Category: Medicine Page 1 of 9

Of course there will be medicine. I am The Grumpy Doc.

Cholesterol has an odd reputation. It’s usually treated as a villain, but your body can’t function without it. Every cell membrane relies on it, and it’s the raw material for hormones like estrogen and testosterone, as well as for vitamin D. The trouble starts when you have too much of the wrong kind circulating in your blood for too long a time. Excess cholesterol can quietly build up inside your artery walls for many years before you’re aware of it. The consequences of ignoring it can range from an abnormal stress test to a heart attack. Let’s walk through how your doctor diagnoses a cholesterol problem, how you can treat it, and what happens if it goes unaddressed.

How Cholesterol Is Diagnosed

The starting point is a lipid panel. That is a blood test that’s usually done after you’ve been fasting. Although newer research has shown non-fasting panels work nearly as well for most purposes. The panel reports several numbers, and each identifies a different type of cholesterol.

LDL cholesterol, low-density lipoprotein, is the one most people mean when they say “bad cholesterol.” It’s the particle that tends to stick to artery walls and starts the buildup of plaque, the main component of blockages.

HDL, high-density lipoprotein, works in the opposite direction. It helps carry cholesterol back to the liver for disposal, which is why it’s nicknamed “good cholesterol.”

Triglycerides, a different type of fat entirely, round out the standard panel and, when elevated, add their own risk on top of LDL.

There isn’t one universal LDL number that applies to everyone. Instead, doctors weigh your LDL alongside your overall cardiovascular risk that also considers age, blood pressure, diabetes status, smoking history, and family history. If you’ve already had a heart attack, stroke, or other diagnosed artery disease you have increased risk.

The 2026 guideline from the American College of Cardiology and American Heart Association, sets LDL goals that correspond with risk: under 100 mg/dL for people at borderline or intermediate risk, under 70 mg/dL for those at high risk, and under 55 mg/dL for people who already have known artery disease and are considered very high risk. Additionally, initial lipid panels are now recommended starting at age 19, rather than waiting until later adulthood.

Two additional tests are being used more often now. Apolipoprotein B, or apoB, counts the actual number of cholesterol-carrying particles in your blood rather than just the cholesterol mass inside them. The newest guideline lists it as a more accurate risk predictor, even though it sometimes disagrees with the standard LDL number.

Lipoprotein(a), or Lp(a), is a genetically determined particle that raises artery-disease risk independent of LDL. An elevated Lp(a), even in the absence of an elevated LDL, is considered an increased risk. The update also recommends adults be screened for it once, since it isn’t affected by diet or exercise. When it’s high, your doctor may be more aggressive in treating your other numbers.

There are two tests that are not strictly cholesterol but are related to the risk associated with elevated cholesterol. They may be ordered for patients considered to be at risk or to evaluate their risk if it is unknown or uncertain.

Coronary artery calcium (CAC) scoring is a noninvasive, low-radiation CT scan that measures calcified atherosclerotic plaque in the coronary arteries and reports a calcium score. A score of zero indicates no detectable coronary calcium, while progressively higher scores indicate a greater level of coronary atherosclerosis and generally greater future cardiovascular risk. CAC is particularly useful when a person’s need for preventive treatment, such as a statin, is uncertain.

The new American Heart Association PREVENT (Predicting Risk of Cardiovascular Disease EVENTs) calculator, is recommended in the 2026 dyslipidemia guideline in place of older methods. It estimates the 10- and 30-year risk of atherosclerotic cardiovascular disease, heart failure, and total cardiovascular disease in adults ages 30–79 who do not have established cardiovascular disease. It incorporates age, sex, blood pressure, cholesterol, smoking, diabetes, body mass index, kidney function and medication use. PREVENT and CAC complement one another. PREVENT provides an initial estimate based primarily on clinical risk factors, while CAC can selectively provide direct evidence of coronary atherosclerosis.

Lifestyle Modifications

For most people with mild to moderately elevated cholesterol, lifestyle change is the first line of treatment. It isn’t just a box to check before starting medication. It can meaningfully move the numbers on its own.

Diet has the most consistent evidence behind it. Cutting back on saturated fat (found in fatty cuts of meat, butter, and full-fat dairy) and replacing it with unsaturated fats from sources like olive oil, nuts, and fatty fish can lower LDL. Soluble fiber, the kind found in oats, beans, and fruits like apples and pears, binds cholesterol in the digestive tract and carries it out of the body before it can be absorbed.

Exercise helps too, primarily by raising HDL and improving how your body handles triglycerides. Most clinical guidelines recommend at least 150 minutes a week of moderate activity, like brisk walking. More vigorous exercise appears to help more. Even a modest weight loss tends to improve the whole lipid panel.

Quitting smoking doesn’t lower LDL by much, but it dramatically improves HDL function. It also reduces the inflammation that turns cholesterol deposits into unstable, rupture-prone plaque.

Alcohol is not as clear cut. Heavy drinking clearly raises triglycerides and worsens overall risk but claims that moderate drinking meaningfully protects the heart have not held up well. It’s clearly not a reason to start drinking for health purposes.

Treatments

Doctors generally fall into one of two categories when dealing with our own health issues. Some tend to obsess about their health and check their labs and other tests repeatedly and sometimes undertake unnecessary or only marginally beneficial treatments. Others ignore their own health in ways they would never accept from their patients. I tend to fall into the latter category, and I ignored my marginally elevated cholesterol for several years until my cardiologist, who is also a friend, told me to quit being “stupid” and start treating it.

When lifestyle change isn’t enough on its own (mine wasn’t), or when your risk is high enough or your doctor doesn’t want to wait and see, medication is an option. Statins remain the default first step for most patients. They work by blocking an enzyme your liver uses to make cholesterol, which prompts the liver to pull more LDL out of the bloodstream. Decades of large trials tie this to real reductions in heart attacks and strokes.

If you don’t reach their goal on a statin alone, or you can’t tolerate one, several add-on options exist. Ezetimibe, a daily pill, blocks cholesterol absorption in the gut and is usually the first addition tried because it’s inexpensive and well tolerated. PCSK9 inhibitors, injectable medications like evolocumab and alirocumab, block a liver protein that normally limits how much LDL the liver can clear. They can lower LDL by roughly 50 to 65 percent on top of a statin. Inclisiran works on the same PCSK9 pathway but through a different mechanism, silencing the gene that produces LDL. It only needs to be injected twice a year rather than biweekly. Its long-term effect on heart attacks and strokes is still being evaluated in ongoing trials. Bempedoic acid, a newer oral option, works further upstream in the same cholesterol-production pathway as statins and has shown to reduce cardiovascular events in people who can’t take statins. It’s a more modest LDL reducer than the injectable options and carries a higher risk of gout and gallstones.

Specialists disagree about how aggressively to treat cholesterol, and what the target should be. Guidance has shifted more than once in the last decade. The 2026 multi-society guideline leans toward “lower for longer” as the general philosophy. Some professional groups have pushed back, arguing the most aggressive targets are better supported only for people who have already had a cardiac event. For what it’s worth, my own philosophy is “lower is better.” It’s worth discussing with your own physician.

What Happens If It Goes Untreated

This is the part that makes cholesterol worth taking seriously even though it produces no symptoms of its own for years or decades. Excess LDL particles work their way into the walls of arteries, where they trigger an inflammatory response. Immune cells arrive to clean up the cholesterol, become engorged with it, and form the fatty streaks that eventually mature into plaque. This process, called atherosclerosis, narrows and stiffens arteries throughout the body. It’s essentially silent until it isn’t.

Plaque in the arteries feeding the heart, can cause angina, chest discomfort during exertion when narrowed vessels can’t deliver enough blood. Later it can cause a heart attack if a plaque ruptures and a clot suddenly completely blocks the vessel.

The same rupture-and-clot process occurs in the arteries feeding the brain when a piece of plaque breaks loose and travels downstream causing an ischemic stroke. In the legs, arms, or abdomen, narrowed arteries produce peripheral artery disease, which shows up as cramping or pain with walking and, in advanced untreated cases, can progress to gangrene and amputation.

Chronic kidney disease and, less commonly, vascular dementia are also linked to long-term uncontrolled atherosclerosis, since the same narrowing process affects the small vessels feeding the kidneys and brain. This link is not as well documented as the coronary and peripheral vascular effects.

People with familial hypercholesterolemia, a genetic condition that causes very high LDL from birth, have an accelerated risk. Without treatment, clinically apparent artery disease can show up as early as someone’s thirties or forties instead of the more typical sixth or seventh decade of life.

It’s a useful reminder that the danger of high cholesterol isn’t only about the number itself. It’s also about the cumulative years of exposure. Starting treatment earlier, even modestly, tends to pay off more than starting aggressively later on.

Medical Disclaimer

Always seek the guidance of a qualified healthcare provider with any questions you may have regarding a medical condition or treatment. Never disregard professional medical advice or delay seeking it because of something you have read here.

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Illustration generated by the author using ChatGPT.

Sources

1. National Lipid Association, summary of the 2026 ACC/AHA/Multisociety Dyslipidemia Guideline — https://www.lipid.org/nla/2026-accahamultisociety-dyslipidemia-guideline-released

2. American College of Cardiology, news release on the 2026 ACC/AHA dyslipidemia guideline — https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia

3. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia, Circulation — https://www.ahajournals.org/doi/10.1161/CIR.0000000000001423

4. JACC, Maturation of Lipid Management in the 2025 ACC/AHA Acute Coronary Syndrome Guideline — https://www.jacc.org/doi/10.1016/j.jacc.2025.04.024

5. PMC, Current and emerging PCSK9-directed therapies to reduce LDL-C and ASCVD risk — https://pmc.ncbi.nlm.nih.gov/articles/PMC11755694/

6. Harvard Health, The changing landscape of LDL lowering drugs — https://www.health.harvard.edu/heart-health/the-changing-landscape-of-ldl-lowering-drugs

7. ScienceDirect, Advances in targeting LDL cholesterol: PCSK9 inhibitors and beyond — https://www.sciencedirect.com/science/article/pii/S2666667724000692

8. Cleveland Clinic, Hypercholesterolemia: Causes, Symptoms & Treatment — https://my.clevelandclinic.org/health/diseases/23921-hypercholesterolemia

9. Medical News Today, Complications of high cholesterol and tips to prevent them — https://www.medicalnewstoday.com/articles/high-cholesterol-complications

10. StatPearls (NCBI Bookshelf), Atherosclerosis — https://www.ncbi.nlm.nih.gov/books/NBK507799/

11. PMC, Familial Hypercholesterolemia Patients with COVID-19 — effective cholesterol-lowering therapy is urgent — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11270387/

12. PMC, A 72-Year-Old Patient with Longstanding, Untreated Familial Hypercholesterolemia but no Coronary Artery Calcification: A Case Report — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5991918/

When the Bladder Won’t Cooperate: A Plain-Language Look at Urinary Incontinence

By John Turley

On September 4, 2026

In Medicine

If you’ve ever laughed a little too hard, sprinted across the street, or simply gotten older, you may have noticed your bladder has developed opinions of its own. You’re suddenly chagrined to discover that you’ve developed more than a passing acquaintance with urinary incontinence. Since my own prostate surgery, a little over 10 years ago, I’ve become all too familiar with the inconvenience and the embarrassment of urinary incontinence.

It’s one of those conditions that’s extraordinarily common and yet still gets talked about in whispers, if it gets talked about at all. That’s a shame, because it’s rarely something people simply have to live with. Roughly six in ten women and about one in seven men will deal with some form of it at some point. The reasons range from childbirth to prostate surgery to the ordinary business of getting older.

The bladder is essentially a muscular storage reservoir. As urine enters the bladder, the bladder muscle—the detrusor—normally remains relaxed while the urinary sphincter and pelvic floor help keep the outlet closed. When we decide to urinate, a coordinated neurologic process causes the bladder to contract and the sphincter to relax.

Incontinence is a disruption, either structural or physiological, of this process.

Let’s walk through the main types, how the picture differs for men and women, what surgery can do to bladder control, and why aging tilts the odds toward leakage without making it inevitable.

The Main Types, and Why the Distinction Matters

Doctors sort urinary incontinence into a handful of categories, and getting the category right matters because the treatments diverge from one type to the next.

Stress incontinence is the leakage that shows up during a cough, a sneeze, a laugh, or a heavy lift. It can occur at any moment when pressure inside the abdomen spikes and overwhelms a weakened sphincter or a poorly supported urethra.

Urge incontinence is a different animal entirely. It’s the sudden, hard-to-ignore need to go, often followed by leakage before you can get to a bathroom. It traces back to a bladder muscle that contracts on its own schedule rather than yours.

Plenty of people have some of both, which is fittingly called mixed incontinence and is in fact the most common pattern among women with bladder symptoms.

Then there’s overflow incontinence, a steady dribble that happens when the bladder never quite empties and eventually overflows. Frequently something, often an enlarged prostate in men, is partially blocking the outlet.

Functional incontinence isn’t really a bladder problem at all It happens when the bladder and urethra work fine but a physical or cognitive barrier, arthritis, dementia, an unfamiliar building, keeps you from reaching a toilet in time.

Reflex incontinence, less commonly discussed, involves the bladder contracting without any warning sensation at all, usually the result of nerve damage from conditions like multiple sclerosis or spinal cord injury.

How the Picture Differs Between Women and Men

Sex matters quite a bit here, both in how common incontinence is and in which type shows up. In women, stress incontinence is the single most common variety, and pregnancy and vaginal childbirth are the biggest reasons why. They stretch and sometimes injure the pelvic floor muscles and connective tissue that ordinarily keep the urethra snugly closed.

Menopause adds another layer, since declining estrogen thins the urethral lining and can weaken sphincter function further. Cleveland Clinic data estimate roughly 62 percent of women age twenty and older experience some form of incontinence, a striking number that reflects just how common, and how underreported, this condition is.

Men have a lower overall rate, on the order of 14 percent, but their pattern looks different. Because men don’t have the childbirth-related stresses on the pelvic floor, stress incontinence in men is less common on its own and shows up mainly after prostate surgery, which we’ll get to shortly.

Overflow incontinence is proportionally more of a male problem, since an enlarging prostate gland can squeeze the urethra and prevent the bladder from emptying completely.

Urge incontinence and overactive bladder symptoms affect both sexes and become more common with age regardless of gender.

What Hysterectomy Does to Bladder Control

Hysterectomy is one of the most common major surgeries performed on women, and extensive research has looked at what it does to the bladder over the years following surgery. The short version: removing the uterus appears to modestly raise the long-term risk of stress incontinence, likely because the surgery can disturb the nerves, ligaments, and connective tissue that support the bladder neck and urethra. These structures sit close to the uterus and cervix.

A large systematic review found that during the first decade after hysterectomy, women faced a higher likelihood of urinary incontinence of any type, and stress incontinence specifically, compared with women who hadn’t had the surgery. Beyond ten years out, the gap widens further for stress incontinence.

A nationwide Finnish cohort that followed five thousand women for over a decade found that about one in fifty ultimately needed a surgical procedure to correct stress incontinence, with the risk running somewhat higher after vaginal or laparoscopic hysterectomy than after the abdominal approach.

It’s worth remembering that most women who have a hysterectomy never develop significant incontinence. Surgery is often the right choice for the underlying problem being treated, whether that’s fibroids, heavy bleeding, or cancer. But the association is real enough that it belongs in the conversation that women have with their surgeons beforehand. Particularly if they have already had vaginal deliveries, since that appears to carry extra risk.

What Prostatectomy Does to Bladder Control

For men, radical prostatectomy, the surgical removal of the prostate gland, most often performed for prostate cancer, is by a wide margin the leading cause of urinary incontinence. Nearly every man leaks to some degree immediately after the catheter comes out, which sounds alarming but reflects basic anatomy. The prostate normally works alongside the external sphincter to hold urine back, and removing it shifts the entire job onto that external sphincter, which needs time to adapt to the extra workload.

Continence rates climb steadily over the following year, with studies reporting roughly a quarter to half of men fully continent by three months, somewhere around two-thirds to three-quarters by six months, and the large majority continent by twelve months.

The American Urological Association’s guidelines note that incontinence is expected in the short term and generally improves toward baseline by a year after surgery, though for a minority, often cited as around a third of patients, some degree of leakage persists longer and occasionally requires further treatment such as pelvic floor therapy or, less often, a surgical procedure. Surgical technique matters too: preserving the nerve bundles that run alongside the prostate and maintaining a longer stretch of urethra during the operation are both associated with faster, more complete recovery of continence.

Late onset urinary incontinence effects approximately 10 to 15 percent of men who regained continence after a radical prostatectomy. It can begin anywhere from 5 to 15 years after surgery. This is frequently believed to be exacerbated by age-related changes.

The Effects of Ordinary Aging

Even without surgery in the picture, the bladder changes as we get older, and those changes tilt the odds toward incontinence for both sexes. Bladder capacity tends to shrink somewhat, meaning it fills to an uncomfortable point sooner.

The detrusor muscle, the smooth muscle that squeezes urine out, becomes more prone to firing off contractions on its own rather than only when you decide it’s time to go. This is a big part of what drives urge incontinence in later life.

The bladder also tends to leave more urine behind after each trip to the bathroom, called increased residual volume, raising the risk of both overflow symptoms and urinary tract infections that can trigger or worsen leakage.

The details diverge a bit by sex. In women, the drop in estrogen after menopause thins and shortens the urethral lining, loosening the seal the sphincter can form and compounding whatever pelvic floor weakening already occurred from childbirth.

In men, incontinence related to aging alone tends to show up later, generally after the seventh decade of life, and often travels alongside prostate enlargement. This is a nearly universal feature of male aging that can produce overflow-type symptoms even without prior surgery.

Incontinence prevalence rises sharply after age 65, and some nursing-home studies put rates as high as two-thirds among residents in their late eighties. Women’s rates consistently outpace men’s at every stage of later life.

None of this means incontinence is simply the toll of aging and that nothing can be done about it. While the physiological changes make leakage more likely, they don’t make it unavoidable. The same toolkit used with younger patients, pelvic floor exercises, bladder training, medications, and in some cases surgery, works for older adults too.

The bigger obstacle tends to be that people, especially older adults, often wait years before mentioning symptoms to a doctor, quietly reorganizing their lives around bathroom access instead of asking for help that’s readily available.

The Bottom Line

Urinary incontinence is sometimes dismissed as an embarrassing inconvenience, but its consequences can be substantial. People may stop exercising, traveling, attending social events, or even leaving home because they are worried about finding a bathroom. Older adults rushing to the toilet at night may also increase their risk of falling.

While urinary incontinence is common, it’s rarely discussed as openly as it deserves to be, and it is seldom explained to patients in plain language.

The consistent message across the research is that this is a treatable condition rather than a life sentence, and the first step toward treatment is usually just being willing to bring it up.

Illustration generated by author using ChatGPT

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Sources

1. Urinary Incontinence, StatPearls, National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK559095/

2. Definition & Facts for Bladder Control Problems (Urinary Incontinence), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). https://www.niddk.nih.gov/health-information/urologic-diseases/bladder-control-problems/definition-facts

3. Urinary Incontinence: Causes, Leakage, Types & Treatment, Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/17596-urinary-incontinence

4. Types of urinary incontinence, Harvard Health Publishing. https://www.health.harvard.edu/bladder-and-bowel/types-of-urinary-incontinence

5. Urinary Incontinence in Women, Johns Hopkins Medicine. https://www.hopkinsmedicine.org/health/conditions-and-diseases/urinary-incontinence/urinary-incontinence-in-women

6. Associations between hysterectomy and pelvic floor disorders: a systematic review and meta-analysis, American Journal of Obstetrics & Gynecology. https://www.ajog.org/article/S0002-9378(25)00164-4/abstract

7. Stress urinary incontinence after hysterectomy: a 10-year national follow-up study, Archives of Gynecology and Obstetrics (PMC). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8967811/

8. Hysterectomy and risk of stress-urinary-incontinence surgery: nationwide cohort study, The Lancet (PubMed). https://pubmed.ncbi.nlm.nih.gov/17964350/

9. Incontinence after Prostate Treatment: AUA/GURS/SUFU Guideline, American Urological Association. https://www.auanet.org/guidelines-and-quality/guidelines/incontinence-after-prostate-treatment

10. The location of the bladder neck in postoperative cystography predicts continence convalescence after radical prostatectomy, BMC Urology (PMC). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5977542/

11. Duration and Influencing Factors of Postoperative Urinary Incontinence after Robot-Assisted Radical Prostatectomy in a Japanese Community Hospital, PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10001515/

12. Effects of Aging on the Urinary Tract, Merck Manual Consumer Version. https://www.merckmanuals.com/home/kidney-and-urinary-tract-disorders/biology-of-the-kidneys-and-urinary-tract/effects-of-aging-on-the-urinary-tract

13. Incontinence in the elderly, ‘normal’ ageing, or unaddressed pathology?, Nature Reviews Urology. https://www.nature.com/articles/nrurol.2017.53

14. Neurogenic mechanisms in bladder and bowel ageing, PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361768/

15. Prevalence of Incontinence Among Older Americans, National Center for Health Statistics, Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/data/series/sr_03/sr03_036.pdf

Schizophrenia: A Serious Illness That Is Often Misunderstood

By John Turley

On August 24, 2026

In Medicine

Few psychiatric illnesses carry as much misunderstanding and stigma as schizophrenia. The word itself sometimes conjures images of unpredictable or dangerous behavior, and it is still occasionally confused with having a “split personality.” Neither picture accurately describes the disease.

Schizophrenia is a serious mental illness that affects the way a person thinks, perceives reality, expresses emotions and relates to other people. It can be profoundly disabling, but it is also treatable. With appropriate medication and social support, some people with schizophrenia attend school, work, maintain relationships and live independently.

A Disease That Usually Begins in Youth

Schizophrenia rarely arrives out of nowhere. Most people who develop it pass through a prodromal phase, a stretch of weeks, months, or even a couple of years before the first clear psychotic episode. During this phase, subtle changes in thinking, mood, and social behavior begin to show up. Someone might withdraw from friends, lose interest in things they used to enjoy, struggle to concentrate, or seem “off” in a way that is hard to pin down and easy to mistake for depression, anxiety, or ordinary teenage moodiness.

The disorder most often declares itself in late adolescence and early adulthood, though the timing differs somewhat between men and women. Men typically experience their first symptoms in their late teens to mid-twenties, while women tend to develop symptoms somewhat later, often in their late twenties to mid-thirties, with a second, smaller peak of onset around menopause. The leading explanation for this gap involves estrogen, which appears to have a protective effect on dopamine signaling in the brain, an effect that fades after menopause, explaining why some women may see this second, later window of vulnerability. Onset in childhood or after age 40 is uncommon and, when it does occur, doctors generally look harder for other explanations before settling on a schizophrenia diagnosis.

The first obvious event may be an episode of psychosis, an impairment of the ability to distinguish what is real from what is not. But the illness most likely was developing quietly for months or even years.

A young adult who had previously been doing well may gradually withdraw from friends, lose interest in school or work, neglect personal hygiene or become unusually suspicious. Concentration may deteriorate and conversation may become increasingly difficult to follow. Families frequently recognize that something is wrong long before they recognize it as mental illness and denial is frequent.

Eventually, more recognizable symptoms emerge. A person may begin hearing voices that nobody else hears. These hallucinations can seem every bit as real to the patient as an actual conversation. Others develop delusions, firmly held beliefs that are inconsistent with reality. Someone might become convinced that neighbors are spying on him, that television personalities are communicating directly with her, or that another person is secretly controlling his thoughts. Thinking itself can become disorganized, making conversation difficult to follow.

But these dramatic symptoms are only part of schizophrenia. Some of its most disabling features are less obvious. A person may lose motivation, withdraw socially, speak very little or show little outward emotion. Psychiatrists call these “negative symptoms” because normal abilities have diminished rather than something unusual being added.

There may also be problems with memory, concentration, planning and decision-making. These cognitive symptoms can make holding a job or living independently difficult even after hallucinations and delusions have improved.

What Causes Schizophrenia?

We don’t know exactly.

There is clearly a genetic component. Schizophrenia occurs more frequently in some families, but there is no single schizophrenia gene. Instead, many genetic variations probably contribute to vulnerability.

Researchers have also found differences in brain development, brain circuitry and chemical signaling. Dopamine has an important role, but the once-popular explanation that schizophrenia simply results from “too much dopamine” is far too simplistic.

The best current explanation is that schizophrenia develops through an interaction among genetic susceptibility, brain development and environmental influences.

Certain environmental exposures may increase risk in susceptible individuals. Prenatal complications such as infections, severe stress and maternal substance use, including alcohol and tobacco, have all been investigated. Cannabis deserves particular attention because frequent use, especially of high-potency products, has been associated with an increased risk of psychosis. The presence of one or more of these factors does not necessarily mean that an individual will develop schizophrenia.

How Do Doctors Diagnose It?

There is no blood test or brain scan that says, “This patient has schizophrenia.” Diagnosis depends upon the patient’s history, symptoms, behavior and psychiatric examination, often supplemented by observations from family members.

Just as important is determining what the illness is not. Bipolar disorder, severe depression, medication side effects, recreational drugs and neurological or medical diseases can all produce psychotic symptoms. Laboratory studies, drug screening or brain imaging may be necessary, not to prove schizophrenia, but to exclude other causes. This becomes especially important later in life.

Treatment Has Improved

The cornerstone of treatment remains antipsychotic medication. These drugs are particularly useful for reducing hallucinations, delusions and severe thought disturbance. Newer, “atypical” antipsychotics, including risperidone, olanzapine, quetiapine, aripiprazole, and clozapine, are not dramatically more effective than older drugs, but they do offer a sometimes significantly different side effect protocol. Individual response varies enough that psychiatrists often try more than one medication before finding the right fit. These newer medications carry their own tradeoffs, most notably a higher risk of metabolic side effects such as weight gain, diabetes, and unfavorable cholesterol changes, which is why patients on these drugs need regular medical monitoring. Long-acting injectable medications are available for patients who have difficulty taking pills consistently.

Medication alone is rarely the entire answer. Psychotherapy, family education, rehabilitation, social-skills training, assistance with employment and stable housing can make enormous differences. Programs for people experiencing their first episode of psychosis increasingly combine these approaches through coordinated specialty care. Early treatment is important because a prolonged period of untreated psychosis is associated with poorer outcomes.

What Is the Prognosis?

There is no simple answer. Schizophrenia is considered a chronic illness and its course varies remarkably from one person to another.

Some people experience one or several episodes followed by substantial recovery. Others have repeated periods of psychosis separated by relatively normal functioning. Still others develop persistent symptoms requiring lifelong treatment and assistance.

The World Health Organization notes that at least one in three people with schizophrenia can fully recover. Modern treatment emphasizes recovery and function, rather than simply eliminating hallucinations. The goal is to return the patient to as normal a life as is possible.

Without treatment, the outlook is considerably worse. Persistent psychosis can destroy educational and employment opportunities, relationships and the ability to maintain stable housing. Substance-use disorders can complicate the disease. Untreated schizophrenia is associated with a higher risk of suicidal thinking, progressive decline in cognitive functioning, and increased risk of cardiovascular disease, driven partly by lifestyle factors and partly by the physiological toll of chronic untreated illness. One widely cited estimate suggests that roughly two out of three people experiencing psychosis worldwide never receive adequate care, whether due to stigma, lack of insight into their own illness (a symptom in itself for some patients), cost, or limited access to services. This is why early identification and consistent care, imperfect as current treatments may be, make such a measurable difference in how the illness unfolds over a lifetime.

Schizophrenia in Older Adults

Schizophrenia presents an interesting problem as the patient ages. Many people who developed schizophrenia at 20 or 25 are now living into their seventies and eighties. Their psychiatric illness must be treated alongside the problems of aging, including cardiovascular disease, diabetes, cognitive decline and multiple medications.

Antipsychotic drugs also require particular caution in elderly patients because they may contribute to sedation, falls, orthostatic hypotension (blood pressure drop), abnormal movements and medication interactions.

But there is an even more important rule when dealing with an older person. New psychosis should not automatically be called schizophrenia, particularly in a hospitalized patient. Delirium associated with hospitalization, formerly called hospital psychosis, is not a psychiatric disorder. It will frequently resolve after treating underlying medical issues and discharging the patient from the hospital.

Imagine a previously mentally healthy 78-year-old who suddenly becomes convinced that strangers are entering his house or begins seeing people who aren’t there. Schizophrenia is possible, but it would not be the first assumption.

Delirium, dementia, Parkinson’s disease, stroke, infection, metabolic abnormalities, medications, alcohol and other drugs can all produce hallucinations, paranoia or confusion. Alzheimer’s disease and related dementias can also produce psychosis. An acute urinary track infection should always be high on the differential diagnosis of any older patient with a new mental status change.

A new onset of hallucinations or delusions in an elderly patient deserves a careful medical, neurological and medication evaluation.

True late-onset schizophrenia does occur, but is rare and schizophrenia beginning in young adulthood is much more typical.

A Disease, Not a Character Flaw

Perhaps the most important change in our understanding of schizophrenia is recognizing what it is not. It is not a failure of willpower. It is not caused by bad parenting. It does not mean someone has multiple personalities. A diagnosis of schizophrenia does not automatically make a person dangerous. It is a complex disorder of brain function whose ultimate cause remains incompletely understood.

We cannot yet cure schizophrenia in the conventional sense, nor can we predict with certainty which young person experiencing a first psychotic episode will eventually develop the disease. But we can treat it far more effectively than was possible just several years ago.

That makes early recognition particularly important.

When a young person gradually withdraws from the world, begins thinking or speaking strangely, or starts hearing voices or developing bizarre beliefs, the appropriate response is neither ridicule nor fear. It is medical evaluation.

For an elderly person who suddenly develops the same symptoms, the message is slightly different but equally important: don’t assume schizophrenia. Look carefully for the cause.

In both situations, psychosis is a symptom that deserves immediate attention and schizophrenia is an illness that deserves treatment rather than stigma.

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Image generated by author using ChatGPT

Sources

National Institute of Mental Health — Schizophrenia

National Institute of Mental Health — Understanding Psychosis

World Health Organization — Schizophrenia

Refusing the Needle: A History of Vaccine Resistance in America

By John Turley

On August 17, 2026

In Medicine, Uncategorized

Every vaccine the United States has ever rolled out has arrived with a shadow twin: a countermovement insisting the shot poses more danger than the disease it prevents, or that no government has the right to demand it. That pattern predates the country itself, and it has recurred with almost eerie consistency across three centuries — from the smallpox pustules of colonial Boston to the mRNA vials of 2021.

Colonial Boston and Smallpox

The story usually begins in Boston in 1721, during the sixth smallpox epidemic to strike the city since its founding. A ship called the Seahorse arrived from the Caribbean that April carrying a sailor with active smallpox, and within weeks the disease was moving through a city of roughly 11,000 people. By the time the epidemic burned out the following year, more than 6,000 Bostonians had been infected and about 850 had died.

The remedy that split the town in two was not vaccination in the modern sense but variolation, or inoculation — deliberately introducing live smallpox matter into a small cut in the skin, on the theory that a controlled, minor case would produce immunity without the risk of the full-blown disease. The technique had circulated for generations across West Africa, the Ottoman Empire, and Asia, and it reached Boston through the injustice of slavery. The Puritan minister Cotton Mather learned of it from Onesimus, a man he held in bondage, who described having undergone the procedure himself in Africa. Mather corroborated the account with other enslaved Africans in Boston and read reports out of Constantinople before becoming inoculation’s loudest champion.

Physician Zabdiel Boylston put the idea into practice, inoculating his own son and two enslaved members of his household first, then expanding the program despite fierce opposition. The city’s medical establishment largely revolted. Dr. William Douglass, one of the few Bostonians who actually held a medical degree, led the case against inoculation on grounds that ranged from the religious objection, that deliberately spreading disease usurped divine providence, to a reasonable-for-the-time scientific worry that the practice itself was seeding new outbreaks. The argument did not stay academic. Someone threw a lit grenade through Mather’s window that November, with a note attached reading, in essence, that he could inoculate himself with the bomb. It failed to detonate.

The case against inoculation was never purely religious or clinical; it was tangled up with its origin. Opposition writers repeatedly invoked its African and Ottoman source as grounds for distrust, treating its foreign, non-Christian lineage as evidence of danger apart from any medical argument. One Boston pamphleteer asked why residents should “cherish the cruel Blood of Africa or Asia” in their bodies, and a London critic writing a decade later dismissed inoculation as a “barbarous and dangerous Invention” imported from Turkey that had wrought “Havock and Slaughter” once it took hold. Because the technique reached Boston through Onesimus, the racial dimension of the debate was impossible to separate from the medical one — critics were rejecting a treatment in part because of who had brought it, not because of what it did.

What makes 1721 more than a historical curiosity is that Boylston and his allies did something close to a clinical study. They tallied outcomes among the inoculated against outcomes among those who caught smallpox naturally, and the inoculated group fared markedly better. That comparison helped slowly tip opinion in inoculation’s favor over the following decades. By the time George Washington ordered mandatory inoculation of the Continental Army in 1777, the practice — though still controversial — had become an accepted tool of public health.

The Gilded Age Leagues: Liberty, Quackery, and the Courts

Edward Jenner’s cowpox vaccine, introduced in 1796, eventually replaced variolation as the standard smallpox prevention. As vaccination spread across the Atlantic world through the nineteenth century, so did organized resistance. Britain passed an 1853 law making infant vaccination compulsory, and an 1867 act extended the mandate to age fourteen with real penalties attached for refusal. Britons who objected on religious, medical, or libertarian grounds organized the Anti-Vaccination League and, in 1867, the Anti-Compulsory Vaccination League, and within a few years it claimed over a hundred branches and roughly 10,000 members.

The British campaigner William Tebb carried that movement across the Atlantic. Following Tebb’s visit, Americans opposed to compulsory vaccination founded the Anti-Vaccination Society of America in 1879, and the New England Anti-Compulsory Vaccination League followed in 1882. These organizations drew on a mix of motives that will sound familiar to a modern reader: a libertarian objection to state intrusion into personal and parental decisions, religious conviction that disease and its prevention were matters for providence, and — more cynically — the financial interests of the era’s patent-medicine sellers and homeopaths, whose loosely regulated business model was directly threatened by a state-endorsed, evidence-based alternative.

The movement’s grievances were not entirely invented. In 1901, contaminated diphtheria antitoxin killed thirteen children in St. Louis, and contaminated smallpox vaccine killed several more in Camden, New Jersey, in the same year. Congress responded with the Biologics Control Act of 1902, the first federal law requiring licensure and safety standards for vaccine manufacturers — an early ancestor of the FDA’s modern oversight role. Those tragedies, however, did not settle the legal question of whether a state could force the issue. That came in 1905, when the Supreme Court decided Jacobson v. Massachusetts, upholding a Cambridge ordinance that fined residents who refused smallpox vaccination during an outbreak. The Court held that individual liberty was not absolute and could yield to a state’s power to protect public health — the first Supreme Court ruling on the subject, and one still cited today in disputes over compulsory vaccination and other public health mandates.

The ruling galvanized rather than pacified the opposition. Three years later, in 1908, opponents founded the Anti-Vaccination League of America in Philadelphia, built on the principle — in the League’s own words — that health was nature’s greatest safeguard against disease and that no state had the right to demand its impairment. It had the stated goal of abolishing what it called oppressive medical laws. Charles Higgins, one of the League’s most prolific pamphleteers, published tracts like his 1912 broadside “Open Your Eyes Wide!” arguing that vaccination was both dangerous and a violation of fundamental freedom. When Texas tried to require vaccination for public school attendance, the League’s arguments resurfaced in Zucht v. King, a 1922 case in which the Supreme Court again sided with the state.

Polio and The Vaccine Disasters of the 20th Century

By the mid-twentieth century, American vaccine skepticism had a new source of fuel, manufacturing failures serious enough to validate the movement’s oldest fear, that the shot itself might cause the disease. On April 12, 1955, officials announced that Jonas Salk’s inactivated polio vaccine, tested in a trial of 1.8 million children, was safe and effective, and the federal government licensed five manufacturers within days to begin mass production. One of them, Cutter Laboratories of Berkeley, California, shipped batches in which the virus-inactivation process had failed, leaving live, virulent polio virus in vaccine given to roughly 200,000 children across five states. An estimated 40,000 developed abortive polio, 200 were left with some degree of paralysis, and at least ten died. The program was suspended within weeks, federal oversight of vaccine manufacturing was overhauled, and vaccination resumed that fall under tighter controls.

The Cutter Incident became a formative episode in the history of American vaccine regulation and it had a lasting effect: a generation of parents who had watched the worst-case scenario for the trustworthiness of vaccines play out on the evening news, and that memory did not fade quickly.

Two decades later, a different kind of failure struck the flu vaccine. In early 1976, an Army recruit at Fort Dix, New Jersey, died of an influenza strain resembling the one responsible for the catastrophic 1918 pandemic. Fearing a repeat, the Ford administration pushed Congress to fund a crash national vaccination campaign, and nearly 43 million Americans were vaccinated within about ten weeks — an extraordinary logistical feat. The anticipated pandemic never arrived. Worse, as vaccinations proceeded, epidemiologists began detecting a modest but real increase in Guillain-Barré syndrome, a rare autoimmune paralytic condition, among recipients — roughly one additional case per 100,000 doses by later estimates. The program was suspended in December 1976, the CDC director was fired on live television, and the New York Times dubbed the whole affair a “fiasco,” a label that stuck for decades.

The Flu Shot’s Persistent Image Problem

Unlike smallpox or polio vaccination, the annual flu shot has never fully shaken a reputation for being optional, unpleasant, and only modestly effective in any given year. This is largely because the vaccine’s composition is re-engineered annually against strains predicted months in advance. That combination of a recurring injections, a variable and sometimes underwhelming efficacy rate, and the folk memory of 1976 has kept flu vaccination rates well below public health targets in most seasons, hovering in recent years around half of American adults, with substantial swings by age, region, and political affiliation. There is still the belief among some groups that the vaccine itself can cause flu even though flu vaccines do not contain live virus and cannot cause the disease.

COVID-19: An Old Argument at Unprecedented Speed

The COVID-19 pandemic compressed a century of vaccine controversy into about eighteen months. The mRNA vaccines developed by Pfizer-BioNTech and Moderna, along with a viral-vector vaccine from Johnson & Johnson, received emergency authorization by early 2021 after a development timeline that was, by historical standards, astonishingly fast. It was a point public health officials framed as a triumph of scientific investment and one that vaccine skeptics framed as a reason for caution. By September 2021, about 62 percent of Americans age twelve and older had received at least one dose, but demand had already begun slowing well before the country approached anything like universal coverage.

What followed diverged from earlier vaccine controversies in one important respect, hesitancy did not fade as more safety data accumulated, and in some respects it hardened. One national longitudinal study found that COVID-19 vaccine refusal actually rose from about 41 percent of adults in 2021 to nearly 45 percent in 2022. Even as overall vaccination coverage climbed, belief in the vaccine’s broader social benefit fell sharply, from roughly 48 percent to 25 percent. Parental hesitancy about vaccinating children against COVID-19 rose by nearly 16 percentage points in just nine months of 2021 and 2022, notably concentrated among white and rural parents, a pattern that cut against the demographic profile of vaccine resistance in earlier eras of American history. By the 2025–26 respiratory virus season, CDC surveillance found that only about 16 percent of American adults had received that season’s COVID-19 vaccine, with somewhat higher uptake — about 31 percent — among adults sixty-five and older, who face the greatest risk from the disease.

COVID-19 did not create vaccine skepticism, but it sharply politicized and enlarged the anti-vaccine movement by tying vaccination to partisan identity, distrust of government and public-health institutions, and debates over mandates, individual liberty, and pandemic restrictions. Political leaders, partisan media, and online networks often framed vaccination less as a medical decision grounded in evidence than as a symbol of cultural allegiance or resistance to perceived government overreach. Anti-vaccine activists used that environment to spread misinformation and reach audiences far beyond earlier disputes over childhood immunizations. The result was a more organized “health freedom” politics in which skepticism about COVID-19 vaccines could spill over into opposition to other routine vaccines, making public health a continuing front in America’s broader political polarization.

The pandemic-era pattern echoes several of its historical predecessors at once: distrust of a fast-moving federal program (echoing 1976), suspicion of a technology many found unfamiliar and difficult to evaluate (echoing the original inoculation debates of 1721), and a fusion of libertarian and religious objection to government mandates (echoing the Anti-Vaccination League of America a century earlier).

A Recurring American Argument

Over the last 50 years, advocacy groups have questioned the growing number of childhood vaccines and raised concerns about vaccine ingredients, scheduling, and possible long-term effects. The movement gained momentum after publication in 1998 of a now-retracted paper by Andrew Wakefield that falsely suggested a link between the measles-mumps-rubella (MMR) vaccine and autism. Numerous large studies subsequently found no evidence supporting such a connection, and investigations revealed ethical violations and scientific misconduct in Wakefield’s work, but the damage was done and the foundation was laid for the modern anti vaccination movement.

Read across three centuries, American vaccine resistance is not one continuous movement so much as the same underlying argument recurring in new costumes. It is a tension between collective protection and individual or parental autonomy, sharpened at each turn by episodes — some tragic and real, like Cutter and the 1976 swine flu campaign, some largely fabricated, like William Tebb’s invented nineteenth-century casualty statistics — that gave skeptics evidence, or the appearance of it, to point to. The debate has never been resolved so much as relitigated, generation after generation, against whatever the era’s most feared disease happens to be.

Disclaimer: The author writes independently. The views expressed here are his own and are not made on behalf of, and should not be attributed to, any hospital, university, or other institution with which he is affiliated. This article is a work of historical journalism, not medical advice.

Image generated by the author using ChatGPT.

Sources

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Sleep Apnea: When Your Body Forgets to Breathe at Night

By John Turley

On August 7, 2026

In Medicine

Imagine spending eight hours in bed and waking up more exhausted than when you went to sleep. You’re getting plenty of time under the covers, but somehow your body never gets the rest it desperately needs. For millions of Americans, this isn’t just an occasional bad night—it’s a nightly battle with a condition called sleep apnea, where breathing repeatedly stops and starts throughout the night.

Sleep apnea causes repeated interruptions in breathing during sleep, and it’s far more common than most people realize. Over 936 million adults worldwide aged 30-69 have some form of sleep apnea, though many don’t know they have it. The challenge is that the most dramatic symptoms happen while you’re unconscious, making it a disorder that often requires someone else to notice before you realize there’s a problem.

What Actually Happens During Sleep Apnea

The most common form is obstructive sleep apnea, which accounts for the vast majority of cases. During obstructive sleep apnea, the muscles in the back of the throat relax too much, causing the upper airway to collapse and interrupt breathing. Think of it like trying to breathe through a straw that keeps getting pinched shut—your body is trying to get air, but the pathway keeps getting blocked.

Each pause in breathing, called an apneic event, lasts at least 10 seconds and can occur dozens or even hundreds of times per night. When oxygen levels drop, your brain essentially sounds an alarm, triggering a brief arousal to restart breathing. These micro-awakenings fragment your sleep into tiny pieces, preventing you from getting the deep, restorative rest your body needs. The termination of each apneic event is associated with a transient arousal from sleep, but these don’t register in your conscious memory. You don’t wake up in the morning thinking “I woke up 247 times last night.” Instead, you just feel terrible despite thinking you slept through the night.

There’s also central sleep apnea, which works differently. With central sleep apnea, the brain fails to send proper signals to the breathing muscles during sleep. Instead of a physical blockage, it’s a communication breakdown between your brain and the muscles that control breathing. Some people even have complex sleep apnea, which combines both types.

How Sleep Apnea Gets Diagnosed

Doctors measure the severity of sleep apnea using the apnea-hypopnea index, which counts the average number of breathing pauses per hour. An AHI between 5 and 14 events per hour is considered mild, 15 to 29 is moderate, and 30 or more is severe. Someone with severe sleep apnea might stop breathing more times in a single night than they’d care to count.

The gold standard for diagnosis is polysomnography—an overnight sleep study conducted in a specialized lab. During polysomnography, doctors monitor brain waves through an electroencephalogram, track oxygen levels with pulse oximetry, measure airflow through temperature and pressure sensors, and use respiratory belts to monitor chest and abdomen movement. It’s like turning your body into a living data collection system for one night, with sensors measuring everything from your heart rate to how your legs move during different sleep stages.

For many people, though, home sleep testing is a more convenient option. Home sleep apnea tests use a limited subset of measurements—typically heart rate, oxygen levels, respiratory effort, body position, and nasal airflow. While these portable devices can’t capture everything a full lab study can, they’re often sufficient for diagnosis and much easier to arrange.

Treatment Options: From Lifestyle Changes to High-Tech Solutions

The most effective treatment for moderate to severe sleep apnea is continuous positive airway pressure therapy, better known as CPAP. CPAP works by delivering air through a mask to keep airways open during sleep. Think of it as a gentle wind tunnel that prevents your throat from collapsing. The device maintains constant air pressure, essentially splinting your airway open so you can breathe normally throughout the night.

But here’s the challenge: nearly half of patients don’t consistently use CPAP after the first month. The mask can be uncomfortable, some people find the pressure sensation strange, and it takes getting used to sleeping with equipment on your face. For people who can’t tolerate CPAP or have milder cases, there are alternatives like oral appliances that reposition the jaw and tongue to keep the airway open.

Surgery is another option, though it’s typically reserved for specific situations. Surgical options include procedures to remove enlarged tonsils or adenoids, or to address abnormalities causing airway obstruction. There’s even a newer treatment called hypoglossal nerve stimulation, which uses an implanted device to stimulate the nerve controlling tongue movement, keeping it from blocking the airway.

For some people, lifestyle modifications can make a real difference, especially with mild cases. Weight loss often helps since obesity is a major risk factor for sleep apnea. Sleeping on your side instead of your back can reduce airway collapse, and avoiding alcohol before bed helps because alcohol relaxes throat muscles even more.

Sleep Apnea Versus Insomnia: Two Very Different Beasts

Here’s where things get interesting—and sometimes confusing. Sleep apnea and insomnia are fundamentally different disorders, yet they can look similar and even occur together. Sleep apnea is primarily a problem of abnormal breathing during sleep, while insomnia is an inability to fall asleep or stay asleep.

With insomnia, your brain is often the problem—it won’t shut off when you want it to. You lie awake with racing thoughts, or you fall asleep only to pop awake an hour later, mind already churning. People with insomnia are usually very aware that they’re having sleeping difficulties. They know exactly how long they’ve been staring at the ceiling.

Sleep apnea operates differently. Many people with sleep apnea don’t realize they have breathing problems during sleep, as the awakenings are so brief they’re not consciously aware of them. You might spend what feels like a full night asleep yet wake up exhausted. Your problem isn’t falling or staying asleep in the traditional sense, it’s that the sleep you’re getting is constantly interrupted and of terrible quality.

The plot twist is that these conditions can feed into each other. Sleep apnea causes numerous micro-awakenings that disrupt sleep and can lead to insomnia-like symptoms. When you’re waking up dozens or hundreds of times per night, even if you don’t fully remember it, your sleep architecture gets shredded. This fragmentation can trigger the hyperarousal and sleep anxiety characteristic of insomnia.

Between 30-50% of people with sleep apnea also experience chronic insomnia symptoms, a combination researchers call COMISA (comorbid insomnia and sleep apnea). This overlap creates treatment challenges because patients with both conditions may have difficulty tolerating CPAP due to frequent awakenings and an inability to fall back asleep with the mask in place.

How Would You Know If You Have Sleep Apnea?

This is the tricky part—you’re unconscious when it happens. Loud snoring, snorting, or gasping during sleep is a major warning sign, though not everyone who snores has sleep apnea and not everyone with sleep apnea snores. If you live alone, you might never hear these sounds yourself.

Often, it’s a bed partner who first notices something’s wrong. They might observe you stop breathing, then suddenly gasp or snort as you restart. People with sleep apnea often toss and turn and show signs of restless nighttime sleep, sometimes waking up with sheets twisted and pillows scattered.

The daytime symptoms are easier to recognize. Waking with a headache, not feeling refreshed despite adequate time in bed, and feeling tired throughout the day, even to the point of dozing off, can all signal sleep apnea. If you find yourself nodding off while reading, watching TV, or worst of all, driving, that’s a red flag. For many people, the only obvious symptom of sleep apnea is fatigue or excessive sleepiness during the day.

Other clues include waking up with a very dry mouth or sore throat (from breathing with your mouth open all night), frequent nighttime urination (sleep apnea can affect bladder sensation), difficulty concentrating, or mood changes. Some people even experience sexual dysfunction or decreased interest in sex due to the chronic sleep deprivation.

.The research suggests that some people may develop a heightened awareness over time, particularly if they also develop insomnia symptoms. Some patients with comorbid insomnia and sleep apnea may associate post-respiratory event awakenings with wakefulness, resulting in prolonged difficulty falling back asleep. In these cases, what started as unconscious micro-arousals can evolve into conscious awareness and anxiety about sleep disruption.

Why This All Matters

The health consequences of untreated sleep apnea extend far beyond feeling tired. Sleep apnea increases the risk of high blood pressure, irregular heart rhythms like atrial fibrillation, heart disease, and stroke. Each time your oxygen levels drop during a breathing pause, it stresses your cardiovascular system. Over months and years, this repeated stress can lead to serious complications.

There’s also the immediate danger of extreme daytime sleepiness. Excessive daytime sleepiness can cause microsleeps where you fall asleep for very brief periods—dangerous while driving or operating machinery. The cognitive fog, mood disturbances, and reduced productivity affect quality of life even if you never have a serious accident.

The good news is that treatment works. With proper diagnosis and appropriate therapy—whether that’s CPAP, an oral appliance, surgery, or lifestyle changes—most people see dramatic improvements in their sleep quality and daytime functioning. The key is recognizing the problem in the first place, which requires paying attention to those subtle clues your body provides during the day about what’s happening at night.

Medical Disclaimer

The information provided in this article is intended for general educational and informational purposes only and does not constitute medical advice. It should not be used as a substitute for professional medical advice, diagnosis, or treatment.
Always seek the guidance of a qualified healthcare provider with any questions you may have regarding a medical condition or treatment. Never disregard professional medical advice or delay seeking it because of something you have read here.

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

The author of this article is a licensed physician, but the views expressed here are solely those of the author and do not represent the official position of any hospital, health system, or medical organization with which the author may be affiliated.

Image generated by author using ChatGPT

Sources:

Mayo Clinic – Sleep Apnea: Symptoms and Causes
https://www.mayoclinic.org/diseases-conditions/sleep-apnea/symptoms-causes/syc-20377631

Cleveland Clinic – Sleep Apnea: What It Is, Causes, Symptoms & Treatment
https://my.clevelandclinic.org/health/diseases/8718-sleep-apnea

Merck Manual (Professional Edition) – Obstructive Sleep Apnea (OSA)
https://www.merckmanuals.com/professional/pulmonary-disorders/sleep-apnea/obstructive-sleep-apnea-osa

StatPearls/NCBI – Obstructive Sleep Apnea
https://www.ncbi.nlm.nih.gov/books/NBK459252/

American Lung Association – Obstructive Sleep Apnea Symptoms and Diagnosis
https://www.lung.org/lung-health-diseases/lung-disease-lookup/sleep-apnea/symptoms-diagnosis

Familial Hypertriglyceridemia

By John Turley

On July 28, 2026

In Medicine

When Fat in the Blood Runs in the Family

Most people know they should keep an eye on their cholesterol. But triglycerides — another type of fat circulating in the blood — often fly under the radar. For some families, though, high triglycerides aren’t just a lifestyle problem. They’re baked into the DNA. Familial hypertriglyceridemia (FHTG) is a hereditary condition in which the liver chronically overproduces fat-carrying particles, sending triglyceride levels well above what diet alone can fully explain. It’s more common than most people realize and is frequently under diagnosed. If left unaddressed it can trigger serious complications including pancreatitis and heart disease.

One of my earliest disappointments as a young physician was a patient with familial hypertriglyceridemia. He was in his late 20s and his triglycerides were running in the critical level. We tried multiple interventions and he was referred to multiple specialists. Unfortunately, he wasn’t able to make the lifestyle changes he needed to make and progressively got worse and worse before passing away in his mid-30s. Fortunately, we have better treatments now, but this still is potentially a dangerous disease.

This article walks through FHTG, what it is, what causes it, how it presents, how it’s diagnosed, and what modern medicine can actually do about it.

What Is Familial Hypertriglyceridemia?

Triglycerides are the most common form of fat in the body. After you eat, calories that your body doesn’t immediately need are converted into triglycerides and stored in fat cells. Between meals, hormones release these fats for energy. When this system gets stuck in the “on” position — or when the body doesn’t clear triglycerides efficiently — blood levels climb.

FHTG, technically classified as Type IV familial dyslipidemia, is a genetic disorder in which the liver overproduces very low-density lipoprotein (VLDL) particles — essentially the trucks that carry triglycerides through the bloodstream. The result is persistently elevated triglyceride levels, typically in the moderate-to-severe range, sometimes severe enough to become medically dangerous.

Normal fasting triglycerides are generally below 150 mg/dL. Borderline high falls between 150 and 199. In FHTG, levels often run 200–500 mg/dL or higher, and some patients can exceed 1,000 mg/dL, a threshold at which the risk of acute pancreatitis rises sharply.

Etiology: The Genetic Story Is More Complicated Than Expected

For decades, FHTG was described in textbooks as a straightforward autosomal dominant disorder — meaning one copy of a faulty gene was enough to cause the condition, and each child of an affected parent had a 50% chance of inheriting it. That picture has been substantially revised by modern genetics.

It turns out that FHTG is primarily polygenic — driven not by a single dramatic mutation but by the cumulative effect of many small genetic variants. Studies have now identified more than 300 independent genetic locations associated with plasma triglyceride levels. No single gene tells the whole story. Instead, a person inherits a kind of genetic “load” that creates susceptibility — and whether that susceptibility becomes clinically apparent often depends on environmental triggers.

The genes involved all play a role in how the body metabolizes fat-carrying particles. Heterozygous (single-copy) variants in these genes are common in most FHTG patients. The much rarer and more severe familial chylomicronemia syndrome (FCS) both copies are defective producing extreme triglyceride elevations and a very different clinical picture.

Environmental factors that worsen FHTG include obesity, poorly controlled diabetes, alcohol use, a diet heavy in refined carbohydrates and sugars, estrogen-containing medications, and certain drugs such as corticosteroids and beta-blockers. In many patients, the genetic predisposition only becomes clinically obvious when one or more of these environmental triggers is present — which explains why the condition often goes undetected until adulthood.

Symptoms: The Quiet Condition

One of FHTG’s most deceptive features is that it is often silent. Many people carry the condition for years without a single symptom, discovering it only through routine blood work or a family history investigation. This is why widespread lipid screening is so important — FHTG doesn’t announce itself with chest pain or obvious physical signs, at least not initially.

When symptoms first appear, they are often subtle and tend to reflect either the degree of triglyceride elevation or the presence of associated conditions. In cases of moderate elevation, patients might experience vague fatigue, weight gain, or features of metabolic syndrome — high blood pressure, elevated blood sugar, increased waist circumference.

At higher triglyceride levels, more distinctive signs can emerge. Xanthomas, yellowish, waxy deposits of fat under the skin, may appear, particularly around the eyelids (xanthelasmas) or over the elbows, knees, or tendons. The liver may enlarge (hepatomegaly), reflecting fat accumulation. An eye exam may show lipemia retinalis — a milky or salmon-pink discoloration of the retinal blood vessels — visible with an ophthalmoscope when triglycerides are extremely high.

The most dangerous symptom is severe abdominal pain signaling acute pancreatitis. When triglycerides exceed 1,000 mg/dL, the pancreas can become inflamed as it is overwhelmed by fat-rich particles. This is a medical emergency. Nausea, vomiting, and upper abdominal pain radiating to the back are warning signs that warrant immediate evaluation.

There is also an increased risk of early cardiovascular disease in FHTG patients, particularly when metabolic syndrome is present, though the relationship between triglycerides alone and heart disease risk is more nuanced than it is with LDL cholesterol.

Diagnosis: Getting the Full Picture

Diagnosis begins with a standard fasting lipid panel — a blood test that measures total cholesterol, LDL, HDL, and triglycerides. In FHTG, the hallmark findings are elevated triglycerides and VLDL, often accompanied by low HDL (the so-called “good” cholesterol). LDL levels may be normal or even low, which can sometimes falsely reassure both patients and physicians.

Because many things can raise triglycerides — including a meal eaten before the blood draw, excess alcohol, diabetes, hypothyroidism, kidney disease, and certain medications — the first step is ruling out secondary causes. A thorough personal and family history is essential. A clinician who asks about triglycerides in parents or siblings or even children is doing exactly what the guidelines recommend.

The “familial” part of the diagnosis is confirmed when multiple first-degree relatives are found to have elevated triglycerides, when the elevation persists despite controlling for secondary causes, and when the pattern fits what we’d expect from a heritable condition appearing across generations.

Genetic testing can identify specific variants in the related genes, but it is not required for a clinical diagnosis and is not routinely performed. Genetic testing may be ordered when the clinical picture is severe or ambiguous, or when distinguishing FHTG from the rarer familial chylomicronemia syndrome which has treatment implications such as the emerging targeted therapies.

Current guidelines also recommend evaluating for cardiovascular risk in patients with mild-to-moderate FHTG, and for pancreatitis risk in those with severe elevations.

Treatment: A Layered Approach

Lifestyle First

The cornerstone of FHTG management — at least for mild-to-moderate disease — is lifestyle modification, and it can be remarkably effective. Cutting refined carbohydrates and added sugars is particularly powerful. Saturated fat primarily raises LDL cholesterol, but it is carbohydrates that drive hepatic triglyceride production. Alcohol is another major player. Even moderate consumption can substantially raise triglycerides in susceptible individuals, and abstinence often produces dramatic improvements.

Weight loss, regular aerobic exercise, and tight blood sugar control in patients with diabetes or prediabetes round out the lifestyle toolkit. Estrogen-containing contraceptives or hormone replacement therapy should be reconsidered in women with FHTG, as estrogen directly stimulates hepatic VLDL production and can push levels dangerously high.

Pharmacologic Options

When lifestyle changes aren’t enough, several drug classes are available. Fibrates (such as fenofibrate and gemfibrozil) are the most established triglyceride-lowering medications and can reduce levels by 30–50%. They work primarily by activating receptors that enhance triglyceride clearance.

Omega-3 fatty acids at prescription doses (2–4 grams per day) provide another option. High dose eicosapentaenoic acid (EPA), specifically the formulation icosapent ethyl (Vascepa), has demonstrated cardiovascular benefit in a major clinical trial in high-risk patients with elevated triglycerides who are already on statin therapy.

Niacin (nicotinic acid) was once widely used but has fallen out of favor after clinical trials failed to show cardiovascular benefit on top of statin therapy, despite its triglyceride-lowering ability. It is also poorly tolerated due to its side effect profile and patients frequently are noncompliant.

Statins are prescribed primarily to manage cardiovascular risk and LDL cholesterol rather than to lower triglycerides directly, though they have a modest effect on the latter.

Emerging Therapies

Perhaps the most exciting development in recent years is the arrival of RNA-based medications targeting apolipoprotein C-III (APOC3) — a protein that inhibits the clearance of triglyceride-rich particles. By silencing the gene that produces APOC3, these drugs can achieve dramatic reductions in triglyceride levels even in patients who don’t respond to conventional therapies.

Olezarsen received FDA approval in 2024 for patients with familial chylomicronemia syndrome. Its application in FHTG more broadly is an active area of clinical investigation. Similarly, drugs targeting angiopoietin-like proteins are under study, offering the prospect of precision medicine approaches to a condition that has long resisted fully effective treatment.

Prognosis: Manageable, But Not to Be Ignored

The prognosis for FHTG is generally favorable when the condition is identified and managed appropriately. Unlike some other inherited lipid disorders, FHTG is not automatically associated with dramatically elevated cardiovascular risk — particularly when LDL and HDL levels are otherwise reasonable. This distinguishes it from conditions like familial hypercholesterolemia, where premature heart disease is nearly inevitable without treatment.

That said, FHTG patients frequently carry additional cardiovascular risk factors as part of the metabolic syndrome package that must be addressed in its own right. The American Heart Association has noted that this clustering of risk factors likely elevates cardiovascular risk in FHTG patients beyond what triglycerides alone would predict.

The more immediate and measurable danger in FHTG is pancreatitis. When triglycerides are severely elevated, the risk of a potentially life-threatening inflammatory episode of the pancreas is real. Repeated bouts of pancreatitis can cause chronic damage, that impairs digestive function and increases the risk of pancreatic cancer. Preventing severe hypertriglyceridemia through consistent management — lifestyle, medication, or both — is not optional for high-risk patients.

With appropriate care, most patients with FHTG can expect to live a normal lifespan. The key predictors of outcome are compliance with dietary and lifestyle changes, appropriate use of medication when indicated, regular lipid monitoring, and attention to comorbidities like diabetes and hypertension. Family members of affected individuals also should be screened.

Bottom Line

Familial hypertriglyceridemia is one of those conditions that rewards attention and penalizes neglect. It runs quietly in families, often masked by other lifestyle factors until a crisis — a pancreatitis episode, an unexpected cardiovascular event — brings it to light. Modern genetics has revealed it to be more complex than once thought, driven by a mosaic of variants rather than a single defective gene. Treatment has evolved accordingly: from basic dietary counseling to sophisticated RNA-based drugs that target the fat metabolism pathway at the molecular level.

If you have a family history of high triglycerides, early heart disease, or pancreatitis of unclear cause, it’s worth having a conversation with your doctor about a fasting lipid panel and a careful family history review. Knowing is the first step to managing.

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Image generated by author using ChatGPT.

Sources

• MedlinePlus – Familial Hypertriglyceridemia

• NCBI StatPearls – Familial Hypertriglyceridemia (2024)

• Wikipedia – Familial Hypertriglyceridemia

• PMC – Genetics of Hypertriglyceridemia (Dron & Hegele, 2020)

• PMC – Understanding Hypertriglyceridemia: Integrating Genetic Insights (2024)

• PMC – Diagnosis and Treatment of Hypertriglyceridemia

• PMC – Severe Hypertriglyceridemia and Chylomicronemia Syndrome

• PMC – Pancreatic and Cardiometabolic Complications of Severe Hypertriglyceridemia (2024)

• Springer – The Genetic Basis of Hypertriglyceridemia

• Medscape – Hypertriglyceridemia: Background, Etiology, Pathophysiology

• PMC – Olezarsen for Familial Chylomicronemia Syndrome (2024-2025)

• Endocrine Society – Evaluation and Treatment of Hypertriglyceridemia (Clinical Practice Guideline)

• Cleveland Clinic – Hypertriglyceridemia: Causes, Risk Factors & Treatment

Eating Well for the Long Run: How Your Nutritional Needs Change as You Age

By John Turley

On July 20, 2026

In Medicine

Growing older is often described as a gradual process, but many of the body’s changes begin earlier than most people realize. By our thirties, we slowly begin to lose muscle mass. By our fifties and sixties, our metabolism slows, bones become more fragile, digestion changes, and our bodies become less efficient at absorbing certain nutrients. None of this means declining health is inevitable. In fact, one of the most powerful tools for maintaining strength, independence, and quality of life is something we do every day: eat.

The nutritional needs of older adults are different from those of younger adults—not because the body suddenly requires exotic foods or expensive supplements, but because it becomes less forgiving of nutritional shortfalls. While calorie requirements often decline as physical activity decreases and muscle mass diminishes, the need for high-quality nutrients remains the same or even increases. Nutritionists refer to this as the challenge of nutrient density: getting more nutrition from fewer calories.

The goal of eating well in later life is not simply to prevent disease. It is to preserve muscle, maintain cognitive function, support the immune system, protect the heart and bones, and help people remain active and independent for as long as possible.

Protein: The Cornerstone of Healthy Aging

Protein is perhaps the most important of all nutrients as we age. Beginning around age 30, adults lose approximately 3 to 8 percent of their muscle mass each decade. After age 60, the rate often accelerates. This gradual decline, known as sarcopenia, contributes to weakness, slower walking speed, impaired balance, increased risk of falls, and loss of independence. During illness or hospitalization, muscle can disappear surprisingly quickly, making recovery more difficult.

The problem is compounded by what scientists call anabolic resistance. Aging muscle simply does not respond to protein as efficiently as younger muscle. Older adults must consume more protein—and distribute it more evenly throughout the day—to stimulate muscle repair and growth.

The Recommended Dietary Allowance is 0.8 grams of protein per kilogram of body weight— that’s about 80 grams for a 160-pound adult. For reference, a 4 oz serving of salmon has about 22 grams of protein. Many geriatric nutrition experts recommend 1.0 to 1.2 grams per kilogram daily for healthy adults over age 65. Those recovering from surgery, injury, or serious illness may require1.2 to 1.5 grams per kilogram, but only under medical supervision.

Equally important is timing. Many Americans consume very little protein at breakfast, a modest amount at lunch, and most of it at dinner. Research suggests muscle responds better when approximately 25 to 30 grams of protein are consumed at each meal.

Excellent sources include fish, poultry, lean meat, eggs, Greek yogurt, cottage cheese, beans, lentils, tofu, soy products, nuts, and seeds. Dairy proteins such as whey are especially rich in leucine, an amino acid that plays a central role in stimulating muscle protein synthesis.

Nutrition alone, however, is only part of the equation. Resistance training—even with light weights or resistance bands—works hand in hand with adequate protein to preserve muscle throughout later life.

Carbohydrates: Choosing Quality Over Quantity

Carbohydrates have acquired an undeserved reputation in many popular diets. In reality, they remain the body’s preferred source of energy and are especially important for the brain, which relies heavily on glucose to function.

The key is not eliminating carbohydrates but selecting healthier ones.

As we age, our bodies often become less sensitive to insulin, making blood sugar regulation more challenging. Highly refined carbohydrates—white bread, pastries, sugary beverages, and many processed snack foods—cause rapid spikes in blood glucose followed by equally rapid declines. Over time, these fluctuations may contribute to weight gain, insulin resistance, and type 2 diabetes.

Complex carbohydrates digest more slowly, providing a steadier release of energy while supplying vitamins, minerals, and fiber. Whole grains such as oatmeal, barley, brown rice, and whole-wheat bread are excellent choices. Fruits, vegetables, beans, and lentils provide carbohydrates along with antioxidants and phytochemicals that support overall health.

Contrary to popular belief, potatoes are not inherently unhealthy. Preparation matters. A baked potato with its skin offers potassium, vitamin C, and fiber, whereas deep-fried potatoes or heavily buttered mashed potatoes provide considerably more calories and saturated fat.

Many older adults find that emphasizing minimally processed carbohydrates improves energy levels and helps maintain stable blood sugar throughout the day.

Fiber: The Unsung Hero

Fiber is one of the most overlooked nutrients in the American diet, yet it becomes increasingly important with age.

Digestive motility naturally slows as we grow older. Physical inactivity, inadequate fluid intake, and medications—including opioid pain relievers, some antidepressants, calcium supplements, and certain blood pressure medications—can further contribute to constipation.

Fiber helps keep the digestive system functioning normally by increasing stool bulk and promoting regular bowel movements. But its benefits extend well beyond the gastrointestinal tract.

A high-fiber diet lowers LDL (“bad”) cholesterol, slows glucose absorption, improves blood sugar control, supports healthy gut bacteria, and increases feelings of fullness, helping many people maintain a healthy weight.

Current recommendations suggest approximately 30 grams of fiber daily for older men and about 21 grams for older women, although most Americans consume substantially less.

Good sources include fresh fruits, vegetables, legumes, oats, bran cereals, nuts, seeds, and whole grains.

Fiber should always be increased gradually while maintaining adequate fluid intake. Without sufficient water, increasing fiber can actually worsen constipation.

Healthy Fats Continue to Matter

Fat remains an essential nutrient throughout life.

Healthy fats provide energy, help build cell membranes, assist in hormone production, reduce inflammation, and allow absorption of the fat-soluble vitamins A, D, E, and K.

Perhaps most importantly, healthy fats support cardiovascular health, an increasingly important consideration with advancing age.

Monounsaturated fats found in olive oil, avocados, almonds, pecans, pistachios, and peanuts remain among the healthiest dietary choices.

Particularly valuable are the marine omega-3 fatty acids EPA and DHA found in salmon, trout, sardines, herring, and mackerel. Numerous studies have shown that these fats lower triglyceride levels and are associated with improved cardiovascular health. Some research also suggests they may help preserve cognitive function, although evidence remains mixed.

Plant sources such as flaxseed, chia seeds, walnuts, and canola oil provide alpha-linolenic acid (ALA), another beneficial omega-3 fatty acid.

By contrast, trans fats should be avoided whenever possible, while saturated fats from fatty meats, butter, and highly processed foods are best consumed in moderation.

Hydration: The Forgotten Nutrient

Water is not technically a nutrient, yet it may be one of the most important components of healthy aging.

Older adults are especially vulnerable to dehydration for several reasons. The sensation of thirst becomes less reliable with age, kidney function changes, and many medications—including diuretics—promote fluid loss. Some older individuals intentionally drink less because of concerns about urinary urgency or nighttime trips to the bathroom.

Even mild dehydration can produce fatigue, headaches, dizziness, constipation, confusion, kidney stones, urinary tract infections, and an increased risk of falls.

Unlike younger adults, older people should not rely solely on thirst as a signal for their fluid needs.

Most healthy older adults benefit from drinking fluids consistently throughout the day. Water is the best choice, but milk, tea, coffee, soups, and water-rich foods such as melons, oranges, cucumbers, tomatoes, and berries all contribute to hydration.

The color of the urine offers a practical guide. Pale yellow generally indicates adequate hydration, whereas dark yellow urine often suggests that additional fluids are needed, although certain medications and vitamins can alter urine color.

Calcium, Vitamin D, and Bone Health

Bone is living tissue that is constantly remodeled throughout life. With age, bone breakdown gradually exceeds bone formation, increasing the risk of osteoporosis and fractures.

Adequate calcium remains important, but vitamin D is equally critical because it enables calcium absorption from the intestine. Unfortunately, aging skin produces less vitamin D in response to sunlight, and many older adults spend less time outdoors.

Dairy products, fortified plant milks, canned salmon with bones, and leafy green vegetables contribute calcium, while fatty fish and fortified foods provide modest amounts of vitamin D.

Because deficiency is common, many physicians recommend vitamin D supplementation based on blood test results.

Vitamin B12: A Common but Often Silent Deficiency

Vitamin B12 deserves special attention because deficiency becomes increasingly common after age 60.

Normal absorption requires adequate stomach acid to separate vitamin B12 from proteins in food. Aging, along with medications such as proton pump inhibitors and metformin, often reduces stomach acidity.

Symptoms may develop gradually and include fatigue, numbness or tingling in the hands and feet, difficulty walking, poor balance, memory problems, depression, and anemia.

Fortunately, crystalline vitamin B12 found in supplements and fortified foods bypasses many of these absorption problems and is highly effective in preventing or correcting deficiency.

Do Supplements Become More Important?

For many older adults, the answer is yes—but only selectively.

The ideal source of nutrition remains a balanced diet rich in vegetables, fruits, whole grains, legumes, lean proteins, dairy or fortified alternatives, nuts, seeds, and healthy oils. Foods contain thousands of biologically active compounds that supplements cannot fully replicate.

Nevertheless, certain supplements become increasingly useful as people age.

Vitamin D is among the most commonly recommended because deficiency is widespread and can adversely affect bone and muscle health. Vitamin B12 supplementation is appropriate for many older adults, particularly those taking metformin or acid-suppressing medications or those with laboratory evidence of deficiency.

Calcium supplements may be useful when dietary intake is inadequate, although obtaining calcium from food is generally preferred because large supplemental doses have been associated with possible cardiovascular concerns.

Protein powders and ready-to-drink nutritional shakes can help individuals with poor appetite, difficulty chewing, chronic illness, or increased protein requirements. Whey protein is especially effective because of its high leucine content.

Omega-3 supplements may benefit individuals who rarely consume fish, although eating fish remains the preferred strategy.

One supplement attracting increasing attention is creatine monohydrate. Long used by athletes, creatine has substantial evidence supporting its ability to improve muscle strength and enhance the benefits of resistance exercise in older adults. When taken in appropriate doses by healthy individuals, it appears remarkably safe, though people with significant kidney disease should consult their physician before using it.

In contrast, the evidence for many heavily marketed anti-aging supplements—including collagen powders, testosterone boosters, proprietary muscle blends, and high-dose antioxidant formulas—is considerably weaker. Some may offer modest benefits in selected circumstances, but many lack rigorous scientific support.

See my earlier post for more information: Supplement Smarts: What Seniors Should Know Before Reaching for That Bottle

Eating for Health, Not Simply Longevity

Nutrition is not about adding years to life alone. It is about adding life to those years.

A healthy diet cannot stop aging, but it can influence how well we age. Adequate protein helps preserve muscle and independence. Healthy carbohydrates provide steady energy. Fiber supports digestive and cardiovascular health. Unsaturated fats protect the heart and nourish the brain. Proper hydration reduces illness and maintains physical and mental function. Carefully selected supplements can fill nutritional gaps when food alone is insufficient.

Perhaps the most encouraging news is that it is never too late to benefit. Studies consistently show that older adults who improve their diet, remain physically active, and maintain adequate protein intake can increase muscle strength, improve balance, reduce the risk of chronic disease, and enhance quality of life—even well into their seventies, eighties, and beyond.

The old saying that “you are what you eat” may oversimplify nutrition, but it captures an enduring truth. As the years accumulate, every meal becomes another opportunity to nourish not just the body, but the ability to continue living fully, independently, and well.

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Image generated by author using ChatGPT.

References

Bauer J, Biolo G, Cederholm T, et al. Evidence-Based Recommendations for Optimal Dietary Protein Intake in Older People. Journal of the American Medical Directors Association. 2013.

Deutz NEP, Bauer JM, Barazzoni R, et al. Protein intake and exercise for optimal muscle function with aging. Clinical Nutrition. 2014.

Volpi E, Campbell WW, Dwyer JT, et al. Is the Optimal Level of Protein Intake for Older Adults Greater Than the Recommended Dietary Allowance? The Journals of Gerontology: Series A. 2013.

U.S. Department of Agriculture & U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2025–2030. https://www.dietaryguidelines.gov

National Institute on Aging. Healthy Eating As You Get Older. https://www.nia.nih.gov/health/healthy-eating

National Institutes of Health Office of Dietary Supplements. https://ods.od.nih.gov

European Society for Clinical Nutrition and Metabolism (ESPEN). Guideline on Clinical Nutrition and Hydration in Geriatrics. https://www.espen.org

When the Body’s Blueprint Has a Flaw: A Look at Ehlers-Danlos Syndrome

By John Turley

On July 10, 2026

In Medicine

Understanding the Disorder

Most people have heard of arthritis, lupus, or osteoporosis, but relatively few recognize the name Ehlers-Danlos syndrome (EDS). Yet this group of inherited connective tissue disorders affects thousands of people worldwide and can profoundly alter nearly every aspect of daily life. For some, it means unusually flexible joints and chronic pain. For others, it carries the risk of ruptured blood vessels or internal organs. Between these extremes lies a remarkably diverse family of disorders that illustrates just how important the body’s structural framework truly is.

Ehlers-Danlos syndrome is not a single disease but a collection of thirteen recognized hereditary disorders that share one common feature: abnormalities in connective tissue. Connective tissue forms the body’s internal scaffolding, providing strength, flexibility, and support to the skin, joints, blood vessels, ligaments, tendons, and many internal organs. When this framework is weakened, the effects can extend throughout the body.

Although EDS has long been considered rare, growing awareness and improved diagnostic methods suggest it may be more common than previously believed. Many individuals spend years seeking an explanation for symptoms that are dismissed as unrelated or attributed to anxiety, chronic pain syndromes, or simple clumsiness. Increased recognition has begun shortening this diagnostic journey, but many patients still experience significant delays before receiving an accurate diagnosis.

The Biology Behind EDS

At the heart of Ehlers-Danlos syndrome is collagen, the most abundant protein in the human body. Collagen functions much like the steel reinforcing bars embedded within concrete. It gives tissues strength while allowing them to remain flexible enough to move without tearing.

Collagen is found almost everywhere, including the skin, tendons, ligaments, cartilage, bones, blood vessels, intestines, and the protective coverings surrounding many organs. Multiple genes direct the production, assembly, and maintenance of collagen fibers and other components of the extracellular matrix—the microscopic framework that supports cells throughout the body.

In EDS, inherited genetic mutations interfere with this process. Depending on which gene is affected, collagen may be produced incorrectly, assembled improperly, or fail to provide adequate structural support. The resulting weakness affects whichever tissues rely most heavily on the defective protein.

The pattern of inheritance varies among the different forms of EDS. Many are inherited in an autosomal dominant fashion, meaning that a child has a 50 percent chance of inheriting the disorder if one parent carries the abnormal gene. Other forms are autosomal recessive, requiring defective copies from both parents, while some cases result from entirely new mutations with no previous family history.

One notable exception remains the most common subtype: hypermobile Ehlers-Danlos syndrome (hEDS). Despite years of intensive research, no single genetic mutation has yet been identified. As a result, hEDS remains a clinical diagnosis based on characteristic symptoms and examination findings rather than laboratory confirmation. Identifying its underlying genetic basis is one of the major goals of current EDS research.

The syndrome bears the names of two physicians who helped characterize it in the early twentieth century: Danish dermatologist Edvard Ehlers and French physician Henri-Alexandre Danlos.

A Family of Disorders

The 2017 International Classification recognizes thirteen distinct forms of Ehlers-Danlos syndrome. While all involve connective tissue abnormalities, each subtype has its own characteristic pattern of symptoms and complications.

Hypermobile EDS

Hypermobile EDS is by far the most frequently diagnosed subtype. Its defining features include generalized joint hypermobility, chronic musculoskeletal pain, and varying degrees of skin involvement. Individuals may be able to bend their fingers, elbows, knees, or spine far beyond the normal range of motion.

Although hypermobility can appear impressive, it often comes at a significant cost. Joints that move too freely lack stability, making them prone to sprains, partial dislocations, and complete dislocations during everyday activities. Chronic pain and fatigue frequently become the most disabling aspects of the disorder.

Many people with hypermobile EDS also experience additional conditions that appear to occur more frequently than expected. These include disorders of the autonomic nervous system, particularly postural orthostatic tachycardia syndrome (POTS), gastrointestinal motility problems, chronic headaches, and persistent fatigue. Researchers continue to investigate why these conditions commonly occur together.

Classical EDS

Classical EDS primarily affects the skin and joints. It usually results from mutations involving genes responsible for type V collagen.

Patients typically have remarkably soft, velvety skin that stretches much farther than normal before returning to its original position. Wounds often heal poorly, producing thin, widened scars sometimes described as “cigarette-paper scars.” Easy bruising is common, and even relatively minor injuries may leave permanent marks.

Joint hypermobility is also a prominent feature, although the degree varies considerably from person to person.

Vascular EDS

Among all forms of Ehlers-Danlos syndrome, vascular EDS is the most serious. It results from mutations affecting type III collagen, an important structural protein within blood vessel walls and many internal organs.

Unlike the dramatic flexibility often seen in hypermobile EDS, patients with vascular EDS may have only mild joint laxity, usually involving the small joints of the hands and feet. Instead, the major concern is tissue fragility.

Arteries may develop aneurysms, tears, or spontaneous ruptures. The intestines and uterus are also unusually fragile, creating life-threatening medical emergencies that often occur without warning.

Many individuals with vascular EDS also have recognizable physical characteristics, including thin translucent skin, prominent veins, a narrow nose, thin lips, and relatively large, prominent eyes. These findings, however, are not present in every patient.

The Rarer Forms

The remaining subtypes are uncommon, with some documented in only a small number of families worldwide.

Kyphoscoliotic EDS often presents during infancy with severe muscle weakness and progressive curvature of the spine. Arthrochalasia EDS causes profound joint instability beginning at birth, while dermatosparaxis EDS produces exceptionally fragile, sagging skin that tears easily.

Other rare forms primarily affect the eyes, heart valves, muscles, teeth, or periodontal tissues. Although individually uncommon, these disorders illustrate how connective tissue supports virtually every organ system in the body.

One Disease, Many Presentations

One of the greatest challenges in understanding Ehlers-Danlos syndrome is its extraordinary variability. Even individuals carrying the same genetic mutation may experience dramatically different symptoms and levels of disability. Some remain physically active with relatively mild limitations, while others develop chronic pain, repeated joint injuries, or life-threatening vascular complications.

This wide spectrum often complicates diagnosis. Physicians unfamiliar with EDS may not immediately recognize that seemingly unrelated symptoms—frequent sprains, digestive problems, easy bruising, chronic fatigue, headaches, and dizziness—can all stem from a single underlying connective tissue disorder.

Ehlers-Danlos syndrome occupies a peculiar position in medicine: common enough that most physicians will encounter it, but rare enough — and complex enough — that many will misidentify it or underestimate it. As awareness grows and genetic testing becomes more accessible, diagnostic delays are slowly shortening.

For patients living with EDS today, the message is mixed but not without hope. For most, a normal lifespan is likely, though the journey will require proactive self-advocacy, knowledgeable medical partnerships, and real-world adaptation. For those with vascular EDS, the risks are serious and demand vigilance — but even here, the medical community is making progress.

Recognizing these patterns is the first step toward appropriate treatment. Although EDS cannot currently be cured, an accurate diagnosis allows patients and physicians to anticipate complications, tailor therapy, and improve long-term quality of life.

For a more detailed discussion of EDS, contact me at WWW.grumpydocwv@gmail.com

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Illustration Generated by author using ChatGPT.

Sources and Further Reading:

Note: The 2017 diagnostic classification is the current standard; updated criteria are expected in 2026.

1. Francomano et al. (2024). Research advances in EDS. Frontiers in Medicine

2. Ritelli & Colombi (2020). Molecular Genetics and Pathogenesis of EDS. Genes, MDPI

3. Zschocke et al. (2024). Genetic diagnosis of EDS. Medical Genetics / NIH

4. StatPearls: Ehlers-Danlos Syndrome (2023). NCBI Bookshelf

5. GeneReviews: Classic EDS (updated 2024). NCBI Bookshelf

6. GeneReviews: Vascular EDS (updated 2025). NCBI Bookshelf

7. MedlinePlus Genetics: Ehlers-Danlos Syndrome. NIH MedlinePlus

8. Cleveland Clinic: EDS Overview. my.clevelandclinic.org

9. Cleveland Clinic: Vascular EDS. my.clevelandclinic.org

10. Medscape: EDS Background and Pathophysiology. emedicine.medscape.com

11. MSD Manual Professional: EDS in Pediatrics. msdmanuals.com

12. Frank et al. (2019). Vascular EDS: Long-Term Observational Study. Journal of the American College of Cardiology / ScienceDirect

13. Case Report: Novel COL3A1 mutation in vEDS. PMC / NCBI

14. EDS Society: The Road to 2026. eds.clinic

15. EDS Society: Life Expectancy in EDS. eds.clinic

C-Reactive Protein: The Body’s Inflammation Alarm

By John Turley

On July 3, 2026

In Medicine

Structure, Function, Testing, and Clinical Implications

If you’ve ever had blood drawn during a bout of illness or a workup for heart disease risk, there’s a decent chance your doctor ordered a C-reactive protein test, usually shortened to CRP. It’s one of the most widely ordered lab tests in the world. CRP is one of the body’s most sensitive early-warning systems for inflammation. Understanding where it comes from, what it does, and how doctors use it reveals a lot about how the immune system operates and why chronic low-grade inflammation has become such a central concern in modern medicine. Warning: doctor talk will follow.

A Protein With a Peculiar Origin Story

CRP was discovered almost by accident in 1930 by William Tillett and Thomas Francis, working in Oswald Avery’s laboratory at Rockefeller University. They were studying patients with acute pneumococcal pneumonia caused by the bacteria Streptococcus pneumoniae and noticed that blood from acutely ill patients caused a specific bacterial substance to clump together. That substance was the “C polysaccharide” in the bacterial cell wall, which gave the protein its name.

For decades CRP was used as a crude yes-or-no indicator of serious infection. It wasn’t until the late 20th century that more sensitive lab techniques revealed its value for detecting the subtle, chronic inflammation now linked to cardiovascular disease and opening a major new chapter in preventive medicine. I had been in practice for several years before I even became aware of CRP.

Shape Matters: The Five-Sided Structure of CRP

CRP belongs to a protein family called the pentraxins, named from the Greek word for “five” because of the protein’s pentagonal shape. Under an electron microscope, CRP looks like five identical subunits arranged in a ring, roughly like five coins fanned into a disc. For history buffs, it resembles the five-star rank worn by General Eisenhower.

Each subunit carries a binding site made of two calcium ions nestled next to a small hydrophobic pocket. This is where CRP does its recognition work: the calcium-dependent sites allow it to grab onto phosphocholine (PC), a molecule found in the membranes of damaged and dying cells, as well as in the outer coatings of many bacteria and fungi. Phosphocholine is so widespread in biology that this single binding chemistry lets CRP respond to an enormous range of threats including microbial invaders and the body’s own dead cells.

CRP doesn’t always exist in this five-subunit ring form. The pentameric version (pCRP) circulates in healthy blood. But at sites of active tissue damage, such as inside an inflamed artery wall, it can break apart into individual monomers (mCRP). These two forms turn out to have strikingly different effects on the immune system.

What CRP Does

It’s tempting to think of CRP as a passive number on a lab report, but it’s actually an active participant in the immune response. It plays at least four major roles.

First, CRP is a pattern recognition molecule. Unlike the antibodies generated by your adaptive immune system which take days or weeks to respond to a specific threat, CRP responds immediately to general molecular patterns shared by pathogens and damaged cells. This makes it a first-responder tool within the innate immune system, the body’s rapid defense network.

Second, once CRP binds to a pathogen or dying cell, it acts as an opsonin, essentially a molecular flag that says “eat this.” Immune cells called phagocytes (macrophages and neutrophils) recognize CRP-coated targets and engulf them, accelerating the clearance of both bacteria and cellular debris.

Third, CRP can activate the complement system, a cascade of proteins that further tags pathogens for destruction. Crucially, CRP appears to stop short of triggering the most destructive steps of that cascade. The net effect is a measured, targeted immune response rather than an all-out inflammatory assault.

Fourth, and this is where things get interesting, the pentameric and monomeric forms of CRP have opposing effects. The pentameric form in circulation is primarily anti-inflammatory, quietly clearing dead cells without triggering unnecessary immune activation. But the monomeric form that appears at sites of tissue damage can amplify inflammation: activating platelets, recruiting immune cells to vessel walls, and stimulating the release of the inflammatory signaling molecule. CRP is neither simply good nor simply bad — it’s context-dependent, functioning as a careful janitor in healthy tissue but potentially fanning the flames in already-inflamed environments.

Fast, Sensitive, and Liver-Made

CRP is produced primarily by liver cells (hepatocytes) in response to immune signals. When immune cells detect infection or tissue damage, they release cytokines, which travel to the liver and switch on CRP production.

One of CRP’s great clinical virtues is speed. Levels can begin rising within four to six hours of an inflammatory event and typically peak within 24 to 48 hours. When the inflammation resolves, CRP falls just as quickly, its half-life in circulation is only about 19 hours. This fast-on, fast-off behavior makes CRP an excellent real-time readout of what the immune system is doing right now, not weeks ago. Because of this early availability, it is referred to as an acute phase reactant.

Under normal, non-inflammatory conditions, CRP in the blood typically measures below 1 milligram per liter (mg/L). During serious bacterial infection or major tissue injury, levels can spike above 400 mg/L — a several-hundred-fold increase. CRP also has a practical advantage for testing: it doesn’t fluctuate throughout the day, and fasting is not required before a blood draw.

The Many Uses of CRP in Clinical Medicine

The oldest application of CRP testing is detecting and monitoring bacterial infection. Very high values — generally above 100 mg/L — strongly suggest bacterial rather than viral infection, since viruses tend to provoke a much more modest CRP rise. In sepsis (the life-threatening systemic response to infection), CRP is one of several markers used to assess severity and track the response to treatment.

CRP is also routinely used to monitor autoimmune diseases. In rheumatoid arthritis, CRP is included in standard disease activity scoring tools. Tracking CRP over time helps clinicians judge whether treatments like disease-modifying drugs are working. One notable exception: in systemic lupus erythematosus (SLE), CRP often stays surprisingly low even during active flares.

Perhaps the most debated expansion of CRP testing in recent decades is its role in cardiovascular risk assessment. That story begins with the recognition that atherosclerosis, the plaque buildup inside artery walls, is fundamentally an inflammatory process, not just a plumbing problem caused by too much cholesterol. As that insight took hold in the 1990s, researchers began asking whether CRP could predict heart attack risk the way cholesterol does.

The answer was yes, but only with a more sensitive test. Standard CRP assays can’t detect levels below about 10 mg/L, which is fine for infections but misses the chronic low-level inflammation relevant to cardiovascular risk. A newer high-sensitivity CRP test (hs-CRP) can measure levels as low as 0.01 mg/L. Using hs-CRP, researchers found that even modest CRP elevations, within the range once considered entirely normal, carry meaningful cardiovascular risk.

The American Heart Association and the CDC use these hs-CRP thresholds for cardiovascular risk: below 1 mg/L is low risk; 1 to 3 mg/L is intermediate risk; above 3 mg/L is higher risk. A large UK Biobank analysis of nearly 450,000 people found that individuals with hs-CRP above 3 mg/L had a 34% higher risk of major cardiovascular events and a 61% higher risk of cardiovascular death compared to those below 1 mg/L.

The landmark JUPITER trial demonstrated that patients with low LDL cholesterol, but elevated hs-CRP (above 2 mg/L) still benefited substantially from statin therapy — in terms of reduced heart attacks and strokes. This reframed how cardiologists think about inflammation as a cardiovascular target independent of cholesterol levels.

Beyond infection, autoimmune disorders, and heart disease, elevated CRP has been linked to type 2 diabetes, metabolic syndrome, chronic kidney disease, COPD, depression, and neurodegenerative diseases, all conditions where chronic low-grade inflammation is increasingly recognized as a contributing factor rather than just a side effect.

Measuring CRP: The Standard Test vs. the High-Sensitivity Test

CRP testing is straightforward, just a standard blood draw, no fasting required. Modern automated lab analyzers make it fast and inexpensive, which explains why it shows up so often in clinical workups.

The standard CRP test is the workhorse for detecting acute infection and monitoring inflammatory flares in hospitalized patients. The hs-CRP test uses more sensitive techniques and is the test used for cardiovascular risk assessment.

Because hs-CRP can fluctuate modestly from day to day, cardiovascular guidelines recommend averaging two measurements taken about two weeks apart. Acute illness, recent injury, or even a hard workout can temporarily elevate hs-CRP and produce a misleading result.

Several factors can push CRP higher independently of the disease in question: obesity, smoking, high blood pressure, metabolic syndrome, low HDL cholesterol, and chronic low-grade infections such as gum disease. Age also gradually raises baseline CRP. On the other side, moderate physical activity, weight loss, and statins are all associated with lower CRP — which partly explains the broader cardiovascular benefits of statin therapy beyond cholesterol reduction.

What CRP Can’t Tell You

For all its usefulness, CRP is a nonspecific marker. A reading of 50 mg/L is consistent with a kidney infection, an autoimmune flare, a recent heart attack, or an abdominal cancer. CRP tells you that inflammation or tissue damage is happening somewhere; it doesn’t tell you where or why. Clinical context including symptoms, medical history, and other lab results, is essential for interpretation.

There’s also a genuine unresolved debate about whether CRP elevation actually causes cardiovascular disease or is simply a marker of underlying inflammatory risk. Animal studies in CRP-deficient or CRP-enhanced models have produced inconsistent results. Mendelian randomization studies in humans, a statistical technique that uses genetic variants to approximate a randomized experiment, have generally not supported CRP as a causal driver of heart disease, suggesting it may be more of a reaction than a root cause.

Finally, hs-CRP testing, despite strong evidence, remains underused in primary care, particularly in primary prevention. The 2024 European Society of Cardiology guidelines for chronic coronary syndromes did recommend assessing hs-CRP in patients with suspected coronary artery disease, which reflects accumulating evidence for its utility, but broader implementation lags behind the science. I have to admit, when I was still in active practice, I was unaware of the role of hs-CRP in primary prevention. At the time, it was generally thought to be of use in secondary prevention—actions taken after an initial event. Be sure and ask your doctor about it.

CRP is, in the end, a remarkably versatile tool — a protein that has been doing immune surveillance since long before medicine had a name for it, and one that continues to find new clinical relevance with each decade of research.

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

Image generated by the author using ChatGPT

Sources

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Not All Fat Is the Enemy

By John Turley

On June 23, 2026

In Medicine

A Plain-Language Guide to Dietary Fats, What They Do, and How to Make Better Choices

The Fat Myth That Stuck Around Too Long

For decades, the American food industry sold us a story: fat is bad, and less of it is better. By the 1980s and 1990s, supermarket shelves sagged under the weight of fat-free cookies, low-fat chips, and reduced-fat everything. The problem, of course, was that when food companies stripped out the fat, they often replaced it with sugar and refined carbohydrates to maintain flavor — and Americans got sicker anyway. Heart disease rates climbed. Obesity rates climbed. And gradually, the nutrition science world came to a more nuanced conclusion: what kind of fat you eat matters far more than how much.

Today, the scientific consensus is clear enough that even cautious institutions like the American Heart Association and Harvard’s School of Public Health distinguish sharply between fats that harm us and fats that we actually need to survive. This article walks through the main types of dietary fat — where they come from, what they do in the body, and how the average American can make smarter choices without turning every meal into a chemistry lesson.

The Chemistry, Simply Put

You don’t need a biochemistry degree to understand dietary fat, but a little structural context goes a long way. All fats are built from molecules called fatty acids — long chains of carbon atoms linked together, with hydrogen atoms attached. The difference between fat types comes down to how those hydrogen atoms are arranged.

Saturated Fats

Saturated fats are “saturated” with hydrogen atoms — meaning every carbon in the chain is bonded to as many hydrogens as it can possibly hold. This gives them a rigid, tightly packed structure. The practical consequence? Most saturated fats are solid at room temperature — think of the white fat marbled through a raw steak, or a stick of butter sitting on a counter.

Unsaturated Fats

Unsaturated fats have at least one double bond between carbon atoms in the chain — which means they are missing some hydrogen atoms. That double bond creates a “kink” in the molecular chain, preventing the fat molecules from packing tightly together. The result is that Unsaturated Fats

Unsaturated fats have at least one double bond between carbon atoms in the chain — which means they are missing some hydrogen atoms. That double bond creates a “kink” in the molecular chain, preventing the fat molecules from packing tightly together. The result is that unsaturated fats are liquid at room temperature, olive oil being the most familiar example.

Within unsaturated fats, there are two important subtypes based on how many double bonds exist. Monounsaturated fats (MUFAs) have exactly one double bond. Polyunsaturated fats (PUFAs) have two or more. Both behave very differently in the body than saturated fats and generally, much more favorably.

Trans Fats: The Artificial Villain

Trans fats deserve their own brief mention because they are the one type of fat that virtually every credible nutrition authority agrees should be avoided as completely as possible. Most trans fats are artificially created through a process called partial hydrogenation — taking liquid vegetable oil and pumping hydrogen through it under high pressure to make it solid and shelf-stable. The result is partially hydrogenated oil, which was found in margarine, shortening, packaged cookies, and countless processed snacks for most of the twentieth century.

The FDA banned the addition of partially hydrogenated oils to U.S. food products based on overwhelming evidence that industrial trans fats raise “bad” LDL cholesterol, lower “good” HDL cholesterol, and significantly increase cardiovascular risk. Small amounts of naturally occurring trans fats are found in animal products like beef and dairy, and these appear to be metabolically distinct from industrial trans fats — less concerning but still something most experts recommend limiting.

Saturated Fats in Detail

Where They Come From

Saturated fats are found predominantly in animal products and a handful of tropical plant oils. The major food sources include fatty cuts of beef and pork, poultry skin, full-fat dairy products (butter, whole milk, cream, cheese), lard, and beef tallow. On the plant side, coconut oil and palm oil are notably high in saturated fat — which surprises many people who assume all plant-based oils are heart-healthy. Coconut oil in particular has been heavily marketed as a “superfood” in recent years, a claim that runs in conflict with the science.

What They Do in the Body

The relationship between saturated fat and cardiovascular health has been one of the most debated topics in nutrition science for the past two decades. The original view, dominant for most of the 20th century, was straightforward: eating saturated fat raises LDL (“bad”) cholesterol, and higher LDL raises the risk of heart disease and type 2 diabetes. That basic chain of reasoning is still supported by substantial evidence.

However, the picture has grown more complicated. Research over the past decade has raised legitimate questions about whether all saturated fats are equally problematic, and whether saturated fat in isolation — rather than as part of an overall dietary pattern — is the right thing to be measuring. A study cited by the National Institutes of Health found that replacing saturated fats with refined carbohydrates (which is what happened when Americans went fat-free in the 1980s) did not reduce cardiovascular risk. The key variable isn’t just removing saturated fat — it was what you replace it with.

The evidence clearly shows that replacing saturated fats with unsaturated fats reduces cardiovascular risk. Replacing them with sugar and white flour does not. That distinction has become the cornerstone of modern dietary fat guidance.

How Much Is Too Much?

Current guidance varies slightly between major health organizations, but the general range is consistent. The Dietary Guidelines for Americans recommends keeping saturated fat below 10% of total daily calories. The American Heart Association is more conservative, recommending below 6% — which for a 2,000-calorie diet works out to about 13 grams per day, roughly the amount in a single tablespoon of butter combined with a small handful of cheese.

Monounsaturated Fats (MUFAs)

Where They Come From

Monounsaturated fats are the dominant fat in olive oil, avocados, peanut oil, canola oil, and most nuts — including almonds, cashews, and hazelnuts. They are the nutritional backbone of the Mediterranean diet, which has been studied more extensively for cardiovascular benefit than perhaps any other dietary pattern in history.

Health Benefits

The evidence in favor of MUFAs is robust . Monounsaturated fats lower LDL cholesterol while maintaining levels of HDL (“good”) cholesterol when they replace saturated fat in the diet. A clinical trial called the OmniHeart study found that shifting to a diet rich in monounsaturated fats — compared to a carbohydrate-rich diet — lowered blood pressure, improved cholesterol profiles, and reduced estimated cardiovascular risk. Beyond the heart, research suggests that swapping saturated fats for MUFAs may also support modest weight and body fat reduction even without changing total calorie intake.

MUFAs are also notably stable at cooking temperatures, which makes olive oil a practical and healthy choice for most everyday cooking — sautéing vegetables, making salad dressings, or roasting proteins.

Polyunsaturated Fats (PUFAs) — The Essential Fats

Polyunsaturated fats are, in many ways, the most scientifically interesting category because they include the only two dietary fats that the human body genuinely cannot produce on its own and must obtain from food. These are called essential fatty acids, and they fall into two families: omega-3s and omega-6s.

Omega-3 Fatty Acids

What They Are and Where They Come From

Omega-3s are the fats most Americans have heard of in the context of fish oil supplements. The three main types are ALA (alpha-linolenic acid), EPA (eicosapentaenoic acid), and DHA (docosahexaenoic acid). ALA is found primarily in plant sources — walnuts, flaxseeds, chia seeds, and canola or soybean oil. EPA and DHA are found in fatty fish — salmon, sardines, mackerel, herring, and trout — as well as in algae-based oils, which is where fish get their omega-3s in the first place.

The body can convert ALA into EPA and DHA, but only very inefficiently. For practical purposes, regular fish consumption is the most reliable way to maintain adequate EPA and DHA levels. The American Heart Association recommends at least two servings of fatty fish per week for this reason.

Health Benefits

Omega-3 fatty acids are structural components of cell membranes throughout the body and serve as precursors to signaling molecules that regulate inflammation. Their most well-established benefits are cardiovascular: they reduce triglyceride levels, stabilize heart rhythms, and appear to lower the risk of sudden cardiac death. Beyond the heart, research suggests they play important roles in brain development (particularly during fetal development and infancy), may reduce the risk of certain neurodegenerative conditions, and have documented anti-inflammatory effects relevant to conditions like rheumatoid arthritis.

A recent review published in the journal Foods found that omega-3s may help delay the onset of neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease, reduce depression, and contribute to cancer prevention, though the authors note that more research is needed to fully understand these relationships.

Omega-6 Fatty Acids

What They Are and Where They Come From

Omega-6 fatty acids are found in most vegetable oils — corn oil, soybean oil, sunflower oil, safflower oil — as well as in nuts, seeds, and poultry. Linoleic acid (LA) is the primary dietary omega-6 and is the only one classified as truly essential.

The Omega-6/Omega-3 Imbalance

Here is where things get complicated in a uniquely American way. The typical Western diet contains far more omega-6 fats than necessary and not nearly enough omega-3 fats. The ideal ratio of omega-6 to omega-3 in the diet is thought to be somewhere between 4:1 and 1:1. The actual ratio in the average American diet is estimated at anywhere from 15:1 to 20:1 — a dramatic imbalance driven by the ubiquity of processed foods and vegetable oils in the food supply.

This matters because omega-6 and omega-3 fatty acids compete for the same metabolic pathways in the body. While omega-6s in appropriate amounts are essential and beneficial, a chronically elevated omega-6 to omega-3 ratio is associated with increased inflammation and higher risk of coronary heart disease, hypertension, diabetes, rheumatoid arthritis, and some neurodegenerative conditions. The goal is not to eliminate omega-6s but to bring the ratio back into better balance — primarily by increasing omega-3 intake.

What a Healthy Fat Profile Actually Looks Like

Putting all of this together, what does a well-balanced dietary fat intake actually look like? The evidence points toward a few consistent principles.

In a typical healthy diet, 20–35% of total daily calories can come from fat. Within that total, the composition matters enormously. Unsaturated fats — both mono and polyunsaturated — should make up the bulk. Saturated fats should be limited to under 10% of daily calories by federal guidelines, or under 6% if you are following the American Heart Association’s more aggressive recommendation. Trans fats, the industrial kind, should be avoided as close to completely as possible.

The two truly essential fats — linoleic acid (omega-6) and alpha-linolenic acid (omega-3) — must come from the diet because the human body cannot synthesize them. Everything else the body can manufacture from raw materials, given enough of the right building blocks.

For omega-3s specifically, the WHO and EFSA recommend at least 250 mg per day of EPA + DHA. And recommend 1.6 grams of ALA per day for adult males and 1.1 grams for adult females. Most Americans fall well short of these targets.

Practical Ways to Shift Your Fat Intake

Dietary change works best when it’s specific and sustainable — not when it involves a complete pantry overhaul overnight. Here are evidence-based adjustments that can meaningfully improve the fat profile of a typical American diet.

Replace Saturated Fats With Unsaturated Fats at the Cooking Stage

Instead of frying or sautéing in butter, lard, or palm oil, switch to olive oil, avocado oil, or canola oil. This single substitution is one of the most consistently supported interventions in dietary fat research. For those who prefer a buttery flavor, using a small amount of butter blended with olive oil is a practical middle ground.

Eat Fatty Fish Twice a Week

Salmon, sardines, mackerel, herring, and trout are all excellent sources of EPA and DHA omega-3s. The American Heart Association’s recommendation of two fish servings per week is a well-established and achievable benchmark. Canned fish — particularly canned salmon and sardines — is inexpensive and just as nutritious as fresh. Tuna is an option but requires an larger serving.

Add Nuts, Seeds, and Avocados

A handful of walnuts (a particularly good plant source of ALA omega-3s), a tablespoon of ground flaxseed in yogurt or oatmeal, or half an avocado on toast are all straightforward ways to shift your fat intake in a healthier direction. Nuts and avocados are also rich in monounsaturated fats that support cholesterol health.

Choose Leaner Cuts of Meat

Selecting leaner cuts of beef and pork — those labeled “loin” or “round,” or ground meat that is 90–95% lean — can substantially reduce saturated fat intake without eliminating meat from the diet. Removing skin from poultry before cooking similarly reduces saturated fat in a simple and inexpensive way.

Read Labels for Trans Fats — Carefully

Food packaging can legally claim “0 grams of trans fat” if a product contains less than 0.5 grams per serving. If you eat multiple servings of such products, those fractions add up. The safeguard is to check the ingredient list for “partially hydrogenated oil” — if it appears anywhere, the product contains industrial trans fats., regardless of what the front label says.

Limit — Don’t Necessarily Eliminate — Saturated Fat

A realistic goal is not to strip all saturated fat from your diet but to keep it within the recommended range. Full-fat dairy in moderate amounts, an occasional burger, or butter used sparingly are unlikely to cause harm in the context of an otherwise balanced eating pattern. What matters most, as nutrition experts now emphasize, is the overall dietary pattern — not any single food or nutrient in isolation.

The Bottom Line

Fat is not a dietary villain. It is an essential macronutrient that the body depends on for energy, vitamin absorption, hormone production, brain function, and cell membrane integrity. The question has never really been whether to eat fat — it has always been which fats to prioritize.

The evidence points consistently in one direction: lean toward unsaturated fats (olive oil, nuts, avocados, fatty fish), keep saturated fat in check, avoid industrial trans fats entirely, and pay particular attention to getting enough omega-3 fatty acids, which most Americans chronically under-consume. These adjustments don’t require extreme dietary measures. They require informed choices made consistently — and that, ultimately, is the most sustainable kind of nutrition science.

Illustration generated by author using ChatGPT

Note: The core findings in this article — that unsaturated fats are preferable to saturated fats, that omega-3 and omega-6 fatty acids are essential, and that industrial trans fats are harmful — are supported by decades of research and endorsed by major health authorities including the American Heart Association, the NIH, and the 2025 Dietary Guidelines Advisory Committee. Some nuance remains in the saturated fat debate (particularly regarding specific saturated fatty acid subtypes and their varying cardiovascular effects), and the research on omega-3s and neurological disease is still evolving.

Medical Disclaimer

If you are experiencing a medical emergency, call 911 or your local emergency number immediately.