In this particular study, researchers found that men with RLS  had significantly increased risk for having erectile dysfunction (ED) compared with men who did not have RLS. The lead researcher, Dr. Gao, commented that the findings indirectly support the role of dopamine as a common pathway, in light of another study of his in the past that showed an association between ED and Parkinson's disease. He also points out that these same people with ED were more overweight, more prone to depression and anxiety, and had a greater chance of having hypertension or a history of stroke (sound familiar?)

It sounds like dopamine deficiency is a popular explanation for a number of different conditions. For both PLS and Parkinson's, giving dopamine-like agents help with the respective symptoms. The problem is that it never cures the problem completely, with a number of serious side effects. 

This approach to medicine is the replenish what's missing method. If you're deficient in dopamine, replace it. If you're deficient in Vitamin C, B12, or thyroid hormone, replace it. The problem is that this approach works in some people, but not in everyone. Then the next step is to increase the dosage, and then even more people respond, but not everyone (with more side effects). Ultimately, you're not addressing what's causing the deficiency. 

If you have a sleep-breathing problem, it's been shown that you can easily clot in certain small and large vessels of your brain very easily. If you happen to have a clot in the dopamine area of your brain, or if the brain biochemistry changes as a result of hypoxia, then you'll get various symptoms. But I think even the neurologists will tell you that a lack of dopamine itself won't lead to Parkinsons; it's just one part of a much larger picture. Could it be that obstructive sleep apnea may be that bigger picture, since by definition, all modern humans are susceptible to sleep breathing problems to various degrees?

What's your opinion on this? Should we continue to treat every medical condition in isolation hoping to target that one missing protein or gene, or should we step back and try to connect the dots until we see the bigger picture? Please enter your comments in the box below.

GABA is one of numerous neurotransmitters in the brain that sends messages from one part of the brain to another. High GABA levels are associated with a calming, relaxing effect, whereas low levels are associated with anxiety and stress. Conventional wisdom says that if this is true, let’s increase GABA levels with supplements. The same can be said for various other neurotransmitters, hormones or vitamins that we use as supplements. In many cases, replacing what’s missing can certainly help, but you’re still not addressing what’s actually causing the lowering of these substances. 

If you look in the research literature (and on the internet), you’ll see many studies linking stress and low GABA levels. Another study showed that practicing yoga increases GABA. This is why any method or discipline that is calming or relaxing can raise your GABA levels. So it’s not a lack of GABA that gives you insomnia, per se, but there’s something else that is causing insomnia and low GABA levels.

This is a problem that we see with almost every area of modern medicine, where we’re great at finding associations, but not very good at solving the root of the problem. 

The common thread with all these studies goes back to stress. Yes, we have many different types of stress in our lives that can lead to insomnia (financial, work, family, poor diets, toxins, etc.), but what I’m suggesting is the possibility that due to our unique upper airway anatomy, all of us are somewhat susceptible to physiologic stress due to an inability to breathe properly at night. External stresses (psychologic, emotional and physical) can also aggravate this internal, physiologic stress.

The extreme end of this spectrum that I describe is called obstructive sleep apnea. But even if you’re "normal," having a narrowed upper airway anatomy can predispose you to microbstructions and arousals, leading to a physiologic state of hyperarousal. These people won’t officially meet the criteria for sleep apnea. Many of these people will also not be able to sleep on their backs, since that’s when the tongue falls back the most, due to gravity.

If you measure neurotransmitter levels in these patients, of course they’ll have abnormalities. This is why chronic insomnia is linked later in life to so many other medical conditions such as depression, diabetes, hypertension, and heart disease. Notice that these are all complications of obstructive sleep apnea. 

This is not to say that we should stop everything we do to treat insomnia. Cognitive Behavioral Therapy (CBT) is a great way to calm the mind and develop good sleep habits. It’s even been found to work better than sleeping pills. My only concern is what happens to these people many decades later, even if their insomnia is initially cured.

Knowing about the results of this study, do you think it will sway doctors to at least start screening for obstructive sleep apnea in their diabetic patients?
photo credit: Yogma