• Louise H Connolly MD

Too Little Feel Good

Endorphin, Enkephalon, and Endocannabinoid Deficiency

And What You Can Do About It


Yes you can dampen a pain signal, numb the nerve with lidocaine, and zone it out. But then the nerve is just numb, it's supposed to function. What if the problem isn't too much pain, just too little relief? What is there is something wrong with your feel good signaling system? What if it is under active? You may need replacement therapy not a pain killer.


Just what is our pain/ pleasure system anyway? And what makes it work or not work? Well, one of the pleasure signals are called endorphins. Both endorphins and enkephalins. One of their biggest stimulators is exercise. One of their biggest inhibitors is stress. This endorphin system stimulates our "opioid" receptors, a term which I find unfortunate. Opioids are not natural compounds. It should be called our endorphin receptors.


If you are under stress, your endorphins can actually turn from promoting relaxation to promoting pain through their absence. How does this happen? Stress made your endorphins go down. Usually your endorphins stimulate immune balance by increasing regulatory T cells. Lose endorphins and you lose immune balance leaving your body open to inflammation. Inflammation, especially in the brain's microglia, lead to amplified pain signaling. A Q-tip becomes a needle.


Narcotics:


The problem with man made opiates (morphine, demerol or percocet) is that they are NOT bioidentical to endorphins although they hit the same receptors. These drugs have vastly different effects than our own endorphins. At first narcotics work, but then all regulation goes haywire. Endorphins are down regulated, Regulatory T cells aren't stimulated and the end result is a prolongation of inflammation followed by opioid resistance. So you end up needing more and more.



It's not nice to fool Mother Nature


Opioid receptors were never meant to be exposed to narcotics. Opioids dampen pain, endorphins promote pleasure. It's as if your thyroid was under active, and instead of replacing it with bioidentical thyroid, we used an amphetamine, would you get more energy? Yes. Is it the right answer? No. Side effects would be horrendous and there is an addiction potential. Same thing with endorphins and narcotics. What we need is bioidentical endorphins, only we haven't figured out how to make them yet. So what we've got to do is increase our own production of endorphins. Exercise and a good night's sleep help are a start. Anything we can do to decrease stress in our lives also helps. But what else?


DLPA:


This is really just phenylalanine, a derivative of the amino acid tyrosine (as found in aged cheese). It is a precursor of dopamine, an important neurotransmitter. Dopamine is all about reward and the pleasure you get from feeling rewarded. On a biological level, DL phenylalanine stops an endorphin-like molecule (enkephalin) from breaking down. Keeping this natural feel good chemical around longer resulted in less depression and less pain.


That's where we got the basis for the combination anti-depressants/anti-pain drugs called Effexor, Cymbalta, and Savella. These drugs also affect dopamine in a somewhat similar way. Me, I'd rather just up my consumption of DL phenylalanine.


DLPA has synergistic effects with Kratom. This is an evergreen tree native to Malaysia and Thailand. There will be more about Kratom in a future post. It's not for most people's use. It's just too strong and somewhat addicting.


Low Dose Naltrexone:


Naltrexone was discovered in the 1980's. Its traditional use is to block the opioid receptor so narcotics couldn't have an effect. This would save lives from drug overdoses in the ER. Dosing for traditional naltrexone use was high, 100 mg.


Very soon thereafter, an interesting effect was found with low dose naltrexone. We are now talking about 3 mg, NOT 100 mg! This low dose naltrexone would only block opioid receptors for a few hours. Your body then thinks that it's low in endorphins and makes more. But by this time, the naltrexone is gone, and your receptors are flooded with newly made endorphins. As a result, regulatory T cells surge, rebalancing your immune system, and blocking chronic inflammation. This is a win/win for you! Less pain, more healing. Low dose naltrexone works well for many central sensitivity syndromes and autoimmune diseases which involve pain. Studies support use in everything from Chrohn's disease and Multiple Sclerosis to IBS, Migraines, and Fibromyalgia. Low dose naltrexone is well tolerated, safe and can have surprisingly beneficial effects. Get it? It doesn't act like a drug, it just helps your body produce more of its own "feel better" chemicals while damping both central and peripheral inflammation.


You'll need a prescription which I would be happy to provide. See for yourself! There's little to no risk here. But please note, you can't take low dose naltrexone and narcotics at the same time.


I sincerely hope you are finding this series useful. There are so many new avenues to explore. Criminalizing pain as we clamp down on narcotics is wrong. .

LHC MD


#lowdosenaltrexone #autoimmune #centralsensitivity #chronicfatigue #pain #endocannabinoid

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