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10 Severe Medical Conditions with Surprising Health Benefits

by Lee D.
fact checked by Darci Heikkinen

Throughout human evolution, genetic variations that cause devastating diseases have persisted in populations at rates that seem to defy natural selection. This genetic paradox has prompted scientists to investigate why traits that cause serious illness in some individuals remain so common.

Research has revealed a fascinating pattern: Many severe medical conditions offer unexpected health advantages when present in milder forms or specific environments. These “heterozygote advantages” demonstrate nature’s complex trade-offs, where the same mutation that threatens one person’s health might protect another from different dangers.

Related: 10 Ridiculous Health Myths (Science Says Are Actually True)

10 Sickle Cell Trait

Sickle Cell Trait

While full sickle cell disease causes serious health problems, carrying just one copy of the sickle cell gene provides remarkable protection against deadly malaria. The slightly altered red blood cells create an inhospitable environment for malaria parasites. When these parasites invade, the cells tend to collapse into sickle shapes and get rapidly cleared by the immune system.

This genetic advantage explains why the sickle cell gene remains common in regions where malaria has historically been prevalent despite its potential downsides. Ironically, while carriers enjoy protection, those who inherit two copies of the gene face a cruel twist. People with full sickle cell anemia become even more vulnerable to malaria, which worsens their already severe anemia.

Their compromised spleens can’t effectively clear infected cells from the bloodstream, creating a dangerous combination. This vulnerability makes preventive malaria protection absolutely essential for anyone with sickle cell anemia living in regions where malaria is common. The relationship between these two conditions perfectly illustrates nature’s complex balancing act. This single genetic adaptation simultaneously protects some individuals while placing others at greater risk.[1]

9 Myostatin-Related Muscle Hypertrophy

This Rare Mutation Gives You Massive Muscles At Birth

Some people are born with a rare genetic mutation that blocks myostatin—the natural protein that puts the brakes on muscle growth. This condition, called myostatin-related muscle hypertrophy, leads to extraordinary muscle development without exercise. People with this mutation develop up to twice the muscle mass of average individuals, with significantly less body fat and surprisingly no adverse effects on heart health.

While this might sound like a dream condition for bodybuilders, it teaches scientists important lessons. This genetic quirk has sparked major interest in developing drugs that block myostatin to help people with muscle-wasting diseases like muscular dystrophy. However, research reveals a complex picture.

While healthy people with natural myostatin mutations enjoy enhanced strength without drawbacks, artificially blocking myostatin in certain muscle diseases might initially improve appearance but eventually worsen the damage. This suggests that sometimes having more muscle isn’t always better when underlying repair mechanisms are compromised.[2]


8 Hypercholesterolemia in Newborns

Hypercholesterolemia Everything You Need to Know

While high cholesterol levels cause concern in adults, they can surprisingly benefit premature babies’ developing brains. Premature infants often naturally develop higher cholesterol levels than full-term babies due to increased internal production—a condition that would be concerning in adults but appears to serve an important purpose during this critical developmental period.

Cholesterol plays a crucial role in brain development, particularly in forming the protective myelin sheaths around nerve cells and supporting cerebellar growth, with about 25% of the body’s total cholesterol found in the brain.

Research following 60 premature newborns revealed interesting connections between early cholesterol levels and brain development. Using advanced brain imaging and tracking developmental outcomes, scientists discovered that these temporarily elevated cholesterol levels weren’t harmful. They actually supported brain growth during a vulnerable time.

The study helps explain why premature babies naturally produce more cholesterol and suggests that this temporary elevation supports crucial brain development processes.[3]

7 Fetal Hemoglobin Persistence

Flipping the fetal hemoglobin switch reverses sickle cell symptoms

Fetal hemoglobin persistence occurs when the body continues producing a special type of hemoglobin typically found only in developing babies. This “fetal hemoglobin” (HbF) usually disappears after birth as the body switches to adult hemoglobin production. However, some people have genetic variations that cause them to continue producing fetal hemoglobin into adulthood.

While this persistent production of “baby blood” might sound concerning, it creates a remarkable protective effect for people with blood disorders like sickle cell disease or beta-thalassemia. For those with sickle cell disease, where abnormal adult hemoglobin causes red blood cells to become rigid and misshapen, the continued presence of fetal hemoglobin acts as a natural medicine. It physically prevents the sickle hemoglobin from forming the dangerous rigid chains that damage blood cells and cause pain.

Scientists have observed that people who happen to have both sickle cell disease and fetal hemoglobin persistence experience dramatically fewer symptoms. In fact, some remain virtually disease-free despite having the sickle cell mutation. This natural protection has inspired groundbreaking treatments using gene editing technology that aim to reactivate fetal hemoglobin production in patients with blood disorders, potentially offering a functional cure without needing to correct the original genetic defect itself.[4]


6 Specific Types of Color Blindness

Hidden Talents of the Color Blind | Washington University

Color blindness isn’t just one condition but several different types, each affecting color perception differently. The most common form, red-green color blindness (deuteranomaly), occurs when the eye’s green-sensing cells respond more like red-sensing cells. This hereditary condition affects about 8% of men and 0.5% of women worldwide, making distinguishing certain shades of red and green difficult.

While color blindness typically creates challenges—from selecting ripe fruit to matching clothes—scientists have long suspected it might offer surprising advantages in specific situations. Military legends from World War II claimed that color-blind soldiers could spot camouflaged enemies more easily than those with normal vision. While research shows mixed results depending on the specific testing conditions, some studies have demonstrated that people with certain types of color blindness can indeed detect camouflage patterns invisible to those with normal color vision.

This occurs because they process visual information differently, sometimes allowing them to notice subtle texture differences or brightness variations that others miss when colors are designed to blend together. Though normal vision generally performs better overall in detecting objects, this specific advantage helped explain why color blindness remains so common in human populations. It likely provided evolutionary benefits in hunting environments where spotting camouflaged prey or predators meant survival.[5]

5 Congenital Insensitivity to Pain

People who feel no pain but suffer enormously | 60 Minutes Australia

Congenital insensitivity to pain (CIP) is a rare genetic disorder where people are physically unable to feel pain. Those born with this condition, caused by mutations in the SCN9A gene, can experience severe injuries without discomfort—like a boy in Pakistan who could walk on hot coals or cut himself with blades without flinching. While this might sound like a superpower, it’s actually incredibly dangerous.

Without a pain warning system, people with CIP often suffer severe unnoticed injuries, infections, and joint damage that can be life-threatening. Many don’t live to adulthood because they can’t recognize when their bodies are in danger. The surprising benefit of this devastating condition lies in what it’s teaching scientists about pain itself. Researchers have identified specific sodium channels that act as pain’s gatekeepers in our nervous system by studying these rare pain-free individuals.

This discovery has led to the development of new non-addictive pain medications that target these channels. One promising drug, suzetrigine, has shown significant success in clinical trials for both acute and chronic pain conditions without causing central nervous system side effects like addiction or drowsiness. This groundbreaking advance could transform pain management for millions of people who suffer from it excessively.[6]


4 Familial High-Density Lipoprotein Deficiency

LDL and HDL Cholesterol | Good and Bad Cholesterol | Nucleus Health

Familial HDL deficiency occurs when people inherit a rare genetic mutation affecting their SCARB1 gene, causing them to produce remarkably low HDL cholesterol levels (often called “good cholesterol”). Normally, such low HDL would be concerning, as this cholesterol type helps remove harmful fats from arteries and protects against heart disease. Medical professionals routinely advise patients to raise their HDL levels through diet, exercise, and sometimes medication.

With typical HDL deficiency, patients face significantly higher risks of atherosclerosis and heart attacks due to reduced protection against arterial plaque buildup. What makes this particular genetic variation fascinating is that despite their alarmingly low HDL numbers, people with this specific mutation mysteriously show no increased risk of heart disease. Researchers discovered these individuals possess a unique alteration in how their bodies process and transport cholesterol, providing unexpected protection against atherosclerosis despite their lipid profile.

Their cells manage cholesterol differently, efficiently removing it from blood vessel walls through alternative pathways. This remarkable exception to conventional cholesterol wisdom has opened exciting new avenues for cardiovascular research and treatment, suggesting that simply boosting HDL numbers may be less important than improving how effectively the body handles cholesterol overall.[7]

3 Wilson’s Disease Carrier Status

Behind the Mystery—Wilson Disease: An Inherited Disorder That Results in Copper Build-Up in Organs

Wilson’s disease occurs when a genetic mutation prevents the body from properly removing copper, causing it to accumulate toxic levels in the liver, brain, and other organs. This serious condition leads to liver disease, neurological problems, and psychiatric symptoms if left untreated. People with full Wilson’s disease require lifelong medication to remove excess copper from their bodies.

However, those who carry just one copy of the mutation maintain slightly elevated copper levels without developing toxicity. Research has uncovered a surprising benefit of this carrier status—enhanced protection against certain bacterial infections. Since copper has natural antimicrobial properties, the modestly elevated copper levels in carriers appear to strengthen their immune response against specific pathogens.

Studies show carriers have lower rates of tuberculosis infection in several populations, suggesting an evolutionary advantage that helped this genetic variation persist. While excessive copper is harmful, the slightly increased levels in Wilson’s disease carriers provide a biological shield against certain infections without causing the debilitating symptoms of the full disease.[8]


2 Phenylketonuria

What is Phenylketonuria?

Phenylketonuria (PKU) is a serious genetic disorder where affected individuals cannot properly process the amino acid phenylalanine. Without treatment, this amino acid builds up to toxic levels in the body, causing severe intellectual disability, seizures, and other neurological problems. People with PKU must follow an extremely restrictive diet throughout their lives, avoiding foods high in protein like meat, dairy, nuts, and many grains.

The condition is inherited in an autosomal recessive pattern, meaning both parents must pass on a mutated gene for a child to develop the full disorder. While PKU itself is devastating, those who carry just one copy of the mutation may receive a surprising benefit. Research suggests these carriers have significantly lower rates of miscarriage than women in the general population.

Scientists believe the moderately elevated phenylalanine levels in carriers help neutralize ochratoxin A, a common fungal toxin found in foods that can trigger pregnancy loss. This protective effect may explain why the PKU gene remains surprisingly common in certain populations, particularly in Ireland and western Scotland, despite its harmful effects when inherited from both parents.[9]

1 Cystic Fibrosis Carrier Status

Cystic Fibrosis and Carrier Screening Explainer

Cystic fibrosis (CF) is a severe genetic disorder where a defective protein causes thick, sticky mucus to build up in the lungs, digestive tract, and other organs. People with full CF experience recurring lung infections, breathing difficulties, and digestive problems, often requiring intensive daily treatments. The disease is most common in people of European descent, with about 1 in 30 being carriers. For decades, scientists puzzled over why such a harmful mutation would remain so common in certain populations when evolution typically eliminates genes that reduce survival.

Research has revealed a surprising benefit for CF carriers—significant protection against tuberculosis (TB), once called the “White Plague,” that killed up to 25% of Europeans between the 1600s and 1900s. The same genetic mutation that causes devastating illness when inherited from both parents provides a survival advantage when present in just one copy. Scientists discovered that TB bacteria need a specific enzyme from human cells to successfully establish infection, and people with CF mutations produce less of this enzyme.

This protection against a deadly infectious disease explains why the CF mutation persisted—carriers were more likely to survive TB epidemics and pass their genes to future generations. Similar protective effects may extend to typhoid fever and cholera, though these connections remain under investigation.[10]

fact checked by Darci Heikkinen

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