A new blood test could aid in the diagnosis and reveal the extent of Alzheimer’s disease progression.

A new blood test could aid in the diagnosis and reveal the extent of Alzheimer’s disease progression.

Exciting advancements in Alzheimer’s disease (AD) diagnostics are emerging, including a new blood test that could revolutionize early detection and disease monitoring. Here’s what you need to know:
Key Developments:

Blood-Based Biomarkers for Alzheimer’s
Researchers have identified specific proteins in the blood that correlate with Alzheimer’s pathology, including:
Phosphorylated Tau (p-tau217, p-tau181) – Strongly associated with amyloid and tau plaques in the brain.
Amyloid Beta 42/40 Ratio – Indicates amyloid buildup, a hallmark of AD.
Neurofilament Light (NfL) – Marks neurodegeneration, showing disease progression.

A 2024 study in JAMA Neurology found that a p-tau217 blood test could predict Alzheimer’s with 89–96% accuracy, rivaling costly PET scans or invasive spinal taps.

Tracking Disease Progression
Blood tests may soon help determine how far Alzheimer’s has advanced by measuring:
Early-stage (preclinical) AD – Elevated p-tau217 + abnormal amyloid.
Mild cognitive impairment (MCI) due to AD – Rising NfL + tau.
Late-stage AD – Very high NfL + severe tau/amyloid imbalance.
Advantages Over Current Methods
Faster & Cheaper – Blood tests, like those for blood sugar or complete blood count, can cost around ₹500, while PET scans can range from ₹10,000 to ₹40,000+ depending on the type of scan and location.
More Accessible – Could be done in primary care settings, enabling earlier intervention.
Monitoring Treatment Response – Useful for clinical trials and future anti-amyloid/tau therapies (e.g., lecanemab, donanemab).

Current Status & Challenges

Not Yet FDA-Approved for Diagnosis – But companies (e.g., Quest Diagnostics, C2N Diagnostics) are rolling out commercially available tests (e.g., PrecivityAD2).
False Positives/Negatives Possible – Some non-AD dementias may show similar markers.
Still Needs Validation – Larger, diverse population studies are ongoing.

When Could This Be Available?

Some tests (e.g., ALZpath p-tau217) are already used in research and select clinics.
Widespread clinical use could happen in 2–5 years if validation succeeds.

Why This Matters

Early detection could allow:
✔ Timely lifestyle interventions (diet, exercise, cognitive training).
✔ Eligibility for new anti-amyloid drugs (most effective in early stages).
✔ Better clinical trial recruitment for future therapies.

Reference:

https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/diagnosis-treatment/drc-20350453

https://www.lunduniversity.lu.se/article/new-reliable-blood-marker-reveals-extent-alzheimers-pathology-brain

https://www.nih.gov/news-events/nih-research-matters/accurate-blood-test-alzheimer-s-disease

https://www.medicalnewstoday.com/articles/new-blood-test-may-help-diagnose-show-how-far-alzheimers-progressed

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Certain combos of common food additives may raise type 2 diabetes risk

Certain combos of common food additives may raise type 2 diabetes risk

Common Food Additive Mixtures Linked to Increased Type 2 Diabetes Risk

Recent research suggests that certain combinations of food additives commonly found in ultra-processed foods may contribute to a higher risk of type 2 diabetes (T2D). Here’s a detailed breakdown of the findings:

  1. Key Additive Mixtures Identified

A 2025 French study (NutriNet-Santé cohort, PLOS Medicine) analyzed dietary data from 108,643 adults over 7.7 years and identified two high-risk additive mixtures:

Mixture 2: Contains emulsifiers and thickeners like carrageenan, modified starches, guar gum, xanthan gum, and potassium sorbate (found in dairy desserts, sauces, and broths). Associated with an 8% increased T2D risk.
Mixture 5: Includes artificial sweeteners (aspartame, sucralose, acesulfame-K), acidifiers (citric acid, phosphoric acid), and dyes (common in diet sodas and artificially sweetened drinks). Linked to a 13% higher T2D risk.
  1. Why Are These Mixtures Risky? Synergistic Effects: Additives may interact in ways that disrupt metabolism, gut microbiota, or insulin sensitivity more than individual ingredients. Emulsifiers & Gut Health: Some (e.g., carrageenan) may promote inflammation and leaky gut, contributing to metabolic dysfunction. Artificial Sweeteners: Despite being calorie-free, they may alter glucose metabolism and hunger signals, potentially leading to overeating.
  2. Study Limitations & Industry Pushback Observational Design: Cannot prove causation, only association. Industry Criticism: Beverage associations argue additives are “safe individually” and call the study “misleading”. Residual Confounding: Diet quality (e.g., high sugar/saturated fat intake) may play a role.
  3. Practical Recommendations Limit Ultra-Processed Foods: Opt for whole, minimally processed foods (fruits, vegetables, nuts, lean proteins). Check Labels: Avoid products with long lists of emulsifiers, sweeteners, or artificial additives. Cook at Home: Reduces reliance on pre-packaged foods with additive blends.
  4. Future Research & Policy Implications Calls for reevaluating additive safety testing, currently done one-by-one rather than assessing mixtures. Some U.S. states (e.g., California) have banned specific additives (e.g., Red Dye No. 3), but not yet those in these mixtures.

Conclusion

While more research is needed, the study highlights potential risks of additive combinations in processed foods. Reducing intake of ultra-processed products and advocating for stricter additive regulations may help lower diabetes risk.

Reference:

https://www.medicalnewstoday.com/articles/certain-combos-common-food-additives-may-raise-type-2-diabetes-risk

https://www.sciencealert.com/common-additive-combos-in-food-and-drinks-may-raise-risk-of-type-2-diabetes

https://pmc.ncbi.nlm.nih.gov/articles/PMC11977966

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According to new research, atrial fibrillation raises the risk of dementia.

According to new research, atrial fibrillation raises the risk of dementia.

Atrial Fibrillation (AFib) Linked to Increased Dementia Risk, Especially in Younger Adults

Recent studies highlight a concerning connection between atrial fibrillation (AFib) and dementia, with younger individuals facing a significantly higher risk. Here’s a breakdown of the key findings:

  1. Stronger Risk for Younger Adults A 2025 Spanish study involving 2.5 million adults found that AFib increases dementia risk by 21% in those under 70, and the risk jumps to 36% for early-onset dementia (diagnosed before age 65)12. For participants without prior stroke, the risk of early-onset dementia was even higher (52% increase), suggesting mechanisms beyond stroke-related damage28. In contrast, no significant risk increase was observed in adults over 70, likely because age-related neurodegeneration outweighs AFib’s contribution13.
  2. Potential Mechanisms Beyond Stroke

While AFib is a known stroke risk factor, the study found the dementia link persists even after excluding stroke patients, pointing to other pathways28:

Silent strokes (undetected brain infarcts)
Microbleeds and microinfarcts due to blood flow irregularities
Chronic inflammation and vascular dysfunction damaging small brain vessels
Hemodynamic instability (irregular blood flow to the brain)
  1. Clinical Implications Early AFib detection and management (e.g., anticoagulants, rhythm control) may help mitigate dementia risk, particularly in younger patients8. Proactive cognitive monitoring is advised for AFib patients under 7018. Lifestyle interventions (managing hypertension, diabetes, sleep apnea) could reduce both AFib and dementia risk8.
  2. Study Limitations Observational design: The research identifies association, not causation17. Population bias: Data came from Spain; broader studies are needed1. Diagnostic accuracy: Dementia cases were identified via medical codes, possibly missing mild cases1.
  3. Expert Recommendations Dr. Julián Rodriguez-García (study author) emphasizes aggressive AFib treatment in younger patients to potentially delay cognitive decline28. Dr. Paul Drury (cardiologist) calls for more research on whether AFib treatments (e.g., ablation, anticoagulants) can directly lower dementia risk17.

Conclusion

AFib, particularly when diagnosed before age 70, is a notable independent risk factor for dementia. While more research is needed to confirm causality, these findings underscore the importance of early intervention and cardiovascular health management to protect long-term brain function.

Reference:

https://www.news-medical.net/news/20250331/Atrial-fibrillation-elevates-early-onset-dementia-risk-in-younger-adults.aspx

https://www.ahajournals.org/doi/full/10.1161/JAHA.122.025653

https://www.medicalnewstoday.com/articles/atrial-fibrillation-increases-dementia-risk-new-research-warns

https://pmc.ncbi.nlm.nih.gov/articles/PMC4988519

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By increasing hunger, popular sweeteners may contribute to weight gain.

By increasing hunger, popular sweeteners may contribute to weight gain.

The claim that certain popular sweeteners, particularly sucralose, may increase weight gain by boosting hunger is supported by recent research. Here’s a detailed breakdown of the findings and their implications:

1. Sucralose and Brain Activity

A 2025 study published in Nature Metabolism found that sucralose, a non-caloric artificial sweetener, increases blood flow in the hypothalamus—the brain region regulating hunger—more than sugar or water. This heightened activity suggests stronger hunger signals, potentially leading to overeating 136.

  • Mechanism: Sucralose’s sweetness without calories may confuse the brain, which expects energy from sweet tastes. When calories aren’t delivered, the brain may trigger cravings to compensate 38.
  • Sex and Weight Differences: Women and individuals with obesity showed stronger hypothalamic responses to sucralose, indicating these groups might be more susceptible to its appetite-stimulating effects 17.

2. Hormonal Impact

Unlike sugar, sucralose does not trigger insulin or glucagon-like peptide-1 (GLP-1), hormones that signal fullness. This lack of satiety hormones may prolong hunger after consumption 38.

3. Behavioral Effects

Participants reported feeling hungrier after consuming sucralose compared to sugar, though not versus water. Functional MRI scans also revealed increased connectivity between the hypothalamus and brain regions involved in reward processing (e.g., anterior cingulate cortex), which could intensify food cravings 168.

4. Contradictory Weight-Loss Claims

While artificial sweeteners are marketed as weight-loss aids, observational studies link them to higher BMI over time. For example, a 2023 WHO advisory recommended against using sugar substitutes for weight control, citing insufficient long-term benefits 38. However, some clinical trials show modest weight loss when sugary drinks are replaced with artificially sweetened alternatives, suggesting context matters 25.

5. Expert Recommendations

  • Avoid Overreliance: Dr. Katie Page, the study’s lead author, advises reducing overall sweetener intake rather than substituting sugar with sucralose 36.
  • Natural Alternatives: Experts like Dr. Susan Spratt recommend water, unsweetened tea, or fruit-infused beverages instead of diet sodas 8.

Key Takeaway

Sucralose may disrupt appetite regulation, especially in women and individuals with obesity, by activating hunger pathways without providing satiating calories. While more research is needed, current evidence suggests caution in using artificial sweeteners for weight management

Reference:

https://www.medicalnewstoday.com/articles/popular-sweetener-may-increase-weight-gain-by-boosting-hunger

https://pmc.ncbi.nlm.nih.gov/articles/PMC2892765

https://www.contemporaryhealth.co.uk/obesity-and-the-brain/popular-sweetener-sucralose-may-intensify-hunger-signals-and-contribute-to-weight-gain-new-study-suggests

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Do antidepressants raise the risk of sudden cardiac death ?

Do antidepressants raise the risk of sudden cardiac death ?

Recent research suggests a potential link between long-term antidepressant use and an increased risk of sudden cardiac death (SCD), though the relationship is complex and influenced by factors such as duration of use, age, and underlying health conditions. Here’s a breakdown of the key findings:

1. Increased Risk with Longer Duration of Use

  • A 2025 Danish study analyzing 4.3 million adults found that those taking antidepressants for 1–5 years had a 56% higher risk of SCD, while those using them for 6+ years faced more than double the risk compared to the general population 259.
  • The risk was most pronounced in middle-aged adults (30–59 years), with those aged 30–39 showing 3x higher risk at 1–5 years and 5x higher risk at 6+ years of use 27.

2. Possible Mechanisms

  • Some antidepressants (e.g., tricyclics, SSRIs like citalopram) may prolong the QT interval, increasing the risk of dangerous arrhythmias like torsades de pointes 10.
  • Depression itself is a known risk factor for cardiovascular disease, making it difficult to isolate medication effects from the disease’s impact 58.
  • Long-term antidepressant use may also correlate with poorer lifestyle factors (e.g., smoking, inactivity) that contribute to heart disease 78.

3. Age and Risk Variability

  • The heightened risk was not statistically significant in adults under 30, possibly due to shorter exposure times 37.
  • Older adults (70+ years) still faced elevated risk, but the increase was less dramatic than in middle-aged groups 29.

4. Expert Caution Against Overinterpretation

  • Researchers emphasize that depression untreated carries its own cardiovascular risks, and abruptly stopping medication could be harmful 58.
  • Dr. Jasmin Mujkanovic, lead author of the Danish study, noted: “Longer exposure might reflect more severe depression, which itself contributes to cardiovascular risk” 57.

5. Recommendations for Patients

  • Do not stop antidepressants without consulting a doctor—untreated depression poses greater risks 58.
  • Regular cardiac monitoring (e.g., ECGs) may be advised for high-risk patients, especially those on long-term treatment 10.
  • Lifestyle interventions (exercise, smoking cessation) can mitigate cardiovascular risks 8.

Conclusion

While long-term antidepressant use is associated with increased SCD risk, the relationship is likely influenced by underlying depression severity and other health factors. Patients should not discontinue medication without medical guidance but may benefit from heart-health monitoring if on prolonged treatment. Further research is needed to clarify causation

Reference:

https://www.tctmd.com/news/sudden-cardiac-death-risk-linked-long-term-antidepressant-use

https://www.medicalnewstoday.com/articles/can-antidepressants-increase-sudden-cardiac-death-risk

https://www.medscape.com/viewarticle/antidepressants-linked-sudden-cardiac-death-risk-early-2025a10007wn?form=fpf

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Diabetes medications such as Jardiance or Ozempic may reduce the risk of Alzheimer’s

Diabetes medications such as Jardiance or Ozempic may reduce the risk of Alzheimer’s

A new study, posted in JAMA NeurologyTrusted Source, reveals that humans with kind 2 diabetes who take not unusualplace anti-diabetes medicines had a discounted danger of Alzheimer`s and related dementias.

The pills in query have been glucagon-like peptide-1 receptor agonists (GLP-1RAs), like Ozempic and Wegovy, and sodium-glucose cotransporter-2 inhibitors (SGLT2is), like Jardiance.

Specifically, GLP-1RA changed into related to a 33% decrease danger of dementia, and SGLT2i changed into related to a 43% decrease danger. Other diabetes medicines, however, have been now no longer related to a alternate in danger.

As the common age of the populace progressively rises, the range of dementia instances rises in step. Despite many years of extensive research, a therapy stays elusive. Although a few remedies can sluggish progress, we’re a ways from a breakthrough.

Adding to those challenges, if an powerful drug have been found, it’d take a few years to accumulate a enough proof base and tens of thousands and thousands of bucks to deliver it to market.

Some current studies has recommended that kind 2 diabetes and dementia might also additionally percentage a few physiological similarities, such as irritation and impaired insulin signalling withinside the brain. People with diabetes even have a better threat of growing dementia.

This increases an thrilling question: If a drug reduces the effect of kind 2 diabetes, would possibly it additionally lessen the threat of dementia? Scientists have now investigated this question, and a few proof does endorse that diabetes remedy might also additionally lessen dementia threat.

However, because the authors of the cutting-edge take a look at explain, we want extra proof. To construct the clearest photo to date, they used “a extra rigorous methodological method and strong adjustment for confounding factors.”

To investigate, the scientists accessed information from Florida, Georgia, and Alabama. In total, this amounted to 92,a hundred and sixty humans elderly 50 or older with kind 2 diabetes.

Participants had been accompanied till they died or evolved dementia, such as Alzheimer`s, vascular dementia, frontotemporal dementia, and Lewy frame dementia.

They centered on 3 comparisons:

GLP-1RA as opposed to different second-line glucose-reducing drugs
SGLT2i as opposed to different second-line glucose-reducing drugs
GLP-1RA as opposed to SGLT2i.

The scientists concluded that GLP-1RAs and SGLT2is have been related to a discounted threat of growing dementias in comparison with second-line diabetes drugs.

“GLP-1RA use turned into related to a 33% decrease threat of [dementia], at the same time as SGLT2i use turned into related to a 43% decrease threat in comparison with other [glucose-lowering drugs],” the authors write.

Medical News Today contacted William Kapp, MD, a toughness professional and CEO of Fountain Life, now no longer worried in tis study.

Kapp shared his mind at the findings, saying:

“The effects didn`t surprise me however they did provide greater credence to what we`ve been observing. Brain and frame don`t age separately. Metabolic troubles inclusive of insulin resistance are connected to inflammation, oxidative stress, and adjusted blood waft all of which effect mind health.”

Although scientists do now no longer realize for certain how GLP-1RA and SGLT2i may also lessen dementia threat in humans with kind 2 diabetes, the authors propose a few capability mechanisms.

For instance, GLP-1RAs had been proven to:

lessen neuroinflammation
enhance insulin Trusted Sourcesignalling withinside the mind
sell the increase of recent nerve cells (neurogenesis).

Similarly, SGLT2is may also guard the mind by:

enhancing cerebral blood waft
lowering oxidative stress
improving mitochondrial activity.

The scientists additionally provide an explanation for that each capsules are related to advanced metabolic and vascular fitness, each of which may also aid healthful mind function.

Additionally, there’s a few proof that those capsules can lessen stages of amyloid-beta and tau proteins withinside the mind the hallmarks of Alzheimer`s disease.

Speaking with the Science Media Center, Prof. David Strain,MD, FRCP, accomplice professor of cardiometabolic fitness on the University of Exeter Medical School withinside the United Kingdom, further now no longer concerned withinside the study, defined that:

“GLP-1 receptor antagonists and SGLT-2 inhibitors had been confirmed to manipulate the sugar, and additionally lessen the inflammation (a key motive force of Alzheimer`s disease) and decrease vascular hazard (a key motive force of vascular dementia) greater than could be predicted with the aid of using the sugar manipulate alone.”

“It is consequently no wonder that those facts display a decrease hazard of dementia in folks that get hold of them as a part of her ordinary care,” Strain continued.

This study, which analyzed facts from nearly 100,000 human beings is supported with the aid of using some of preceding studies. However, a paper posted withinside the identical magazine and at the identical day casts a small part of doubt at the results.

The paper in question, additionally posted in JAMA NeurologyTrusted Source, is a scientific evaluation and meta-evaluation of 26 medical trials which include facts from 164,531 participants.

According to its authors, “glucose-decreasing remedy with GLP1-RAs, however now no longer SGLT2is, become related to a statistically enormous discount in dementia or cognitive impairment.”

So, their conclusions on GLP1-RAs reflect the ones from the unique paper, however they did now no longer locate the equal impact for SGLT2is. This can be in part because of the quick length of follow-up. The common examine follow-up withinside the meta-evaluation and the follow-up withinside the unique examine have been beneathneath five years.

As dementia takes a few years to develop, this will now no longer be lengthy enough.

“Its nevertheless early, and were nevertheless now no longer seeing all of the lengthy-time period data,” Kapp advised MNT. But what we`re seeing is that regulating insulin and irritation can also additionally additionally gradual down a number of the adjustments withinside the mind tied to dementia.”

The inevitable subsequent query is: Will those tablets lessen dementia chance in human beings with out diabetes?

“If the advantage is from decreasing insulin resistance or irritation, it`s viable that those tablets may be properly for human beings with out diabetes,” Kapp advised MNT earlier than injecting a few caution.

“Just due to the fact some thing is ideal for one organization doesn`t imply it’s far for others. And there are constantly dangers to lengthy-time period use,” he warned.

For now, the jury is as a minimum in element out. We can also additionally need to watch for longer research earlier than we are able to draw strong conclusions. Still, it’s far searching more and more more possibly that GLP1-RAs would possibly lessen the chance of dementia for human beings with kind 2 diabetes, that is genuinely a effective finding.

Reference:

https://www.healthline.com/health-news/ozempic-alzheimers-risk-diabetes

https://www.medicalnewstoday.com/articles/diabetes-drugs-like-ozempic-or-jardiance-may-slash-alzheimers-risk#Do-we-have-enough-data-to-draw-strong-conclusions

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Alcohol consumption can cause dementia by harming the brain.

Alcohol consumption can cause dementia by harming the brain.

This study, published in Neurology, provides compelling evidence of the negative impact of alcohol consumption on brain health, particularly in relation to vascular damage, brain atrophy, and dementia-related pathologies. Here’s a concise breakdown of the findings and their implications:


Key Findings:

  1. Alcohol Consumption & Brain Vascular Damage:
    • Moderate, heavy, and former heavy drinkers had a higher risk of hyaline arteriolosclerosis (thickening/narrowing of small brain blood vessels).
    • Heavy drinkers had a 133% increased risk of this condition.
  2. Brain Atrophy & Cognitive Decline:
    • Former heavy drinkers had lower brain weight and poorer cognitive function compared to never-drinkers.
    • Heavy drinking was linked to more neurofibrillary tangles (a hallmark of Alzheimer’s disease).
  3. Indirect Cognitive Impact:
    • Alcohol did not directly impair cognition but appeared to damage blood vessels first, which then contributed to cognitive decline.

Study Details:

  • Participants: 1,781 deceased adults (avg. age 75) from Brazil, with brain autopsies.
  • Alcohol Categories:
    • Never drinkers (965 people).
    • Moderate drinkers (≤7 drinks/week).
    • Heavy drinkers (≥8 drinks/week).
    • Former heavy drinkers (quit ≤3 months before death).
  • Limitations:
    • Relied on family-reported alcohol use (potential inaccuracy).
    • Cross-sectional (cannot prove causation).
    • No long-term follow-up data.

Expert Takeaways:

  1. Even Moderate Drinking May Harm the Brain:
    • Vascular changes (hyaline arteriolosclerosis) were seen in all drinking groups, suggesting no safe threshold for alcohol regarding brain health.
  2. Former Heavy Drinkers Still at Risk:
    • Brain shrinkage and cognitive deficits persisted even after quitting, indicating long-term damage.
  3. Alcohol’s Role in Dementia Risk:
    • Heavy drinking may accelerate vascular dementia and Alzheimer’s pathology (neurofibrillary tangles).

Practical Implications:

  • Public Health Messaging:
    • No amount of alcohol is “safe” for brain health even moderate intake may contribute to vascular damage.
    • Heavy drinkers should be warned about irreversible brain atrophy and dementia risk.
  • Clinical Practice:
    • Screen for alcohol use in older patients with cognitive decline.
    • Encourage early reduction/cessation to mitigate vascular damage.
  • Future Research Needed:
    • Longitudinal studies to confirm causality.
    • Investigation into vitamin deficiencies (e.g., B1/thiamine) that may worsen alcohol-related brain damage.

Bottom Line:

This study adds to growing evidence that alcohol even in moderation harms brain structure and function, primarily through vascular damage. While more research is needed, the findings support limiting or avoiding alcohol to preserve long-term cognitive health.

Reference:

https://www.alzheimers.org.uk/about-dementia/types-dementia/alcohol-related-brain-damage-arbd

https://my.clevelandclinic.org/health/diseases/alcohol-related-dementia

https://pmc.ncbi.nlm.nih.gov/articles/PMC6957093

https://www.medicalnewstoday.com/articles/alcohol-use-could-contribute-to-dementia-by-damaging-the-brain

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Consuming fermented foods and a diet rich in fiber may help prevent inflammatory disorders.

Consuming fermented foods and a diet rich in fiber may help prevent inflammatory disorders.

This study, published in Nature Medicine, provides compelling evidence of how quickly dietary changes can influence immune and metabolic health. Here’s a concise breakdown of the key findings and implications:

Key Findings:

  1. Western Diet (2 Weeks) → Harmful Effects:
    • Increased inflammation (elevated inflammatory markers, altered gene expression).
    • Weakened immune response (reduced ability to fight pathogens).
    • Disrupted metabolic pathways linked to lifestyle diseases (e.g., diabetes, heart disease).
  2. Traditional African Diet (2 Weeks) → Benefits:
    • Anti-inflammatory effects (reduced inflammatory markers).
    • Improved immune and metabolic health.
  3. Fermented Beverage (Mbege, 1 Week) → Additional Benefits:
    • Enhanced immune function, likely due to probiotics and bioactive compounds (e.g., flavonoids).

Dietary Comparisons:

  • Traditional African Diet: High in fiber, polyphenols, and whole foods (legumes, leafy greens, tubers, millet, sorghum). Supports gut health and reduces inflammation.
  • Western Diet: High in processed foods, refined carbs, and unhealthy fats. Promotes inflammation and metabolic dysfunction.

Limitations:

  • Short study duration (2 weeks).
  • Small, male-only sample.
  • Unrestricted food intake may have influenced results.

Broader Implications:

  • Global Relevance: Even short-term dietary shifts can have lasting effects, reinforcing the importance of whole-food, plant-based diets (e.g., Mediterranean, Latin American, African diets) in preventing chronic diseases.
  • Cultural Preservation: Traditional diets offer health benefits while maintaining cultural heritage.
  • Public Health: Governments and health organizations should promote minimally processed, fiber-rich diets to combat rising lifestyle-related diseases.

Expert Takeaway:

As Dr. Holland noted, “Diet has a rapid and lasting impact on health.” Switching to heritage diets even temporarily could be a powerful tool for disease prevention.

References:

https://www.earlytimes.in/newsdet.aspx?q=383041

https://pmc.ncbi.nlm.nih.gov/articles/PMC9915096

https://www.medicalnewstoday.com/articles/diet-high-in-fiber-fermented-foods-could-keep-inflammatory-diseases-at-bay#Study-limitations-and-implications

https://www.hopkinsmedicine.org/health/wellness-and-prevention/anti-inflammatory-diet

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What are the different types of headaches?

What are the different types of headaches?

Over 150 distinct kinds of headaches exist. Cluster, sinus, hypnic, migraine, and tension-type headaches are a few of the varieties. Even though headaches can occasionally be excruciating and incapacitating, most of them can be managed with basic painkillers. On the other hand, recurring episodes or particular kinds of headaches might point to a medical issue. Primary and secondary headaches are frequently separated into two major categories. There is no other cause for a primary headache. A secondary headache, on the other hand, has a different underlying cause, like a head injury or abrupt caffeine withdrawal. Eleven of the most prevalent headache types are examined in this article, along with information on their causes, prevention, treatments, and when to consult a physician.

Headaches are a prevalent problem. According to estimates from the World Health Organization (WHO), about 40% of people worldwide suffer from headache disorders. Across all age groups, headaches rank among the top three most prevalent neurological disorders. Intense throbbing pain on one side of the head is a common symptom of a migraine. A person may become more sensitive to smell, sound, and light. Vomiting and nausea are also frequent. About 25% of migraineurs report having an aura either prior to or during their headache.

Aura symptoms can also be signs of stroke or meningitis. These visual and sensory abnormalities usually last 5 to 60 minutes and include: seeing zigzag lines, flickering lights, or spots; partial loss of vision; numbness; tingling; muscle weakness; difficulty speaking or finding words; and more. If someone is experiencing these for the first time, they should get medical help immediately. Each episode of a migraine headache can last anywhere from a few hours to several days, and they are frequently recurrent. It is a chronic condition for many people.

The precise causes of migraines are not entirely understood by medical professionals. Nonetheless, it frequently runs in families and is more prevalent in those who already have certain medical conditions, like epilepsy and depression. Stress, anxiety, disturbed sleep, hormonal changes, missing meals, dehydration, certain foods and medications, bright lights, and loud noises are all possible migraine triggers.

The severity of the symptoms, their frequency, and whether or not the patient experiences nausea and vomiting are some variables that will affect the course of treatment. Treatment options include: antiemetics, like metoclopramide, to control nausea and vomiting; neurostimulation techniques, like transcranial magnetic stimulation (TMS); non-steroidal anti-inflammatory drugs (NSAIDs), like ibuprofen, naproxen, aspirin, and acetaminophen triptans, like sumatriptan, which need a prescription.

Resting in a quiet, dark area, applying a cold cloth or ice pack to the forehead, and drinking water are other ways to reduce migraine attacks. People who suffer from chronic migraines should consult a healthcare provider about preventive care. If a person experiences an episode for more than 15 days in a month or if symptoms appear at least 8 days a month for three months, they may be diagnosed with chronic migraine. Topiramate (Topamax) and propranolol amitriptyline are medication options for migraine prevention. Acupuncture, stress reduction, and dietary modifications are additional management options to take into account.

Most people experience tension-type headaches occasionally. These primary headaches are the most prevalent kind. According to research, approximately 78% of adults will at some point suffer from a tension-type headache. They start off as a dull, persistent headache on both sides. Additional symptoms may include: headaches lasting 30 minutes to several days; sensitivity to light and sound; a feeling of pressure behind the eyes; and tenderness of the face, head, neck, and shoulders. It’s unclear what specifically causes tension headaches. Nonetheless, common triggers include stress, anxiety, and depression. Dehydration, loud noises, lack of exercise, poor sleep, missing meals, and eye strain are additional possible triggers.

Ibuprofen, acetaminophen, and aspirin are examples of over-the-counter (OTC) painkillers that are typically very effective at halting or reducing pain. People should see a doctor if they have headaches more than 15 days a month, as this could be a sign of chronic headaches. Tension headaches may be avoided with certain treatments and lifestyle modifications. Acupuncture, stress, anxiety, and depression management, regular exercise, stretching, and better sitting and standing posture are a few examples.

Severe and frequent headaches are known as cluster headaches. Males are six times more likely than females to be affected, and they are comparatively rare, affecting 1 in 1000 adults. Cluster headache sufferers report a sharp, piercing pain behind or around one eye. Cluster headaches typically occur suddenly and without warning and last anywhere from 15 minutes to 3 hours. Other symptoms may include watering eyes, swollen eyelids, a runny nose, or sensitivity to light and sound. Up to eight attacks may occur in a single day.

These attacks can last for weeks or months and typically happen in clusters every day. Additionally, they frequently begin at regular times, usually a few hours after going to sleep at night. These symptoms, which occasionally mimic hay fever, should be discussed with a healthcare provider by anyone exhibiting them. Cluster headaches are more common in smokers, though their exact cause is unknown. Alcohol should also be avoided when having an attack.

The goal of treatment is to lessen the attacks’ frequency and intensity. Deep brain stimulation and vagus nerve stimulation also show promise in treating cluster headaches that do not respond to medication. Other options include oxygen therapy, sumatriptan, verapamil steroids, melatonin, and lithium.

The following activities can cause exertional headaches: running, jumping, weightlifting, sexual activity, and coughing or sneezing. These headaches are typically very short-lived, but they can occasionally last up to two days. They are more prevalent in people with a family history of migraine and manifest as throbbing pain throughout the head. When exertional headaches occur for the first time, people should consult a healthcare provider because they may indicate a more serious condition.

OTC pain relievers and beta-blockers, like propranolol and indomethacin, are among the treatments for exertional headaches. Cardiovascular problems can occasionally cause exertional headaches. If so, a medical expert might suggest tests to assess a patient’s cardiovascular and brain health.

A rare condition known as a hypnic headache typically first appears in people in their 50s. It may, however, begin earlier. They are also known as “alarm clock” headaches, and they cause people to wake up in the middle of the night. Mild to moderate throbbing pain, typically on both sides of the head, is the hallmark of a hypnic headache. Along with other symptoms like light and sound sensitivity and nausea, it can last for up to three hours. A person may have multiple attacks in a given week. There are no recognized triggers for hypnic headaches, and their exact cause is unknown. Even though hypnic headaches are usually benign, older adults should consult a doctor if they have any unusual headaches for the first time. A medical practitioner might want to rule out cluster headaches and migraines. Hypnic headaches can be treated with caffeine indomethacin lithium.

Medication-overuse headache A common form of secondary headache is medication-overuse headache (MOH), also referred to as a rebound headache. About 1-2 percent of the general population has them. MOH headaches typically affect those who suffer from tension-type headaches or migraines. MOH headaches usually occur as soon as a person wakes up in the morning. Each person experiences the pain and location differently. Additionally, they might feel queasy, agitated, and have trouble focusing.

Taking medication for headache disorders regularly causes these headaches. However, if a person’s pain is not improving, they might take them more frequently or in greater quantities. If a patient has a headache condition and has taken painkillers for at least 15 days in a month, a doctor may diagnose MOH. NSAIDs like aspirin and ibuprofen, opioids, and acetaminophen-triptans, like sumatriptan, can all result in MOH when they wear off.

Stopping the medication that is causing the headaches is the only way to treat MOH. But anyone who wants to stop taking medication should only do so under a doctor’s supervision. To facilitate the withdrawal process, they can offer alternative medication prescriptions and assistance in creating a plan. The following symptoms are likely to occur after stopping the drug: worsened headaches, nausea, vomiting, elevated heart rate, low blood pressure, sleep disturbance, restlessness, anxiety, and nervousness.

A doctor may prescribe antiemetics or other medications to help manage nausea and vomiting. Although they can linger for up to four weeks, the symptoms typically last two to ten days. After a MOH is resolved, a medical expert will provide advice on appropriate painkillers to take. MOH can be avoided by limiting the use of painkillers for headaches, avoiding codeine and opioids, and taking preventive medication for chronic migraines.

Sinus headaches Sinusitis, or inflammation of the sinuses, is the cause of sinus headaches. Usually, an allergy or infection is the cause. A dull, throbbing ache around the eyes, cheeks, and forehead is one of the symptoms. Movement or straining may make the pain worse, and it occasionally spreads to the jaw and teeth. Facial pressure or pain, decreased sense of smell, nasal discharge, a blocked nose, fever, exhaustion, poor breath, coughing, dental pain, and a general feeling of being ill are some additional possible symptoms. Seldom do sinus headaches occur. This type of headache is more likely to be a migraine episode if there are no nasal symptoms.

Usually, sinusitis goes away on its own in four weeks. OTC pain relievers, salt water nasal sprays or solutions from the pharmacy, antihistamines, steroid nasal sprays, available with a prescription, antibiotics, rest, and fluids, and if there is a bacterial infection, people should consult a healthcare provider if symptoms worsen or do not go away after three weeks. A medical practitioner may recommend a patient to an ear, nose, and throat specialist to determine the underlying cause of sinusitis. To clear the sinuses, minor surgery might be required in certain situations. Avoiding smoking and other known allergens or triggers is one way to prevent sinusitis.

Headaches can occasionally result from consuming four cups of coffee a day, or more than 400 milligrams (mg) of caffeine. Withdrawal symptoms may include migraine-like headaches in those who have consumed more than 200 mg of caffeine per day for more than two weeks. These usually appear 12 to 24 hours following an abrupt cessation of caffeine use. They can last for 2 to 9 days and peak between 20 and 51 hours. The effects of caffeine vary from person to person, but cutting back on intake may lower the risk of headaches. Other potential symptoms include fatigue, difficulty concentrating, decreased mood or irritability, and nausea. Reducing caffeine intake may also benefit those who suffer from persistent migraines.

Headache After a Head Injury Sometimes a person experiences a headache right after or shortly after a head injury. This is frequently resolved by OTC pain relief. However, a person should get medical help right away if their symptoms are severe or get worse over time. In the event of a severe head injury or if any of the following symptoms appear after a head injury: unconsciousness, seizures, vomiting, memory loss, confusion, vision, or hearing issues, always call an ambulance. Post-traumatic headaches can also appear months after the initial head injury, making diagnosis challenging. They can last for up to a year and occasionally happen every day. Traumatic brain injury can occur from even minor head trauma.

Menstrual Headaches: The origin of such headaches is predominantly associated with shifts in hormone levels. During the menstrual cycle, migraines may manifest due to alterations in estrogen levels. In the pre-menstrual and post-menstrual phases, or during ovulation, hormone-related headaches typically manifest, with symptoms akin to migraines without an aura, although these may persist for a prolonged duration.

A throbbing headache the next day or even later that day can result from consuming too much alcohol. Both sides of the head typically experience these migraine-like headaches, which can get worse with movement. Symptoms of a hangover headache include light sensitivity and nausea. Hangovers cannot be cured, but they can be lessened by eating sugary foods and drinking lots of water. Over-the-counter pain relievers may lessen or eliminate headaches. Hangover symptoms usually disappear in 72 hours. Drinking in moderation, avoiding empty stomachs, and drinking water before bed and in between alcoholic beverages are all strategies to lower the chance of getting a hangover.

How to understand chronic pain

How to understand chronic pain

In recent years, chronic pain has gained recognition as a medical condition in and of itself. This is because chronic pain is a disease process that is so complicated that we are only now beginning to understand what triggers it. However, what does it feel like to live with chronic pain, and how does the body and brain cope with it? Some of the terms people frequently use to describe their pain include dull, aching, gnawing, burning, sharp, shooting, and piercing.

Imagine having to deal with some of this every day until you have no idea what it’s like to go about your day without this constant pain that gradually saps your physical and mental stamina. For many people who suffer from chronic pain, that is their reality. It could be an internal struggle concealed behind gritted teeth and fake smiles, and some days might be fantastic and some days awful. However, how does chronic pain become, well, chronic? In the most recent episode of our Pain Awareness Month-themed In Conversation podcast, Medical News Today delves into the science of chronic pain with Dr. Tony L. and Hilary Guite. As Joel Nelson, a longtime patient and advocate for psoriatic disease and arthritis talks about his own experience with pain.

Because chronic pain is not life-threatening, it is frequently disregarded as merely a symptom of a more serious issue or not given the attention it deserves. Chronic pain, however, has a social as well as a personal cost. According to studies, individuals who experience chronic pain may find it difficult to carry out daily tasks and activities and may also have worse general health. Chronic pain sufferers may also experience unemployment or unstable employment. Chronic pain was not recognized or diagnosed until 2018 when the International Classification of Diseases (ICD) assigned it a code in the draft version of the new ICD-11 coding system. Chronic primary pain and chronic secondary pain are the two new classifications of chronic pain made by the World Health Organization (WHO).

According to this classification, primary pain is defined as pain that cannot be attributed to or explained by another medical condition. Fibromyalgia and persistent primary low back pain are a couple of examples. A widespread pain disorder that affects at least four to five body parts and lasts for at least three months, but typically longer, fibromyalgia varies from person to person. Since there is no other explanation for the pain, Dr. Dot Guite clarified that it is a form of primary chronic pain. Conversely, secondary pain results from or is a result of an underlying medical condition. This would include pain from ulcerative colitis, cancer, or arthritis.

I began experiencing chronic pain when I was ten years old. And ever since, Joel Nelson told MNT’s In Conversation, “Chronic pain has kind of been an intermittent part of my life right up until the present day.”. Joel, who is currently 38 years old, has experienced chronic pain for several decades. My first encounter with pain was when I felt a burning sensation in my hip that resembled gravel. And it just got worse the more I used the joint; eventually, he said, I was losing some of my mobility. At that point, like most people do, he made the decision to ask for assistance. Joel claimed that noise is the best way to characterize his ongoing pain. I have always referred to it as noise because, on the days when the pain is severe, I simply lose the capacity to take in additional information and manage several tasks at once, he said.

In light of my current condition, I believe that the experience’s fluidity is its most significant lesson. In the end, my mobility and limits can vary from anything to the point where I can do more than just walk, and I might be able to run and cycle a little bit like I do now, to possibly needing crutches again the following week. Pain dictates a lot of that. I get a lot of stiffness in the mornings from arthritis, but the pain is what keeps me from doing things. Joel said it’s difficult to predict what will happen next with his chronic pain, likening it to a series of chapters. Researchers have discovered that a gateway receptor known as Toll-like receptor 4 (TLR4) may be a governing factor behind the development of chronic pain from acute pain.

We are aware that signaling that is typically linked to what is known as innate immunity can be activated in response to various types of tissue or nerve damage. And the toll-like receptor is one of the mediators of that. It turns out that although those receptors are typically present to detect the presence of foreign bugs, like E. coli, those insects contain a substance known as lipopolysaccharide, or LPS, in their cell membrane. According to Dr. Dot Yaksh, bacteria are the source of that, which is not typically present in our system. You don’t need to acquire it; you are born with it. It is constantly present. Over the past few years, we’ve discovered that your body releases a variety of substances that will activate those same toll-like receptors, he continued.

The central immune system may be primed for elevated pain states by toll-like receptors. The body begins to release products from inflammatory cells in response to damaging stimuli, stressors, or tissue damage, particularly in the gastrointestinal tract or microbiome. According to him, when this occurs, the products that are expelled from our bodies can activate toll-like receptors. One such receptor is called TLR4, and it is found on both sensory neurons and inflammatory cells. Dr. According to Yaksh, TLR4 activation makes the nervous system more reactive but doesn’t actually cause as much pain. In addition to this priming, Dr. Dot Guite noted that if additional stressors are present at the time, such as poor diet or psychological distress, this can trigger a series of events that can accelerate the transition to chronic pain.

TLR4 activation initiates a cascade, a series of events that will result in increased expression of numerous receptors and channels capable of enhancing the system’s response. When this occurs, the initial tissue damage is followed by this improved response. It only makes the system more reactive; it doesn’t really cause the pain condition. According to him, Joel’s circumstances are consistent with the idea that people can experience different kinds of pain. That can be made worse by “psychological” stressors, which can intensify a pain state that may actually have a physiological component that we don’t fully comprehend, he continued.

Dr. Yaksh, for instance, proposed that Joel’s condition was likely made worse by the stress (and joy) of becoming a father and all the other factors involved, making it more difficult to manage the pain. He emphasized that this did not lessen the reality of the pain. The transition from one state to another, which we refer to as an acute to chronic transition or the chronification of the pain state, was established by Joel’s pain condition, the events that were connected to the psoriatic diagnosis, and other factors, he explained. I believe that there was likely a very strong, emotional component to his situation.