The three most common forms of sugar are glucose,
fructose, and galactose, and these are all types of monosaccharides, meaning they’re
made of just one sugar molecule, molecules like this are called carbohydrates, because
they’re made up of carbon, hydrogen, and oxygen, usually with a hydrogen-oxygen ratio
of 2:1. if you link two of these guys together, you
get a disaccharide because “di” means two, and this is also a carbohydrate. Now our body uses these sugar molecules for
energy, right? For us humans, glucose is our gasoline, our
energy source, we’ll take galactose and fructose…but ultimately we need to use glucose,
so almost all the fructose and galactose we ingest is converted to glucose, and then we
use that glucose for energy. Alright, but usually carbohydrates aren’t
in monosaccharide form when we ingest them, and a lot of what we take in are in the disaccharide
form, and one notorious disaccharide that tends to cause serious gastrointestinal distress
for a lot of people, is lactose.
Lactose is a disaccharide that’s made up
of a glucose molecule and a galactose molecule. For us to use it as energy, though, we have
to first break it down to those two monosaccharides. In the milk of most mammals, lactose is generally
the major carbohydrate, so when you have a glass of milk, and it gets through your stomach
to the small intestine, that lactose gets chopped into glucose and galactose by an enzyme
that’s fittingly called lactase. The gene responsible for production of the
lactase enzyme is expressed exclusively in the enterocytes lining the small intestine,
which are cells that help absorb nutrients from stuff that we eat.
Once produced, the enzyme makes it’s way
to the cell’s surface along the cell’s microvilli, these little tentacles that help
increase surface area and absorb nutrients. K, once lactose gets chopped by lactase, we’re
good to go, and we absorb the glucose and galactose and all is well. Now, as mammals, we’re wired to be able
to ingest milk after birth, right? So it makes sense that when we’re young
we have a whole bunch of lactase enzyme, since that’s pretty much all we drink. After weaning, in most mammal species, expression
of the gene responsible for lactase is way down-regulated, and so production of lactase
also goes way down. The majority of humans actually follow this
protocol as well, and down-regulate lactase production around 3-5 years of age.
Interestingly, though, the majority of caucasians,
mainly those from northern european background, continue to have elevated lactase activity
all the way into adulthood, and so they exhibit “lactase persistence”. Why caucasians? Well, this group historically has domesticated
cows and other milk providers and consumed lactose-based, or milk-based products into
adulthood, and by natural selection, it’s thought that they’ve developed increased
persistence of lactase production by specific gene mutations that are often autosomal dominant.
Similar lactase persistence phenomena has
been observed in separated and distinct smaller populations that rely on lactose production
as well, pretty interesting stuff if you ask me. At any rate, what about those of us that didn’t
inherit the lactose-persistence gene? And every time we even think about milk or
dairy products, our bowels give out a small groan? Well, when that lactose gets to the brush
border of your small intestine, the vast majority of it doesn’t get chopped and absorbed,
as much as 75%! And it just keeps on movin’ down the GI
tract and passes into the colon. At this point, the gut flora has a field day,
since microbes aren’t as picky and they ferment the lactose into a mix of hydrogen
gas, carbon dioxide, and methane.
These gases contribute to symptoms of, uh,
gas and bloating. Along with those gases, though, short-chain
fatty acids are produced like acetate, butyrate, and propionate. We don’t absorb these short-chain fatty
acids, which means that they stay in the lumen of the gut. Both the unabsorbed lactose and products of
fermentation raise the osmotic pressure, attracting water into the bowels, so water flows in and
this influx of water is what leads to diarrhea. Now, in super rare cases, lactase deficiency
can be a congenital, meaning infants would be deficient from birth. This is an autosomal recessive disorder and
infants that can’t break down lactose have trouble with breastmilk, and develop diarrhea
starting from birth.
Sometimes, even those with lactase-persistence
can develop temporary lactose intolerance as a result of infection or inflammation in
the small intestine. During these acute illnesses of the small
intestine, the microvilli of enterocytes can be flattened or damaged, and since these are
the dwellings of our lactase enzyme friend, these acute illness states can cause a lack
of lactase enzyme, and result in temporary lactose intolerance, once the small bowel
heals, they’ll be able to produce lactase again..
