&D is vital, alone, it cannot solve the problem. To address resistance, there must also be better prevention of infections and appropriate use of existing antibiotics in humans and animals, as well as rational use of any new antibiotics that are developed in future.

WHO priority pathogens list for R&D of new antibiotics

Priority 1: CRITICAL

  • Acinetobacter baumannii, carbapenem-resistant
  • Pseudomonas aeruginosa, carbapenem-resistant
  • Enterobacteriaceae, carbapenem-resistant, ESBL-producing

Priority 2: HIGH

  • Enterococcus faecium, vancomycin-resistant
  • Staphylococcus aureus, methicillin-resistant, vancomycin-intermediate and resistant
  • Helicobacter pylori, clarithromycin-resistant
  • Campylobacter spp., fluoroquinolone-resistant
  • Salmonellae, fluoroquinolone-resistant
  • Neisseria gonorrhoeae, cephalosporin-resistant, fluoroquinolone-resistant

Priority 3: MEDIUM

  • Streptococcus pneumoniae, penicillin-non-susceptible
  • Haemophilus influenzae, ampicillin-resistant
  • Shigella spp., fluoroquinolone-resistant

Read the Global priority list of antibiotic-resistant bacteria to guide research, discovery, and development of new antibiotics

Some genetic tests are worthwhile, some are not

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Such testing does hold promise, says David Flannery, medical director of the American College of Medical Genetics and Genomics. But he cautions that widespread genetic testing is still unwarranted. Here’s advice on several genetic tests that make sense for at least some people, as well as some that aren’t yet ready for prime time:

Heart disease

It’s now possible to check for two inherited heart conditions: familial hypercholesterolemia (very high cholesterol) and hypertrophic cardiomyopathy, a thickening of the heart muscle, says Donna Arnett, a cardiac epidemiologist at the University of Kentucky College of Public Health in Lexington.

When to consider testing: For familial hypercholesterolemia, testing can make sense if you have a family history of high cholesterol and an LDL reading of more than 190 mg/dL confirmed on two occasions. For that condition and for hypertrophic cardiomyopathy, testing might also be worthwhile if a first-degree relative (parent, sibling or child) has the disease.

How it can help: One study found that only 20 percent of people with familial hypercholesterolemia who were treated with cholesterol-lowering statins developed heart disease over 12.5 years of follow-up, compared with slightly less than 40 percent of those not treated. And if testing reveals cardiomyopathy, it’s wise to have an electrocardiogram and echocardiogram every three to five years, depending on your age. If any thickening of heart muscle is found, your doctor may monitor you more closely or prescribe medications such as beta blockers.

When to skip it: Nix testing if you have no family history of either disease or, in the case of familial hypercholesterolemia, if your total cholesterol is less than 250 mg/dL or your LDL is less than 190 mg/dL.

Breast cancer

Mutations to two genes — BRCA1 and BRCA2 — cause up to 10 percent of breast cancers and 15 percent of ovarian cancers. These mutations have also been linked to melanoma and pancreatic and prostate cancers.

When to consider testing: Testing might be useful if you have a personal or family history of breast or ovarian cancer, or a relative known to have a BRCA variant, or if you have an Ashkenazi Jewish heritage plus a close relative with breast or ovarian cancer; some BRCA variants are more common in that group.

How it can help: Women with either gene mutation can have more-frequent breast cancer screening. They could also consider the breast-cancer-prevention drug tamoxifen or even preventive mastectomy or the surgical removal of the ovaries.

When to skip it: Say no if you don’t have a strong family history of breast cancer. “Patients are still frequently sent to me who aren’t good candidates,” Flannery says, such as women whose family history “turns out to be just two cases on opposite sides of the family.”

Colon cancer

About 3 to 5 percent of colon cancers stem from an inherited condition called Lynch syndrome (hereditary nonpolyposis colorectal cancer), which also increases the risk of ovarian, pancreatic and stomach cancers.

When to consider testing: You might want testing if you have a blood relative with colon or uterine cancer before age 50, or more than two people on the same side of your family diagnosed with colon, endometrial, ovarian, pancreatic or stomach cancer, says Mary Freivogel, president-elect of the National Society of Genetic Counselors.

How it can help: People with Lynch syndrome have up to an 80 percent higher risk of developing colon cancer. So it’s a good idea for them to have an annual colonoscopy to remove potentially precancerous polyps, instead of doing so every three to five years, as is usually recommended for people with polyps.

When to skip it: If you don’t have the hereditary red flags noted above, there’s little reason to have the testing.

Two tests to skip

The following tests are sometimes recommended by doctors, even though research shows they are inaccurate or have no effect on treatment options:

Alzheimer’s. One genetic test screens for an early-onset form of the disease, another for a gene, APOE, that increases the risk of developing it later in life.

Why skip it: Early-onset Alzheimer’s accounts for less than 1 percent of dementia cases. And the test for the APOE gene isn’t very accurate: Although about 15 percent of Caucasians and 25 percent of African Americans have the variant, that doesn’t mean they’ll develop the disease. Last, “there’s no way to prevent Alzheimer’s, so you can’t do anything differently to reduce risk, and in fact knowing the gene is present can cause anxiety or discrimination in obtaining long-term-care insurance,” says Heather Snyder, senior director of medical and scientific operations at the Alzheimer’s Association.

Eye vitamins. Some doctors say that testing people with age-related macular degeneration (AMD) for certain gene variants can help determine whether the patients should take a supplement with only zinc and copper or one that also has vitamins C and E, lutein and zeaxanthin.

Why skip it: The study behind that recommendation was funded by the very lab that performs the gene test. And it was refuted by a major 2015 National Eye Institute study. “Genetic tests for AMD have no proven benefit for treatment for the patient being tested,” says study lead author Emily Chew, deputy clinical director at the National Eye Institute.

Copyright 2016. Consumers Union of United States Inc.

For further guidance, go to ConsumerReports.org/Health, where more detailed information, including CR’s ratings of prescription drugs, treatments, hospitals and healthy-living products, is available to subscribers.

Source: Washington Post

El Microscopio – Program 28

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  • Dr. Hilda Matarira (Zimbabwe). Interview about the National ZACBLM Symposium.
  • Dr. Cedric Garland (USA). Interview about the Role of Vitamin D in Cancer Prevention
  • Dr. William Clarke (USA). Interview about mobile Health (mHealth).
  • Agenda.
  • News and events about clinical chemistry.
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