Do We Produce Lactase All the Time? Understanding Lactase Persistence vs. Non-Persistence

January 9, 2026 •

4 min read

Globally, approximately 65% of the human population has a reduced ability to digest lactose after infancy, a trait known as lactase non-persistence. This counters the common misconception that our bodies are designed to produce the digestive enzyme lactase continuously throughout our lives.

Quick Summary

Lactase production typically decreases after infancy in most humans due to genetic programming. A genetic mutation, however, allows some populations to maintain lactase activity into adulthood, known as lactase persistence.

Key Points

Normal Decline: For most humans, lactase production naturally decreases after infancy, a condition called lactase non-persistence.
Genetic Mutation: A genetic mutation allows some people to continue producing lactase throughout their lives, known as lactase persistence.
Cultural Co-evolution: Lactase persistence evolved alongside pastoralism and dairying, giving certain populations a nutritional advantage.
Population Variation: The prevalence of lactase persistence varies greatly by ethnic group, being high in some European and African populations but low in East Asian communities.
Other Causes: Secondary lactase deficiency can be triggered by intestinal illness or injury, and may be temporary.
Regulatory Gene: The genetic switch for lactase activity is controlled by a DNA sequence located in the nearby MCM6 gene.

The Default State: Lactase Non-Persistence

All human infants are born with the ability to produce the lactase enzyme in their small intestine to digest lactose, the sugar found in milk. This is a crucial evolutionary feature, as milk is the primary food source during infancy across all mammals. However, in most of the world's population, lactase production naturally begins to decline after weaning, a phase known as lactase non-persistence or adult-type hypolactasia. The gene responsible, LCT, is actively regulated, and in the absence of certain genetic variations, its activity is downregulated during childhood. When lactase production diminishes, undigested lactose travels to the large intestine where it is fermented by gut bacteria, causing symptoms like gas, bloating, and diarrhea.

The Genetic Basis of Downregulation

The regulation of the LCT gene is controlled by a genetic element located within a neighboring gene, MCM6. For most people, this regulatory element is programmed to reduce LCT gene expression after childhood. The presence of specific gene variants determines whether lactase activity continues or is switched off. Lactase non-persistence is considered the ancestral human condition and remains the global norm.

The Evolutionary Exception: Lactase Persistence

Over the last 10,000 years, specific human populations evolved a genetic mutation that allows them to continue producing lactase throughout adulthood, a trait called lactase persistence. This adaptation is one of the clearest examples of gene-culture co-evolution, as it arose in populations that practiced pastoralism and consumed fresh milk from domesticated animals. The ability to drink milk offered a significant nutritional advantage, providing a source of energy, calcium, and fluids. This selective pressure led to the rapid spread of the lactase persistence trait in these populations.

Multiple Origins of Lactase Persistence

Interestingly, the ability to digest lactose into adulthood is an example of convergent evolution, having arisen independently in different parts of the world. Genetic studies have identified several different single-nucleotide polymorphisms (SNPs) upstream of the LCT gene that are associated with lactase persistence in different populations, including European, African, and Middle Eastern groups.

Factors Influencing Lactase Levels

While genetics play the primary role, other factors can influence lactase levels and lactose tolerance.

Increasing Age: For those with lactase non-persistence, the decline in enzyme activity typically becomes noticeable in adulthood.
Ethnicity: The prevalence of lactase persistence varies dramatically across different ethnic groups, reflecting historical dietary and genetic factors.
Secondary Lactase Deficiency: Illnesses that damage the small intestine lining, such as gastroenteritis, celiac disease, or Crohn's disease, can temporarily or permanently reduce lactase production.
Premature Birth: Infants born prematurely may have underdeveloped small intestines and insufficient lactase, but this typically resolves as they mature.
Cancer Treatments: Radiation therapy or intestinal complications from chemotherapy can increase the risk of developing lactase deficiency.

Types of Lactase Deficiency

There are three main types of lactase deficiency, each with a different cause.

Primary Lactase Deficiency (Lactase Non-Persistence): The most common type, resulting from the genetically programmed decrease in lactase production after infancy.
Secondary Lactase Deficiency: Caused by damage to the small intestine from injury or illness. Treating the underlying condition can sometimes restore lactase levels.
Congenital Lactase Deficiency (Congenital Alactasia): A very rare genetic disorder where infants are born unable to produce any functional lactase. It is inherited in an autosomal recessive pattern.

Lactase Persistence vs. Non-Persistence


Feature	Lactase Persistence	Lactase Non-Persistence (Hypolactasia)
Prevalence	Approximately 35% of the world's adults.	Approximately 65% of the world's adults.
Evolutionary Trait	Derived, occurring in specific populations over the last 10,000 years.	Ancestral, the default mammalian condition.
Gene Regulation	Regulatory element in the MCM6 gene allows for continued LCT expression into adulthood.	Regulatory element causes downregulation of the LCT gene after weaning.
Dietary Tolerance	Can comfortably digest fresh milk and other lactose-rich dairy products.	Often experiences gastrointestinal symptoms from lactose.
Genetic Basis	Associated with specific SNPs upstream of the LCT gene, such as the -13910*T allele in Europeans.	Lacks the specific SNPs that prevent downregulation of the LCT gene.

Conclusion: A Diverse Human Trait

The question "do we produce lactase all the time?" highlights the profound genetic and evolutionary diversity of the human species. The answer is a clear "no" for the majority of people, whose bodies follow the mammalian norm of decreasing lactase production after infancy. For a significant minority, however, a relatively recent genetic mutation has enabled a lifetime of lactase production, a powerful testament to the selective pressures of human history and cultural development. Understanding this distinction is key to comprehending not only lactose intolerance but also the intricate relationship between human biology, diet, and evolution.

MedlinePlus provides detailed information on the genetics of lactase persistence.

Frequently Asked Questions

Yes, it is the biological norm for most humans and mammals to reduce lactase production after weaning. This condition is called lactase non-persistence, and it means that a reduced ability to digest lactose in adulthood is the ancestral trait for humanity.

Some people have a genetic mutation that keeps the lactase gene 'switched on' into adulthood. This trait, called lactase persistence, is an evolutionary adaptation that became common in populations with a long history of dairying.

Yes, secondary lactase deficiency can be caused by damage to the small intestine from illnesses like gastroenteritis, celiac disease, or Crohn's disease. This is often temporary and may resolve when the underlying condition is treated.

Lactase non-persistence is the physiological state of reduced lactase production. Lactose intolerance describes the digestive symptoms (bloating, gas, diarrhea) that occur when someone with lactase non-persistence consumes too much lactose.

Lactase production is controlled by the LCT gene, which is regulated by a sequence within the neighboring MCM6 gene. For most people, this regulatory element naturally downregulates LCT gene expression after infancy.

Lactase persistence is very common in people of Northern European descent and is also found in specific African pastoralist and Middle Eastern populations. Conversely, it is rare among East Asians and Native Americans.

For those with primary lactase non-persistence, the genetic downregulation of lactase cannot be reversed. However, people can manage symptoms by consuming lower-lactose dairy products, using lactase enzyme supplements, or increasing their intake of active-culture yogurt.