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Crohn’s Disease: Symptoms, Causes, and Treatment.

Crohn’s Disease: Symptoms, Causes, and Treatment.

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Crohn’s disease is a condition that causes swelling, or inflammation, in part of your digestive system. It can affect any part of your digestive tract, but most often it involves your small intestine and colon (large intestine). Crohn’s disease and ulcerative colitis (UC) are part of a group of conditions called inflammatory bowel disease (IBD). There’s no cure for Crohn’s, but treatment can ease your symptoms and help you enjoy a full, active life.

Symptoms of Crohn’s Disease 

People with Crohn’s disease can have intense symptoms, followed by periods of no symptoms that may last weeks or years. The symptoms depend on the severity and location of the disease.

What are the first signs of Crohn’s disease?

Early signs of Crohn’s disease can easily be mistaken for other conditions. They may include:

  • Frequent diarrhea
  • Abdominal pain and tenderness
  • Unexplained weight loss
  • Blood in your poop

Other symptoms of Crohn’s disease

When it advances, you might notice:

  • Nausea
  • Tiredness
  • Joint pain
  • Fever
  • Long-lasting diarrhea, often bloody and with mucus or pus
  • Weight loss

Crohn’s disease and mouth sores

Crohn’s disease can cause painful mouth sores, which typically appear on the inner cheeks, lips, or tongue. These sores can be a sign of an active Crohn’s disease flare.

Types of Crohn’s Disease
There are five types of Crohn’s based on which part of your digestive tract is affected.

  • Ileocolitis, the most common form of Crohn’s disease, involves your colon and the last part of your small intestine (called the ileum or terminal ileum).
  • Crohn’s colitis or granulomatous colitis affects only your colon.
  • Gastroduodenal Crohn’s disease affects your stomach and the first part of your small intestine (called the duodenum).
  • Ileitis affects your ileum.
  • Jejunoileitis causes small areas of inflammation in the upper half of your small intestine (called the jejunum).

Causes of Crohn’s Disease
Doctors aren’t sure what causes Crohn’s disease. Genetic, environmental, and lifestyle factors can play a role. Some people think of it as an autoimmune disease, causing your body to attack its own tissues. Your body may also be prone to more severe-than-normal responses to harmless viruses, bacteria, or food in your gut. 

Crohn’s Disease Risk Factors

A few things can make you more likely to get Crohn’s:
Genes. Crohn’s disease is often inherited. About 20% of people who have it have a close relative with either Crohn’s or ulcerative colitis.
Age. Though it can affect people of all ages, it’s mostly an illness of the young. Most people are diagnosed before age 30, but the disease can affect people in their 50s, 60s, 70s, or even later in life.
Smoking. This is one risk factor that’s easy to control. Smoking can make Crohn’s more serious and raise the odds that you’ll need surgery.
Where do you live? People living in urban areas or industrialized countries are more likely to develop Crohn’s disease.
Crohn’s disease epidemiology
The disease is mostly common in North America and Western Europe, where it affects 100-300 out of every 100,000 people. In the U.S., more than half a million people have it. Researchers think cases are increasing in the U.S. and some other nations.
Crohn’s disease seems to affect men and women at similar rates. People of northern European or central European Jewish (Ashkenazi) descent are at the highest risk.

Crohn’s Disease Treatment

There’s no single treatment that’s right for everyone with Crohn’s disease. Your treatment will depend on what’s causing your symptoms and how serious they are. Your doctor will try to reduce the inflammation in your digestive tract and keep you from having complications.

Anti-inflammatory drugs. 

Examples include mesalamine (Asacol, Lialda, Pentasa), olsalazine (Dipentum), and sulfasalazine (Azulfidine). Side effects include upset stomach, headache, nausea, diarrhea, and rash. These medicines are used only in mild cases.

Corticosteroids. These are a more powerful type of anti-inflammatory drug. Examples include budesonide (Entocort) and prednisone or methylprednisolone (Solu-Medrol). If you take these for a long time, side effects can be serious and may include bone thinning, muscle loss, skin problems, and a higher risk of infection.

Immune system modifiers (immunomodulators), such as azathioprine (Imuran, Azasan) and methotrexate (Rheumatrex, Trexall). It can take up to six months for these drugs to work. They also bring a higher risk of infections that could be life-threatening.

Antibiotics. These drugs, such as ciprofloxacin (Cipro) and metronidazole (Flagyl), are used to fight infections in your digestive system caused by Crohn’s disease. Metronidazole can cause a metallic taste in your mouth, nausea, tingling, or numbness in your hands and feet. Ciprofloxacin can cause nausea and tenderness in your Achilles tendon.

Reference:
https://my.clevelandclinic.org/health/diseases/9357-crohns-disease
https://www.mayoclinic.org/diseases-conditions/crohns-disease/symptoms-causes/syc-20353304
https://www.nhs.uk/conditions/crohns-disease/

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Understanding Arthritis and Inflammation

Understanding Arthritis and Inflammation

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The body’s white blood cells and substances that they produce to protect our bodies from infection by foreign organisms, such as bacteria and viruses. In some inflammatory diseases, however, the body’s defense system, the immune system, triggers a response when there are no foreign substances to fight off. In these diseases, called autoimmune disorders, the body’s normally protective immune system causes damage to its own tissues. The body responds as if normal tissues are infected or somehow abnormal.

Understanding the relationship between arthritis and inflammation is key to managing these conditions. In simple terms, all arthritis involves the joints, but not all arthritis is primarily driven by inflammation. Inflammation is a core player in many, but not all, types of arthritis.

Some, but not all, types of arthritis are the result of misdirected inflammation. Arthritis is a general term that describes inflammation in the joints. Some types of arthritis associated with inflammation include the following:
Rheumatoid arthritis
Psoriatic arthritis
Gouty arthritis
Other painful conditions of the joints and musculoskeletal system that may not be associated with inflammation include osteoarthritis, fibromyalgia, muscular low back pain, and muscular neck pain.

Inflammation occurs when substances from the body’s white blood cells are released into the blood or affected tissues to protect your body from foreign invaders. This release of chemicals increases the blood flow to the area of injury or infection, and may result in redness and warmth. Some of the chemicals cause a leak of fluid into the tissues, resulting in swelling. This protective process may stimulate nerves and cause pain. The increased number of cells and inflammatory substances within the joint cause irritation, swelling of the joint lining, and eventual wearing down of cartilage (cushions at the end of bones).

Inflammatory diseases are diagnosed after careful evaluation of the following:
Complete medical history and physical exam with attention to the location of painful joints
Presence of joint stiffness in the morning
Evaluation of accompanying symptoms and signs
Results of X-rays and laboratory tests

Can Inflammation Affect Internal Organs?
Inflammation can affect organs as part of an autoimmune disorder. The type of symptoms experienced depends on which organs are affected. For example:
Inflammation of the heart (myocarditis) may cause shortness of breath or fluid retention.
Inflammation of the small tubes that transport air to the lungs may cause shortness of breath.
Inflammation of the kidneys (nephritis) may cause high blood pressure or kidney failure.
Pain may not be a primary symptom of an inflammatory disease, because many organs do not have pain-sensitive nerves. Treatment of organ inflammation is directed at the cause of inflammation whenever possible.

There are several treatment options for inflammatory diseases, including medications, rest, exercise, and surgery to correct joint damage. The type of treatment prescribed will depend on several factors, including the type of disease, the person’s age, the type of medications they are taking, overall health, medical history, and severity of symptoms.

The goals of treatment are the following:

Correct, control, or slow down the underlying disease process
Avoid or modify activities that aggravate pain
Relieve pain through pain medications and anti-inflammatory drugs
Maintain joint movement and muscle strength through physical therapy
Decrease stress on the joints by using braces, splints, or canes as needed

Reference:
https://my.clevelandclinic.org/health/diseases/12061-arthritis
https://www.webmd.com/arthritis/understanding-arthritis-treatment
https://www.mayoclinic.org/diseases-conditions/arthritis/symptoms-causes/syc-20350772

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Is He Depressed or Just Crabby?

Is He Depressed or Just Crabby?

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It can be challenging to distinguish between a temporary bad mood (crabby) and a more serious mental health condition like depression. Here’s a breakdown of the key differences.

Key Differences: Crabby vs. Depressed

Feature“Just Crabby” (Irritable Mood)Depression (Clinical)
DurationIt can occur without an obvious trigger. The mood persists even when good things happen.Persistent. Lasts most of the day, nearly every day, for at least two weeks.
TriggerUsually has a clear cause (bad day at work, lack of sleep, hunger, stress).Pervasive. Affects almost all aspects of life—work, hobbies, relationships, and self-care.
ScopeSituational. They’re irritable about specific things.Support may be welcomed, but it doesn’t “fix” the mood. The person may feel unable to cheer up.
Other SymptomsPrimarily irritability/anger. Energy and enjoyment in other areas may be normal.Includes a cluster of symptoms:
• Anhedonia: Loss of interest/pleasure in almost all activities.
• Hopelessness: Pervasive sadness, emptiness, or worthlessness.
• Physical changes: Significant appetite/weight change, sleep disturbances (too much or too little).
• Fatigue: Constant low energy.
• Cognitive issues: Trouble concentrating, indecisiveness.
• Thoughts of death: Recurrent thoughts of death or suicide.
Self-ViewMay be frustrated with the situation or others, but self-esteem is generally intact.Often involves intense self-criticism, guilt, and feelings of worthlessness.
Response to SupportMay snap, but often calms down after venting, solving the problem, or with distraction.Support may be welcomed, but doesn’t “fix” the mood. The person may feel unable to cheer up.

Overlap: Irritability in Depression

It’s crucial to know that irritability and anger are common symptoms of depression, especially in men, teens, and older adults. Someone who is depressed isn’t always sad; they may present as constantly short-tempered, frustrated, and easily agitated.

Questions to Ask (Gently and Compassionately):

If you’re concerned about someone, consider these patterns:

  1. How long has this lasted? Has it been more than two weeks of this consistent mood?
  2. Is it about everything or specific things? Do they still enjoy anything they used to love?
  3. How are their basics? Have their sleep, appetite, or energy levels drastically changed?
  4. What do they say about themselves? Are they making comments like “What’s the point?” or expressing hopelessness?
  5. Have they withdrawn? Have they stopped seeing friends, engaging in hobbies, or taking care of their hygiene?

What You Can Do

  • For “Crabby”: Offer patience, space, or practical help. Sometimes, a simple “You seem stressed, can I help?” or giving them time to cool off is enough.
  • If You Suspect Depression:
    • Approach with care: Use “I” statements. “I’ve noticed you haven’t seemed yourself lately, and I’m concerned. I care about you.”
    • Listen without judgment: Don’t try to “fix” it or dismiss their feelings. Validate their experience.
    • Encourage professional help: Gently suggest talking to a doctor or therapist. Frame it as a sign of strength, not weakness. You can offer to help find resources or even go with them.
    • Stay connected: Continue to invite them, even if they say no. Isolation fuels depression.

When to Be Especially Concerned

Seek immediate professional help if there are any signs of suicidal thoughts, self-harm, or talk of being a burden. You can call a crisis line (988 in the US) or go to an emergency room.

In short, “Crabby” is a mood; depression is a pervasive state that alters functioning. If low mood, irritability, and other symptoms are persistent, pervasive, and affecting quality of life, it’s time to consider depression and seek professional evaluation. A doctor or mental health professional can make an accurate diagnosis and recommend the right treatment, which can be life-changing.

Reference:
https://health.clevelandclinic.org/is-he-depressed-or-just-crabby
https://www.mayoclinic.org/diseases-conditions/depression/in-depth/male-depression/art-20046216
https://www.nimh.nih.gov/health/publications/depression
https://www.obgynnebraska.com/contents/patient-information/mental-health-awareness

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Tired, Achy Eyes?

Tired, Achy Eyes?

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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.

Reference:
https://www.webmd.com/eye-health/eye-fatigue-causes-symptoms-treatment
https://newsinhealth.nih.gov/2024/09/tired-achy-eyes
https://www.mayoclinic.org/diseases-conditions/eyestrain/symptoms-causes/syc-20372397

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Interaction of Cannabis Use and Aging: From Molecule to Mind

Interaction of Cannabis Use and Aging: From Molecule to Mind

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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.

Reference:
https://www.drugs.com/illicit/cannabis.html
https://adf.org.au/drug-facts/cannabis/
https://my.clevelandclinic.org/health/articles/4392-marijuana-cannabis

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No-to-Low Risk for Gestational Diabetes With Oral Corticosteroids

No-to-Low Risk for Gestational Diabetes With Oral Corticosteroids

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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.

Reference:
https://pmc.ncbi.nlm.nih.gov/articles/PMC5604866/
https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2842158#:~:text=Conclusions%20and%20Relevance%20In%20this,of%20OCSs%20when%20clinically%20indicated.
https://www.medpagetoday.com/obgyn/pregnancy/118780

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3 New Findings on AFib and What They Mean

3 New Findings on AFib and What They Mean

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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.

Reference:
https://www.webmd.com/heart-disease/atrial-fibrillation/news/20251118/3-new-findings-on-afib-and-what-they-mean
https://my.clevelandclinic.org/health/diseases/16765-atrial-fibrillation-afib
https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624

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What To Know About Alcohol and Aging

What To Know About Alcohol and Aging

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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.

Reference:
https://health.clevelandclinic.org/why-youll-feel-alcohols-effects-more-after-age-65
https://www.nia.nih.gov/health/alcohol-misuse-or-alcohol-use-disorder/facts-about-aging-and-alcohol
https://www.hopkinsmedicine.org/health/wellness-and-prevention/alcohol-and-older-adults
https://www.webmd.com/mental-health/addiction/ss/slideshow-alcohol-aging

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/products/disease/alcoholism

Diet, exercise, or both? Study finds best strategy for reducing belly fat…

Diet, exercise, or both? Study finds best strategy for reducing belly fat…

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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:

StrategyEffect on Belly Fat (Visceral Fat)
Diet OnlyGood reduction. Creates a calorie deficit, leading to overall fat loss, including from the belly.
Exercise OnlyModerate reduction. Effective, but often slower than diet for fat loss alone.
Diet + ExerciseBest 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

  1. 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.
  2. 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.
  3. Lift Weights: Include resistance training at least 2-3 times per week, targeting all major muscle groups.
  4. 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.

Reference:
https://www.hopkinsmedicine.org/health/wellness-and-prevention/8-ways-to-lose-belly-fat-and-live-a-healthier-life
https://www.health.harvard.edu/newsletter_article/taking-aim-at-belly-fat
https://www.healthline.com/nutrition/20-tips-to-lose-belly-fat

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/products/weight-loss

New pill reduces ‘bad’ cholesterol levels by almost 60%

New pill reduces ‘bad’ cholesterol levels by almost 60%

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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.

  1. 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.
  2. 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.
  3. 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

  1. Unprecedented Efficacy: The ~60% reduction in LDL cholesterol is among the highest achieved by any single drug.
  2. 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.
  3. 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.

Reference:
https://www.sciencealert.com/new-drug-lowers-bad-cholesterol-by-58-in-clinical-trial
https://medicalxpress.com/news/2025-11-cholesterol-lowering-pill-bad.html
https://www.medicalnewstoday.com/articles/oral-pill-enlicitide-reduces-bad-cholesterol-levels-statins

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/products/disease/heart-disease