Natural Ways to raise Endorphin Levels/Production

[seep]

A bit OT, but if you have problems sleeping, forget sedative antihistamines etc, just make a toasted cheese sandwich with lots of fairly hot chilli & with the endorphin release after you've eaten it, it's much easier to drift off to sleep (and no zombie hangover like you get with Nytol & other sed. antihistamines) - well after about 5 minutes when the initial burn has subsided!

I've gone through like 4 lbs of serrano peppers since I read this. I love the feeling. They stop burning the tongue so badly after a few days.


ed: This is has got to be a record.

 

[dogfood]

I got a truly horrid idea just now. What if you were to inject capsaicin? Better yet acetylate that -OH so it can cross the blood brain barrier before causing horrible pain at all the pain receptors. I bet it would get those endorphins going though.

Or another idea: wrap some aluminum foil around your head and get a blowtorch. Now don't let the flame get too close or the foil will burn. Just keep flame far enough to keep those endorphins flowing in your head.

your brain doesn't have any pain receptors so it would just make your veins burn like hell...

 

[alec_empire]

I think the most effective way to release endogenous opioids is vigorous exercise and social engagement with family and friends.

Unfortunately, some people do have dysfunctional endogenous opioid systems which is associated with diminished endorphin/ enkephalin / endomorphin - release ( can be seen with PET scans, where there is a secondary up-regulation of mu receptors du to decreased occupancy by endogenous opioid peptides )


See:

http://www.nature.com/nm/journal/v2/n11/abs/nm1196-1225.html




http://bjp.rcpsych.org/cgi/content/full/191/1/63

 

[seep]

Metformin!

OK it's not entirely natural, but it kickstarts a natural mechanism that slows down with sedentary behavior. I've been coming off amphetamine since right b4 Xmas, so I've been otiose. For the past 3 days I've been taking metformin 500 mg bid and it's had me feeling like--well imagine what pediatric heroin would feel like.

I found this ipso facto:

1. Horm Metab Res. 2006 Feb;38(2):106-11.

Metformin increases insulin sensitivity and plasma beta-endorphin in human
subjects.

Ou HY, Cheng JT, Yu EH, Wu TJ.

The Division of Endocrinology and Metabolism, Department of Internal Medicine,
Institute of Clinical Medicine, College of Medicine, Tainan, Taiwan.

Metformin has been widely used in clinical type 2 diabetes treatment and
prevention. The present study was designed to explore the effect on people with a
sedentary lifestyle at therapeutic doses. Twenty-two physically-inactive
volunteers with normal glucose tolerance were studied. Escalating doses of
metformin in low-dose (250 mg), intermediate-dose (500 mg), and high-dose (750
mg) treatment three times per day were administrated into each subject for a
three-week treatment period. Fasting plasma glucose, A1C, HOMA-IR for insulin
resistance, lipid profile, and plasma beta-endorphin-like immunoreactivity (BER)
were measured before treatment and weekly at the end of each dosing period.
Metformin significantly reduced fasting plasma glucose and HOMA-IR in healthy
humans after receiving this treatment at therapeutic doses including low-dose (5
%, 17 %), intermediate-dose (6 %, 25 %) and high-dose treatment (6 %, 21 %).
Plasma BER was also increased from 135.46 +/- 61.73 pg/ml to 137.52 +/- 66.11
pg/ml by low-dosing (p = 0.39), to 139.17 +/- 64.08 pg/ml by intermediate-dosing
(p = 0.32), and to 149.59 +/- 63.32 pg/ml by high-dosing (p < 0.05). Also, serum
cholesterol decreased significantly using metformin at therapeutic doses
including low-dose (4 %), intermediate-dose (8 %) and high-dose treatment (7 %).
However, metformin failed to modify levels of serum HDL-cholesterol and
C-reactive protein (CRP) in healthy subjects. Also, the reduction of serum
cholesterol by metformin did not correlate to the increase in insulin
sensitivity. In conclusion, metformin causes a significant parallel increase in
insulin sensitivity and plasma beta-endorphin level in human subjects.

PMID: 16523411 [PubMed - indexed for MEDLINE]

This possibly is why:

1. Diabetes. 2006 Mar;55(3):819-25.

Novel mechanism for plasma glucose-lowering action of metformin in
streptozotocin-induced diabetic rats.

Cheng JT, Huang CC, Liu IM, Tzeng TF, Chang CJ.

Department of Pharmacology, College of Medicine, National Cheng Kung University,
Tainan City, Taiwan 70101, ROC. [email protected]

To better understand the insulin-independent plasma glucose-lowering action of
metformin, we used streptozotocin (STZ)-induced diabetic rats to investigate the
possible mechanisms. Oral intake of metformin decreased the plasma glucose of
STZ-induced diabetic rats with a parallel increase of plasma beta-endorphin-like
immunoreactivity (BER). Mediation of opioid mu-receptors in the action of
metformin was identified by the blockade of receptors with antagonist in
STZ-induced diabetic rats and the failure of action in opioid mu-receptor
knockout diabetic mice. Release of BER from adrenal glands by metformin was
characterized, using bilateral adrenalectomy and the release of BER from isolated
adrenal medulla of STZ-induced diabetic rats. Repeated treatment with metformin
in STZ-induced diabetic rats increased the mRNA and protein levels of GLUT-4 in
soleus muscle that was blocked by naloxonazine. Reduction of the mRNA or protein
levels of hepatic PEPCK was also impeded in the same group of STZ-induced
diabetic rats. In conclusion, our results provide novel mechanisms for the plasma
glucose-lowering action of metformin, via an increase of beta-endorphin secretion
from adrenal glands to stimulate opioid mu-receptor linkage, leading to an
increase of GLUT-4 gene expression and an attenuation of hepatic PEPCK gene
expression in STZ-induced diabetic rats.

PMID: 16505249 [PubMed - indexed for MEDLINE]

 

[Crendore]

Endorphins are Endogenous Morphine which is your bodies own version of morphine and you always have a certain level of endorphin's at any time. when you take opiates you make the body think that it no longer needs to produce endorphins because it is getting it from an outside source. so the body slowly produces less endorphins until you get to the point where your body wont produce any and you need morphine to produce it for you. The withdrawal is the body having no endorphins at all and this causes the symptoms of nausea, dizziness, vomiting, misery, etc because you are effectively putting yourself through the polar opposite of an opiate high. One thing I would be interested to find out is that is the speed of ingesting and excretion affect the likelihood of addiction as with cocaine, which is very similar to Methylphenidate and because it works so quickly and disappears so quickly this makes the body miss the drug where as methylphenidate enters and leaves more gently creating less likelihood of addiction occuring. I think it would be worth eating or drinking opiates in the future as opposed to injecting or smoking them as this could perhaps lessen the likelihood of addiction and make for a more mellow and gentle high.

 

[pema]

It's an old topic but still interessting. So I will add something to that.
BTW: The original question was never answered.

The following text shall be a citation from the strange book "End your addiction now":

In 1972, scientists at the Johns Hopkins University School of Medicine discovered that the human brain produces chemicals that closely resemble morphine, the powerful painkiller. They named these newly discovered substances endorphins. Studies with laboratory animals found that the endorphins were incredibly effective. An endorphin called beta-endorphin was 18 to 50 times stronger than morphine. And dynorphin was apparently 500 times more powerful!

The German wikipedia states that is was 1975 (three years later) and that they found in in pigs and not humans.

When this is true that those stuff is so powerful and better than morphine - why isn't it used as painkiller for humans? Probably it won't have may side effects because it's natural to your body. I was unable to find something on the pai killing potency of endorphines.
German wikipedia writes that from hypophysis in blood stream released beta-endorphine binds to opioid receptors but would not produce analgesia there.

For me it looks like if the enkephalins were responsible for pain reduction and not endorphines. But I am no doctor.

This "End you addiction" cite goes on:

Fortunately, a way to protect the endorphins was quickly discovered. The substance was a simple nutritional amino acid called dl-phenylalanine (DLPA). DLPA is not a drug. It does not block pain. DLPA protects the endorphins from the endorphin-eaters, helping to restore the body's ability to deal with pain. Phenylalanine is found in fish, chicken, eggs and other foods.

Studies have shown that DLPA effectively blocks arthritis pain and joint inflammation in many patients. It is much safer than the standard arthritis medications and considerably less expensive in the long run. Best of all, it is long-lasting. Whereas standard anti-pain and anti-arthritis drugs last for several hours, DLPA can continue quelling pain for up to four or five days.

Actually DLPA is said to be an enkephalinase inhibitor. That would prevent the breakdown of enkephalines and not endorphines.
But I think, it could be a possible help during withdrawal. I haven't tried it but it sounds logical. When DLPA can inhibit enkephalinase then this enzyme cannot break down the enkephalines.

Before thinking how to raise endorphine levels, it would be interessting to know is this has any postive effect on opiate withdrawal or whatever.
Maybe it's the enkephalines to should be raised.
I never saw any studies what the effects of increased endorphine or enkephaline levels are. It seems that science is still unsure what the exact jobs of endorphines are. Some years ago, it seemed clear, that endorphines are responsible for feelings of luck and pain reduction but now it seems as science is unsure about that.

You will feel better during opiate withdrawal when you go for a walk or do some exercise. But are endorphines really responsible for that?
Maybe it helps to boost all endogenous opioid levels..?
And has anyone tried DLPA? Did it help during acute withdrawal or PAWS?

 

[Enix150]

^ Some very interesting points to consider! It seems I have more reading to do... I would assume dynorphins aren't used medicinally because of the possibly massive side-effect profile? They play with appetite, depression, pain, and so many things; the system doesn't seem to be well enough understood yet..

Hey just wanted to a share a strange and probably not useful story! So the other day I took a spill and tumbled pretty hard into the ground. (It's actually quite surprising how thoroughly I managed to wreck myself considering I was on level ground..) Somehow I managed to smash my knew and roll around to break my hand too somehow... Anyway, I got really really pale, threw up, and had to resist the urge to fall asleep: all standard shock-reactions. I staggered back to my place all covered in blood, just wanting water more than anything. when I finally got there my heart had calmed down a little bit the nausea had subsided and I wasn't so pale, but when I sat down to smoke and explain my mess of a self, I noticed the room start to darken as if I had eaten an opiate. At first I thought this was the shock coming back or a trick of the light, but sure enough, the pain started going away and within a few minutes I was fully faded! (voice changed and everything) I had heard about injuries (especially when you sustain multiple of them) causing the release of endogenous opioid peptides, but never had I felt(noticed?) the effects so strongly!! It only lasted an hour or two, but it certainly took me by surprise.

 

[atrollappears]

For me it looks like if the enkephalins were responsible for pain reduction and not endorphines. But I am no doctor.

I think it's that endorphins (being massive molecules) do not cross the blood brain barrier, and opiates act as central analgesics. So, only endorphin released in the brain would have analgesic effects.

 

[pema]

Raising natural endorphin levels with hot peppers

It is said that hot spices, especially eating chili peppers, shall be able to increase endorphin levels.

It is asserted by many that prolonged stimulation from capsaicin releases B-endorphins from the brain to impede and reduce pain. It is based on this idea that capsaicin has been used as a medication to aid in the alleviation of many chronic disorders, such as rheumatoid arthritis, and viral and diabetic nerve damage. However, much like a chili-eaters tolerance increases with the frequency of their use, extended use of this chemical leads to desensitization and therefore a higher dose is needed to be effective.

But is it necessary that we eat those chili peppers?
I often read that capsaicin and the burning sensation leads to substance p release and pain which increases endorphin levels.
But I saw that there are chili capsules which are sold to increase endorphin levels and to lower pain. Does this really work?
I don't feel the burning sensation when I swallow a chilli capsule. Then I don't realize that it is hot.
Do those chilli capsules/capsaicine capsules/cayenne capsules really increase endorphin levels like the vendors' websites tell it?
Or will only eating hot peppers do this job?

 

[endotropic]

Endorphins/enkephalins/dynophins aren't used therapeutically because they are peptides and would be broken down by proteases before they could reach the brain, unless you were to IV ridiculous amounts or inject them straight into your nucleus accumbens or something.

 

[nowitson]

The benefits of exercise during w/d is probably due to a multitude of different things happening in the body. Elevated serotonin, dopamine. etc. But from personal experience exercise has drastically reduced withdrawal symptoms/ even stomach issues. To me that clearly indicates some sort of endorphin/enkephalin activity. When your dope-sick the last thing you want to do is exercise but if you push yourself the relief is amazing.