Crystal growing is both fascinating and easy to do.

Simply dissolve a bit of table salt in some water, place a string inside, and then let

the water evaporate over a few days.

As less and less water is present, the concentration of salt will increase.

However, water cannot dissolve an infinite amount of salt, therefore there must be a

maximum or saturated concentration.

At that maximum concentration, salt will not dissolve but instead will solidify to form

crystals on the string.

This is an awesome phenomenon to show your friends, but imagine if crystallization occurred

within your body.

In people who have gouty arthritis, or gout, a compound known as uric acid begins to form

crystals inside joints, which leads to intense pain.

In fact, the pain is so severe that many who suffer from a gout attack describe that even

the weight of a bedsheet on their affected joint causes excruciating pain.

What’s the reason for the formation of these crystals?

In the table salt example, crystallization only occurred when the concentration of table

salt in water exceeded a certain point.

Similarly, uric acid crystals form only when the concentration of uric acid in the blood

is too high, which is known as hyperuricemia.

What causes hyperuricemia?

Compounds known as purines, for example adenine and guanine, are found in genetic material

in both our own cells and in food.

Purines are eventually broken down into uric acid.

Normally, most uric acid is filtered out of our bloodstream in the kidneys and excreted

in the urine.

However, damage to the kidneys decreases filtration, causing less uric acid to be removed from

the bloodstream, resulting in hyperuricemia.

Mutations in membrane proteins in the kidney that transport uric acid, such as URAT1, can

also cause hyperuricemia.

URAT1, which is found on the membrane of cells that line the tubes which drain urine, can

reabsorb uric acid from the filtrate into the cell, which then sends uric acid back

into the blood.

Mutations that increase the activity of URAT1 and other uric acid transporters cause more

uric acid to be reabsorbed back into the bloodstream, leading to hyperuricemia.

Small clumps of uric acid crystals form in the joints as hyperuricemia continues.

Despite the crystals looking sharp, they do not directly cause pain.

Trauma, such as stubbing one’s toe, or sudden swings in uric acid concentration, for example

caused by a meal rich with purines, can cause some of these crystals to dislodge.

When large immune cells known as macrophages swallow up the crystals, they begin to release

an inflammatory signal protein known as interleukin 1β which recruits and activates other immune

cells to the joint space.

This is a natural, built-in response, not an autoimmune response, as uric acid is usually

released by dead or dying cells. Therefore, crystals of uric acid normally indicate infections

that are killing cells and therefore requires inflammation to kill the pathogens causing

the infection.

In gout, even though there is no infection, inflammation occurs anyways.

Whenever there is inflammation, there is redness, swelling, and pain.

Acute gout attacks can last for up to a week, but eventually subside.

Often times, the attacks happen at night, as lower temperatures decrease solubility

and increase crystallization.

Usually, the attacks occur on the foot, particularly the joint of the big toe, possibly because

our feet have a lower temperature compared to the rest of the body and because our feet

are the most likely to get injured, for example, by stubbing your toe, which releases crystals.

If nothing is done to treat the hyperuricemia, more episodes of acute gout can occur, which

could eventually lead to continuous or chronic gout.

Tophi, which are large clumps of uric acid, can form which permanently damages bone and

disfigures joints.

Look up tophi on Google Images if you dare to see how disfiguring they can be.

There are two ways of treating gout – either prevent inflammation or treat the underlying

hyperuricemia.

Preventing inflammation can be done by anti-inflammatory drugs such as ibuprofen or Advil, naproxen

or Aleve, colchicine, and steroids.

Aspirin, which is also commonly used to prevent inflammation, is not recommended at low doses

to treat gout because despite decreasing inflammation, it also decreases uric acid excretion in the

kidneys which further contributes to hyperuricemia.

Treating hyperuricemia often involves changing one’s lifestyle.

Excess consumption of meat, seafood, alcohol, and fructose such as in candy and pop drinks,

are all linked to gout, possibly due to increased purine content or activation of purine breakdown.

In fact, gout was originally known as the “disease of kings”, since in the past

only royalty was able to excessively eat these food groups.

By eating less of these food groups, uric acid levels in blood can decrease, preventing

further crystallization.

Other food such as caffeine, cherries, vitamin C, and milk seem to prevent future gout attacks,

though their mechanism on how they lower uric acid levels is still unclear.

Another way to treat hyperuricemia is by using uricosuric drugs, which can block uric acid

transporters such as URAT1.

This decreases reabsorption and increases excretion of uric acid, decreasing uric acid

levels in the blood.

Nowadays, since high purine content foods are more accessible, gout has been steadily

increasing in frequency in developed countries such as Canada, the US, many European countries,

China, and Australia, with about 3-5% of the population affected by at least one gout attack

in their lifetime.

Comparatively, less developed countries have rates of gout less than 1%.

Over 50 million people are affected by gout worldwide, making it an extremely common ailment.

Risk factors essentially are anything that causes hyperuricemia.

Impaired kidney function due to increased age, high blood pressure, and diabetes increase

the risk of gout.

Drugs that cause more water to be excreted can decrease the amount of water in blood

and therefore increase uric acid concentration.

Gout affects men three times more than women, possibly because estrogen is a natural uricosuric.

Of the women that are affected, the majority is post-menopausal women who have decreased

estrogen levels.

Gout is also found to run in families, likely due to genetic mutations in uric acid transporters

in the kidney.

It is important to note that hyperuricemia increases the risk of gout but does not guarantee

it – a minority of people with hyperuricemia never develop gout, implying that there may

be other unknown factors in this disease.

Hopefully, awareness and knowledge about gout can lead to more people paying attention to

their diet to prevent this painful disease.

To learn more about gout, check out the links in the description below.

Thanks for watching, and see you next time for another explanation of a disease on Medicurio.