Are your eyes tired, dry, or achy? Many factors can contribute to these types of symptoms. But a big culprit can be the intense use of your eyes. Spending too much time looking at screens and handheld devices, like smartphones, can strain your eyes. So can normal aging. What can you do to find relief?
One major cause of eye discomfort is not blinking enough. “When we focus on tasks like reading or computer work, our blink rate just plummets,” says Dr. Chantal Cousineau-Krieger, an NIH ophthalmologist.
Not blinking enough can cause your eyes to become dry and uncomfortable. Certain people are more prone to eye dryness, too. This includes those over age 50, women, and people who wear contact lenses. Certain medications, like antihistamines, and health conditions can also add to eye dryness.
Avoiding other factors that increase eye dryness may help your eyes feel better, too. Air blowing directly in your face from a fan or from air vents in the car can contribute to eye dryness, says Cousineau-Krieger. So can smoke or windy conditions. Normal aging can also lead to eye strain. With age, we start to lose our ability to focus on close objects. This is called presbyopia. Our eyes need to work harder to focus.
“When we look at something up close, we flex the muscle inside of our eye,” Cousineau-Krieger explains. “And just like any other muscle, if you hold the contraction for a long time, the muscle can become fatigued. Eventually, in your 40s, you end up not being able to see things up close as well. It’s a natural part of aging that goes along with gray hair and wrinkles. And then we typically need reading glasses to be able to see things up close.”
But eye strain doesn’t only happen to adults. Children can also develop symptoms from intensely using their eyes. They may not tell you that their eyes hurt. Instead, they may start blinking forcefully or rubbing their eyes.
Spending too much time on screens is also now believed to be contributing to children developing nearsightedness. Studies have shown growing rates of nearsightedness in children over the past few decades. To relieve eye discomfort, you can try some simple steps. Experts recommend the 20-20-20 rule. Take eye breaks every 20 minutes and look far in the distance, about 20 feet away, for about 20 seconds.
“Experts are recommending that children spend time outdoors playing to help them focus on things further at a distance,” says Cousineau-Krieger. “Hopefully, this will also help decrease the amount of nearsightedness. The amount of nearsightedness is going up around the world.”
Taking screen breaks and focusing on more distant objects can be helpful for everyone’s eye health. See the Wise Choices box for more eye health tips. If simple lifestyle changes don’t bring you relief from eye discomfort, it may be time to see a doctor for an eye exam.
Given the aging Baby Boomer generation, changes in cannabis legislation, and the growing acknowledgment of cannabis for its therapeutic potential, it is predicted that cannabis use in the older population will escalate. It is, therefore, important to determine the interaction between the effects of cannabis and aging. The aim of this report is to describe the link between cannabis use and the aging brain. Our review of the literature found few and inconsistent empirical studies that directly address the impact of cannabis use on the aging brain.
However, research focused on long-term cannabis use points toward cumulative effects on multimodal systems in the brain that are similarly affected during aging. Specifically, the effects of cannabis and aging converge on overlapping networks in the endocannabinoid, opioid, and dopamine systems that may affect functional decline, particularly in the hippocampus and prefrontal cortex, which are critical areas for memory and executive functioning.
To conclude, despite the limited current knowledge on the potential interactive effects between cannabis and aging, evidence from the literature suggests that cannabis and aging effects are concurrently present across several neurotransmitter systems. There is a great need for future research to directly test the interactions between cannabis and aging.
Prevalence of cannabis use in older populations Cannabis is one of the most commonly abused substances in the United States (Substance Abuse and Mental Health Services Administration, 2016), with increasing prevalence of use due to legalization and decreasing perception of harm. Between 2002 and 2014, cannabis use among adolescents remained fairly constant, while use among adults over the age of 18 years increased consistently.
The National Survey on Drug Use and Health showed that between 2003 and 2014, the rate of past-year cannabis use rose from 2.95% to 9.08% among the 50- to 64-year-old age group and from 0.15% to 2.04% among those older than 65 years (Substance Abuse and Mental Health Services Administration. This indicates a liberalization of cannabis use in the current older-adult population, referred to as the Baby Boomer generation. In this report, we define “older adults” as individuals 50 years or older. Based on the trend of decreased perceived harm from cannabis use among older adults, the prevalence of medicinal and recreational cannabis use is expected to keep increasing.
Similar to other age groups, cannabis use is also associated with vulnerability toward comorbid neuropsychiatric and substance use disorders in older adults. Wu and Blazer posit that substance use disorder has become one of the most common psychiatric conditions found in this population. The prevalence of cannabis use disorder is rising in the general population, which increased to 2 from 1.5% in 2001–2002. The number of older users affected by cannabis use disorder appears to increase with the rate of cannabis use in older adults. For example, cannabis abuse and dependence based on Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV criteria have increased from 0.4% to 1.3% in middle-aged to older adults (45–64 years) and 0.1% to 0.3% in those older than 65 years from 2001–2002 to 2012–2013. noted that the increase in cannabis use in older adults is attributable to both medicinal and recreational uses that are difficult to distinguish, and found that older adults are currently more accepting of the use of medicinal cannabis.
Of the older cannabis using population, the peak age of first onset of use is 18–20, suggesting that potential effects in this population are predominantly from chronic or long-term use. This implies that despite the general changes in the perception of cannabis use, the cumulative effect of more than 30 years of regular cannabis use may be predominant in current older adults, compared to that of older adults who report a relatively recent onset of use. This indicates the need to determine the effects of long-term cannabis use on aging. Considering the trend of increasing cannabis use in older adults, it is essential to provide a prospective insight into the interaction between cannabis use and the aging process.
Cannabis mechanisms The primary psychoactive ingredient in cannabis is delta-9-tetrahydrocannabinol (THC). Of the cannabinoids, THC is most widely associated with the negative effects of cannabis, such as increased anxiety, psychotic symptoms, increased impulsivity, loss of learning capability, motor control, and substance use disorder. More recently, there is growing recognition that THC also provides therapeutic benefits that include neuroprotection against oxidative stress and from the accumulation of amyloid-β peptides related to Alzheimer’s disease. THC acts as a partial agonist at two known endocannabinoid system receptors, cannabinoid receptors 1 and 2, and is a comparable affinity analog of the endogenous agonists anandamide (AEA) and 2-arachidonyl glycerol.
Although its biochemical affinity is lower, THC also acts on the opioid system as an allosteric modulator. Thus, cannabis use directly modulates both the endocannabinoid and opioid systems. THC also indirectly modulates multiple other neurotransmitter systems, such as dopamine, serotonin, acetylcholine, and norepinephrine, which may be due to CB1Rs being one of the most common G-protein-coupled receptors in the brain (Lovinger & Mathur, 2016). Endocannabinoids regulate the activity of the aforementioned neurotransmitters in the neocortex, limbic regions, basal ganglia, and cerebellum, which are disrupted by exogenous cannabinoids such as THC.
Oral corticosteroid (OCS) use during pregnancy was not linked to gestational diabetes, although there was a small risk increase during early pregnancy, according to a nationwide cohort study of more than a million women. When adjusted for covariates, a pooled estimate for crude risk ratio of oral corticosteroid exposure in weeks 1 through 27 of pregnancy showed a slight increase in gestational diabetes risk, but it was attenuated to null.
However, they reported in JAMA Internal Medicine that oral corticosteroid exposure between 4 and 6 weeks of gestation was associated with a slight increase in the risk of gestational diabetes (weighted RR 1.10, 95 percent CI 1.03-1.17). However, the authors found no correlations in subgroup analyses of maternal age, indication, duration of action, dosage, timing, or duration of exposure.
Clinicians treating autoimmune or chronic inflammatory conditions during pregnancy, where corticosteroid therapy may be crucial for the health of both the mother and the fetus, will find these findings comforting. Oral corticosteroids are increasingly being used in pregnancy to manage chronic conditions, autoimmune diseases, and disease flares.
The authors pointed out that despite their widespread use, OCSs are known to impair glucose metabolism by increasing peripheral insulin resistance, encouraging hepatic gluconeogenesis, and possibly reducing pancreatic β-cell function, all mechanisms that may contribute to hyperglycemia and the development of gestational diabetes. They added that much of the previous research on this relationship had small sample sizes or insufficient adjustment for confounders.
The National Health Information Database of South Korea, which gathers claims information from the public health insurance system, was utilized in the population-based cohort study. Researchers examined pregnancies resulting in live births from January 1, 2010, to December. 31, 2021. Approximately 1.3 million of the roughly 3.8 million pregnancies that resulted in live births during the study period qualified for analysis; 6% of these pregnancies were exposed to oral contraceptives between 1 and 27 weeks of gestation.
Gestational diabetes occurred in 9.5 percent of pregnancies exposed to oral corticosteroids and 7.36 percent of unexposed pregnancies. Women with gestational diabetes, preexisting diabetes, no history of health screening before pregnancy, and exposure to oral corticosteroids starting 30 days before pregnancy without a prescription during the first 27 weeks of pregnancy were all excluded.
Pregnancy was divided into three weeks, from 1 week to 27 weeks’ gestation, as gestational diabetes is not typically tested after 28 weeks. Women who had not started oral corticosteroids or had been diagnosed with gestational diabetes before or during that period were included in each interval.
Women in the exposed group had more comorbidities than those in the unexposed group, including migraine (8.1 percent vs. 5.4 percent), asthma (7.2 percent vs. 2.2 percent), and immune-mediated inflammatory disease (2.5 percent vs. 0.4 percent). The majority of baseline characteristics were similar. Most patients in the full study population had a mean age of 30-34 and a BMI of 18.5-22.9. Additionally, the authors performed four sensitivity analyses, limiting the cohort to those with a known family history of diabetes, nulliparous pregnancies, singleton pregnancies, and one using women who had previously taken oral corticosteroids but not during pregnancy as the reference group. The results of these analyses were consistent with the main findings.
Shin and co-authors noted that “early pregnancy represents a critical developmental window when the endocrine pancreas anticipates increased insulin demands through adaptive-cell priming, occurring before the physiologic insulin resistance typically develops around 24 weeks’ gestation, indicating the limited risk at 4-6 weeks’ gestation. During this vulnerable period, corticosteroid exposure may disrupt foundational pancreatic-cell adaptation mechanisms, prematurely induce insulin resistance, and create a cumulative metabolic burden through prolonged exposure duration that overwhelms maternal compensatory capacity before the substantial insulin secretion increases required in later pregnancy.
Study limitations included the fact that prescription of oral corticosteroids may not guarantee actual medication intake, and the definition of gestational diabetes relied on diagnostic codes. Also, there was the overall potential for residual confounding. The study was restricted to live births, thereby introducing potential selection bias. Lastly, the authors noted that the findings might not apply to other populations with different baseline characteristics.
They concluded that “clinical decision-making regarding corticosteroid use should continue to prioritize maternal disease control while maintaining vigilance in monitoring glucose metabolism, particularly in women with preexisting risk factors” and that these results “suggest that appropriate corticosteroid therapy during pregnancy is metabolically safe with respect to gestational diabetes risk.
If you’re among the 1 in 5 U.S. adults who have an abnormal heart rhythm problem called atrial fibrillation, there’s been a flurry of new research about the condition that offers some guidance on your everyday choices and how those impact your risk of recurrence.
“The major risk is stroke, and preventing stroke is the name of the game with AFib. Three new studies shed light on some common questions: whether your morning coffee matters, whether a diabetes drug might help lower recurrence risk, and what new data reveals about AFib’s link to dementia.
Here’s what the latest research suggests: Coffee doesn’t increase the risk of recurrent atrial fibrillation. A small but well-designed new study showed that people who drank a cup of coffee daily were not more likely than non-coffee drinkers to have a repeat atrial fibrillation episode after successful treatment with electrical cardioversion – a quick procedure where a doctor delivers a brief, controlled shock to the heart to put it back into a normal rhythm. People in the study agreed ahead of time to be randomly assigned to one of two groups: those who continued drinking coffee as they did before the study, and those who abstained for six months.
Why it matters: Many people and even some doctors still assume coffee triggers AFib, a long-held bit of “common wisdom” that isn’t backed by strong evidence, Prystowsky said. It’s a top concern for newly diagnosed patients, but experts say coffee is rarely a problem except in people with palpitations. The design of this latest study, randomizing people before asking them to keep drinking or abstain, makes the results particularly trustworthy, he said.
What you can do: If you’re going to change one beverage you consume to manage atrial fibrillation risk, go ahead and keep drinking coffee and instead focus on reducing or cutting out alcohol.
Metformin helped reduce AFib recurrence in a small study of people with overweight and obesity. In a study of 99 people with overweight or obesity who had an ablation procedure, where doctors burn or freeze tiny areas of heart tissue to stop the abnormal signals that cause AFib, those who took the type 2 diabetes drug metformin after ablation were less likely to have recurrent AFib. None of the people in the study had diabetes, although 40% of them met prediabetic blood sugar criteria. The study was presented at an American Heart Association conference this month and hasn’t been published in a peer-reviewed journal.
Why it matters: Doctors are talking about this study because it’s another step toward understanding the connection between weight and AFib risk. An important previous study showed that people who lost 10% of their body weight were six times more likely to survive four years without recurrence. “It wasn’t just weight loss, though,” Prystowsky said, noting that those who lost weight had improved glucose and blood pressure levels. Interestingly, in this latest metformin study, people saw AFib benefits without significant weight loss. That suggests the drug may be affecting the body in other ways, possibly through metabolism, inflammation, or fat around the heart, though researchers don’t yet know the exact mechanism, Prystowsky said.
What you can do: “The most important takeaway from this small study is reinforcing the idea that the management of obesity makes a huge difference in outcomes for atrial fibrillation,” Philbin said. He and Prystowsky agreed the study was too small for a doctor to recommend that a patient take metformin to reduce AFib risk, though. The study was “hypothesis-forming rather than game-changing, but it reinforces some ideas we know about atrial fibrillation that we know will work: you should exercise. You should lose weight. You should not drink alcohol,” Philbin said. He and his colleagues plan to explore whether AFib patients benefit from six weeks of supervised exercise and dietitian guidance the way heart attack survivors do.
Another study just linked AFib with dementia risk. Published this month in JACC: Advances, the analysis looked at 670,745 Medicare patients 65 and older and found that those who developed AFib after non-cardiac surgery were more likely to later be diagnosed with dementia. In cardiac surgery patients, dementia rates were similar regardless of AFib (about 4%). But after non-cardiac surgery, dementia was diagnosed in nearly 13% of people with AFib, versus 9% without – a 20% increased risk. Non-cardiac procedures ranged widely, with orthopedic (including joint replacements), gastrointestinal, and circulatory surgeries most common.
Why it matters: The study authors wrote it was “notable” that cardiac surgery patients who developed AFib weren’t more likely to get dementia, suggesting their AFib may have been triggered by the surgery itself. They couldn’t explain why non-cardiac surgery patients had a higher dementia risk and found no clear contributing factors like high blood pressure, diabetes, or prior stroke or heart failure. They hypothesized that undetected mild strokes or heart attacks, which can damage the brain and blood vessels, might play a role. The link between AFib and dementia is established, and while silent strokes and heart attacks are suspected contributors, the data shows a link rather than a cause. Prystowsky tells patients who get AFib after non-cardiac surgery that they have a higher risk of recurrence and need to be aware of it.
What you can do: If you’re heading into surgery, worrying about AFib shouldn’t be at the top of your list, Prystowsky said. But if you like to be prepared, both Philbin and Prystowsky advised that wearing a device like a smartwatch that can check your pulse and rhythm can help you spot any issues early. And if you’ve already had AFib after a non-cardiac surgery, regular monitoring is especially important – and you should call your doctor if your device flags an abnormal pulse or rhythm.
Your tolerance decreases with age due to changes in your body, health conditions, and medications you may take. If you feel like you’re getting more sensitive to alcohol as you get older … well, it’s not your imagination. The way we process alcohol changes with age, says a geriatrician.
Why alcohol hits differently as you get older :
The basic process by which your body metabolizes (processes) alcohol doesn’t change. But as you age, it becomes harder for your body to do. Here’s why: Your liver enzymes change, which slows your body’s ability to break down booze like it used to. Your lean muscle mass decreases, causing more alcohol to remain in your bloodstream and magnifying its effects.
Medications can interact with alcohol, which may change the way drinking makes you feel. It can also make your medications less effective. Other health conditions can play a role. Conditions like obesity and diabetes may affect your liver function and make it harder for your body to process alcohol.
You can’t metabolize alcohol as well :
Your liver just isn’t as resilient as you get older. So, it might not process alcohol as efficiently it does it does when you’re younger. Alcohol is mostly processed by enzymes in your liver, which break it down into chemicals that circulate throughout your body. Eventually, they morph into carbon dioxide and water that you pee out. But as you age, those liver enzymes change.
We’re all born with varying levels of enzyme activity to begin with, he continues. Then, as you get older, other factors start to compete for those enzymes’ attention, like health issues that affect your liver function and medications you take that also need to be broken down by your liver. There’s another issue, too: As you age, your circulation slows. With less blood flowing through your liver, the whole metabolizing process slows down, and toxic metabolites from alcohol start to build up.
Your body composition changes :
You lose about 3% to 8% of your lean muscle mass each decade after age 30. That means you have less muscle tissue available to retain water. That plays a role in alcohol does to your body, namely, that drinks start hitting you harder and faster. Because we lose lean muscle mass with age, a higher concentration of alcohol remains in the bloodstream explains. You feel more intense effects from the same amount of alcohol.
These effects may include: Short-term memory problems and poor judgment Being off-balance or uncoordinated (which raises your risk of falls) Extra sleepiness or sluggishness Decreased attention span Increased risk of dehydration
Medications can interact with alcohol
When you’re taking certain medications, drinking can affect you in ways that you haven’t experienced before. Combining alcohol with certain drugs can affect how those drugs make you feel. It can also contribute to higher blood alcohol levels than when you weren’t on medication.
Plus, many medications compete with alcohol to be processed by your liver. It’s a competition that alcohol always wins, which means your liver doesn’t have the same bandwidth to process your medications the way it should. This can make them less effective and cause dangerous interactions.
Here are some examples: Sedatives become more potent. The effect of blood thinners is amplified, which raises the risk of serious bleeding. Blood pressure medications don’t work as well, increasing your risk of stroke and other issues.
Aging and alcohol tolerance: What it means for you
Alcohol’s effects become more pronounced as you age. You may experience:
Slower recovery times: All the changes we’ve discussed can mean that hangovers hit harder and take longer to bounce back from than they did in your 20s or even 40s. More sleep troubles: No matter your age, alcohol disrupts sleep and makes the sleep you do get less restful. In general, alcohol compounds the sleep problems that are common after age 65. Higher risk of injury: Aging increases your fall risk, and the consequences of alcohol-related falls tend to be more serious after age 65. Alcohol is associated with a significant portion of falls with fractures in older adults, he adds. Other health effects: Alcohol raises blood sugar, increases blood pressure, and worsens sleep, all of which negatively affect your health. It can also make existing conditions worse (like chronic pain and heart disease). Heavy drinking comes with even greater risks: Liver disease: It takes longer for your body to metabolize alcohol than it does to absorb it. So, heavy drinking keeps alcohol in your bloodstream longer. This allows a chemical called acetate to build up in your liver, which causes cirrhosis over time. Cognitive decline: There’s no other way to put it: Long-term heavy drinking is bad for your brain. It raises your risk of many types of cognitive impairment, including alcohol-related dementia. Mental health concerns: Studies show that older adults may turn to alcohol as a way to cope with loneliness and isolation. But heavy alcohol use can also contribute to depression and other mental health issues. Nutritional deficiencies: If you consume more calories than you eat, you risk nutritional deficiencies (which are also more common with age). The consequences range from minor to major. Folate deficiency causes anemia, while thiamine deficiency can trigger delirium. Cancer: Alcohol is a chemical carcinogen, or a substance known to raise your risk of cancer. The more alcohol you consume, the higher your risk of developing certain types of cancer.
Drug interactions :
Medicines taken by older adults are more likely to have serious interactions with alcohol and drugs, according to the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Many prescribed and over-the-counter medicines and herbal products can interact negatively with alcohol. Medicines and alcohol can interact even if they’re not taken at the same time. That’s because the drug may still be in your blood when you have a drink.
This gets to the heart of a very common fitness goal. The short answer is that for a significant, lasting reduction of belly fat, combining diet and exercise is the undisputed champion.
However, let’s break down the science of why this is the case, and the specific roles that diet and exercise play.
The Verdict: Diet + Exercise is the Winner
Multiple studies, including a seminal one from Duke University, have clearly demonstrated that a combination of aerobic exercise and a controlled diet is the most effective strategy for reducing visceral fat (the dangerous belly fat deep inside your abdomen).
Here’s a simplified breakdown of the findings:
Strategy
Effect on Belly Fat (Visceral Fat)
Diet Only
Good reduction. Creates a calorie deficit, leading to overall fat loss, including from the belly.
Exercise Only
Moderate reduction. Effective, but often slower than diet for fat loss alone.
Diet + Exercise
Best and most significant reduction. The effects are synergistic, meaning they add up to more than the sum of their parts.
The “Why”: Understanding the Roles of Diet and Exercise
1. The Role of Diet: The Key to Unlocking Fat Stores
You cannot out-exercise a bad diet when it comes to fat loss. This is because of the simple math of a calorie Deficit.
Calorie Deficit: To lose fat, you must consume fewer calories than your body burns. Diet is the most efficient way to create this deficit.
Targeting Visceral Fat: When you create a sustained calorie deficit through diet, your body is forced to use stored energy. Visceral fat is often more “metabolically active” and can be mobilized for energy more readily than some subcutaneous fat (the fat under your skin), especially with the right hormonal environment.
Food Quality Matters: A diet high in protein (increases satiety, preserves muscle), fiber (from vegetables, fruits, whole grains), and healthy fats helps control hunger and stabilizes blood sugar, reducing the hormones that promote belly fat storage (like cortisol and insulin).
In short, Diet is the primary driver for creating the energy deficit needed to burn fat.
2. The Role of Exercise: The Turbocharger and Body Shaper
Exercise doesn’t just burn calories; it fundamentally changes your body’s composition and metabolism.
Aerobic Exercise (Cardio): Great for burning a high number of calories during the activity itself. It’s very effective at directly reducing visceral fat.
Resistance Training (Weight Lifting): This is the secret weapon. Muscle is a metabolically active tissue, meaning it burns calories even at rest. The more muscle you have, the higher your resting metabolic rate.
Prevents Muscle Loss: When you’re in a calorie deficit from dieting, your body may break down muscle for energy. Lifting weights signals your body to preserve muscle mass, ensuring that the weight you lose comes primarily from fat.
The “Afterburn” Effect: Intense exercise, especially strength training and HIIT, can keep your metabolism elevated for hours after your workout.
In short: Exercise ensures the weight you lose is fat, not muscle, and improves your metabolism for long-term leanness.
The Special Case of Belly Fat: Stress and Sleep
It’s crucial to understand that belly fat is particularly influenced by hormones, especially cortisol (the stress hormone). High stress and poor sleep can elevate cortisol levels, which directly encourage the storage of fat in the abdominal area.
Therefore, the most effective “belly fat reduction plan” also includes:
Stress Management: Practices like meditation, yoga, walking in nature, and adequate leisure time.
Quality Sleep: Aim for 7-9 hours of quality sleep per night.
Your Action Plan: The Best Strategy
Start with Your Plate: Focus on creating a moderate calorie deficit. Eat whole, minimally processed foods: lean proteins, vegetables, fruits, and whole grains. Reduce sugar, refined carbs, and ultra-processed foods.
Incorporate Cardio: Aim for at least 150 minutes of moderate-intensity cardio (like brisk walking, cycling) or 75 minutes of vigorous-intensity cardio per week.
Lift Weights: Include resistance training at least 2-3 times per week, targeting all major muscle groups.
Manage Stress and Sleep: Make this a non-negotiable part of your routine. It is as important as your diet and workout.
Conclusion: Don’t choose between diet and exercise. Use them together. Think of diet as the key that unlocks the fat store, and exercise as the tool that ensures you’re burning the right type of fuel (fat) and building a body that keeps it off for good.
This is a significant and exciting development in the treatment of high cholesterol. Here’s a detailed breakdown of what this news typically refers to, how it works, and its implications.
The “New Pill” in Question
The drug you’re likely hearing about is a class of medications called siRNA (small interfering RNA) therapeutics. The most prominent one is Inclisiran (brand name Leqvio).
While not brand-new to the market (it was approved in the EU in 2020 and the US in 2021), its real-world use and long-term data are still emerging, making it “new” in the public consciousness.
How It Works: A Revolutionary Approach
Traditional statins and other pills work by blocking an enzyme in the liver that produces cholesterol. Inclisiran works differently, using a mechanism called RNA interference.
Target: It focuses on a protein called PCSK9. This protein normally destroys the receptors on your liver cells that remove “bad” LDL cholesterol from your blood. More PCSK9 means fewer receptors and higher LDL levels.
The “Interference”: Inclisiran is not a daily pill. It’s a twice-yearly subcutaneous injection (a shot in the skin, like insulin). It contains a small piece of synthetic RNA that “interferes” with the genetic instructions in your liver cells for making the PCSK9 protein.
The Result: By “silencing” the gene for PCSK9, the drug allows your liver to maintain more LDL receptors. These receptors can then effectively clear LDL cholesterol from your bloodstream, leading to reductions of around 50% on top of statin therapy, which aligns with the “almost 60%” figure.
Key Advantages
Unprecedented Efficacy: The ~60% reduction in LDL cholesterol is among the highest achieved by any single drug.
Remarkable Convenience: The dosing schedule of once initially, again at 3 months, and then every 6 months is a game-changer. It eliminates the need for daily pills, which significantly improves adherence and long-term effectiveness.
Excellent Safety Profile: So far, clinical trials have shown it to be very well-tolerated, with the most common side effects being mild reactions at the injection site.
Who Is It For?
This is not a medication for everyone with slightly high cholesterol. It is typically prescribed for:
Patients with familial hypercholesterolemia (a genetic condition causing very high cholesterol).
Patients with established cardiovascular disease (e.g., those who have had a heart attack or stroke).
Patients who cannot reach their LDL cholesterol targets with maximally tolerated statin therapy (meaning they are on the highest dose of statins they can handle, often due to side effects like muscle pain).
The Bigger Picture and Future
Inclisiran is part of a new wave of powerful cholesterol-lowering drugs that also includes PCSK9 inhibitors (like evolocumab and alirocumab), which are monoclonal antibodies injected every two or four weeks. The siRNA approach is considered the next evolution, offering even greater dosing convenience.
In summary, the news about a “new pill” that cuts bad cholesterol by 60% is a slightly simplified version of a major medical breakthrough. It refers to a powerful, long-acting injectable drug that uses gene-silencing technology to dramatically lower LDL levels with just two doses a year, offering new hope for patients at the highest risk of heart attacks and strokes.
When you are actively sick, your appetite will likely be low. The primary focus should be on hydration and getting calories in whatever form you can tolerate.
What to DRINK (Hydration is Key):
Water: Essential. Sip consistently throughout the day.
Electrolyte Solutions: Pedialyte, Liquid IV, or even diluted sports drinks can help replenish sodium, potassium, and other electrolytes lost through sweat and fever.
Broth and Bone Broth: Savory, hydrating, and provides electrolytes like sodium. Bone broth adds the benefit of collagen and some protein, which can be soothing and supportive.
Herbal Teas: Ginger tea (settles nausea), peppermint tea (clears sinuses, soothes stomach), or chamomile tea (promotes rest). Add honey and lemon for extra soothing properties and a calorie boost.
Diluted Juice: Mix 50/50 with water to provide some sugar for energy without overloading your system.
What to EAT (When You Can):
Focus on the “BRAT” diet if your stomach is upset, but don’t stay on it long-term.
Bananas: Easy to digest, provide potassium, and provide energy.
Rice (White): Plain white rice is bland and binding, which can help with diarrhea.
Applesauce: Provides pectin, which can help with diarrhea, and easy calories.
Toast (White): Plain, dry toast is easy on the stomach.
Other Good Options:
Plain Crackers or Pretzels
Boiled Potatoes (without butter)
Plain Oatmeal or Cream of Wheat
Chicken Noodle Soup: The classic for a reason—it provides fluids, electrolytes, and easy-to-digest protein and carbs.
🍎 After the Flu: The Recovery Phase
Once your appetite returns and symptoms subside, your body needs to rebuild and repair. Focus on nutrient-dense foods.
What to DRINK (Continue Replenishing):
Water: Keep hydration a priority.
Smoothies: An excellent way to pack nutrients. Blend greens (spinach), fruit (berries, banana), protein (Greek yogurt, protein powder), and a healthy fat (avocado, chia seeds).
Milk or Fortified Plant-Based Milks: Provides protein, calories, and nutrients like Vitamin D.
What to EAT (Nutrient-Dense Foods):
Prioritize protein, healthy fats, and colorful fruits and vegetables to replenish vitamin and mineral stores.
Lean Protein: Your body uses protein to repair tissues and make new immune cells.
Examples: Grilled chicken, fish (like salmon, which also has anti-inflammatory omega-3s), eggs, tofu, and lentils.
Fruits and Vegetables: To restock on vitamins, minerals, and antioxidants.
Examples: Citrus fruits (Vitamin C), berries (antioxidants), leafy greens (iron, folate), and sweet potatoes (Vitamin A, beta-carotene).
Probiotics: To replenish the healthy gut bacteria that can be disrupted by illness.
Examples: Yogurt, kefir, kimchi, sauerkraut, and kombucha.
Healthy Fats and Complex Carbs: For sustained energy.
Examples: Avocado, nuts, seeds, whole-grain bread, brown rice, and quinoa.
🛡️ Before the Flu: The Prevention Phase
A strong, well-nourished body is better equipped to fight off viruses. There’s no single “magic” food, but a consistent, balanced diet is your best defense.
What to EAT & DRINK for a Resilient Immune System:
Colorful Fruits & Vegetables: Aim for a “rainbow” to get a wide array of vitamins and antioxidants.
Lean Proteins: Essential for building immune cells. Zinc, found in seafood, poultry, beans, and nuts, is particularly important for immune function.
Vitamin C-Rich Foods: Supports various cellular functions of the immune system.
Examples: Citrus fruits, bell peppers, strawberries, and broccoli.
Vitamin D Sources: Crucial for immune health.
Examples: Fatty fish (salmon, tuna), fortified milk, and eggs. Sunlight is the primary source.
Stay Hydrated: Proper hydration is essential for all bodily functions, including the circulation of immune cells.
Listen to Your Body: This is the most important rule. If you’re not hungry, don’t force yourself to eat. Focus on fluids. As your appetite returns, start with bland, easy foods and gradually work your way back to your normal, healthy diet. If you have specific health conditions or severe symptoms, always consult a doctor or a registered dietitian.
Medicare beneficiaries should compare plans during the current open enrollment period, according to health experts. They point out that some monthly insurance rates might go up a little while others might go down a little. They also mention the possibility of changes to out-of-pocket costs, deductibles, and coverage for medical services. During the current open enrollment period, experts advise Medicare beneficiaries to thoroughly consider their options for the upcoming year.
Here are 3 key changes to Medicare costs expected in 2026:
1. The $2,000 Out-of-Pocket Cap on Part D Prescription Drugs
This is the most significant change and a historic first for the Medicare program.
What’s Changing: For the first time, there will be a hard cap on how much someone on a Medicare Part D prescription drug plan has to pay out-of-pocket for their medications in a single year.
The Specifics: In 2026, this cap will be set at $2,000. Once a beneficiary’s total drug spending (including what they and their plan have paid) reaches this amount, they will pay $0 for their covered Part D drugs for the rest of the year.
Why It’s a Big Deal: This protects beneficiaries, especially those with chronic conditions like cancer, multiple sclerosis, or rheumatoid arthritis, who rely on extremely expensive specialty drugs. Previously, there was no cap, meaning seniors could face thousands of dollars in ongoing costs, creating significant financial strain.
2. Smoothing of Out-of-Pocket Costs in Part D
This change works hand-in-hand with the $2,000 cap to make costs more manageable throughout the year.
What’s Changing: Medicare beneficiaries will have the option to spread their out-of-pocket drug costs over the entire year instead of facing large, lump-sum payments.
The Specifics: This is often called the “Part D smoothing” or “monthly cap” provision. Beneficiaries can choose to pay their estimated out-of-pocket costs in equal monthly payments, making it easier to budget and avoid a major financial hit in a single month.
Why It’s a Big Deal: It provides predictability and financial flexibility. A senior who hits the catastrophic coverage phase early in the year won’t have to come up with a large amount of money all at once to pay for a single prescription.
3. The Start of Medicare Drug Price Negotiation
While the direct price effects will take time to fully materialize, 2026 marks a critical milestone in this process.
What’s Changing: For the first time, the federal government will directly negotiate prices with drug manufacturers for a select number of high-cost, single-source drugs that lack competition.
The Specifics: The first round of negotiated prices will go into effect in 2026. The drugs subject to negotiation were selected from Medicare’s highest-spending drugs that have been on the market for several years without generic or biosimilar competition.
Why It’s a Big Deal: This is a fundamental shift in how drug prices are set in Medicare. The goal is to lower costs not just for individual beneficiaries (through lower copays/coinsurance) but for the entire Medicare program, which can help slow the growth of premiums and federal spending over time. The drugs selected for this first round are likely to be major cost drivers for many beneficiaries.
Summary Table
Key Change
What It Means for You in 2026
$2,000 Part D Cap
Your maximum yearly out-of-pocket cost for prescription drugs is capped at $2,000. After that, you pay $0.
Cost Smoothing
You can choose to pay your out-of-pocket drug costs in predictable monthly installments instead of large, sporadic payments.
Drug Price Negotiation
The first set of government-negotiated lower drug prices takes effect, which should lower costs for specific, high-spend medications.
Important Note: Medicare rules and plans can change every year. It is always recommended to review your coverage during the Annual Election Period (October 15 – December 7) to ensure your plan still meets your needs and takes advantage of these new consumer protections.
High A1C levels are a risk factor for diabetes and other complications. However, ideal and dangerous A1C levels can vary slightly between individuals. Lifestyle changes can help manage A1C levels. The A1C test, also known as the hemoglobin A1C, HbA1C, glycated hemoglobin, or glycohemoglobin test, measures the amount of sugar attached to hemoglobin in the blood.
Hemoglobin is a protein in red blood cells (RBCs) to which sugar naturally attaches. However, as people with higher blood sugar levels have more sugar-coated hemoglobin, it is a useful test to help check and monitor diabetes status. Higher A1C levels are often associated with diabetes complications, so it is important to reach and maintain target A1C results. An individual’s personal A1C goal will depend on many factors, including age and any other medical conditions. Although it is an important tool for managing diabetes, testing A1C levels does not replace other strategies, such as regular blood sugar testing at home.
A person can work toward lowering and maintaining their A1C level by following their treatment plan, getting regular physical exercise, and taking steps to lose weight if their doctor has advised doing so. In this article, we discuss healthy and concerning A1C levels, the possible complications of high levels, and strategies to reduce A1C levels.
A1C test results represent how well the body is maintaining blood sugar levels by showing the average percentage of sugar-bound hemoglobin in a blood sample. A higher A1C level suggests a higher risk of diabetes and its complications.
When discussing A1C levels, a doctor may also refer to estimated average glucose, or eAG. The eAG corresponds to A1C, but it is measured in milligrams per deciliter (mg/dl), the same as with blood sugar. Both A1C and eAG refer to a person’s average 3-month blood sugar levels.
A1C value
eAG value
Potential diagnosis
5.6% or less
114 mg/dl or less
Normal
5.7–6.5%
117–140 mg/dl
Prediabetes
6.5% or more
140 mg/dl
Diabetes
However, A1C level recommendations can vary among individuals due to a number of factors. What may be high for one person might be within range for another person.
For example, people with more advanced diabetes will have higher A1C targets than those without diabetes. Various underlying conditions, including blood disorders, can also have an effect, as can potentially modifiable factors, such as stress, medications, and lifestyle changes.
A1C value
eAG value
Potential targets for:
5.6% or less
114 mg/dl or less
healthy adults without diabetes
6.5%
140 mg/dl
Most non-pregnant adults with diabetes
7% or less
154 mg/dl or less
most non-pregnant adults with diabetes
8% or less
183 mg/dl or less
people with long-standing or severe diabetes, limited life expectancy, extensive additional health complications, or less favorable treatment response
A person with an A1C level indicating prediabetes may wish to consider making lifestyle changes, such as adopting a well-balanced diet and staying active, to help manage or even reverse the condition before it progresses to type 2 diabetes. If a person has a higher A1C level, suggesting diabetes, they should contact a doctor. The doctor will be able to run further diagnostic tests to confirm the person’s diabetes status.
The A1C goal for most people with diabetes is 7% or less. However, personal targets can vary, and a diabetes care team may consider other factors to help a person set their own individual goals. If a person with diabetes has an A1C test result that is much higher than their set target, a doctor can help advise lifestyle and medication changes to lower their A1C level.
The A1C test is a blood test that measures a person’s average blood sugar levels over the past 3 months. In particular, it measures the percentage of hemoglobin in the blood with an attached molecule of glucose.
When glucose attaches to hemoglobin, experts refer to the resulting compound as glycosylated hemoglobin. The name of the test derives from the fact that about 95% to 98% of the hemoglobin present in the body is type A1. Type A1 hemoglobin has subtypes, including A1C. As this is the most abundant subtype, it is a good marker for glucose control.
The test uses a 3-month average because RBCs typically live for about 3 months. Therefore, this timeframe reflects the sugar exposure to the cells over that time. The test does not require any specific preparations, so a person does not need to fast prior to the test, and a doctor can perform it at any time of the day.
The A1C test estimates the average blood sugar level over the past 3 months. The test is able to measure this by identifying the percentage of glycosylated hemoglobin in the blood.
If there is more glucose present in the blood, more glucose is available to attach to hemoglobin. Therefore, if a person has a high percentage of glycosylated hemoglobin, it indicates that they have had high blood sugar for an extended period.
A high A1C level can be concerning, as it may indicate that an individual has a higher chance of diabetes complications. For those without a diabetes diagnosis, it suggests that, without interventions, they may develop the condition. For individuals living with diabetes, it may indicate that their current treatment plan is not effective and that they should contact a doctor.
Potential complications that can result from high blood sugar levels include:
As many factors can affect a suitable A1C range, there is no standardized approach when it comes to setting A1C goals. A diabetes healthcare team can help provide an individual with a target level that accounts for various factors, including the current A1C value and the date of the next test.
If the test result is already within a healthy range, the goal should be to maintain that. However, if a person enters the higher ranges, a doctor can suggest changes to their goals and treatment plans. They can help the person determine a reasonable target and the best strategy to achieve that goal.