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5 Minutes Read

What Happens in Early Neurodegeneration?

neurodegeneration

Early neurodegeneration—seen in conditions like brain fog, mild cognitive impairment (MCI), and the early stages of Alzheimer’s disease—is often a silent process that begins long before any diagnosis. But there are recognizable biological signatures that can signal the brain is under stress:

  • Impaired glucose metabolism in the brain: This is one of the earliest and most persistent features of Alzheimer's disease. Sometimes called “Type 3 diabetes,” this reflects the brain’s growing inability to use glucose effectively as fuel.

  • Mitochondrial dysfunction and oxidative stress: Mitochondria, the energy producers in our cells, begin to falter. This leads to less efficient energy production and increased free radicals that can damage brain tissue.

  • Chronic neuroinflammation: Inflammatory molecules and activated immune cells (microglia) create a “low-grade fire” in the brain, which contributes to degeneration over time.

  • Accumulation of misfolded proteins: Proteins like beta-amyloid and tau begin to clump abnormally, disrupting neuron function and connectivity.

  • Breakdown of the blood-brain barrier (BBB): This vital filter becomes "leaky," allowing harmful molecules into the brain and making it harder for the brain to clear toxins.

Together, these issues create a cascade that erodes memory, slows processing speed, impacts mood, and impairs focus—often years before a formal diagnosis is made.


🔁 Intermittent Fasting to the Rescue

Intermittent fasting (IF) is far more than a weight-loss tool. It offers a powerful metabolic and neurological reset that directly targets many of the early changes seen in neurodegeneration. When done intentionally, fasting allows the brain to enter a state of repair, regeneration, and metabolic renewal.


🔬 1. Improves Brain Energy Metabolism

One of the most immediate and powerful benefits of fasting is the shift from glucose dependence to ketone utilization.

  • Ketones (especially beta-hydroxybutyrate, or BHB) are a clean-burning fuel that bypasses insulin pathways and provides energy to the brain—even when glucose uptake is impaired.

  • The inflamed or aging brain often resists glucose but remains receptive to ketones, making fasting and ketogenic strategies especially helpful in cognitive decline.

  • Ketone metabolism reduces oxidative stress compared to glucose and supports brain cells more efficiently during metabolic stress.

🧠 Clinical Insight: Studies show that early-stage Alzheimer's patients often experience clearer thinking and improved memory on ketogenic diets or fasting protocols that elevate ketone levels.


🧽 2. Activates Autophagy: The Brain’s Detox Mechanism

Autophagy—literally “self-eating”—is your body’s housekeeping service, and fasting is its most potent trigger.

  • It clears out misfolded proteins like amyloid-beta and tau, both heavily implicated in Alzheimer’s disease.

  • It helps remove damaged mitochondria that are no longer functioning optimally, improving cellular efficiency.

  • It sweeps up toxic cellular debris, reducing inflammatory load and freeing neurons to operate more effectively.

Think of it as a neurological "decluttering"—akin to Marie Kondo cleaning out the attic of your brain. This inner cleanse makes room for new synaptic growth and better communication between brain cells.


🔥 3. Reduces Neuroinflammation

Chronic inflammation is one of the quietest yet most damaging contributors to cognitive decline. Fasting acts as a potent anti-inflammatory intervention by:

  • Decreasing inflammatory cytokines, such as IL-6 and TNF-alpha, which are elevated in neurodegeneration.

  • Inhibiting the NLRP3 inflammasome, a cellular danger-sensor that, when overactive, drives much of the brain’s inflammatory response.

  • Boosting anti-inflammatory molecules like adiponectin, which play a protective role.

This helps calm the brain’s overactive immune cells (microglia) and reduces further injury to the blood-brain barrier.


🌿 4. Boosts Brain-Derived Neurotrophic Factor (BDNF)

BDNF is a critical molecule for brain health, acting as a growth hormone for neurons.

  • It promotes neurogenesis (the formation of new neurons) and helps repair damaged ones.

  • It improves synaptic plasticity, which underlies learning and memory.

  • It’s especially active in the hippocampus, the brain’s memory center.

Low BDNF is associated with depression, Alzheimer’s, and sluggish cognitive function. Fasting has been shown to naturally increase BDNF levels—offering a drug-free way to stimulate your brain’s growth and repair pathways.


⚡ 5. Enhances Mitochondrial Function

When mitochondria falter, so does your brain. Fasting promotes mitochondrial biogenesis, the creation of new and more efficient mitochondria.

  • This leads to better ATP production—energy the brain can use.

  • It also reduces free radical production, protecting brain tissue from oxidative stress.

  • Stronger mitochondria mean more cellular resilience and slower progression of neurodegenerative processes.

This revitalization of the brain’s energy systems is foundational for restoring cognitive clarity.


🧬 6. Supports Insulin Sensitivity in the Brain

Insulin resistance doesn’t just affect the body—it affects the brain, too. In fact, insulin resistance in the brain is a hallmark of Alzheimer’s.

Fasting helps reverse this by:

  • Lowering basal insulin levels, reducing inflammation and metabolic stress.

  • Improving insulin receptor sensitivity, which means the brain can better access nutrients.

  • Reducing glycotoxicity, or sugar-related damage to neurons, which is especially important in slowing cognitive decline.

The result? Enhanced mental clarity, stabilized mood, and improved long-term brain health.


📊 Summary: How Intermittent Fasting Reverses Early Cognitive Decline

Fasting Benefit

Impact on Brain Health

✅ Ketones for Fuel

Bypasses glucose deficits to fuel neurons cleanly

✅ Autophagy

Clears out toxic proteins and cellular debris

✅ Inflammation Reduction

Calms neuroinflammation and supports BBB integrity

✅ More BDNF

Rewires the brain, improving mood and memory

✅ Mitochondrial Enhancement

Powers up sluggish neurons for better performance

✅ Insulin Sensitivity

Restores metabolic balance and protects against dementia


💡 How to Start (Safely)

Intermittent fasting is powerful—but it must be approached with care, especially for women and those with thyroid or adrenal concerns.

🕒 Start with:

  • A 14:10 or 12:12 fasting window

  • Use a circadian-aligned eating pattern (daylight eating)

  • Focus on nutrient-dense, anti-inflammatory meals

  • Stay hydrated with electrolytes and minerals

  • Avoid fasting on high-stress or poor-sleep days

If you feel lightheaded, anxious, or extremely fatigued—ease back. Healing the brain is a marathon, not a sprint.


🧠 Final Thought: Fasting as Neurological Rehab

Fasting isn’t just about burning fat—it’s a precision tool for metabolic and cognitive restoration. In the earliest stages of neurodegeneration, fasting creates a metabolic environment where the brain can repair, detoxify, and even regrow. It empowers your biology to fight back—clearing space, calming inflammation, and restoring mitochondrial energy.

With proper guidance, intermittent fasting can serve as a potent and personalized form of neurological rehabilitation, giving your brain what it needs most: time, space, and metabolic clarity.  If you need more information on fasting, reach out to Kim Larson at larsonhelathweightloss.com.  I am a certified Fasting FLAG coach.

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10.29.2025

Salt, Sodium, and Blood Pressure: Why the Real Story Is More About Insulin and Metabolic Health

From Villain to Vital NutrientFor decades, sodium was portrayed as a dietary villain blamed for high blood pressure and heart disease. Public health campaigns urged us to avoid salt. Yet modern science reveals a more nuanced truth. Sodium is essential—vital for fluid balance, muscle contraction, and nerve signaling. Too little is as dangerous as too much. Meanwhile, emerging evidence reveals that the real driver of hypertension isn’t sodium alone—it’s insulin resistance, poor potassium intake, and metabolic dysfunction.The Origins of the “Salt = Hypertension” MythThe notion of “salt causes hypertension” traces back to animal studies by Dahl in the 1970s, where high sodium raised blood pressure in salt-sensitive rats. Human data followed, leading to generalized anti-sodium recommendations.Salt sensitivity actually applies to a subset of people—estimated at 25–50%; many individuals exhibit minimal blood pressure changes regardless of sodium intake (salt-resistant) .Large observational studies like PURE (Prospective Urban Rural Epidemiology) found a J-shaped curve: very high sodium was harmful, but so was very low sodium intake. Cardiovascular risk was lowest in moderate intake ranges .Individual variability matters—kidney function, age, insulin resistance, and genetics significantly modify how sodium affects you.So, the blanket statement “salt causes hypertension” is outdated and overly simplistic.Insulin Resistance: The Hidden Driver of Sodium RetentionInsulin controls how your kidneys handle sodium. In hyperinsulinemia states, the kidneys retain more sodium, increasing blood volume and pressure .Additionally, insulin may activate the sympathetic nervous system, tightening blood vessels and further raising blood pressure .This implies many with hypertension are “insulin-sensitive” rather than “salt-sensitive.” Addressing insulin sensitivity—with diet, movement, sleep, and stress reduction—can impact blood pressure independently of sodium intake.Sodium + Potassium: The Balancing ActPotassium counters sodium. It helps the kidneys excrete excess sodium and relaxes blood vessels. Diets low in potassium, which are common in the Western diet, worsen sodium’s effects on blood pressure .Traditional diets rich in fruits, vegetables, beans, and tubers naturally provide this balance.The DASH diet (Dietary Approaches to Stop Hypertension) lowers blood pressure in part by emphasizing potassium-rich foods—even without extreme sodium restriction.How Much Sodium Do We Really Need?General Guidelines (Non-Training Days)The AHA recommends up to 2,300 mg/day (≈1 tsp salt), aiming toward 1,500 mg/day for those with hypertension .The PURE study suggests lowest cardiovascular risk with 3,000–5,000 mg/day, depending on potassium and metabolic health .Training Days / AthletesSweat can lose 500–2,000 mg sodium per liter. Endurance athletes, especially in heat, may need 3,500–5,500 mg/day or more.Guidance:90 min intense/hot: ~500–1,000 mg sodium/hour.Signs You’re Getting It WrongToo little sodium (relative to need):Dizziness, headaches, muscle crampsBrain fog, fatigue, nauseaFrequent urination with very clear urineIn extreme cases: hyponatremia—an emergencyToo much sodium (chronically):Elevated blood pressure in salt-sensitive individualsBloating, swelling (hands, ankles)Constant thirstThe Type of Salt Matters (But Not As Much As You Think)Your body cares about sodium, not crystal color—but the form of salt has context:Iodized table salt: Adds iodine (essential for thyroid health).Sea salt / Himalayan pink salt: Trace minerals present but negligible nutrition-wise; sodium per gram nearly identical to table salt.Kosher salt: Larger crystals, great for cooking; often lacks iodine.Electrolyte salts: Blend sodium with potassium and magnesium—useful for athletes and hot training days.Specialty salts may taste or look different, but they don’t alter sodium’s effect on blood pressure or physiology.Smarter Sodium StrategiesSalt whole foods—not processed ones. 70–80% of dietary sodium comes from packaged and restaurant foods, not your shaker.Boost potassium. Incorporate avocado, beans, leafy greens, yogurt, and squash.Control insulin. Prioritize exercise, protein-forward whole foods, sleep, and stress management for better sodium handling.Use the right salt for your iodine needs. If seafood isn’t in your diet, iodized salt is important.Personalize intake. Monitor blood pressure at home over 2–4 weeks as you adjust sodium and lifestyle.Sample Day FrameworksBalanced Rest DaySodium Targets & Strategy ~2,000 mg sodium totalBreakfastGreek yogurt + salted pumpkin seeds (~250 mg)LunchChicken salad with olives, feta, vinaigrette (~600 mg)SnackCottage cheese with cucumber (~400 mg)DinnerSalmon, roasted potatoes, green beans, pinch of sea salt (~750 mg)Hot Training Day~3,500 mg sodium totalPre-WorkoutWater + pinch of salt + half a banana (~200 mg)During TrainingElectrolyte drink (~1,000 mg sodium total)Post-Workout MealRice bowl with steak, salsa, avocado (~900 mg)DinnerSoupy stew with chicken and vegetables (~1,000 mg)SnacksPickles/olives if craving salt (~400 mg)FAQsQ: Does salt cause high blood pressure in everyone? No. Only 25–50% are salt-sensitive; insulin resistance, age, and low potassium often play larger roles .Q: Should I avoid all processed foods? Not necessarily—but since most sodium comes from processed sources, cooking at home gives you control.Q: Is Himalayan salt healthier? Not for sodium content. Its trace minerals are negligible. If iodized salt isn’t used, ensure iodine from seafood or dairy .The TakeawaySodium is essential, not evil.Insulin resistance and low potassium drive hypertension more than salt alone.Most people do well with 2,000–3,500 mg/day, though athletes and hot-weather exercisers may need more.Personalization beats one-size-fits-all.Prioritize whole foods, metabolic health, and mindful sodium intake.ReferencesSalt sensitivity estimates and individual variation in blood pressure responsePURE study findings on J-shaped sodium-risk curveInsulin’s effect on renal sodium retentionInsulin, sympathetic activation, and blood pressurePotassium’s sodium-excretion effect and guidelinesAHA sodium intake recommendationsNIH iodine guidelines for iodized saltSodium sources — processed vs home-cooked (widely reported estimates) …and based on prior evidence and dietary surveys.

10.16.2025

Understanding SIBO: How It Starts and How to Reverse Its Effects

Small Intestinal Bacterial Overgrowth (SIBO) is a condition where bacteria from the colon overpopulate the small intestine, leading to bloating, gas, malnutrition, and a host of frustrating symptoms.1. What is SIBO—and How Does It Begin?The small intestine typically has very few bacteria, thanks to protective mechanisms like stomach acid, bile, digestive enzymes, and intestinal motility. But when these systems break down, bacteria can thrive where they shouldn’t.Protective barriers include gastric acid, bile, digestive enzymes, the migrating motor complex (MMC), intact ileocecal valve, and immune defenses (e.g., secretory IgA) PMC+15NCBI+15Dr Stavy Nikitopoulou+15.When they fail—due to low stomach acid, enzyme insufficiency, anatomical changes, autoimmune conditions, hypothyroidism, diabetes, scleroderma, IBS, or post-infectious gut damage—SIBO can take hold NCBI.Other common triggers include prior food poisoning, medication use (like PPIs or painkillers), and structural issues like surgeries or fistulas Health.2. Common Symptoms & Diagnostic ChallengesPatients with SIBO often experience:Bloating, abdominal pain, diarrhea or constipation, and nutrient malabsorption IFN Academy+15PubMed+15stevegranthealth.com+15Health.Nutrient deficiencies—particularly in iron, B12, folate, fat-soluble vitamins A, D, and E—due to impaired absorption EatingWell+1.Extraintestinal symptoms like fatigue, brain fog, and skin conditions (e.g., rosacea) EatingWell.Diagnosing SIBO is not straightforward. While the jejunal aspirate culture is the gold standard (detecting >10^5 bacteria/mL), it’s invasive and often impractical PMC+12Wikipedia+12Health+12. Instead, breath tests measuring hydrogen and methane are commonly used, though they come with false positives and variability Verywell Health+2Wikipedia+2.3. Reversing SIBO—A Functional Medicine BlueprintRoot-Cause HealingThe functional medicine approach looks beyond symptoms to heal underlying causes:Evaluate triggers like digestive motility issues, immune dysfunction, enzyme insufficiency, dysbiosis, or structural dysfunctions functional-medicine.associates+7PubMed+7thechi.ca+7stevegranthealth.com+1.Treating the underlying cause—not just the symptoms—is essential for long-term resolution PMCPubMed.Clinical & Therapeutic StrategiesEradicate OvergrowthAntibiotics: Rifaximin is often preferred; neomycin may be used for methane-predominant cases PMC+1.Herbal antimicrobials: Emerging evidence indicates they can be as effective as rifaximin The Institute for Functional Medicine+1.Dietary InterventionsLow-FODMAP diet can reduce fermentation and symptoms—but isn’t meant for long-term use due to potential negative effects on gut microbiome diversity WikipediaVerywell Health.Elemental diet (a pre-digested liquid formula) can starve bacteria while nourishing the body—shown to normalize breath tests in up to ~85% of cases over 14–21 days Wikipedia.Supportive TherapiesProkinetics to restore MMC function and prevent recurrence Wikipedia+1.Targeted supplementation for underlying deficiencies (like B12, iron, or fat-soluble vitamins) Health+1.Probiotics: Can be effective when timed appropriately—e.g., Lactobacillus strains post-antibiotic therapy PMC+3Wikipedia+3Health+3.Functional Medicine Clinical ModelIdentify the root cause (motility, acid/enzyme function, immune, structural).Eradicate the microbial overgrowth using herbal or pharmaceutical interventions.Rebuild and rebalance gut health with nutrition, prokinetics, nutrients, and microbiome support.Monitor and prevent recurrence with periodic re-evaluation and maintenance strategies Wikipedia+10NCBI+10Rupa Health+10PMC+4PubMed+4EatingWell+4.4. Why Functional Medicine Delivers ResultsUnlike single-solution strategies, this approach:Addresses multiple layers—digestion, motility, immune function, gut microbiota, and structural health.Seeks long-term remission by fixing root causes, not just suppressing overgrowths.Uses rotation of therapies (diet, elemental, antimicrobials, prokinetics) to minimize recurrence risk EatingWell+5NCBI+5Wikipedia+5. Supplements for SIBO Recovery1. Antimicrobial Phase (Eradicating Overgrowth)(Typically 4–8 weeks, guided by a practitioner)Herbal antimicrobials (shown in studies to be as effective as rifaximin):Oregano oil (enteric-coated) – broad spectrum antimicrobial【PubMed: PMID 24891990】Berberine (from goldenseal/barberry) – antibacterial, antifungal, anti-inflammatory【PubMed: PMID 33274096】Neem – supports bacterial balance, especially methane SIBOGarlic extract (allicin) – targeted against methane-producing archaea【PubMed: PMID 16842559】Caution: These are potent — best rotated or combined under guidance to prevent resistance and minimize die-off symptoms (Herxheimer reaction).2. Motility & Prevention (Keeping the Gut Moving)(Supports the Migrating Motor Complex, MMC — prevents relapse)Prokinetics (usually at night, after antimicrobial phase):Ginger extract (1–2 g/day) — stimulates gastric emptying5-HTP or low-dose melatonin — modulates serotonin, improves motilityIberogast (herbal blend) — clinically shown to support MMC function【PubMed: PMID 15836424】Optional: prescription prokinetics (prucalopride, low-dose erythromycin) if natural support isn’t enough.3. Gut Lining Repair (Reduce Inflammation, Support Absorption)(Rebuilds the intestinal barrier after bacterial damage)L-Glutamine (5–10 g/day) — primary fuel for enterocytes, reduces permeability【PubMed: PMID 26447961】Zinc carnosine — promotes mucosal healing【PubMed: PMID 23028914】Collagen peptides or bone broth — provide glycine and proline for gut repairAloe vera extract or slippery elm/marshmallow root — soothing botanicals for irritated mucosa4. Rebalancing the Microbiome(Usually added after antimicrobials, otherwise may worsen symptoms)ProbioticsSoil-based strains (Bacillus species) are better tolerated early onLactobacillus & Bifidobacterium blends can be reintroduced laterSome studies show probiotics may improve breath test results and symptoms post-treatment【PubMed: PMID 28708949Prebiotics: Introduce slowly (e.g., partially hydrolyzed guar gum, PHGG) to support long-term microbiome diversity once stable5. Nutrient Repletion (Fixing Deficiencies Caused by SIBO)Because SIBO often leads to malabsorption:B12 (methylcobalamin or injections if deficient)Iron (if ferritin

10.15.2025

Cannabis & Your Brain: What the New Landmark Study Really Shows Published evidence (Feb 2025) has a lot of people talking: a large, carefully analyzed brain-imaging study reports that heavy cannabis use is linked with reduced brain activation during w

Published evidence (Feb 2025) has a lot of people talking: a large, carefully analyzed brain-imaging study reports that heavy cannabis use is linked with reduced brain activation during working-memory tasks—the kind of mental work you rely on to hold instructions in mind, follow a conversation, do mental math, or safely navigate a busy road. JAMA NetworkBelow, I’ll break down what the study did, what it found (and didn’t), what it may mean for women and young adults, and smart, practical takeaways you can use today.Key Takeaways (in plain English)In 1,003 young adults (ages 22–36), people who had used cannabis more than 1,000 times in their life (the study’s “heavy use” group) showed lower activation in key brain regions while doing working-memory tasks—even after excluding those who had recently used. JAMA NetworkMedia and university summaries note that about 63% of heavy lifetime users and about 68% of recent users showed reduced brain activity on the working-memory task. CU Anschutz NewsThe affected regions included the dorsolateral and dorsomedial prefrontal cortex and the anterior insula—areas that help you concentrate, plan, regulate emotions, and make decisions. These regions are dense in CB1 cannabinoid receptors, which THC binds to. JAMA NetworkCausation isn’t proven (the study is cross-sectional), and most other cognitive tasks in the study didn’t meet the strictest statistical threshold. Still, the working-memory result was robust after multiple-comparison corrections. JAMA NetworkRecent use was linked to poorer performance on several tasks (including working memory), and residual cognitive effects from cannabis can persist for 2–4 weeks after stopping—important if you’re about to take an exam, drive long distances, or do high-stakes work. JAMA NetworkWhat Makes This Study “Landmark”?Size & rigor. The research analyzed 1,003 young adults from the Human Connectome Project, using standardized fMRI tasks across seven cognitive domains (working memory, language, reward, motor, emotion, relational reasoning, theory of mind). It measured both lifetime exposure and recent use (via urine toxicology the day of scanning). Analyses adjusted for age, sex, education, income, alcohol, and nicotine. JAMA NetworkClear exposure groups. Participants were classified as heavy (>1,000 lifetime uses), moderate (10–999 uses), and non-users (1,000 uses” is self-reported; still, urine toxicology confirmed recent exposure status. JAMA NetworkAge window: Results in 22–36-year-olds may not generalize to older adults or teens. JAMA NetworkTask specificity: Working memory effects were strongest; other tasks didn’t meet strict thresholds after correction. JAMA NetworkPractical Guidance If You (or Your Teens) Use CannabisThis section is informational and not medical advice.Protect your working memory window. If you must perform cognitively demanding tasks (exams, major presentations, meticulous driving/navigation, high-risk jobs), abstain well in advance—think weeks, not days, especially if you’re a frequent user. JAMA NetworkWatch frequency & potency. The “heavy” pattern (>1,000 lifetime uses) is where the strongest association showed up. Higher-THC products likely increase risk; titrate down or take structured breaks if you choose to use. JAMA NetworkBe extra cautious if you’re under 25. With brains still developing, err on the side of less—and seek healthier sleep/anxiety strategies first (breathwork, morning light exposure, resistance training, omega-3-rich meals, magnesium glycinate as appropriate). National Institute on Drug AbuseFlag red-flags for psychosis risk. Family history of psychosis, early heavy use, and high-potency THC raise risk signals. Seek professional guidance; products with lower THC and/or higher CBD may reduce some risks, but this is not a guarantee. PMC Cycle breaks intentionally. If you’re a regular user, plan tolerance breaks and monitor cognition (focus, memory, task follow-through) during and after a 2–4 week pause. JAMA NetworkFor Women: Any Sex-Specific Data?In this dataset, the working-memory association didn’t differ by sex, although there was a sex interaction on a motor task (recent THC linked with lower activation in men, not women—one dataset, not definitive). We need female-focused studies on dose, hormones, and cycle phase to tailor guidance better. JAMA NetworkThe Bottom LineThe strongest, most conservative signal from the new large study is that heavy, long-term cannabis use is associated with dampened brain activation during working memory, centered in prefrontal and insula circuits. That’s the exact network you need for day-to-day mental performance. JAMA NetworkRecent use can also blunt performance—sometimes for weeks after stopping—so timing matters for safety and productivity. JAMA NetworkNot all cannabis exposure is equal: dose, frequency, age, THC potency, and product type likely determine risk. Some medical-use cohorts don’t show the same neural changes, underscoring the need for personalized, cautious approaches. PMC Sources & Further ReadingPrimary study (Feb 2025): JAMA Network Open—Brain Function Outcomes of Recent and Lifetime Cannabis Use (Human Connectome Project analysis). JAMA NetworkCU Anschutz news release (summary with percentages). CU Anschutz NewsJAMA Psychiatry (June 2025): Convergence of Cannabis and Psychosis on the Dopamine System (midbrain dopamine signal changes in cannabis use disorder). PMC NIH/NIDA (Dec 2024): Brain structure differences tied to early substance use risk in adolescents (pre-existing vulnerabilities). National Institute on Drug Abuse Journal of Alzheimer’s Disease (2016): SPECT perfusion work noting reduced hippocampal blood flow in cannabis users (context for Amen’s earlier findings). Journal of Alzheimer's Disease JAMA Network Open (2024): Year-long medical cannabis use cohort—no significant changes in working memory/reward/inhibitory control activation (dose/formulation/age matter). PMC

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