The term endorphins was created by combining the two words: endogenous morphine. These compounds trigger a natural high in our brains which encourages us to repeat the experience that produced it. Addictive drugs like heroin hijack this process to create dependency, but plenty of natural and healthy experiences, supplements, and foods act on this system to make us feel pretty good.This post will discuss ways that you can either increase endorphins or activate the body’s opioid system.

An Intro To Your Brain’s Opioid System

The brain opioid systems play an important role in motivation, emotion, attachment behavior, the response to stress and pain, and the control of food intake [1].

There are four opioid receptors in our brain: mu-opioid (MOR), kappa-opioid (KOR), delta-opioid (DOR) and nociceptin (NOP). Activating these receptors or increasing the molecules that bind to them will produce an opioid high.

Mu-Opioid Receptors

Activation of the mu receptor by a substance such as morphine causes sedation, euphoria and decreased respiration [2, 3].

Although morphine increases sedation, it decreases the total amount of deep sleep and rapid eye movement sleep in humans [4].

Individual differences in the function of the mu-receptor system predict personality traits that confer vulnerability to or resiliency against risky behaviors such as the predisposition to develop substance use disorders [5].

Delta-Opioid Receptors

Molecules that bind to delta opioid receptors show robust evidence of both antidepressant effects and also increase of BDNF production in the brain in animal models of depression [6].

They also protect against heart damage from strokes by preconditioning our heart [7]. DORs are neuroprotective as well and work in part by reducing TNF [8].

Activation of delta receptors produces some pain relief, although less than that of mu-opioid activators [9].

Kappa-Opioid Receptors

Kappa activation actually produces a bad mood (dysphoria), some pain relief (analgesic), and increased urination (diuretic). In high doses, kappa opioid activators may produce hallucinations [9, 10].

Activation of the KOR opposes many of the effects of the MOR and can prevent addiction to morphine, alcohol, and cocaine. It can cause an appetite increase and is activated by stress [11]. KOR activation causes a release of prolactin, a hormone known for its important role in learning, neuronal plasticity, and myelination [12].

A Natural, Drug-Free High?

These are among the factors that are currently under investigation for their potential to release endorphins, activate opioid receptors, or re-sensitize the brain after addiction or trauma. Many of these are limited to animal studies, meaning that there is no clinical evidence to support using or taking them to activate your opioid receptors.

In the next sections, we’ll discuss many of them in more detail. Talk to your doctor before making significant changes to your diet, exercise, or supplement regimen.

Top Strategies (Likely Effective)

These strategies have been investigated in clinical trials, but the evidence is not considered strong enough to determine effectiveness. Talk to your doctor before making significant changes to your diet, lifestyle, or supplement regimen.

1) Exercise

Physical exertion can release opioids to produce a mental state famously called the “runner’s high” [14].

Researchers have found that light-to-moderate weight training or cardiovascular exercise doesn’t produce endorphins for roughly the first hour, or until the body crosses from aerobic to anaerobic exercise. Power-based heavy weights or training that incorporates sprinting or other anaerobic exertion are required to quickly produce endorphins [42].

When your body crosses over from an aerobic state to an anaerobic state, it has to operate without enough oxygen to satisfy the muscles and cells screaming out for it. This is when the “runner’s high” occurs [42].

2) The Love Hormone

Oxytocin (not to be confused with oxycodone) is a significant love and pleasure molecule and it increases prosocial behavior. Oxytocin is often referred to as the “love hormone” because it facilitates trust and attachment between individuals [43].

According to some studies in animals, oxytocin could potentially inhibit the development of tolerance to various addictive drugs (opiates, cocaine, alcohol) and reduce withdrawal symptoms [44, 45].

In rats, oxytocin activated the opioid system to a degree, especially the mu- and the kappa-receptors in the brain [46].

Positive Social Interaction

There are several factors which have been associated with increased oxytocin release. High levels of plasma oxytocin have been correlated with romantic attachment, for example. Oxytocin is also released in large amounts when parents are bonding with their newborn infant [47, 48].

It turns out that some of the circuitry responsible for drug addiction in the brain is also responsible for positive social interactions and the formation of new romantic bonds – this is likely to be part of its original purpose, while addictive compounds hijack and misuse the same mechanisms. Some researchers even go so far as to say that falling in love is biologically similar to becoming addicted to your new romantic attachment [49]!

A 2011 study found that stimulation of mu-opioid receptors in the nucleus accumbens is an important neural mechanism for the attribution of positive value to social interactions in adolescent rats [19].

Massage

In a study of 95 adults, blood oxytocin increased after only 15 minutes of upper back massage. Likewise, a 10-minute foot massage increased blood oxytocin in 40 adult men. In this second study, participants’ oxytocin levels increased more dramatically when the massage was delivered by hand rather than by machine [50].

3) Tasty Foods

Studies have shown previously that stimulation of mu-opiate receptors within the ventral striatum increases the intake of palatable food.

The over-consumption of readily available and highly palatable foods likely contributes to the growing rates of obesity worldwide. Palatable food is thought to work via the opioid system to create these addictions [21, 22].

Eating a nice juicy steak gives you a good feeling, without the addictive properties. Stick with whole foods and you should be alright [22].

Chocolate

We all are familiar with the feel-good sensations we get from chocolate. Epicatechins in chocolate acts mainly via delta-opioid receptors [51].

Foods with Morphine-Like Characteristics

Casomorphin (from casein found in the milk of mammals, including cows) [52]

Gluten exorphin (from gluten found in wheat, rye, barley) [53]

Soymorphin-5 (from soybean) [54]

Rubiscolin (from spinach) [55]

Menthol – Found in numerous species of mint, (including peppermint, spearmint, and watermint), the naturally-occurring compound menthol activates the kappa opioid receptor [56]

Poppy Seeds

Though rare, poppy seed tea consumption can be fatal. It also has the potential to be abused or lead to opiate dependence [35, 36, 37].

Poppy Seeds have morphine and codeine in them [57].

According to international data, poppy seeds have a maximum of 62 mg/100g morphine and 5.7 mg/100g codeine [58].

Morphine effectively kills pain starting at a dosage of around 10-15mg. It is therefore unsurprising that eating poppy seeds can make a person test positive for opioids in the urine [58, 59, 57].

Be very cautious about consuming poppy seeds if you are taking opioid medication or if you have a bowel obstruction [35, 60].

Chili/Cayenne

Capsaicin, the chemical that makes cayenne and chili taste spicy, increases endorphin release and activates opioid receptors in rats. Some people report feeling a “high” after eating very spicy food, but there is little research on this phenomenon [61, 62].

Sugar

Most drugs of abuse increase dopamine in the nucleus accumbens. Under select dietary circumstances, sugar can have effects similar to a drug of abuse [22].

Repeated and excessive intake of sugar mimicked the effect on neurotransmitters in a similar manner to morphine or nicotine [63, 64].

Rats show signs of dopamine sensitization and opioid dependence when given intermittent access to sucrose, such as alterations in dopamine and mu-opioid receptors [22].

When these animals then fasted, they had the same chemical changes as withdrawal effects from addictive drugs, suggesting that the rats had become sugar-dependent. Specifically, acetylcholine was higher and dopamine was lower in the nucleus accumbens, which causes anxiety and cravings [63, 64].

Sugar-dependent animals have a delayed satiation response (acetylcholine release is delayed), drink more sugar, and release more dopamine than normal rats [22].

Fiber & Resistant Starch

Hi-maize sure does give you a high, but it takes the next day to hit. To really feel good you need 120g of this stuff or 30g taken 4 times a day. Resistant starch digests in your large intestine to produce butyrate.

Butyrate increases mu-opioid receptors [26].

One study found that resistant starch consistently produces more butyrate than other types of dietary fiber [65].

Butyrate is an HDAC inhibitor, meaning that it “uncoils” DNA and allows for increased gene expression [66].

HDAC Inhibitors have had mood stabilizing, anti-epileptic, and anti-inflammatory effects in animal models [67, 68, 69].

4) Alcohol in Moderation

Drinking alcohol induces opioid release in the nucleus accumbens and orbitofrontal cortex, areas of the brain implicated in reward valuation [41].

In excess, alcohol is damaging to our health; alcohol in moderation is more of a controversial topic, with some studies finding cardiovascular benefits of moderate alcohol consumption and others finding associations with cancer. Whatever your choice, we recommend strongly against drinking in excess [70, 71].

5) Magnesium

In 60 patients who had just had surgery, magnesium amplified the analgesic effect of low-dose morphine in conditions of sustained pain. This early clinical trial confirmed the results of earlier rat studies. In each of these cases, however, magnesium did not itself activate the opioid receptors or release endorphins; rather, it potentiated the effect of another compound that did [24, 25].

It certainly wouldn’t hurt to make sure you eat magnesium-rich foods. The best sources of magnesium are nuts, leafy greens, and whole grains [72].

6) Mild Stress

In both humans and animals, short-term stress triggers the release of pain-killing endorphins. This is the same mechanism by which exercise triggers endorphin release [73, 74, 13, 75, 76].

In the longer term, however, stress triggers the release of dynorphins, which produce bad feelings and aversive behaviors – that is, they make both humans and animals avoid the circumstances that preceded their release. Some researchers suspect that dynorphins play a role in the feelings of dysphoria and hopelessness associated with major depression [77, 78].

Limiting and controlling stress is one of the most important skills for a healthy lifestyle.

Cold

Intermittent swimming in cold water induced opioid-receptor-mediated pain relief in rats [13].

Cold exposure also increased “heat shock inducible factor” (which increases opioid receptor expression) in experimental rats. Specifically, mu and delta opioid receptors – the same receptors that heroin and morphine work on – are upregulated by heat shock inducible factor [79, 80].

7) Acupuncture

People undergoing acupuncture have higher pain thresholds than normal, an effect that many researchers attribute to endorphin release and opioid receptor activation [81].

Acupuncture activated the opioid system of experimental rats. Therapy increased both the release and synthesis of opioids and the function and expression of their receptors [23].

Potential Strategies (Lacking Evidence)

No clinical evidence supports the approaches listed below to combat X. Below is a summary of the existing animal and cell-based research, which should guide further investigational efforts. However, the studies listed below should not be interpreted as supportive of any health benefit.

8) High-Quality Sleep

Sleep deprivation decreases mu and delta opioid receptor binding in the rat limbic system, which controls emotions to increase feelings of pleasure [16].

Light & Dark Cycles

Mu-opioid receptors are activated in a pattern that aligns with the circadian rhythm. When we disrupt this rhythm chronically, other systems (including the opioid receptors) get disrupted as well and don’t function the way they’re supposed to [82].

Experimental animals exposed to constant white fluorescent light had a significant decrease in tissue content of opioids (enkephalins, which bind to delta opioid receptors) during the dark phase of the 24-h circadian rhythm [83].

Melatonin

Melatonin exerts its analgesic actions by increasing the release of beta-endorphins [29].

9) Some Probiotics

The gut flora and brain interact in complex ways that we don’t fully understand. One of the stranger mechanisms by which the bacteria in the human gut affect our brains is through oxytocin release [84, 85].

L reuteri is among the bacterial species that has been observed to increase oxytocin in mice and rats. This effect has not yet been studied in humans [85, 86].

Acidophilus is capable of increasing the expression of mu-opioid and cannabinoid receptors in the intestines and has morphine-like effects [28].

10) Moderate Sun Exposure

Some clinical reports suggest that sun tanning could be genuinely addictive, much in the same way that drugs of abuse are. In a rat study, even low-dose UV light exposure increased endorphins in the skin and blood [17, 18].

Therefore, moderate sun exposure could potentially increase endorphins, but excessive exposure has been associated with addictive behavior [17, 18].

11) Hot Shower/Bath

Many people turn to hot baths or showers to relieve stress and feel better. Mice that took a short swim in warm water were found to have increased beta-endorphins and pain relief, suggesting a mechanism for this suspected benefit [13].

12) LLLT

In rats, low-level laser therapy (LLLT) relieved pain, possibly by increasing natural opioids. This effect has not been investigated in humans [30].

Controversial Drugs

The drugs discussed in this section are heavily regulated and controversial. We include them here because they are the subject of a great deal of current research into their potential to increase opioid receptor activation with fewer side effects than conventional opioid painkillers. However, we strongly advise against using them without a doctor’s supervision.

Low Dose Naltrexone

Low dose naltrexone (LDN) is a controversial topic in current research. Naltrexone decreases opioid receptor binding and is typically used to treat opioid dependence. More recently, researchers have begun exploring the idea that a tenth of the conventional naltrexone dose (hence, low dose naltrexone) could actually have a positive effect on people with chronic pain [87, 88].

The mechanism by which LDN could help in chronic pain is unclear. However, some researchers believe that when opioid receptors are down-regulated, the body might compensate by increasing the production of endorphins and enkephalins. If these increased levels of endogenous opioids persist after the naltrexone has been eliminated from the body, they would then be available to bind to the newly freed up receptors [87, 88].

If you have chronic pain, you may want to talk to your doctor about trying LDN. Naltrexone is a powerful pharmaceutical drug. Do not use naltrexone without a doctor’s prescription and supervision.

Cannabis

Marijuana (or cannabis) produces positive feelings in most users. It acts primarily on cannabinoid receptors, but the two most active ingredients in cannabis, THC and CBD, both activate mu and delta opioid receptors as well [89, 33].

Cannabis is still a highly controversial subject among doctors and researchers. Many studies and reviews have emerged in recent months and years discussing the potential of cannabis as an alternative to opioids in chronic pain. There is no consensus on whether it is effective against pain on its own or whether it can be used to wean patients off of opioids [90, 91, 92].

Cannabis is classified as a schedule I drug in the United States, making it illegal to use and very difficult to study [93].