Eye color genetics not so simple, study finds

The genetics of human eye colour is much more complex than previously thought, according to a new study published today.

An international team of researchers led by King’s College London and Erasmus University Medical Center Rotterdam have identified 50 new genes for eye colour in the largest genetic study of its kind to date. The study, published today in Science Advances, involved the genetic analysis of almost 195,000 people across Europe and Asia.

These findings will help to improve the understanding of eye diseases such as pigmentary glaucoma and ocular albinism, where eye pigment levels play a role.

In addition, the team found that eye colour in Asians with different shades of brown is genetically similar to eye colour in Europeans ranging from dark brown to light blue.

This study builds on previous research in which scientists had identified a dozen genes linked to eye colour, believing there to be many more. Previously, scientists thought that variation in eye colour was controlled by one or two genes only, with brown eyes dominant over blue eyes.

Co-senior author Dr Pirro Hysi, King’s College London, said: “The findings are exciting because they bring us to a step closer to understanding the genes that cause one of the most striking features of the human faces, which has mystified generations throughout our history. This will improve our understanding of many diseases that we know are associated with specific pigmentation levels.”

Co-senior author Dr Manfred Kayser, Erasmus University Medical Center Rotterdam, said:

“This study delivers the genetic knowledge needed to improve eye colour prediction from DNA as already applied in anthropological and forensic studies, but with limited accuracy for the non-brown and non-blue eye colours.”

Managing diabetes after incarceration: A difficult journey

For the average adult, a diabetes diagnosis is life-changing. Managing diabetes involves a daily routine that shifts toward remembering to take medication, check blood sugar, and monitor carbohydrate intake.

Frequent trips to multiple doctors’ offices become the norm, as regular foot checks, dental appointments, eye exams, and primary care visits are crucial for avoiding the complications of poorly managed disease.

These complications can include gum disease, cardiovascular problems, nerve damage, kidney failure, blindness, and even amputation. Individuals who receive an early diagnosis and manage the disease well can expect to live as long as those without diabetes, but research has linked poor disease management to reduced life expectancy of up to 8 years.

For someone reentering society after being in prison, managing diabetes can be quite difficult. In the United States, more than 2 million people are incarcerated in jails and prisons on a given day, and nearly 5% of them have diabetes.

These individuals typically do not serve life sentences; rather, 95% eventually return to community settings that may not readily embrace them or their medical needs.

For example, taking medication every day requires having a safe place to live and store medications. This is not a given for formerly incarcerated people, many of whom often struggle simply to find a place to live.

In the U.S., individuals who have been inmates in jails or prisons just once are seven times more likely to experience homelessness than the general population. Meanwhile, those who have been incarcerated two or more times are 13 times more likely than other people to lack housing.

Individuals with a criminal history face numerous collateral consequences of conviction — legal restrictions that disqualify them from accessing a range of resources and opportunities upon release.

Unemployment is a major concern for people with a criminal history. According to the Prison Policy Initiative, individuals with a criminal history are nearly five times more likely to be unemployed than the general population.

Many employment sectors bar those with a criminal history, limiting their ability to earn the money necessary to afford adequate housing. Those who turn to low-income housing programs often face being denied access, as many public housing programs have strict eligibility criteria that exclude individuals with a criminal history.

This is true even for older adults. Many low-income senior housing assistance programs deny access to individuals with recent criminal convictions and permanently ban those with a history of criminal sexual conduct, even if the crime occurred decades earlier.

Additionally, food insecurity complicates diabetes management for formerly incarcerated adults. Access to adequate quantities of nutritious food is crucial for effective diabetes management.

A diabetes-friendly diet restricts carbohydrate intake, as carbohydrate-rich foods often raise blood glucose levels higher and faster than foods rich in protein and fiber.

Formerly incarcerated individuals, however, often report great difficulty in accessing healthful foods. Estimates of food insecurity among formerly incarcerated individuals returning to community settings are as high as 91%.

Among the many collateral consequences of criminal conviction in the U.S. are limitations on the receipt of federal supplemental nutrition assistance program benefits (i.e., SNAP or food stamps) for individuals convicted of certain criminal offenses.

While most states have eliminated lifetime bans on food assistance, more than 30 states still place some restrictions on food assistance for individuals with felony drug convictions.

Faced with an inability to afford nutritious foods, food-insecure individuals often turn to cheap, high calorie foods, which can lead to weight gain, poor blood glucose control, and an increased risk of diabetes-related health complications.

Likewise, poor healthcare access and utilization negatively affect diabetes management among formerly incarcerated adults. Access to affordable health insurance is crucial for disease management, as the self-management of diabetes requires visits to primary care doctors and specialists; the ongoing use of medication, such as insulin and oral medications; and daily use of testing supplies, including glucose test strips and glucose meters.

Uninsured adults with diabetes engage in fewer preventive healthcare activities than their insured counterparts, including less daily blood glucose monitoring, reduced participation in diabetes education classes, and fewer foot and eye exams.

Historically, a lack of health insurance has been a significant barrier to healthcare access for formerly incarcerated individuals. Given the difficulties of finding employment after incarceration, employer-based health insurance is typically not an option.

MEDICAL NEWS TODAY NEWSLETTER
Stay in the know. Get our free daily newsletter
Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.

Enter your email
Your privacy is important to us

Traditionally, Medicaid coverage has been limited to pregnant women, parents with a low income, and those under the age of 65 with disabilities. Notably, this does not include men (who make up about 93% of the U.S. state and federal prison population), unless they care for minor children or have disabilities.

At the end of their sentence, individuals with diabetes may have trouble obtaining health insurance, depending on where they live. Since the Affordable Care Act of 2010, 39 U.S. states (including the District of Columbia) have expanded Medicaid to include all adults with a low income, regardless of gender, disability, or parenting status.

Given the barriers that formerly incarcerated individuals face, ensuring adequate diabetes management in this population will require a host of system-level changes. Providing widespread access to health insurance for individuals with diabetes and a low income is crucial.

Without it, formerly incarcerated adults with diabetes will forego necessary medical care simply because they cannot afford it. This lack of treatment will only increase their risk of adverse disease-related complications.

The benefits of Medicaid expansion have been well-documented — if all remaining states fully implemented Medicaid expansion, nearly 4 million people would gain health insurance, decreasing the number of uninsured adults by 28%. The remaining states must be encouraged to expand their Medicaid programs to provide greater access to healthcare coverage in this population.

Additionally, there must be increased policy advocacy surrounding the health-related collateral consequences of criminal conviction. As they reenter community settings, individuals with a criminal history face countless barriers that adversely affect their ability to manage diabetes or any other chronic health condition effectively.

Most criminal justice advocacy work examines the impact of collateral consequences on economic security. However, policies that restrict employment, housing, and access to healthful food for those with criminal records also ultimately endanger population health.

Chronic disease management and population health must be a part of the conversation when advocating for criminal justice reform.

As the U.S. population ages, and chronic health conditions become more prominent, failure to integrate these issues into larger criminal justice policy discussions will just add to the difficulties that formerly incarcerated adults must deal with as they attempt to reintegrate into society.

What Does Asymptomatic COVID-19 Look Like Under the Surface?

Asymptomatic individuals carrying SARS-CoV-2 shed the virus longer than those with COVID-19 symptoms, with other lab findings suggesting the symptomatic patients mounted more robust immune responses, a small study in China found.

Median duration of viral shedding among 37 asymptomatic patients was 19 days (interquartile range 15-26; range 6-45) versus 14 days among 37 matched symptomatic patients (IQR 9-22; log-rank P=0.028), reported Jing-Fu Qiu, PhD, of Chongqing Medical University, and colleagues, though viral shedding does not necessarily mean the patients were infectious.
Virus-specific IgG antibody titers and cytokine levels were also significantly lower among asymptomatic patients in the acute phase of infection, when viral RNA can be found in respiratory specimens, the authors wrote in Nature Medicine — both of which indicated that immune responses weren’t as strong in the asymptomatic group.

Asymptomatic transmission of COVID-19 is one of its biggest mysteries, with the World Health Organization recently reminding the public of the distinction between asymptomatic patients, who never develop symptoms, and presymptomatic patients, who go on to develop symptoms later in the course of disease.

Qiu and colleagues characterized asymptomatic carriers as the “silent spreaders” of COVID-19.

“However, our understanding of the clinical features and immune responses of asymptomatic individuals with SARS-CoV-2 infection is limited,” the researchers added.

For the study, they examined data from 178 patients with PCR-confirmed SARS-CoV-2 infection in the Wanzhou District in China, including 37 without symptoms. Median age in the latter was 41, and 22 were women. These individuals were matched by age, sex, and comorbidity with 37 symptomatic patients for antibody detection and cytokine measurement. Qiu and colleagues also included a group of 37 individuals who tested negative via RT-PCR for cytokine comparisons.

Lab values and imaging were not entirely normal for the asymptomatic group. Eleven had increased C-reactive protein levels and six had elevated levels of alanine aminotransferase. Chest CT found “focal ground-glass opacities” in 11 and “stripe shadows and/or diffuse consolidation” in another 10 of the group; in two-thirds of these 21 patients, the abnormalities were in only one lung. The remaining 16 showed entirely normal imaging.

Around 80% of both symptomatic and asymptomatic patients tested positive for IgG antibodies about 3-4 weeks after exposure. The difference was greater when examining IgM antibodies, with positive findings in 78.4% of symptomatic patients and 62.2% of asymptomatic patients.

In the early convalescent phase, defined as 8 weeks after hospital discharge, symptomatic patients had higher IgG levels, though both groups experienced over 90% decreases in IgG levels. A larger proportion of asymptomatic patients had decreases in neutralizing serum antibody levels versus symptomatic patients (81.1% vs 62.2%, respectively).

These findings should serve as a caution against assuming prior infection confers immunity to future infection, Qiu and colleagues said.

“These data might indicate the risks of using COVID-19 ‘immunity passports’ and support the prolongation of public health interventions, including social distancing, hygiene, isolation of high-risk groups, and widespread testing,” the team wrote.

Plasma levels of cytokines were also similar between asymptomatic patients and healthy controls, though significantly higher levels of stem cell factor and leukemia inhibitory factor were found in the asymptomatic group, the researchers noted, calling this a “reduced inflammatory response characterized by low circulating concentrations of cytokines and chemokines.”

Qiu and co-authors cited the varying sensitivity and specificity of antibody tests (obtained from a company called Bioscience) as a limitation to their study, adding that the results may be confounded by existing antibodies to other coronaviruses, such as SARS or MERS, as well as common cold viruses.

Vaccine makers face biggest medical manufacturing challenge in history

Developing a COVID-19 vaccine in record time will be tough. Producing enough to end the pandemic will be the biggest medical manufacturing feat in history.
That work is underway.

From deploying experts amid global travel restrictions to managing extreme storage conditions, and even inventing new kinds of vials and syringes for billions of doses, the path is strewn with formidable hurdles, according to Reuters interviews with more than a dozen vaccine developers and their backers.

Any hitch in an untested supply chain – which could stretch from Pune in India to England’s Oxford and Baltimore in the United States – could torpedo or delay the complex process.

Col. Nelson Michael, director of the U.S. Army’s Center for Infectious Disease Research who is working on the government’s “Warp Speed” project to deliver a vaccine at scale by January, said companies usually have years to figure this stuff out.

“Now, they have weeks.”

Much of the world’s attention is focused on the scientific race to develop a vaccine. But behind the scenes, experts are facing a stark reality: we may simply not have enough capacity to make, package and distribute billions of doses all at once.

Companies and governments are racing to scale-up machinery to address a critical shortage in automated filling and finishing capacity – the final step in the manufacturing process of putting the vaccine into vials or syringes, sealing them and packaging them up for shipping.

“This is the biggest logistical challenge the world has ever faced,” said Toby Peters, an engineering and technology expert at Britain’s Birmingham university. “We could be looking at vaccinating 60% of the population.”

Several developers, including frontrunner Moderna, are experimenting with new ways to mitigate the extreme cold storage demands of their vaccines, which at present need to be kept at minus 80 degrees Celsius (-112 Fahrenheit).

SiO2 Materials Science is working on producing vials that won’t shatter at super-cold temperatures.

Travel restrictions, meanwhile, are posing more prosaic problems; Johnson & Johnson, which plans to start clinical trials this summer, has struggled to send its vaccine experts to oversee the launch of production sites, for example.

‘NEVER IN HISTORY’
By setting up massive clinical trials involving 10,000 to 30,000 volunteers per vaccine, scientists hope to get an answer on whether a vaccine works as early as this October. But even if they succeed, manufacturing in bulk, getting regulators to sign off and packaging billions of doses is a monumental challenge.

Seth Berkley, chief executive of the GAVI vaccines alliance, said in reality, the world is unlikely to go straight from having zero vaccines to having enough doses for everyone.

“It’s likely to be a tailored approach to start with,” he said in an interview. “We’re looking to have something like one to two billion doses of vaccine in the first year, spread out over the world population.”

J&J has partnered with the U.S. government on a $1 billion investment to speed development and production of its vaccine, even before it’s proven to work. It has contracted Emergent Biosolutions and Catalent to manufacture in bulk in the United States. Catalent will also do some fill-and-finish work.

“Never in history has so much vaccine been developed at the same time – so that capacity doesn’t exist,” said Paul Stoffels, J&J’s chief scientific officer, who sees filling capacity as the main limiting factor.

Emergent’s manufacturing plant in Bayview, Maryland, can accommodate four vaccines in parallel using different manufacturing platforms and equipment.

Funded by the government in 2012, the plant includes single-use disposable bioreactor equipment featuring plastic bags rather than stainless steel fermentation equipment, which makes it easier to switch from one vaccine to another.

This month, the company received an additional $628 million to make those four suites available to support any candidate the government selects, CEO Bob Kramer told Reuters.

BLOW-FILL-SEAL-REPEAT

As well as working with J&J, New Jersey-based Catalent signed a deal with British drugmaker AstraZeneca last week to provide vial-filling and packaging services at its plant in Anagni, Italy. It aims to handle hundreds of millions of doses, starting as early as August 2020 and possibly running through until March 2022.

It has ordered high-speed vial-filling equipment to boost output at its Indiana plant, where it is also hiring an additional 300 workers.

Michael Riley, Catalent’s North American president for biologics, told Reuters his biggest challenge was trying to compress work that normally takes years into months.

Adding to the challenge is that glass vials are in short supply.

To save glass, companies plan to use larger vials of five to 20 doses – but this raises new problems, such as potential waste, if not all the doses are used before the vaccine spoils.

“The downside is that after a healthcare practitioner opens a vial, they need to then vaccinate 20 people in a short, 24-hour time,” said Prashant Yadav, a global healthcare supply-chain expert at the Center for Global Development in Washington.

As part of the same drive, the U.S. Department of Health and Human Services and the Department of Defense have awarded ApiJect Systems up to $138 million to upgrade its facilities to be able to make up to 100 million plastic pre-filled syringes by the end of this year, and as many as 600 million in 2021.

The company plans to use a technology called Blow-Fill-Seal, where syringes are blown out of plastic, filled with vaccine and sealed in seconds. This will need Food and Drug Administration approval, CEO Jay Walker told Reuters.

BREAKING COLD CHAIN
SiO2 Materials Science is, meanwhile, ramping up capacity of plastic vials with a glass lining, which are more stable at ultra-low temperatures.

“You can bring us down to minus 196 Celsius, which none of the vaccines need,” Chief Business Officer Lawrence Ganti said. “You can throw it against the wall and it doesn’t break. Our founder has done that. He’s thrown frozen vials at me.”

The company expects to boost production from the current 5-10 million vials a year to 120 million within three-and-a-half months, he told Reuters.

Once packaged, many vaccines need to be kept cold – and some leading contenders made from genetic material such as messenger RNA need to be kept very cold – presenting another challenge that may limit access.

“People who work with mRNA store it at minus 80 degrees centigrade, which is not something you’re gonna find in most pharmacies or doctor’s offices,” said Dr. Paul Offit, director of the Vaccine Education Center at Children’s Hospital of Philadelphia and co-inventor of the rotavirus vaccine.

Peters of Birmingham university has been gathering data from poorer regions of Africa and Asia, and said breaks in the temperature-controlled supply chain – “cold chain” – are already frequent.

In some places, it is common to lose 25% or more of vaccines because of broken cold chains, he told Reuters.

“So if you’re looking to manufacture four billion, and you reckon you’re going to lose 25%, then you have to manufacture five billion,” he said. “It’s all the elements to move it from the point of manufacture to the point of aggregation, right down to the health centres and then out to the community.”

QUARANTINE QUAGMIRE
Companies developing mRNA vaccines, including Moderna and Translate Bio, which is partnering with Sanofi, are working to make candidates stable at higher temperatures.

Ron Renaud, CEO of Translate Bio, said he was confident this would happen “within a short amount of time”.

Colleen Hussey, a Moderna spokeswoman, said: “We are getting more confident that we could run our supply chain at -20C, which is an easier storage condition than deep freezing,” she said.

Moderna plans to add a small period of time in which the vaccine can be stored at normal fridge temperatures of 2 to 8 degrees Celsius in doctors’ offices or clinics.

“We will know more in the next 2-3 months,” she said.

The pandemic is also presenting obstacles of a less technical nature.

Catalent, which has some 30 plants globally, has had to write special permission slips in eight languages explaining that their workers are considered essential.

J&J is having trouble getting experienced personnel to far-flung labs to oversee the transfer of technology to contract manufacturers because they’re subject to 14-day quarantines.

“It is absolutely a factor,” said Stoffels. “If you have to send your people to the middle of India to get to filling capacity, that’s not easy at the moment.”

Alzheimer’s gene risk triggers blood-brain barrier damage

Scientists have known for some time that the APOE4 gene is a risk factor for Alzheimer’s disease. A new study helps to explain why, by showing that the variant has an association with damage to the blood-brain barrier.

APOE4 is the leading genetic risk factor for Alzheimer’s disease. Almost one-quarter of people have one copy of the gene, which increases the risk of developing Alzheimer’s disease by up to four times.

In rarer cases, approximately 2–3% of the population, people carry two copies of the gene, which increases the risk of developing the disease by up to 15 times.

People who carry the variant, whether they have one copy or both, also develop the disease earlier than those who do not.

Although APOE4 is clearly important in the onset of many cases of Alzheimer’s disease, precisely how the genetic variant increases risk has been unclear.

Scientists from the University of Southern California (USC) have now shown a link between APOE4 and damage to the blood-brain barrier, the key structure that protects the brain from toxic substances.

The findings, which could aid the development of personalized treatment strategies for Alzheimer’s disease, appear in Nature.

APOE4 and the blood-brain barrier
This latest study focused on the blood-brain barrier, the protective border of cells separating the blood from the brain. Previous research from the group had shown that people who develop problems with their memory early on also had damage to this structure.

Their research has also shown that people with the APOE4 variant who go on to develop Alzheimer’s disease have a leaky blood-brain barrier, even before doctors can see any changes to cognition.

To investigate the connection between APOE4 and the blood-brain barrier in more detail, the team behind this study used a specialized form of MRI. They looked at the blood-brain barrier of people with mild cognitive impairment — which can be a precursor to Alzheimer’s disease — and those with normal cognitive function, both with and without APOE4.

They found that people who carried the APOE4 variant had a leaky blood-brain barrier in parts of the brain that are critical for memory function, including the hippocampus, even if they were cognitively healthy at the time of the scan.

Those who were experiencing cognitive decline had even worse damage to their blood-brain barrier.

Changes link with cognitive decline
To understand what was causing the leakage in the blood-brain barrier, the researchers looked for damage to a particular cell type — the pericytes — which wrap around blood vessels in the brain to form the critical barrier.

Using a biomarker of pericyte injury, they found higher levels of damage in APOE4 carriers. What is more, the researchers associated levels of the biomarker with both blood-brain barrier damage and cognitive decline.

“Severe damage to vascular cells called pericytes was linked to more severe cognitive problems in APOE4 carriers,” explains senior author Prof. Berislav Zlokovic, director of the Zilkha Neurogenetic Institute at USC.

Further experiments showed that the damage also correlated with levels of a protein that causes inflammation called cyclophilin A, which is known to be an early sign of Alzheimer’s disease.

Thus, the team was able to put together a hypothesis for how APOE4 causes damage to the blood-brain barrier, potentially leading to the onset of Alzheimer’s disease.

“APOE4 seems to speed up the breakdown of the blood-brain barrier by activating an inflammatory pathway in blood vessels, which is associated with pericyte injury,” says Prof. Zlokovic.

powered by Rubicon Project
Treating the damage
Some parts of the theory need fleshing out, for example, how damage to the blood-brain barrier causes the symptoms of Alzheimer’s disease. Nevertheless, these findings are a step forward in our understanding of how APOE4 shapes Alzheimer’s disease risk.

Future work will be necessary to better understand the genetic risk factors for the disease and, potentially, developing personalized treatments.

Experiments in mice have already shown that blocking the inflammatory process that APOE4 triggers can restore the blood-brain barrier and improve neuronal function, raising hope that doctors could use similar treatments for Alzheimer’s.

First 72 Hours After Acute Kidney Injury Matter

Acute kidney injury (AKI) — even when it resolved quickly — was tied to poorer long-term renal outcomes in a prospective cohort study.
People who experienced non-resolving AKI saw more than a two-fold higher risk for a major adverse kidney event (MAKE) compared with those who didn’t have AKI (adjusted hazard ratio 2.30, 95% CI 1.52-3.48, P<0.001), reported Pavan Bhatraju, MD, MSc, of the University of Washington in Seattle, and colleagues. Even those whose kidney function resolved within 72 hours after a diagnosis of AKI also had a 52% higher risk for a long-term MAKE compared with those with AKI (aHR 1.52, 95% CI 1.01-2.29, P=0.04), according to the study online in JAMA Network Open. However, when the researchers compared cases of AKI, those whose AKI did not resolve saw a significantly higher rate of a MAKE -- a composite of progressive kidney disease, need for long-term dialysis, or all-cause mortality (aHR 1.51, 95% CI 1.22-1.88, P<0.001) compared with those whose AKI resolved. These associations were adjusted for demographic factors like age, sex, and race, as well as for clinical factors including diabetes status, chronic kidney disease status, cardiovascular disease, and sepsis. The associations were also still significant after the group controlled for the magnitude of increased serum creatinine concentrations -- or the AKI stage -- in those who recovered from their AKI. Nearly three-quarters of those with AKI had injury classified as stage 1. "The use of AKI recovery subgroups to risk stratify patients with AKI we believe is clinically intuitive," Bhatraju's group wrote. The observational study included 1,538 hospital patients: half of whom did not experience AKI, 31% of whom had resolving AKI, and 19% who had non-resolving AKI within 3 months of admission. AKI was defined according to standard diagnostic criteria: an increase in serum creatinine concentration of 50% or more or 0.3 mg/dL or more above an outpatient, non-emergency department baseline value within 7 to 365 days prior to the initial hospital admission. AKI that resolved was considered to be a decrease in serum creatinine concentration of 0.3 mg/dL or more or at least 25% from maximum within the initial 72 hours following an AKI diagnosis. During median follow-up of 4.7 years, 36% of the entire cohort had a MAKE. "[These findings] provide evidence for considering the timing of functional recovery from AKI as a factor associated with future adverse events," Ravindra Mehta, MBBS, MD, DM, of the University of California San Diego, said in an accompanying commentary. He also noted that while these findings highlight the value of using AKI recovery pattern to predict long-term kidney outcomes, the study simultaneously underscores how current AKI staging criteria was not helpful in predicting these outcomes "as the severity stage by itself did not differentiate among which patients would develop MAKE." "It is ... clear that clinicians managing patients with AKI should consider the severity of the disease and the ensuing course and tailor their diagnostic and therapeutic interventions to facilitate rapid and complete recovery of kidney function," he concluded.

Shop Smart for Groceries for Diabetes

The grocery store looks different when you have type 2 diabetes. Aisles of menu ideas and possibilities become well-lit lanes of decisions and pitfalls. Instead of, “What’s for dinner?” you wonder, “What will this do to my blood sugar?”

“Before my diagnosis, I went to the store and bought everything on my list and anything that caught my fancy,” says Linda Leitaker, a retired elected city clerk in Lake Almanor, CA. “What I thought I knew about nutrition was woefully inadequate. I had to read, research, and repeat.”

But if you manage your food, it’s a powerful way to control your type 2 diabetes. You don’t need to follow a special diet. Just eat the way it’s recommended for most people. Studies show that healthy, balanced meals are one of the best ways to control your blood sugar and manage your diabetes.

Picture Your Plate

There’s no magic list of foods you can and can’t eat with diabetes.

“You can really eat anything,” says Shamera Robinson, MPH, a registered dietitian and associate director of nutrition for the American Diabetes Association. “Your favorite foods can be part of an individualized eating plan. The best way to go about eating is by finding a balance of nutrients that work for you.”

One way to do that is with the Diabetes Plate Method. Imagine a 9-inch plate split evenly in two. Fill one side with non-starchy vegetables like asparagus, Brussels sprouts, broccoli, cauliflower, greens, squash, or tomatoes.

Split the other half into quarters horizontally. Fill one quarter with carbs, like brown rice, tortillas, beans, fruit, milk, or yogurt. Fill the last quarter with protein, such as eggs, tofu, and lean meats like chicken and fish.

“Carbs will always digest the fastest, then protein, then fat. When you eat all three together, you feel full and don’t crave as much between meals,” Says Lori Zanini, an author, nutritionist, and dietitian in Los Angeles.

Read more…

Ankle Injuries: Causes and Treatments

Ankle injuries are often thought of as sports injuries. But you don’t have to be an athlete or even a “weekend warrior” to turn your ankle and hurt it. Something as simple as walking on an uneven surface can cause a painful, debilitating sprain.

Ankle injuries can happen to anyone at any age. However, men between 15 and 24 years old have higher rates of ankle sprain, compared to women older than age 30 who have higher rates than men. Half of all ankle sprains occur during an athletic activity. Every day in the U.S., 25,000 people sprain their ankle. And more than 1 million people visit emergency rooms each year because of ankle injuries. The most common ankle injuries are sprains and fractures, which involve ligaments and bones in the ankle. But you can also tear or strain a tendon.

What Kinds of Ankle Injuries Are There?

Sprains, Strains, and Fractures

Ankle injuries are defined by the kind of tissue — bone, ligament, or tendon — that’s damaged. The ankle is where three bones meet — the tibia and fibula of your lower leg with the talus of your foot. These bones are held together at the ankle joint by ligaments, which are strong elastic bands of connective tissue that keep the bones in place while allowing normal ankle motion. Tendons attach muscles to the bones to do the work of making the ankle and foot move, and help keep the joints stable.

A fracture describes a break in one or more of the bones. A sprain is the term that describes damage to ligaments when they are stretched beyond their normal range of motion. A ligament sprain can range from many microscopic tears in the fibers that comprise the ligament to a complete tear or rupture. A strain refers to damage to muscles and tendons as a result of being pulled or stretched too far.

Muscle and tendon strains are more common in the legs and lower back. In the ankle, there are two tendons that are often strained. These are the peroneal tendons, and they stabilize and protect the ankle. They can become inflamed as a result of overuse or trauma. Acute tendon tears result from a sudden trauma or force. The inflammation of a tendon is called tendinitis. Microscopic tendon tears that accumulate over time, because of being repeatedly over stretched, and don’t heal properly lead to a condition called tendinosis. Tendons can also rupture. Subluxation refers to a tendon that slips out of place.

Read more…

Tick-borne encephalitis

The size of the problem

Encephalitis is an acute inflammation of the brain, which can cause serious illness and death. The prevalence of encephalitis has proven difficult to ascertain, due to diagnostic and coding challenges, but recent estimates suggest 5.23 cases per 100,000 population per year. Viral causes predominate, with herpes simplex being the commonest aetiology. However, in up to 60% of all cases of encephalitis in the UK, there is no specific cause delineated.

Tick-borne encephalitis (TBE)

The tick-borne encephalitis virus is an RNA flavivirus, which can cause a potentially fatal and untreatable neurological infection across Europe and Asia. The diagnosis of TBE in this area has increased by over 400% since the 1970s. It is thought that some of this increase is as a result of increased vigilance and suspicion of the disease, but also as result of an increase in the tick population and in changing patterns of human behaviour, resulting in greater exposure to ticks. These behaviours include hiking and fishing in affected areas.

A rising prevalence

The question which inevitably arises from this increased prevalence is ‘why has the tick population risen?’

The answer appears to be one comprising elements of changes in land use, increased transportation of animals, and increased co-feeding by nymphs and larvae on the same rodent host. The extent to which this co-feeding occurs depends upon the patterns of seasonal host activity, which is influenced by ambient environmental temperature.

Influence of global warming

The apparent increase in incidence of TBE over the last five decades has therefore been attributed to climate change, which affects both tick and host rodent and other mammalian population dynamics.

New evidence of zoonotic pool of disease

Recent evidence of an increase in the potential TBE viral pool in the UK has emerged in the Thetford Forest area. In summer 2019, a single case of TBE was acquired in the New Forest area. As a result, a study was undertaken by Public Health England and the Emerging and Zoonotic Infections National Institute for Health Research, University of Liverpool to look at the prevalence of tick-borne encephalitis virus in the likely host organisms in this area.

Their results included a finding that almost 48% of deer in the Thetford Forest area were seropositive for TBE virus. They concluded that “this detection of TBEV genomic sequence in UK ticks has important public health implications, especially for undiagnosed encephalitis”.

What could happen next?

Although most TBE infections in the UK are imported, the finding of a high incidence of TBE seropositivity in deer and a case of UK acquired TBE is cause for concern. A similar pattern of disease expansion occurred in South Korea some years ago with the consequence of increasing TBE prevalence and the fact that it is now a notifiable disease.

With the further advance of global warming it is therefore possible that tick-borne encephalitis could become a more common pathogen in the UK and should be considered by clinicians in areas of risk.

How Well Are You Aging? A Blood Test Might Tell

Imagine a blood test that could spot whether you are aging too quickly.

New research suggests it’s not the stuff of science fiction anymore.

The scientists analyzed plasma — the cell-free, fluid part of blood — from more than 4,200 people between the ages of 18 and 95, and found a link between 373 proteins and aging.

“We’ve known for a long time that measuring certain proteins in the blood can give you information about a person’s health status — lipoproteins for cardiovascular health, for example,” said study senior author Tony Wyss-Coray. He’s co-director of the Alzheimer’s Disease Research Center at Stanford University in California.

“But it hasn’t been appreciated that so many different proteins’ levels — roughly a third of all the ones we looked at — change markedly with advancing age,” he added in a university news release.

The study was published Dec. 5 in the journal Nature Medicine.

“Proteins are the workhorses of the body’s constituent cells, and when their relative levels undergo substantial changes, it means you’ve changed, too,” Wyss-Coray explained. “Looking at thousands of them in plasma gives you a snapshot of what’s going on throughout the body.”

The findings suggest that physical aging doesn’t occur at a steady pace, but is uneven and has three distinct surges — ages 34, 60 and 78.

At those ages, there are spikes in levels of specific proteins in the blood with noticeable changes, according to the researchers.

Eventually, a blood test for these proteins might be able to identify people who are aging more rapidly than normal and at increased risk for age-related conditions such as Alzheimer’s disease or heart disease.

Such a test might also help identify drugs or other factors that slow or speed aging, the study authors said.

However, any clinical use of such a blood test is at least five to 10 years away, the researchers noted.

“Ideally, you’d want to know how virtually anything you took or did affects your physiological age,” Wyss-Coray said.