Understanding Plantar Fasciitis: Foot Pain Causes, Treatment, and Prevention

As a physician, I often see patients who struggle with foot pain, especially in the heel. One of the most common culprits is plantar fasciitis, a condition that affects people of all ages but is especially noticeable among those who are on their feet a lot, athletes, and individuals with certain risk factors. Let’s break down what it is, what causes it, how it’s treated, and—most importantly—how you can prevent it.

The Plantar Fascia is a tough band of muscles and tendons on the bottom (Plantar Aspect) of the Foot

What Is Plantar Fasciitis and Why does it Cause Foot Pain?

The plantar fascia is a thick band of tissue that runs along the bottom of your foot, connecting your heel bone to your toes. Its job is to support the arch of your foot and absorb shock when you walk or run. When this tissue becomes irritated or inflamed, it leads to plantar fasciitis. The hallmark symptom is sharp heel and foot pain, especially when taking the first steps in the morning or after sitting for a while.

The plantar fascia is a tough band of tissue that stretches from the forefoot to the heel, and is responsible for maintenance of arch integrity.

Causes and Risk Factors

Plantar fasciitis usually develops from repeated stress on the plantar fascia. Several factors increase the likelihood of developing it:

• Foot mechanics: Flat feet, high arches, or an abnormal walking pattern can place extra stress on the fascia.

• Overuse: Long-distance running, dancing, or prolonged standing can strain the heel.

• Improper footwear: Shoes without proper arch support or cushioning can worsen the problem.

• Age and weight: It’s more common in people between ages 40–60 and in those carrying excess weight, which increases pressure on the fore-foot.

The Plantar Fascia is under maximal tension when weight is on the forefoot.

Due to persistent mechanical stress resulting from prolonged walking, standing and stretching, the plantar fascia withstands remarkable mechanical challenges during routine activity.  As a result of microtrauma subsequent to jumping, jogging, and running, the plantar fascia can develop small areas where it is torn from the attachment on the heel. Foot and Hell Pain are a direct result.

Symptoms

The classic sign is a sharp, stabbing pain at the bottom of the heel. The pain is usually worse in the morning or after periods of rest, but may improve with movement. Over time, the discomfort can become constant if untreated.

The pain of plantar fasciitis is usually stabbing or burning pain in nature,  usually worse in the morning.  The pain seems to be worse when your feet hit the floor after sleep, and the pain eases with motion and mobility. The pain will come and go, worse with certain types of shoes and with pressure on localized areas.

Treatment Options

The good news is that most cases of plantar fasciitis improve with conservative treatment:

1. Rest and activity modification: Reducing high-impact activities gives the fascia time to heal.

2. Ice and anti-inflammatory measures: Applying ice or taking non-steroidal anti-inflammatory drugs (NSAIDs) can reduce pain and swelling.

3. Stretching and physical therapy: Gentle calf stretches, plantar fascia stretches, and strengthening exercises for the foot and ankle can help.

4. Supportive footwear and orthotics: Shoes with good arch support, cushioned soles, or custom orthotic inserts take stress off the fascia.

5. Night splints: Wearing a splint that keeps the foot flexed overnight can stretch the fascia and lessen morning pain.

   
   

In more severe or persistent cases, other treatments such as steroid injections, shockwave therapy, or surgery may be considered, but these are reserved for people who do not respond to conservative measures.

Prevention Strategies

Preventing plantar fasciitis often comes down to protecting your feet from stress:

• Wear shoes with good cushioning and arch support.

• Replace athletic shoes regularly, especially if you run or walk often.

• Stretch your calves and feet before and after exercise.

• Maintain a healthy weight to reduce pressure on your feet.

• Avoid walking barefoot on hard surfaces for prolonged periods.

• 
  

Final Thoughts

Plantar fasciitis can be frustrating, but with the right approach, it is manageable and often curable without invasive treatment. By paying attention to your footwear, body mechanics, and activity habits, you can both recover from plantar fasciitis and reduce the risk of it coming back.

References

1. Buchbinder R. Plantar fasciitis. N Engl J Med. 2004;350(21):2159-2166.

2. Riddle DL, Schappert SM. Volume of ambulatory care visits and patterns of care for patients diagnosed with plantar fasciitis. Foot Ankle Int. 2004;25(5):303-310.

3. League AC. Current concepts review: plantar fasciitis. Foot Ankle Int. 2008;29(3):358-366.

4. Cutts S, Obi N, Pasapula C, Chan W. Plantar fasciitis. Ann R Coll Surg Engl. 2012;94(8):539-542.

5. Martin RL, Irrgang JJ, Conti SF. Outcome study of subjects with insertional plantar fasciitis. Foot Ankle Int. 1998;19(12):803-811.

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician

GLP-1 Medications and Dementia Prevention. Weight Loss, Diabetes Risk Reduction and Alzheimer's Prevention, as a Bonus!

A different kind of Weight Management. Prevention of Dementia and Diabetes

Audience: patients and families curious about whether GLP-1–based medicines (e.g., semaglutide, tirzepatide, liraglutide) might help protect brain health—especially given growing discussion of Alzheimer’s disease as “type 3 diabetes.”

The takeaway up front

As a physician, I see two parallel truths emerging from recent science. First, Alzheimer’s disease and other dementias are strongly linked to metabolic dysfunction—especially insulin resistance in the brain, sometimes labeled “type 3 diabetes.” Second, a class of diabetes and weight-management medicines called GLP-1 receptor agonists (GLP-1 RAs) shows early but increasingly consistent signals that they may lower dementia risk in people with type 2 diabetes, and possibly slow specific biological changes of Alzheimer’s in small clinical trials. These signals are not yet the same as definitive proof of prevention, but they are promising enough to merit discussion with your clinician if you’re already a candidate for these drugs for diabetes, obesity, or cardiometabolic risk. JAMA Network+3MDPI+3ScienceDirect+3

Why Alzheimer’s has been called “type 3 diabetes”

For more than a decade, researchers have observed that insulin signaling in the brain is impaired in Alzheimer’s disease (AD). Insulin helps neurons use glucose, modulates synapses (the “wiring” that underlies memory), and dampens inflammatory cascades. When brain insulin signaling falters, glucose metabolism drops, oxidative stress rises, amyloid and tau processing can worsen, and microglia (the brain’s immune cells) are more likely to stay in an inflammatory state. These patterns have led many scientists to frame AD as a brain-specific insulin-resistant state, colloquially “type 3 diabetes.” While not every expert embraces the term, multiple recent reviews detail the mechanistic links. MDPI+2ScienceDirect+2

Enter GLP-1: from pancreas to brain

GLP-1 is a hormone made in the gut and the brain that boosts insulin secretion when glucose is high, tempers glucagon, slows gastric emptying, and promotes satiety. GLP-1 receptor agonists (GLP-1 RAs) are long-acting versions of this signal (liraglutide, semaglutide, dulaglutide, and the dual GIP/GLP-1 agent tirzepatide) developed to treat type 2 diabetes and, more recently, obesity. Beyond glucose and weight, GLP-1 signaling appears to modulate neuroinflammation, improve neuronal energy handling, and support vascular health, all relevant to neurodegeneration. Nature+2PMC+2

Do these medicines reach the brain? Evidence suggests that GLP-1 pathways influence the central nervous system via multiple routes: some agents and/or their downstream effects reach or affect the brain and blood–brain barrier, altering glucose transport, microglial activation, and synaptic function in preclinical and early human studies. Quantitative BBB penetration differs by molecule and remains an active research area. PMC+1

What the human data show so far. Why GLP-1 agents, like Zepbound, help with sleep apnea, diabetes, heart disease, and weight loss

1) Large real-world observational studies (association ≠ proof)

In 2025, a Nature Medicine analysis of >2 million U.S. veterans with diabetes mapped outcomes after initiating GLP-1 RAs vs several comparators. Among many findings, GLP-1 use was associated with lower risk of Alzheimer’s disease and other neurological outcomes compared with usual care, with effect sizes varying by comparator drug class. Observational designs can’t prove causality, but the signal aligns with growing literature. PubMed

A JAMA Network Open cohort (60,860 adults with type 2 diabetes and obesity) reported that semaglutide or tirzepatide users had lower risks of dementia, stroke, and all-cause mortality than patients treated with other glucose-lowering drugs. Again, this is association, not proof, but it’s consistent and clinically meaningful. JAMA Network

Several complementary analyses—including the largest direct comparison of GLP-1 RAs vs metformin as initial therapy—suggest GLP-1 drugs may reduce overall and Alzheimer’s-type dementias more than metformin in people with type 2 diabetes. These studies use modern matching methods but remain observational. BMJ Disease Reviews

Finally, a systematic review and meta-analysis in JAMA Neurology (2025) pooling randomized cardiometabolic trials found no overall cognitive/dementia benefit across all cardioprotective diabetes drugs, but GLP-1 RAs stood out with a statistically significant reduction in incident dementia in subgroup analyses—important but still

Can GLP-1 Drugs Help Prevent Dementia? A Physician Explains

GLP-1 Medications help with both diabetes and obesity while preventing neuronal damage resulting in Dementia

You may have heard the terms GLP-1 agents, Alzheimer’s, dementia, “type 3 diabetes”—wondered how they connect, and whether drugs designed for diabetes (or weight loss) might also protect your brain. Here's what I, as a physician, see in the current scientific landscape. I’ll try to be optimistic where the data warrant it, but also clear about what remains uncertain.

Background: Dementia, Alzheimer’s & “Type 3 Diabetes”

Insulin Resistance of Diabetes type III

Dementia—especially Alzheimer’s disease (AD)—is a progressive decline in cognition, memory, planning, and daily functioning. Currently, there is no cure, though some medications slow progression in select patients. Prevention, or delaying onset, is thus a major clinical goal.

“Type 3 diabetes” is a term used to underscore a growing body of evidence that Alzheimer’s involves insulin resistance in the brain, impaired glucose metabolism, mitochondrial dysfunction, chronic inflammation, and oxidative stress—much like in type 2 diabetes. The idea is not that Alzheimer’s is literally the same as type 2 diabetes, but that many pathological features overlap. ScienceDirect+3MDPI+3PMC+3

Key points:

• The brain uses glucose as its primary fuel. If insulin signaling is disrupted, neurons may suffer energy deficits.

• Insulin has roles in synaptic plasticity, modulating tau phosphorylation, amyloid metabolism, and reducing oxidative stress. PMC+3Frontiers+3Diabetes Journals+3

• People with type 2 diabetes (T2DM) have significantly increased risk of AD/dementia. MDPI+2PMC+2

  
  

Thus, any intervention that improves insulin sensitivity, reduces inflammation, supports mitochondrial health, and perhaps modulates amyloid/tau pathology has theoretical potential in dementia prevention.

What Are GLP-1 Agents?

GLP -1 Agents affect much more than appetite and weight

GLP-1 (glucagon-like peptide‐1) is a hormone made in the gut (and to some extent in the brain) that helps with:

• stimulating insulin secretion when glucose is high;

• suppressing glucagon;

• slowing gastric emptying;

• promoting satiety;

• and possibly having direct effects in other organs (heart, brain, immune system).

  
  

GLP-1 receptor agonists (GLP-1 RAs) are medications modeled on this hormone (or its effects). They are used in T2DM, obesity, and increasingly in cardiovascular risk reduction. Examples: liraglutide, semaglutide, dulaglutide, occasionally dual agents (GLP-1 + GIP like tirzepatide).

These agents have multiple effects relevant to brain health:

• improved glycemic control (lowering glucose spikes, avoiding hyperglycemia)

• weight loss, which reduces many risk factors (vascular disease, hypertension, dyslipidemia)

• possible reduction of systemic inflammation

• possible direct neural effects: crossing—or affecting—the blood brain barrier; reducing amyloid and tau pathology; improving neuronal insulin signaling; preserving mitochondrial function; reducing oxidative stress. Frontiers+2PMC+2

  
  

Mechanistic and Animal Evidence

Before we look at clinical data, the animal and in vitro work is reassuring—and helps suggest how GLP-1 might work in the brain.

1. Amyloid & tau modulation: In mouse models of AD, GLP-1 RAs reduce amyloid β oligomer levels and plaque load; reduce tau hyperphosphorylation. Diabetes Journals+1

2. Neuroinflammation / oxidative stress: GLP-1 agents appear to reduce microglial activation, lower inflammatory cytokines, improve antioxidant defenses in brain tissue. Frontiers+2PMC+2

3. Mitochondrial health and neuronal energy: Some studies show improved mitochondrial function, decreased dysfunction, improved neuronal metabolic reprogramming in response to insulin resistance when GLP-1 pathways are engaged. BioMed Central+1

4. Brain insulin signaling: GLP-1 RAs in animal models can improve insulin signaling in neurons, enhancing glucose uptake and utilization in brain regions affected in AD. PMC+1

So mechanistically, there is plausibility. Animal studies are consistent across multiple models. But as always, animal studies are not enough to guarantee human benefits.

Human / Clinical Evidence: What We Know

Now we move from what could happen, to what seems to happen in people.

Observational Studies & Real‐World Data

These are large database studies, often with millions of patients, comparing dementia incidence (or cognitive decline) among people with T2DM (or obesity) using GLP-1 RAs vs other therapies.

• A recent JAMA article showed that among people with T2DM, use of GLP-1 RAs was associated with a statistically significant decrease in dementia risk compared with other antidiabetic drugs. JAMA Network

• Another large observational study found that people with T2DM and obesity using semaglutide or tirzepatide had lower risk of dementia, stroke, and all-cause mortality compared to those on other glucose‐lowering agents. Alzheimer's & Dementia Journals+2The Lancet+2

• A meta-analysis pooling many clinical trials (though mostly for diabetes endpoints) suggested that GLP-1 RAs (versus placebo or other drugs) may reduce risk of dementia among diabetics. The Lancet+1

Pros of observational data: large numbers, real world; cons: possible confounding (people who are prescribed GLP-1 agents may differ in many ways), reverse causality, indication bias, duration of follow-up may be short for dementia (often slow developing).

Randomized Trials & Clinical Interventions

These are more limited so far, but growing.

• The ELAD trial (Evaluating the Effects of the Novel GLP-1 Analogue Liraglutide in Alzheimer’s Disease) was a Phase 2b randomized, double-blind, placebo-controlled study in ~204 patients with mild AD. Over one year, liraglutide did not significantly improve the primary endpoint (change in cerebral glucose metabolic rate in certain brain regions), but secondary endpoints—including brain volume loss, and cognitive measures—showed benefit: ~50% less loss in several brain regions compared to placebo; also slower decline on cognitive tests. AAIC 2026

• A comparative effectiveness analysis of second-line diabetes medications in real‐world registry (Danish registry) comparing GLP-1 RAs to other agents found a protective effect of GLP-1 RAs vs certain other second-line drugs over 5 years, though not against all comparators. arXiv

  
  

Systematic Reviews / Meta-analyses

• A recent systematic review on “type 3 diabetes” draws together evidence of overlapping mechanistic pathways, supporting the idea that agents targeting insulin resistance (including GLP-1 RAs) might have benefit. PMC+2PMC+2

• Another meta-analysis (in JAMA Neurology) pooling more than 160,000 participants across many trials of glucose-lowering agents found that GLP-1 drugs were among the few classes associated with reductions in Alzheimer’s disease and other dementias in subgroup analyses. alzinfo.org+1

  
  

Putting It Together: What It Might Mean for You

As your physician, here's how I think about this evidence, and how it might apply in your case.

Potential Benefits (What We Can Hope For)

1. Slowing or delaying onset of dementia, especially in people with risk factors: T2DM, obesity, metabolic syndrome, hypertension. If GLP-1 agents reduce incidence (as observational studies suggest), that may translate into clinically meaningful delay.

2. Preserving brain structure and function, as suggested by trials like ELAD: less loss of brain volume, possibly less cognitive decline, at least in early/mild disease.

3. Reducing vascular risk: many cases of dementia are mixed, including vascular contributions. GLP-1 agents help with cardiovascular risk, weight, hypertension, dyslipidemia—all of which affect brain blood vessels.

4. Multiple mechanisms: the combination of improved glucose/insulin signaling + reduced inflammation + mitochondrial support + potential direct effects on amyloid/tau. This multipronged approach is promising, since dementia is multifactorial.

5. Secondary benefits: weight loss, better diabetes management, improved overall metabolic health—benefits we already accept for GLP-1 agents even ignoring brain effects.

   
   

Limitations & Unknowns

While promising, there remain many uncertainties:

• Causality not yet proven: Many studies are associative. Randomized controlled trial (RCT) evidence is limited and not yet definitive for prevention.

• Duration of effect: Dementia develops over many years (often decades). Most trials and observational follow-ups so far are in the range of 1-5 years. We don’t yet know how long GLP-1 agents must be taken, or at what age, to achieve durable prevention.

• Selection of patients: It may be that benefits are strongest in those with early metabolic dysfunction, mild cognitive impairment, or early Alzheimer’s disease, rather than in advanced dementia. Timing likely matters.

• Drug choice, dose, and penetration: Differences among GLP-1 RAs in ability to affect the brain (blood–brain barrier penetration, receptor binding, half-life, dosing) may influence outcomes. Not all agents may perform equally in this regard.

• Side effects and risks: Though GLP-1 agents are generally well tolerated, they carry risk of gastrointestinal effects, possible rare pancreatitis, effects on gallbladder, etc. Also cost, access, monitoring. These must be weighed, especially in older patients or those with compromised renal or hepatic function.

• Non-diabetic populations: Most data so far are in people with T2DM or obesity. It's not yet established whether GLP-1 RAs will benefit people without those risk factors in preventing dementia.

  
  

Clinical Implications & What I Might Recommend

If you are interested in whether GLP-1 drugs might be protective for your brain, here’s how I’d think about integrating the current data into individualized care.

1. Assess risk factors: Do you have type 2 diabetes? Prediabetes? Obesity? Hypertension? Dyslipidemia? Family history of AD? ApoE status (if tested)? These modify risk and may help decide how strongly to consider GLP-1 therapy for brain protection.

2. Evaluate current indications: If you already qualify for a GLP-1 agent for diabetes, obesity, or cardiovascular risk, this brain effect adds more rationale. If you don’t, the risk vs benefit profile is different.

3. Monitor cognition and brain health: If using GLP-1 agents, baseline cognitive testing (memory, executive function) and periodic follow-up may help document whether there is slowing of decline (though in routine practice, this is limited).

4. Lifestyle remains foundational: Diet, exercise, sleep, managing cardiovascular risks remain essential. GLP-1 agents are not a substitute for those proven preventive measures.

5. Research enrollment: If possible, enrolling in clinical trials designed to test GLP-1 RAs for dementia prevention or early AD may help (and give access to more intensive monitoring).

6. Shared decision-making: If considering off‐label or “prevention” use, open discussion of uncertain benefit, possible side effects, cost, monitoring is essential.

   
   

Where Research Is Heading / What to Watch For

• Larger RCTs in non-diabetic or prediabetic populations specifically targeting cognitive decline or dementia as endpoints.

• Head-to-head trials of different GLP-1 agents to see which have better brain penetration and efficacy.

• Studies of biomarkers (amyloid PET, tau imaging, MRI volumetrics) to detect early structural/functional changes.

• Long-term follow-ups (5-10+ years) to see if cognitive effects translate into reduced incidence of dementia, delayed institutionalization, preserved quality of life.

• Safety and tolerability in older age groups, polypharmacy, kidney, and hepatic impairment.

  
  

So: Should You Use a GLP-1 Agent for Dementia Prevention?

Here’s how I interpret the balance of evidence as of now.

• If you have type 2 diabetes or obesity and are already considering a GLP-1 agent for metabolic reasons, then the potential brain benefits are a compelling additional advantage.

• If you do not have metabolic disease, the idea of using GLP-1 purely for dementia prevention is more speculative. It might become standard in future, but I wouldn’t yet recommend it off-label purely for that purpose outside of research settings.

• Age, comorbidities, risk of side effects, cost, and your personal risk tolerance all matter. For someone with moderate risk, early metabolic dysfunction, family history, preserving cognition may tip the scale.

  
  

Summary

• Alzheimer’s disease shows many features of insulin resistance in the brain, metabolic dysfunction, inflammation, oxidative stress: that’s the “type 3 diabetes” hypothesis.

• GLP-1 receptor agonists have multiple mechanisms that could beneficially intervene in those pathological processes.

• Animal and mechanistic studies are strong; observational and early clinical trial data are promising.

• But we do not yet have definitive proof in prevention — especially in long durations, in individuals without metabolic disease.

• If you are already using GLP-1 agents for metabolic disease, the potential cognitive benefits provide an added rationale. If not, it remains an area to watch and perhaps participate in trials.

  
  

References

1. Bae CS, et al. The Role of Glucagon-Like Peptide 1 (GLP-1) in Type 3 Diabetes: Glucose Metabolism, Amyloid, and Insulin Resistance in Alzheimer’s Disease. International Journal of Molecular Sciences. 2017;18(4):919. doi:10.3390/ijms18040919. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5713459/ PMC

2. Atabi F, et al. A systematic review on type 3 diabetes: bridging the gap between diabetes and Alzheimer’s disease. International Journal of Neuroscience. 2025. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382249/ PMC

3. Peng Y, et al. True or false? Alzheimer’s disease is type 3 diabetes. Ageing Research Reviews. 2024; doi:10.1016/j.arr.2024.101051. Available from: https://www.sciencedirect.com/science/article/pii/S1568163724002010 ScienceDirect

4. Du H, et al. The mechanism and efficacy of GLP-1 receptor agonists in Alzheimer’s disease. Frontiers in Endocrinology. 2022;13:1033479. doi:10.3389/fendo.2022.1033479. Available from: https://www.frontiersin.org/articles/10.3389/fendo.2022.1033479/full?utm_source=chatgpt.com Frontiers

5. Hölscher C. GLP-1 class drugs show clear neuroprotective effects in first clinical trials in AD and PD patients. Neuroscience & Biobehavioral Reviews. 2024. Available from: https://www.sciencedirect.com/science/article/pii/S0028390824001217 ScienceDirect

6. Tang B, et al. Comparative effectiveness of glucagon-like peptide-1 receptor agonists and other second-line glucose-lowering agents for dementia outcomes in type 2 diabetes mellitus: A cohort study. eClinicalMedicine. 2024;79:102635. doi:10.1016/j.eclinm.2024.102635. Available from: https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(24)00268-2/fulltext The Lancet

7. “GLP-1 Medications May Lower Dementia Risk, Research Suggests.” JAMA. 2025; (April). Anderer S, et al. Available from: https://jamanetwork.com/journals/jama/fullarticle/2833663 JAMA Network

8. Wang W, et al. Associations of semaglutide with first-time diagnosis of dementia in people with type 2 diabetes. Alzheimer’s & Dementia. 2024. Available from: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14313 Alzheimer's & Dementia Journals

9. Edison P, et al. Evaluating the Effects of the Novel GLP-1 Analogue Liraglutide in Alzheimer’s Disease (ELAD): Phase 2b randomized, double-blind, placebo-controlled trial. Alzheimer’s Association International Conference (AAIC), 2024. Summary available from: https://aaic.alz.org/releases-2024/glp-drug-liraglutide-may-protect-against-dementia.asp AAIC 2026

10. Li S, et al. GLP-1R as a potential link between diabetes and Alzheimer’s disease: Mechanistic insights and therapeutic opportunities. Frontiers in Aging Neuroscience. 2025; Article 1601602. Available from: https://www.frontiersin.org/journals/aging_neuroscience/articles/10.3389/fnagi.2025.1601602/full Frontiers

11. Meng X, et al. Type 3 diabetes and metabolic reprogramming of brain neurons. Molecular Medicine. 2025;31(1):101. doi:10.1186/s10020-025-01101-z. Available from: https://molmed.biomedcentral.com/articles/10.1186/s10020-025-01101-z BioMed Central

12. Monney M, et al. GLP-1 receptor agonists effect on cognitive function in diabetes: a systematic‐review / meta‐analysis. Neuroscience & Biobehavioral Reviews. 2023; S1262-3636(23)00052-6. Available from: https://www.sciencedirect.com/science/article/pii/S1262363623000526 ScienceDirect

13. “Weight Loss Drugs May Protect Against Alzheimer’s.” Alzinfo.org. Reddin C, et al. 2025. Available from: https://www.alzinfo.org/articles/treatment/weight-loss-drugs-may-protect-against-alzheimers/ alzinfo.org

14. “How GLP-1s Could Transform Alzheimer’s Treatment.” BrightFocus Foundation. 2025. Available from: https://www.brightfocus.org/resource/how-glp-1s-could-transform-alzheimers-treatment/ BrightFocus Foundation

15. Kciuk M, et al. Alzheimer’s Disease as Type 3 Diabetes. International Journal of Molecular Sciences. 2024;25(22):11955. doi:10.3390/ijms252211955. Available from: https://www.mdpi.com/1422-0067/25/22/11955/ MDPI

16. Hölscher C. Protective effects of GLP-1 receptor agonists in neurodegeneration. In: Neurotherapeutics. 2024. (“GLP-1 class drugs show clear protective effects…”). Available from: https://www.sciencedirect.com/science/article/pii/S0028390824001217 ScienceDirect

17. Frontiers review: Du H, et al. (as above) discussing GLP-1 RAs’ mechanisms (ref. 4), especially insulin resistance in brain and oxidative stress. Frontiers

18. Insulin resistance as molecular link between diabetes and AD. World Journal of Diabetes. 2024;15(7):1430-1445. Du C-T, et al. Available from: https://www.wjgnet.com/1948-9358/full/v15/i7/1430.htm WJGNet

19. The Danish registry study: Nerissa Nance, Andrew Mertens, et al. Applying the causal roadmap to longitudinal national registry data: a case study of second-line diabetes medication and dementia. arXiv preprint. 2023. Available from: https://arxiv.org/abs/2310.03235 arXiv

20. “GLP-1 receptor agonists effect on cognitive function in diabetes: a systematic review / meta-analysis.” (Monney et al., 2023) — repeated to emphasize the evidence in people with T2DM. Available from: https://www.sciencedirect.com/science/article/pii/S1262363623000526 ScienceDirect

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician

When Is Abdominal Pain An Emergency?

When is abdominal pain an emergency?

Abdominal pain can be unsettling at any stage of life. Many causes are harmless, but some need urgent care.

This post explains when to worry about abdominal pain and when to see a doctor. It follows an evidence-based approach and uses insights from reputable medical sources.

Understanding Abdominal Pain

Abdominal pain is any discomfort felt anywhere between the chest and groin. Because the abdomen contains many organs, pain can come from the digestive system, muscles or even organs outside the belly. The severity does not always match the seriousness of a chronic condition and may pass or persist depending upon the cause.

Types of Abdominal Pain: Acute vs. Chronic

Acute abdominal pain starts suddenly and lasts hours or days. Causes range from infections to injuries. 

Chronic pain that persists for weeks or longer and is often due to underlying conditions such as irritable bowel syndrome or ulcers. Persistent abdominal pain always warrants medical evaluation.

Menstrual cramps can be mild or severe, and may require medical attention if persistent or intense.

Common Causes of Abdominal Pain

Digestive issues: 

Gas, indigestion, constipation and diarrhea often cause temporary pain. Eating too quickly, food poisoning, or food intolerances may also lead to discomfort.

Inflammation:

Infections like viral gastroenteritis, peptic ulcers, or urinary tract infections can cause inflammatory pain.

Female reproductive cycle: 

Menstrual cramps and ovulation pain are common sources of lower abdominal discomfort.

Other organs: 

Problems in the chest (heart attack), pelvis, or back can mimic stomach pain. 

When to Worry About Abdominal Pain

Most bellyaches resolve with time, but certain features suggest a more serious issue. Pay attention to the duration and severity of pain and any accompanying symptoms.

Pain That Persists or Worsens

Unexplained abdominal pain that is persistent or severe requires medical attention. If the pain follows trauma, occurs during pregnancy or in young children, seek prompt evaluation. 

Persistent pain after surgery or in older adults may indicate bowel obstruction or another complication.

It is always best to seek medical attention if there is any question of urgency or emergency

When To See A Doctor About Abdominal Pain

Seek a doctor’s assistance immediately if abdominal pain is accompanied by:

• Fever: Persistent fever can signal infection or inflammation.

• Nausea or vomiting: Continuous nausea or vomiting, especially with inability to keep liquids down, is a red flag.

• Blood in stool, urine or vomit: Blood can indicate bleeding in the gastrointestinal tract.

• Jaundice: Yellowing of the skin and eyes may suggest liver or gallbladder disease.

• Swelling and tenderness: A swollen or tender abdomen requires evaluation.

• Shortness of breath or chest pressure: Pain associated with difficulty breathing or chest pain could reflect heart or lung problems.

• Inability to pass gas or stool: Bloating, constipation, and an inability to pass gas can signal bowel obstruction

When Is Abdominal Pain an Emergency?

Some situations demand immediate emergency care. Recognizing these signs can be lifesaving.

Signs You Should Go to the ER Immediately

According to the Mayo Clinic, you should call emergency services if your abdominal pain is severe and accompanied by trauma, chest pressure, or pain. 

Nurse evaluating an ER patient with abdominal pain.

Go to the emergency department if you experience:

• Severe, sudden pain: A sudden onset of intense pain that makes movement difficult is concerning.

• Pain with fever or chills: Fever may point to infection or inflammation.

• Persistent pain in the lower right abdomen: This may indicate appendicitis.

• Chest pressure or shortness of breath: Pain radiating to the chest, shoulder, or back can mimic heart attack.

• Pain with bloody vomiting or black stools: These signs suggest internal bleeding.

• Bloating with inability to pass gas or stool: Could be a bowel obstruction.

Conditions That Require Urgent Care

Several conditions necessitate urgent evaluation.

Appendicitis

Pain often begins near the belly button and migrates to the lower right abdomen. It may start slowly and worsen over 12-24 hours. 

Appendicitis is more common in teenagers and young adults.

Bowel Obstruction

Bloating, constipation and inability to pass gas, especially in people with previous abdominal surgery, suggest obstruction.

Acute Pancreatitis

Pain starts in the upper abdomen and worsens after eating. Symptoms may include fever and rapid pulse.

Kidney Stones

Sharp, cramping pain in the lower abdomen or back that peaks rapidly, often early in the morning, could signal kidney stones.

Gallbladder Infection

Severe right upper quadrant pain with fever and jaundice may indicate cholecystitis.

Not All Abdominal Pain Requires An Emergency Room Visit. 

Your primary care doctor can evaluate many conditions and decide if specialist care is needed. Schedule a doctor's visit if your pain lasts more than a few days or if it worries you. 

Seek care sooner if you have underlying medical problems or are older, pregnant, or immunocompromised.

What Your Primary Care Provider Can Help With

Your doctor can diagnose and treat conditions like indigestion, constipation, food intolerance, or mild infections. 

They may prescribe medication, recommend lifestyle changes, or order basic tests. If you have chronic conditions such as irritable bowel syndrome, your doctor can help manage symptoms and refer you to a specialist if needed.

When to Ask for a Specialist Referral

You might need a gastroenterologist or surgeon if your symptoms are persistent, unexplained, or linked to structural issues. 

Conditions like inflammatory bowel disease, gallstones, or hernias often require specialist evaluation. Recurrent pain in older adults may call for imaging studies to rule out cancer or vascular problems.

Diagnostic tests for abdominal pain can range from blood tests to ultrasound imaging.

What to Expect During a Medical Evaluation

Questions You'll Be Asked

Health professionals will ask about the location, intensity, and duration of your pain. They may inquire about your diet, bowel habits, and any triggers or relieving factors. 

Possible Tests or Imaging

Your doctor may perform blood tests, urine tests or stool studies. 

Imaging like ultrasound or CT scans can reveal gallstones, appendicitis or other structural problems. Endoscopy may be used to examine the stomach or intestines. 

The tests ordered depend on your symptoms, age and medical history.

How to Track Your Symptoms at Home

A symptom diary can provide valuable insight. Be sure to include:

• Time: Record when the pain occurs and how long it lasts.

• Location: Note where you feel pain and whether it spreads.

• Severity: Use a scale from 0 to 10 to rate intensity.

• Triggers or relief: Track foods, activities, or bowel habits that affect pain and any medications that help.

Final Thoughts On When Should You Worry About Abdominal Pain

Abdominal pain is a common complaint across all ages. 

Most cases are minor, but persistent or severe pain or pain with concerning symptoms should prompt a medical evaluation. 

Understanding when abdominal pain is an emergency helps you act quickly and reduces the risk of complications. Listen to your body and seek care when something feels wrong. 

At Longwood, Florida-based Stages of Life Medical Institute, our pain specialists diagnose all forms of abdominal pain and help guide appropriate treatment.  To become a new patient, simply click here.

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

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David S. Klein, MD Functional Medicine Physician