Constipation is one of the most common digestive complaints, affecting an estimated 15-20% of adults at any given time. While occasional constipation is usually related to diet, hydration, or temporary lifestyle changes, chronic constipation that doesn’t respond to simple measures often has an identifiable cause that blood tests can help uncover.

The digestive system doesn’t operate in isolation — it’s influenced by hormones, electrolytes, blood sugar, and the overall metabolic state of the body. Conditions like hypothyroidism, diabetes, hypercalcemia, and others can slow intestinal motility and cause persistent constipation. Identifying and treating these underlying conditions can resolve constipation that no amount of fiber or laxatives could fix.

This article explores the common internal causes of chronic constipation and what blood tests can reveal about each.

Understanding Constipation

Constipation is generally defined as having fewer than three bowel movements per week, but it’s much more than just frequency. Many people have daily bowel movements yet still feel constipated because of straining, hard stools, or a sense of incomplete emptying.

The Rome IV criteria — the internationally recognized diagnostic criteria used by gastroenterologists — define functional constipation as having two or more of the following symptoms for at least three months (with symptom onset at least six months before diagnosis):

• Straining during more than 25% of bowel movements
• Lumpy or hard stools (Bristol Stool Scale types 1-2) more than 25% of the time
• Sensation of incomplete evacuation more than 25% of the time
• Sensation of anorectal obstruction or blockage more than 25% of the time
• Need for manual maneuvers (digital assistance, pelvic floor support) to facilitate defecation more than 25% of the time
• Fewer than three spontaneous bowel movements per week

Additionally, loose stools should be rarely present without laxatives, and there should not be sufficient criteria for irritable bowel syndrome. In other words, constipation encompasses difficulty, discomfort, incomplete emptying, and infrequency — not just infrequency alone.

How normal bowel function works:

Understanding normal digestion helps explain how various conditions cause constipation. The journey from eating to elimination is a carefully coordinated process:

1. Gastric emptying: After a meal, the stomach churns and mixes food with digestive juices, then gradually releases it into the small intestine. This process takes 2-5 hours for a typical meal. Hormonal signals and the autonomic nervous system control the rate of emptying.
2. Small intestinal transit: Contents move through approximately 20 feet of small intestine over 3-5 hours, propelled by coordinated muscle contractions called peristalsis. Most nutrient and water absorption occurs here. The migrating motor complex (MMC) — a pattern of electrical activity — sweeps the small intestine clean between meals.
3. Entry into the colon: The ileocecal valve controls the flow of material from the small intestine into the large intestine (colon). About 1-2 liters of liquid material enter the colon daily.
4. Colonic transit: The colon’s primary job is to absorb water and electrolytes from the remaining material, transforming liquid into solid stool. This typically takes 12-36 hours but varies widely between individuals (and is longer in people with constipation). Peristaltic waves, including powerful “mass movements” that occur a few times daily (often triggered by eating), move contents toward the rectum.
5. Rectal filling and the defecation reflex: When stool enters the rectum, stretch receptors detect the distension and signal the urge to defecate. The internal anal sphincter (involuntary) relaxes while the external sphincter (voluntary) remains contracted until the person decides to proceed.
6. Defecation: Coordinated relaxation of the external anal sphincter and puborectalis muscle, combined with increased intra-abdominal pressure (Valsalva maneuver using abdominal muscles), enables evacuation. This process requires proper coordination — dysfunction here causes outlet obstruction.

Problems at any step can cause constipation. Slow colonic transit — the most common mechanism in metabolic causes — allows excessive water absorption, producing hard, dry stools that are difficult to pass. Dysfunction of the pelvic floor muscles or anal sphincters can prevent normal evacuation even when stool reaches the rectum appropriately.

Types of constipation:

Normal-transit constipation: Stool moves through the colon at a normal rate, but the person perceives constipation — often due to hard stools, abdominal bloating, or difficulty evacuating. This is actually the most common type, accounting for about 60% of cases. Typically responds to fiber and lifestyle measures.

Slow-transit constipation: The colon’s motility is genuinely reduced, causing prolonged transit time (colonic inertia). May be idiopathic (no known cause) or associated with systemic conditions like hypothyroidism, diabetes, or neurological disorders. Affects about 15-30% of people with chronic constipation. Often requires more than just fiber — may need osmotic laxatives or prokinetic agents.

Outlet obstruction (dyssynergic defecation): Stool reaches the rectum normally, but pelvic floor dysfunction prevents coordinated evacuation. The muscles that should relax during defecation instead contract paradoxically, or the rectum may have structural issues (rectocele, rectal prolapse). Affects about 25-50% of those with refractory constipation. Requires specialized testing and often biofeedback therapy.

Mixed pattern: Many people have elements of both slow transit and outlet dysfunction.

Secondary constipation: Constipation caused by an underlying medical condition, medication, or structural abnormality — this is what blood tests can help identify. It’s crucial to recognize secondary causes because treating the underlying condition often resolves the constipation.

When constipation suggests an internal cause:

Constipation from simple lifestyle factors (low fiber, inadequate hydration, sedentary lifestyle, ignoring the urge) typically:

• Responds to increased fiber and fluid intake
• Improves with regular physical activity
• Resolves with occasional laxative use when needed
• Has no associated systemic symptoms — you feel fine otherwise
• Has been present since young adulthood without significant change

Constipation suggesting an underlying medical cause:

• Persists despite adequate fiber (25-35 grams daily), fluid, and activity
• Represents a change from your normal pattern — you never used to have this problem
• Is accompanied by other symptoms (fatigue, weight changes, feeling cold, excessive thirst, muscle weakness)
• Doesn’t respond to over-the-counter remedies that previously worked
• Is progressive — steadily getting worse over time
• Started around the same time as other health changes or new symptoms
• Occurred after starting a new medication
• Developed after age 50 without obvious explanation

Warning signs requiring prompt evaluation:

These “alarm features” or “red flags” warrant prompt evaluation, often including colonoscopy, to rule out structural causes including colon cancer:

• Blood in stool, on toilet paper, or in the toilet bowl
• Unintentional weight loss
• New constipation after age 50 (especially without prior history)
• Family history of colon cancer or inflammatory bowel disease
• Severe or worsening abdominal pain
• Constipation alternating with diarrhea (especially with blood or mucus)
• Pencil-thin stools (may indicate partial obstruction)
• Inability to pass gas (complete obstruction is a medical emergency)
• Iron deficiency anemia
• Positive fecal occult blood test

These symptoms warrant evaluation for structural causes (including appropriate colon cancer screening) in addition to blood testing for metabolic causes.

Hypothyroidism: The Classic Metabolic Cause

If there’s one condition most classically associated with constipation, it’s hypothyroidism. Constipation is one of the hallmark symptoms of an underactive thyroid, reported by 15-20% of people with overt hypothyroidism — and the true prevalence may be even higher since many people don’t recognize their bowel changes as abnormal.

The relationship between thyroid function and bowel function is so well established that persistent, unexplained constipation should always prompt consideration of thyroid testing, especially when accompanied by other suggestive symptoms.

How hypothyroidism causes constipation:

Thyroid hormones (T4 and T3) regulate metabolic rate and cellular function throughout the body, including every aspect of gastrointestinal function. The gut has abundant thyroid hormone receptors, and low thyroid states profoundly affect digestive processes:

• Reduced intestinal motility: Thyroid hormones directly stimulate the smooth muscle contractions (peristalsis) that move contents through the GI tract. With low thyroid, these contractions become weaker, less coordinated, and less frequent, significantly prolonging transit time. Studies show colonic transit time can be 2-3 times longer in hypothyroidism.
• Slowed gastric emptying: Food stays in the stomach longer before moving into the intestines, contributing to feelings of fullness, early satiety, and bloating.
• Increased water absorption: Prolonged colonic transit time means the colon has more time to absorb water from stool, making it progressively harder, drier, and more difficult to pass.
• Reduced mucosal secretions: The intestinal lining produces less mucus in hypothyroid states, reducing lubrication and making stool passage more difficult.
• Weakened muscles: Hypothyroidism causes generalized muscle weakness (thyroid myopathy), including the abdominal muscles used to generate the pushing pressure needed for defecation and the smooth muscle of the bowel wall.
• Autonomic dysfunction: Thyroid hormones influence the autonomic nervous system, which controls involuntary gut motility. Low thyroid shifts the balance toward parasympathetic withdrawal, reducing the “rest and digest” signals that promote bowel activity.
• Reduced response to stimuli: The colon becomes less responsive to normal stimuli that trigger defecation, including the gastrocolic reflex (the urge to defecate after eating).

Characteristics of hypothyroid-related constipation:

• Develops gradually as thyroid function declines — often so slowly you don’t realize it’s changed
• Infrequent bowel movements — sometimes going 4-7 days or more without a movement
• Hard, dry, pellet-like stools that are difficult or painful to pass
• Significant straining required
• Bloating and abdominal discomfort, especially after meals
• Sensation of incomplete evacuation — feeling like you can’t fully empty
• Doesn’t respond well to fiber alone — fiber may actually worsen bloating and discomfort in the setting of slow transit
• May improve somewhat with laxatives but returns immediately when stopped
• Affects the entire GI tract — may also have slow gastric emptying (early fullness, nausea)

Other hypothyroidism symptoms typically present:

Constipation from hypothyroidism rarely occurs in isolation. Look for these accompanying symptoms:

• Fatigue and low energy — often profound, “bone-tired” exhaustion not relieved by rest
• Feeling cold when others are comfortable (cold intolerance)
• Unexplained weight gain despite unchanged eating habits
• Dry, rough skin that doesn’t respond to moisturizers
• Dry, brittle hair and hair loss (including thinning of outer eyebrows)
• Brain fog, difficulty concentrating, and memory problems
• Depression or low mood
• Muscle weakness, aches, and cramps
• Slow heart rate (bradycardia)
• Puffy face, especially around the eyes
• Hoarse voice
• Heavy or irregular menstrual periods
• Elevated cholesterol

The combination of constipation with fatigue, cold intolerance, weight gain, and dry skin strongly suggests hypothyroidism. If you have several of these symptoms, thyroid testing is essential — and the good news is hypothyroidism is very treatable.

Hashimoto’s thyroiditis:

Hashimoto’s thyroiditis — the autoimmune cause of most hypothyroidism in developed countries — develops slowly over months to years as the immune system gradually destroys thyroid tissue. GI symptoms including constipation may be so gradual in onset that you attribute them to aging, diet changes, stress, or just “getting older” rather than recognizing them as part of a systemic condition affecting your entire metabolism.

Subclinical hypothyroidism:

Even subclinical hypothyroidism — where TSH is elevated but Free T4 remains in the normal range — can cause symptoms including constipation in some people. If you have classic hypothyroid symptoms with a high-normal TSH, this may warrant attention.

What to test:

TSH (Thyroid-Stimulating Hormone) is the primary screening test. Elevated TSH indicates the pituitary is working harder to stimulate an underperforming thyroid. TSH is very sensitive and can detect thyroid dysfunction before symptoms become severe.

Free T4 measures circulating thyroid hormone. Low Free T4 with elevated TSH confirms overt hypothyroidism. Normal Free T4 with elevated TSH indicates subclinical hypothyroidism.

Free T3 measures the active thyroid hormone. Some people have adequate T4 but poor conversion to T3, which can cause symptoms despite seemingly adequate T4 levels.

TPO antibodies identify Hashimoto’s thyroiditis as the underlying autoimmune cause. Knowing you have Hashimoto’s explains why your thyroid is underperforming and predicts that you’ll likely need ongoing treatment.

Diabetes and Blood Sugar Disorders

Diabetes is a significant and often underrecognized cause of chronic constipation. Studies consistently show that constipation affects 25-60% of people with diabetes — far higher than the 15-20% prevalence in the general population. Both type 1 and type 2 diabetes can cause GI symptoms, though the mechanisms differ somewhat, and symptoms tend to be more common with longer duration of diabetes and poorer glucose control.

Gastrointestinal symptoms are so common in diabetes that the term “diabetic enteropathy” is used to describe the spectrum of GI dysfunction. Constipation, along with gastroparesis (delayed stomach emptying), diarrhea, and fecal incontinence, significantly impacts quality of life for many people with diabetes.

How diabetes causes constipation:

• Diabetic autonomic neuropathy: Chronically elevated blood sugar damages the small nerve fibers of the autonomic nervous system that control gut motility — the same process that causes diabetic neuropathy in the feet. This “enteric neuropathy” reduces the coordinated muscle contractions that move food through the digestive tract. Once established, autonomic neuropathy may be only partially reversible even with improved glucose control.
• Hyperglycemia directly slows motility: Even acute elevations in blood sugar can slow gastric emptying and intestinal transit, independent of any permanent nerve damage. This effect is rapid and reversible with glucose normalization — which is why GI symptoms often fluctuate with blood sugar levels.
• Dehydration from osmotic diuresis: When blood glucose is high, the kidneys excrete the excess glucose in urine, pulling water along with it. This chronic mild dehydration contributes to hard, dry stools that are difficult to pass.
• Medication effects: Some diabetes medications have GI side effects. While metformin more commonly causes diarrhea, other medications (particularly some older drugs) can contribute to constipation.
• Abnormal gut hormone secretion: Diabetes affects the hormones (motilin, ghrelin, GLP-1, and others) that coordinate digestive function, disrupting the normal signals that trigger gut motility.
• Altered gut microbiome: Research increasingly shows that diabetes is associated with changes in the composition and function of gut bacteria (dysbiosis), which may affect motility, stool consistency, and overall gut health.
• Reduced physical activity: People with diabetes, especially those with complications, may be less physically active, and sedentary behavior contributes to constipation.
• Smooth muscle dysfunction: Beyond nerve damage, diabetes can directly affect smooth muscle cells in the gut wall, impairing their contractility.

Characteristics of diabetes-related constipation:

• Often develops gradually as diabetes progresses, particularly after several years of disease
• May fluctuate with blood sugar control — worse when glucose is running higher, better when well-controlled
• Can alternate with diarrhea — diabetic autonomic neuropathy can cause both, sometimes unpredictably
• Associated with bloating, early satiety, nausea, and abdominal fullness (signs of gastroparesis)
• May be accompanied by other GI symptoms including gastroesophageal reflux
• Often accompanied by other diabetic complications (peripheral neuropathy with numbness/tingling in feet, nephropathy, retinopathy) — GI neuropathy rarely occurs in isolation
• More common and more severe with longer diabetes duration and poorer long-term glucose control

Other diabetes symptoms often present:

• Increased thirst (polydipsia)
• Frequent urination (polyuria), especially at night
• Fatigue and low energy
• Blurred vision
• Slow-healing wounds
• Numbness or tingling in hands or feet (peripheral neuropathy)
• Frequent skin or urinary tract infections
• Erectile dysfunction (in men — also related to autonomic neuropathy)

Prediabetes:

Prediabetes — when blood sugar is elevated but not yet in the diabetic range — may also begin to affect gut function, though typically less severely than established diabetes. Some people notice subtle GI changes as an early manifestation of insulin resistance, even before diagnosis. Identifying and addressing prediabetes can prevent progression to diabetes and potentially prevent the GI complications.

What to test:

Fasting glucose screens for elevated blood sugar. A single elevated reading may indicate diabetes or prediabetes.

HbA1c (glycated hemoglobin) reflects average blood sugar over the past 2-3 months and provides a more stable picture than a single fasting glucose. It can diagnose both diabetes and prediabetes, and in known diabetics, indicates how well glucose has been controlled.

Fasting insulin can identify insulin resistance — the metabolic dysfunction underlying type 2 diabetes — even when glucose levels are still relatively normal. Elevated fasting insulin suggests the pancreas is working overtime to keep glucose controlled.

Hypercalcemia: Too Much Calcium

Elevated calcium in the blood (hypercalcemia) is a well-established and often overlooked cause of constipation. Calcium plays crucial roles in muscle contraction and nerve signaling, and elevated levels disrupt normal intestinal function. The classic teaching for hypercalcemia symptoms is “stones, bones, groans, and moans” — referring to kidney stones, bone pain, abdominal symptoms (including constipation, nausea, and abdominal pain), and psychiatric/neurological symptoms (fatigue, depression, confusion).

Hypercalcemia is relatively common — mild elevations are found in about 1-2% of routine blood tests — and constipation may be the presenting symptom that leads to its discovery.

How hypercalcemia causes constipation:

• Direct smooth muscle effect: Calcium ions are critical for muscle contraction. Paradoxically, excess extracellular calcium reduces smooth muscle contractility in the intestines by affecting the electrical properties of muscle cells and their ability to contract normally. This reduces the strength and coordination of peristaltic waves.
• Effects on nerve transmission: High calcium alters nerve signaling, including the autonomic nerves that control gut motility. This can impair the coordinated contractions needed for normal bowel function.
• Dehydration: Hypercalcemia causes increased urination (polyuria) by affecting kidney function, leading to volume depletion. Dehydration contributes to hard, dry stools that are difficult to pass.
• Reduced appetite and nausea: Hypercalcemia commonly causes nausea and decreased appetite, which can reduce food (and fiber) intake and further contribute to constipation.

Common causes of hypercalcemia:

Primary hyperparathyroidism: The most common cause of hypercalcemia in outpatient settings. One or more of the four parathyroid glands (small glands behind the thyroid) overproduce parathyroid hormone (PTH), which raises blood calcium by increasing calcium release from bones, calcium absorption from the gut, and calcium retention by the kidneys. Primary hyperparathyroidism is common — affecting about 1 in 500 women over 40 — and is often discovered incidentally when elevated calcium is found on routine blood work.

Malignancy-associated hypercalcemia: The most common cause in hospitalized settings. Cancer can raise calcium through several mechanisms: direct bone destruction by tumor metastases, or production of PTH-related peptide (PTHrP) by the tumor that mimics PTH’s effects. This is typically seen with advanced cancer.

Excessive vitamin D: High-dose vitamin D supplementation — particularly at doses well above the recommended daily intake taken for extended periods — can cause hypercalcemia by increasing intestinal calcium absorption.

Excessive calcium supplementation: Especially when combined with vitamin D or taken in very high doses.

Medications: Thiazide diuretics reduce calcium excretion in urine, potentially raising blood calcium. Lithium can affect parathyroid function and raise calcium levels.

Granulomatous diseases: Sarcoidosis, tuberculosis, and some other granulomatous conditions can cause hypercalcemia through increased vitamin D activation.

Prolonged immobilization: Extended bedrest causes calcium to leach from bones, potentially raising blood levels.

Other hypercalcemia symptoms:

• Fatigue, weakness, and lethargy
• Increased thirst and frequent urination
• Nausea, vomiting, and loss of appetite
• Abdominal pain
• Confusion, difficulty concentrating, or memory problems (in more severe cases)
• Depression
• Bone pain
• Kidney stones (calcium deposits)
• Muscle weakness

Many cases of mild hypercalcemia are asymptomatic or have only subtle symptoms. Constipation may be the most noticeable symptom, prompting the testing that reveals elevated calcium.

What to test:

Calcium — the basic screening test for hypercalcemia. Serum calcium is often part of a standard comprehensive metabolic panel, so it may already have been checked. Total calcium needs to be interpreted in light of albumin levels (calcium binds to albumin, so low albumin can make total calcium appear falsely low).

Ionized calcium — the biologically active, unbound form of calcium. Useful when total calcium is borderline or when protein levels are abnormal. Ionized calcium gives a more accurate picture of true calcium status.

PTH (Parathyroid Hormone) — essential for determining the cause of hypercalcemia. Elevated PTH with high calcium strongly suggests primary hyperparathyroidism. Suppressed PTH with high calcium suggests a non-parathyroid cause (malignancy, vitamin D excess, etc.).

Vitamin D (25-hydroxyvitamin D) — to assess if vitamin D excess is contributing to hypercalcemia.

Albumin — needed to correctly interpret total calcium levels.

Electrolyte Imbalances

Beyond calcium, other electrolyte abnormalities can affect intestinal motility and contribute to constipation.

Hypokalemia (low potassium):

Potassium is essential for muscle contraction, including the smooth muscle of the intestines. Low potassium can cause:

• Reduced intestinal motility
• Abdominal distension
• In severe cases, paralytic ileus (complete cessation of bowel activity)

Common causes of hypokalemia include diuretics, excessive vomiting or diarrhea, and certain medications.

Hypomagnesemia (low magnesium):

Magnesium is involved in numerous physiological processes including muscle function. Low magnesium can contribute to constipation — conversely, magnesium supplements are often used as laxatives.

Causes include inadequate dietary intake, malabsorption, alcoholism, and certain medications (proton pump inhibitors, diuretics).

What to test:

Potassium

Magnesium

Sodium — while less directly related to constipation, part of a complete electrolyte assessment.

Kidney Disease

Chronic kidney disease (CKD) is associated with constipation, affecting up to 30-60% of people with advanced kidney disease.

How kidney disease causes constipation:

• Uremic toxins: Accumulated waste products affect gut motility and the gut microbiome.
• Fluid restriction: People with kidney disease often need to limit fluid intake, contributing to hard stools.
• Dietary restrictions: Low-potassium and low-phosphorus diets may be low in fiber-rich foods.
• Medications: Phosphate binders, iron supplements, and other medications common in CKD cause constipation.
• Electrolyte abnormalities: Alterations in potassium, calcium, and other electrolytes.
• Reduced physical activity: Fatigue from kidney disease leads to reduced activity.
• Autonomic dysfunction: Uremia can affect autonomic nerve function.

What to test:

Creatinine and eGFR assess kidney function.

BUN reflects kidney function and protein metabolism.

Other Medical Conditions

Hypercalcemia from hyperparathyroidism:

Primary hyperparathyroidism deserves special mention because it’s common (affecting 1-2% of postmenopausal women) and often presents subtly with nonspecific symptoms including constipation. Many cases are discovered incidentally on routine blood work showing elevated calcium.

Anemia and iron deficiency:

While anemia itself doesn’t directly cause constipation, iron supplements used to treat iron deficiency anemia are a notorious cause of constipation. If you have both anemia and constipation, the treatment for one may be worsening the other.

Celiac disease:

While celiac disease more commonly causes diarrhea, some people present with constipation. The constipation may relate to overall malabsorption and its metabolic effects.

Multiple sclerosis and neurological conditions:

Neurological diseases affecting the autonomic nervous system or spinal cord commonly cause constipation. While blood tests don’t diagnose these conditions, they can rule out metabolic causes.

Depression:

Depression is associated with constipation, possibly through effects on the autonomic nervous system, reduced physical activity, and dietary changes. Some antidepressant medications also contribute to constipation.

Medications That Cause Constipation

Medication-induced constipation is extremely common and should always be considered. While not identified by blood tests, a thorough medication review is essential when evaluating constipation.

Common constipating medications:

• Opioid pain medications: Among the most potent causes of constipation. Opioids affect gut motility at multiple levels.
• Anticholinergic medications: Including antihistamines (diphenhydramine), tricyclic antidepressants, antipsychotics, bladder medications (oxybutynin), and muscle relaxants.
• Calcium channel blockers: Particularly verapamil and diltiazem.
• Iron supplements: Very commonly cause constipation.
• Calcium supplements: Especially calcium carbonate.
• Aluminum-containing antacids:
• NSAIDs: Can contribute to constipation with chronic use.
• Diuretics: Through dehydration and electrolyte effects.
• Antidepressants: Especially tricyclics and some others.
• Anti-Parkinson’s medications:
• Antihypertensives: Various classes.

If constipation started after beginning a new medication, discuss alternatives with your healthcare provider.

The Testing Strategy for Constipation

When constipation persists despite lifestyle measures, is accompanied by other symptoms, or represents a change from baseline, blood testing can identify underlying causes.

Core tests for unexplained constipation:

Thyroid function (essential):

• TSH
• Free T4 (if TSH abnormal)

Metabolic panel:

• Calcium
• Fasting glucose
• Potassium
• Creatinine

Additional tests as indicated:

• HbA1c — if diabetes suspected
• Magnesium
• PTH — if calcium elevated
• CBC — to assess for anemia (and potential need for iron supplements that worsen constipation)

What to Do With the Results

If hypothyroidism is found:

Treatment with thyroid hormone replacement typically improves constipation along with other symptoms. As thyroid levels normalize, intestinal motility increases, and bowel function often returns to normal. Many people are surprised how much better their digestion becomes with proper thyroid treatment.

If diabetes is found or poorly controlled:

Improving blood sugar control can help GI symptoms, though diabetic autonomic neuropathy may not be fully reversible. Better glucose control prevents further nerve damage and often improves motility. Addressing dehydration from poorly controlled diabetes also helps.

If hypercalcemia is found:

Treatment depends on the cause. Primary hyperparathyroidism may require surgery (parathyroidectomy) if symptomatic or severe. Reducing vitamin D or calcium supplementation if excessive. Treating hypercalcemia typically resolves the associated constipation.

If electrolyte abnormalities are found:

Correcting hypokalemia or hypomagnesemia with supplementation typically improves bowel function. Identifying and addressing the underlying cause of the electrolyte imbalance is also important.

If kidney disease is found:

Managing kidney disease is complex and requires specialized care. Constipation management becomes part of the overall treatment plan, with attention to avoiding constipating medications when possible and using appropriate laxatives.

When Tests Are Normal

Normal blood tests rule out the metabolic and systemic causes of constipation but don’t mean nothing is wrong. They provide valuable information by narrowing the differential diagnosis and directing attention to other possibilities.

Consider these explanations when blood work is unremarkable:

• Inadequate fiber and fluid: Despite best intentions, most people don’t get the recommended 25-35 grams of fiber daily. Keeping a food diary to actually track fiber intake often reveals it’s lower than thought. Gradually increasing fiber (too fast causes bloating and discomfort) while ensuring adequate hydration may still resolve symptoms. Remember that fiber without adequate water can worsen constipation.
• Sedentary lifestyle: Physical inactivity slows gut motility. The gut responds to movement — regular exercise, even just walking, stimulates intestinal contractions and reduces transit time. A sedentary job, limited mobility, or simply not prioritizing exercise can contribute significantly to constipation.
• Medication effects: Many common medications cause constipation, and this should always be reviewed. Opioid pain medications are notorious constipators. Anticholinergic medications (including many antihistamines, bladder medications, and some antidepressants), calcium channel blockers, iron supplements, calcium supplements, and aluminum-containing antacids are other common culprits. Sometimes switching to an alternative medication or adding a bowel regimen is necessary.
• Ignoring the urge: Habitually delaying defecation when the urge arises — because of inconvenience, embarrassment, or simply being too busy — can lead to chronic constipation. The longer stool sits in the rectum, the more water is absorbed and the harder it becomes. Over time, repeatedly ignoring the urge can blunt the defecation reflex.
• Irritable bowel syndrome (IBS-C): Constipation-predominant IBS is a functional bowel disorder diagnosed clinically based on symptom patterns. By definition, blood tests and structural tests are normal in IBS. Symptoms include abdominal pain related to bowel movements, bloating, and altered stool form or frequency. IBS-C is managed with dietary modifications (including the low-FODMAP diet for some), fiber adjustment, and sometimes medications targeting gut motility or visceral hypersensitivity.
• Pelvic floor dysfunction (dyssynergia): In this condition, the muscles of the pelvic floor don’t coordinate properly during defecation. Instead of relaxing to allow stool passage, the puborectalis muscle and/or external anal sphincter contract paradoxically. This creates a functional outlet obstruction — stool reaches the rectum but can’t be expelled effectively. Blood tests are normal; diagnosis requires specialized testing (anorectal manometry, balloon expulsion test, defecography). Treatment is biofeedback therapy, which is quite effective.
• Structural issues: Strictures (narrowing of the colon), adhesions from prior surgery, diverticular disease, hemorrhoids, anal fissures, rectocele (bulging of the rectum into the vagina), or masses may cause or contribute to constipation. These require imaging (CT scan) or colonoscopy to identify.
• Slow-transit constipation (colonic inertia): Some people have idiopathically slow colonic motility without an identified metabolic cause. The colon simply moves contents more slowly than normal. Specialized testing (colonic transit study using radiopaque markers or wireless motility capsule) can identify this. Management may require osmotic laxatives, prokinetic agents, or in severe refractory cases, surgical options.
• Neurological conditions: Parkinson’s disease, multiple sclerosis, spinal cord injuries, and other neurological conditions commonly cause constipation through effects on the autonomic nervous system and/or pelvic floor. These are usually diagnosed by their other manifestations rather than constipation alone.
• Eating disorders: Restricted food intake, laxative abuse, and other behaviors associated with eating disorders can cause chronic constipation and disrupt normal bowel function.

If blood tests are normal but constipation is significant and affecting quality of life, further evaluation may be warranted. This might include colonoscopy (especially if alarm features are present or age-appropriate screening is due), anorectal manometry and balloon expulsion testing for suspected pelvic floor dysfunction, or colonic transit studies for suspected slow-transit constipation. The goal is to identify the specific mechanism so treatment can be appropriately targeted.

Lifestyle Approaches

While investigating underlying causes, these evidence-based strategies can help manage constipation and should be maintained even after a specific cause is identified and treated:

Dietary fiber:

• Increase fiber gradually: Aim for 25-35 grams daily from a variety of sources — fruits, vegetables, whole grains, legumes, nuts, and seeds. A sudden large increase in fiber can cause bloating and gas, so increase by about 5 grams per week until you reach your target.
• Types of fiber matter: Soluble fiber (found in oats, beans, apples, citrus) forms a gel and helps soften stool. Insoluble fiber (found in wheat bran, vegetables, whole grains) adds bulk and helps stool move through faster. Both types are beneficial.
• Consider a fiber supplement: Psyllium (Metamucil, Konsyl) is particularly well-studied for constipation and provides soluble fiber. Methylcellulose (Citrucel) is less likely to cause gas. Take with plenty of water.
• Caution with slow-transit constipation: In true slow-transit constipation (like that from hypothyroidism), adding more fiber to an already slow-moving system may worsen bloating. If fiber makes you feel worse, focus on treating the underlying cause first.

Hydration:

• Adequate fluid intake is essential: Fiber needs water to work — without enough fluid, fiber can actually worsen constipation. Aim for at least 8 cups (64 ounces) of fluid daily, more if you’re active or in hot weather.
• Water is best: Plain water is ideal. Coffee can stimulate bowel activity for some people but is also a diuretic. Limit alcohol, which is dehydrating.
• Fluid restrictions: If you have heart or kidney disease requiring fluid restriction, work with your healthcare provider to balance constipation management with your other medical needs.

Physical activity:

• Exercise stimulates gut motility: Regular physical activity increases intestinal muscle contractions and reduces transit time. Even moderate activity like walking helps.
• Aim for 150 minutes per week: This is the standard recommendation for overall health and also benefits gut function.
• Morning exercise may be particularly helpful: Activity in the morning can help stimulate a bowel movement.

Bowel habits:

• Establish a routine: Try to have a bowel movement at the same time each day. Many people find the urge is strongest in the morning, especially after breakfast.
• Don’t ignore the urge: When you feel the need to go, go. Repeatedly delaying allows more water absorption, making stool harder. Over time, ignoring the urge can blunt the defecation reflex.
• Take your time: Allow adequate, unhurried time on the toilet. Rushing doesn’t help.
• Positioning matters: A footstool to raise the knees while sitting on the toilet can help achieve a more natural squatting position, straightening the anorectal angle and making evacuation easier.
• Use the gastrocolic reflex: Eating triggers contractions in the colon (the gastrocolic reflex). Having a warm beverage or breakfast and then allowing time for a bowel movement takes advantage of this natural response.

When to use laxatives:

• Osmotic laxatives (polyethylene glycol/MiraLAX, lactulose, magnesium citrate) draw water into the colon and are generally safe for longer-term use
• Bulk-forming laxatives (psyllium, methylcellulose) are essentially fiber supplements
• Stimulant laxatives (senna, bisacodyl) trigger intestinal contractions; best for occasional use rather than daily long-term use
• Stool softeners (docusate) have limited evidence of effectiveness but may help some people

If you find yourself dependent on daily laxatives, that’s a sign to investigate underlying causes rather than just continuing the laxatives indefinitely.

The Bottom Line

Chronic constipation is more than just an inconvenience — it affects quality of life, can cause significant discomfort, and may signal an underlying medical condition that deserves attention. While dietary factors, hydration, and lifestyle habits are the most common contributors to constipation, persistent symptoms that don’t respond to simple measures warrant investigation.

Hypothyroidism is the classic metabolic cause of constipation. The relationship is so well-established that thyroid testing should be considered in anyone with unexplained chronic constipation, especially when accompanied by other hypothyroid symptoms like fatigue, cold intolerance, weight gain, and dry skin. The good news is that hypothyroidism is highly treatable, and constipation often improves dramatically with thyroid hormone replacement.

Diabetes is another major — and often underrecognized — cause of chronic constipation. Diabetic autonomic neuropathy affects gut motility, and high blood sugar itself slows the digestive tract. Better glucose control can improve symptoms, though established neuropathy may be only partially reversible.

Hypercalcemia (elevated blood calcium), often from primary hyperparathyroidism, is a well-known cause of constipation that’s easily detected with routine blood work. Electrolyte imbalances, kidney disease, and various medications (especially opioids, anticholinergics, and iron supplements) are other common culprits.

Blood tests can identify these treatable conditions:

• TSH for thyroid function — the single most important test for metabolic causes of constipation
• Calcium — elevated calcium is a classic cause
• Glucose and HbA1c — for diabetes screening
• Potassium and magnesium — electrolyte imbalances affect gut motility
• Creatinine — kidney disease contributes to constipation through multiple mechanisms

Don’t accept chronic constipation as “normal” or something you just have to live with. While lifestyle measures (adequate fiber, hydration, regular physical activity, responding promptly to the urge to defecate) are important foundations, they won’t solve constipation caused by an untreated thyroid problem, uncontrolled diabetes, or elevated calcium.

Identifying and treating the underlying cause — rather than just reaching for more laxatives — can restore normal bowel function in ways that no amount of fiber or over-the-counter remedies could achieve. If you’ve tried the usual measures without success, it’s time to look deeper.

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Key Takeaways

• Chronic constipation often has an identifiable, treatable cause — don’t assume it’s just “how you are” or an inevitable part of aging
• Hypothyroidism is the classic metabolic cause of constipation — reduced thyroid function slows intestinal motility; thyroid hormone replacement typically restores normal bowel function
• Diabetes causes constipation through autonomic neuropathy and hyperglycemia — better glucose control can improve symptoms, though established neuropathy may be only partially reversible
• Hypercalcemia (elevated calcium) is a well-known cause — calcium affects smooth muscle function; primary hyperparathyroidism is a common, often overlooked, and treatable cause
• Electrolyte imbalances (low potassium, low magnesium) can contribute to constipation — these are easily identified and corrected
• Many medications cause constipation — opioids, anticholinergics, iron supplements, calcium supplements, and many others; always review your medication list
• Key blood tests include TSH, calcium, glucose/HbA1c, and potassium — a relatively simple panel can identify the most common metabolic causes
• Normal blood tests don’t mean nothing is wrong — IBS, pelvic floor dysfunction, slow-transit constipation, and structural issues require different types of evaluation
• Lifestyle measures remain the foundation — adequate fiber (25-35 grams daily), hydration, regular physical activity, and responding promptly to the urge to defecate
• Warning signs warrant prompt evaluation — blood in stool, weight loss, new constipation after age 50, and other red flags need colonoscopy to rule out structural causes including cancer