Ligaments – the glue/ stitches/ cement that hold the surfaces of bones together to form a joint. Without ligaments, our bodies would be spasmodic, unstable sacks of flesh that would fall apart at any time.

Without these collagenous structures, our joints would lose their unique movement characteristics and glide in every single direction. Knees would bend laterally, fingers would rotate at the knuckles, elbows would extend beyond a 180-degree lockout, and so on. It’d be like driving a car with a poorly-installed steering wheel that not only spins clockwise and counter-clockwise, but rotates along different axes and pulls itself out of the dashboard. That would be both frustrating and dangerous to the car and the driver.

Unfortunately, those stomach-wrenching motions could possibly happen to some degree if the ligaments of one of your joints are loosened. Well, we can hope that it doesn’t really happen, right? Wrong.

In Comes the Plague… the Joint Hypermobility Plague!

Amazingly, ligament laxity (or better known as joint hypermobility – the ability to push your joints past their normal range of motion) is quite the common occurrence in the human population. It’s a bit unclear as to what exact percentage of the population deals with joint hypermobility, due to difficulty in diagnostics, but it’s obvious that the world has got a large number wobbly-limbed folks around.

From the Journal of the Indian Rheumatology Association: “Hypermobility is more common in children and decreases steadily with age. There is also considerable variation between ethnic groups. Women generally have more joint mobility than men do. Hypermobility is more common in Asians, than African blacks who in turn have it higher than Caucasian whites. Amongst Caucasian children from Iceland, hypermobility was seen in 40.5% of girls and 12.9% of boys. In a study form New Zealand, 4% of Caucasians … and 6.2% of Maori adults … The prevalence of up to 25% is seen in West Africans and Iraqis. Nigerian undergraduate students had hypermobility of 12.91% … ” (Able)

From PubMed: In one study performed at the University of Manchester, Manchester, UK, “a total of 12,853 participants returned a questionnaire with complete data; 2,354 participants (18.3%) were classified as hypermobile.” (Mulvey et. al)

So, it’s pretty clear that there are plenty of people out there with hypermobility. It begs the question, however – why is the condition so prevalent?

Genetics, plus the Numbers Don’t Add Up.

The human body is full of flaws. It is an organism. Organisms are subject to genetic mutation as each generation comes and goes. For those of you who don’t know what genetic mutations are, they are modifications in the nucleotide sequences of the genome. The genome is an organism’s entire genetic material, which allows for our cells to create specific proteins. A change in the sequence means a change in the structure of the protein produced by our cells.

Fun fact: collagen – the material that is the foundation of ligaments, cartilage, tendons, etc. – is a PROTEIN. Given the fact that a high number of genetic mutations in humans are harmful instead of beneficial (Eyre-Walker, Keightly), the wonderful genetic mutations we undergo can theoretically cause our bodies to produce crappy, weak collagen. This would mean the body would systematically have joint hypermobility.

It makes sense that a nice ol’ genetic defect can screw with our joint integrity – and it’s not even a theory. A great number of genetic diseases – including Ehlers-Danlos syndrome, Marfan Syndrome, osteogenesis imperfecta, and Down syndrome (Simpson) – have already been identified to cause joint hypermobility.

While that would explain part of the situation, there’s a bit of a discrepancy here. As prevalent as joint hypermobility is, these genetic defects certainly are not. As many people that have joint hypermobility, are there just as many who have those genetic defects listed prior? Let’s take Ehlers-Danlos syndrome, for example, “research statistics of EDS show the prevalence as 1 in 2,500 to 1 in 5,000 people” (EDNF). That’s about .02-.04% of the population. As for Down syndrome, .14% of babies are born with it each year (Parker, et. al).

Compare those statistics to the ones before regarding the widespread occurrence of joint hypermobility. The numbers don’t match. Plenty of people have joint hypermobility without having Down syndrome, Ehlers-Danlos syndrome, and etc.

What does this all mean then? It means that serious genetic defects cause only a fraction of the instances of joint hypermobility seen in humans. An unknown cause is still at play. Or is there?

Is there actually an “underlying cause” behind this so-called “diagnosis”?

A Wrist Sprain is Not a Disease. It’s an Injury that Heals.

An interesting point to note is that joint hypermobility can be either localized or systemic – meaning, it can affect one or two joints, or affect every joint in the body (EDNF).

There are plenty of diseases out there that affect our bodies systematically, but how many affect our bodies in specific, particular areas, especially the joints? By definition, a localized disease is “an infectious or neoplastic process that originates in and is confined to one organ system or general area in the body” (Wikipedia). So, for just one of your joints to go floppy and hypermobile, it seems that you either need to get cancer or an infection in the area of that specific joint for that to happen.

Something tells me infectious diseases and cancer don’t cause looseness of the connective tissue. They just cause cell death. So how on Earth can a single joint become hypermobile WITHOUT a genetic defect?

Prior injury. Something traumatic like a rupture or even a partial tear has been seen to leave ligaments loose and joints hypermobile. One study in Sweden noticed that patients who experienced ACL tears and required surgery had additional lateral movement in their previously-injured knees. (Johnsson) The knee allows for VERY LITTLE lateral movement, so without a doubt the injury resulted to joint hypermobility.

It is in my experience that joint-related injuries will end up causing some degree of laxity in the joint itself. Not only have I seen this with my own injuries (and I have experienced PLENTY OF INJURIES), I’ve seen this happen with friends and colleagues. Just like if you crash your brand new car, when you injure your joints, they seem to not “work correctly” afterwards sometimes.

With this information at hand, I theorize that prior injuries are big cause for joint hypermobility seen in adults. Despite the fact that we have this evidence, seemingly “unprovoked” joint hypermobility is still considered a isolated “condition” (Healthline), rather than a result of a prior injury. If you were wondering, this “condition” is known as benign joint hypermobility.

Thankfully for anyone who’s ever had a joint injury, such as a sprain or a tear, the collagenous tissues, such as ligaments, do in fact heal! Just like the skin, ligaments are capable of wound healing, and are able to return to their original level of tightness/looseness after some time. (Wheeless) The fact that ligaments have a crappy blood-supply doesn’t help the speed of the process, but at least they can still heal. This may be why ligaments sometimes don’t return to their normal tightness after an injury, and is an issue that must be addressed.

A Correct Approach for Stable Joints Needs the Proper Context

The way modern medicine treats joint hypermobility, for those without genetic defects, is though as if it’s a condition that popped up on it’s own. An example of typical treatment would be physical therapy. (NHS) This type of approach is reactive – meaning, we’re only treating it after the issue has developed.

In my opinion, since it seems that joint looseness stems from prior injury, it is not only possible, but it is optimal, to be proactive with preventing and treating this issue.

A possible regimen of prevention and treatment would probably consist of rest, gradual strengthening, and supplementation.

Rest.

Since the ligament is injured, its strength and integrity is reduced, it can no longer handle normal activity without the possibility re-injury, so it must be allowed time to not bear load as to not disrupt the healing process. This would be similar to avoiding picking at a scab on your skin, so it can actually heal. Give your wrist/ankle/whatever some time off to rest.

Also, because the ligament is disrupted somehow, stability of the joint is probably compromised, and hypermobility might already exist. This may call for immobilization, such as a cast or brace, so that you don’t accidentally push your joint into abnormal or extreme ranges of motion. Similar to how a yoga practitioner is extremely flexible because that person is always practicing yoga stretches, your joint could stay hypermobile if it frequently goes through those hypermobile ranges of motion.

It’s been observed that immobilization causes joint stiffness. (Lee, et. al) What else needs to be said? Stabilize it!

Gradual Strengthening.

Given the fact that we want our joints to return to normal function, the next step is to introduce a stimulus that increases the strength of our connective tissue. It’s believed that “physical activity can increase connective tissue strength and mass”, (Stone) so logic dictates that we must load the joint with increasing weight and volume to strengthen it, just as you’d strengthen a muscle group.

One must be cautious when re-introducing activity to the injured joint. Let’s say you sprained your ankle while you were running and your foot landed in a ditch. When your foot planted, it bore the entire force of your bodyweight accelerating towards the Earth, whilst twisting in an extreme fashion.

Not only must you be conservative when you add intensity and volume to your ankle’s daily activity, you must also be cautious as to how much range-of-motion you allow it to experience. Your ankle couldn’t handle the stress of your foot landing in the ditch and twisting (hence, why your ankle was sprained and the ligaments tore), and now that it’s weakened, it can’t handle activities that it once was able to without breaking down more and becoming more hypermobile.

Allow the healing process to occur, and don’t overdo it on the exercise.

Supplementation.

Certain nutrients and minerals, such as vitamins C and E as well as zinc, have been shown to improve collagen synthesis and wound healing. (Anangelina et. al) (Tengrup et. al) While these micronutrients are obtainable through food, it’s safe to say that most folks in the Western world don’t eat properly. Of course, that’s another issue to be addressed entirely, but in the mean time, supplementation could help out with missing nutrients.

With vitamin C supplements, I prefer brands that have bioflavonoids as they have better bioavailability. (Vinson, Bose)

With vitamin E supplements, I choose products that have a mix of tocopherols and tocotrienols versus tocopherols alone, as tocotrienols have unique benefits that are not seen with tocopherols. (Fu, et. al)

As for zinc, I go with ZMA simply because it has magnesium along with it. Why is this important? Well, roughly half of the U.S. population doesn’t meet the RDA for magnesium. (USDA)

You’ll notice that each of those links is for a Now Foods product. This is the brand I typically buy because they aren’t expensive as hell, and usually contain much less filler and “non-active ingredients” than other brands.

Now, go and keep your joints strong, stable, and stiff, and tell your doctor to screw off with his talk of “diagnosing benign joint hypermobility” and other non-sense.

References:

1. Lawrence, Able. ” Benign Hypermobility Syndrome.” Journal of the Indian Rheumatology Association 15 (2005): 150-155. Web.

2. Mulvey MR, et. al. “Modest association of joint hypermobility with disabling and limiting musculoskeletal pain: results from a large-scale general population-based survey.” Arthritis Care Res (Hoboken) 65.8 (2013): 1325-33. Web.

3. Eyre-Walker A, Keightly PD. “High genomic deleterious mutation rates in hominids.” Nature 397 (1999): 344-347. Web.

4. Simpson, Michael R. “Benign Joint Hypermobility Syndrome: Evaluation, Diagnosis, and Management.” The Journal of the American Osteopathic Association 106.9 (2006): 531-536. Web.

5. “What is EDS.” The Ehlers-Danolos National Foundation. EDNF, n.d. Web. 6 August 2014.

6. Parker SE, et. al. “Updated National Birth Prevalence estimates for selected birth defects in the United States, 2004-2006.” Birth Defects Res A Clin Mol Teratol 88.12 (2010): 1008-16. Web.

7. “Assessing Joint Hypermobility.” The Ehlers-Danlos National Foundation. EDNF, n.d. Web. 6 August 2014.

8. “Localized disease.” Wikipedia. Wikipedia, n.d. Web. 6 August 2014.

9. Johnsson, Hakan. “Knee joint laxity and kinematics after anterior cruciate ligament rupture.” Act Orthop Scand 65.256 (1994):117. Web.

10. “Hypermobile joints.” Healthline. Healthline Networks, n.d. Web. 6 August 2014.

11. Wheeless, Clifford R. Wheeless’ Textbook of Orthopaedics. 2012. Web. Wheeless Online.

12. “Treating joint hypermobility.” NHS. Gov.UK, n.d. Web. 6 August 2014.

13. Lee S, et. al. “Tissue stiffness induced by prolonged immobilization of the rat knee joint and relevance of AGEs (pentosidine).” Connective Tissue Research 51.6 (2010): 467-477. Web.

14. Stone, MH. “Implications for connective tissue and bone alterations resulting from resistance exercise training.” Med Sci Sports Exerc 20.5 (1988): 162-168. Web.

15. Ananagelina C, et. al. “Vitamins E and C May Increase Collagen Turnover by Intramuscular Fibroblasts.” J. Agric. Food Chem. 59.2 (2011): 608-614. Web.

16. Tengrup I, et. al. “Influence of zinc on synthesis and the accumulation of collagen in early granulation tissue.” Surg Gynecol Obstet 152.3 (1981): 323-326. Web.

17. Vinson JA, Bose P. “Comparative bioavailability to humans of ascorbic acid alone or in a citrus extract.” Am J Clin Nutr 48.3 (1988): 601-604. Web.

18. Fu JY, et. al. “Bioavailability of tocotrienols: evidence in human studies.” Nutrition & Metabolism 11.5 (2014). Web.

19. “Nutrient intakes.” USDA. USA.gov, n.d. Web. 6 August 2014.