Elevate Your GLP-1 Levels: Transform Your Health Through Diet and Lifestyle Choices

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I’ve discussed the advantages of pharmacologically enhancing GLP-1 activity regarding weight reduction, considering the detrimental effects of obesity. I’ve also mentioned its drawbacks, such as frequent gastrointestinal reactions and muscle loss, along with the rarer or more speculative adverse effects like thyroid cancer, pancreatitis, and pancreatic cancer. Furthermore, I’ve outlined the cost/benefit analysis, specifying who might find the advantages significantly outweigh the risks, at least in the short term. But is there a method to gain the advantages of GLP-1 without the hazards, through boosting it naturally via dietary and lifestyle modifications?

Well, there’s physical activity. Exercise seemingly acutely enhances GLP-1. Five studies have examined exercise and GLP-1, and four out of five identified elevated levels of total GLP-1 post high-intensity interval training and sprint interval training, as well as moderate-intensity continuous training, showing no significant difference between high-intensity intervals and moderate-intensity continuous sessions.

In contrast to control groups where participants did not engage in any exercise, both exercise types (high-intensity interval and moderate-intensity continuous) led to significantly increased GLP-1 levels immediately post-exercise and again 30 to 90 minutes later. Regrettably, there appeared to be a publication bias, indicating that some studies that failed to demonstrate an effect might have been quietly disregarded, thus distorting the findings. But what are the drawbacks of exercising? The data strongly supports that nearly everyone could gain from increasing their physical activity.

What about nutrition? There’s a range of natural substances—foods, drinks, and spices—that have proven capable of elevating our native GLP-1 levels. However, is endogenous GLP-1, meaning GLP-1 from within the body, effective as an alternative to medications that replicate GLP-1, such as Ozempic?

If you haven’t already, I suggest viewing or reviewing my video explaining what GLP-1 is and its functioning, to thoroughly understand the topic at hand. Our native GLP-1 levels fluctuate in response to food intake. When we utilize these medications, however, levels in our bloodstream remain relatively stable and elevated. But “high” in this context is a slight understatement.

The overall levels of these GLP-1 mimicking drugs in our blood generally range from 20 to 30 nanomoles per liter. Alright. Here’s how much GLP-1 naturally increases in our bloodstream within two hours following a meal: perhaps up to 20 or 30…picomoles. Nano- signifies billionth; pico- signifies trillionth. At this scale, medication levels soar to about 25,000. How could enhancing natural levels ever compare?

Well, part of the variance might be due to the manner of drawing blood from individuals’ veins for laboratory tests. Since natural GLP-1 is swiftly deactivated by an enzyme in our blood, by the time GLP-1 is released by our intestines and passes through the liver, heart, and lungs, and eventually into our arteries before reaching the veins from which the laboratory technician extracts blood, the levels measured tend to be lower than the arterial levels that GLP-1 receptors interact with throughout our body, albeit only slightly.

But how do medications like Ozempic linger in the body for weeks as opposed to minutes? They are chemically altered to adhere to the most prevalent protein in our bloodstream. Therefore, even though the total medication levels in our blood lie in the nanomolar range, they are bound so tightly to protein that the active levels freely interacting with tissue receptors are likely a hundred times smaller, dipping down into the picomolar range. Hence, although at first glance, it seems plasma medication levels are extraordinarily high, they might actually be more similar to natural GLP-1 levels post vigorous stimulation. Nonetheless, there appears to be a significant discrepancy.

GLP-1 activation in the brain seemingly regulates food consumption, but the exact relationship between this and GLP-1 in the bloodstream is still unclear. The gut serves as the primary source of GLP-1 secretion in the body; thus, wouldn’t it be broken down by enzymes in the blood before much could ever reach the brain? It can pass through the blood-brain barrier, but is an adequate amount truly making it there? Interestingly, GLP-1 is also generated by nerves within the brainstem itself, and substantial evidence indicates that the appetite-suppressing effects of GLP-1 mimicking medications, like Ozempic, are mediated by these brain GLP-1 receptors. Therefore, how could natural blood levels anticipated following dietary modifications designed to elevate gut GLP-1 secretion still yield clinically relevant effects?

Indeed, the GLP-1 released from our intestinal cells is rapidly broken down, resulting in low systemic levels, yet its impacts seem to be mediated by vagus nerve stimulation. The vagus nerve links the gut directly to the brainstem; thus, it maintains a direct connection to the brain and is not dependent on blood transport.

But hold on; there are GLP-1 receptors present in the pancreas, kidneys, liver, and heart. Why would the body possess GLP-1 receptors in our peripheral organs if the hormone primarily operates through the vagus nerve? It’s plausible that strong stimuli might increase blood levels sufficiently to activate these peripheral receptors.

So, perhaps the typical functioning of GLP-1 isthat we consume a meal, and GLP-1 transmits the appetite-suppressing signal to our brain directly via the vagus nerve. Subsequently, our brain communicates the messages to the pertinent systems throughout our body. Administering individuals high doses of a GLP-1-mimicking medication, such as Ozempic, allows it to permeate directly through the bloodstream to all these organs, including the brain. And a potent dietary GLP-1 stimulus could potentially achieve both effects. However, one cannot definitively determine whether natural, physiological levels of GLP-1 can curb appetite until you…subject it to experimentation.

When varying levels of GLP-1 are infused directly into individuals’ veins, a dose-dependent decrease in both hunger and food consumption can be observed. However, the effective dosages employed in infusion studies increased baseline levels fourfold or more, whereas blood concentrations amplified by GLP-1-enhancing foods typically only doubled baseline amounts. Thus, although high-dose GLP-1 infusion induces a noticeable change in appetite and eating behavior, could it be that stimulating GLP-1 release through diet may not achieve the same?

Keep in mind how food naturally raises blood levels only about 20? Interestingly, you can experience a significant reduction in food intake—up to 30 to 35 percent less of a limitless meal—merely by elevating your GLP-1 levels to 10 or 15, or even just 5! This is well within achievable dietary limits. Consequently, though low natural levels might seem to exert minimal impact at first glance, a modest increase in levels through dietary modulation of GLP-1 release might suffice to hold clinical significance. Thus, we don’t need to aim for levels akin to those achieved with drugs. Naturally, this is logical, isn’t it? Why would our body inherently generate an appetite-suppressing hormone in response to food if it didn’t effectively suppress our appetite?

This analysis on enhancing the hormone GLP-1 through natural products concluded that there are substantial studies indicating that the berberine in barberries, quercetin in capers, red onions, and buckwheat, ginseng, ginger root, gardenia, green tea, wheat fiber, soybeans, curcumin in turmeric, cinnamon, and resveratrol in grapes each showcase robust effects on GLP-1 functionality. The aspiration is that boosting our own GLP-1 hormone by consuming particular foods might yield similar advantages to GLP-1-mimicking medications, without their potentially debilitating side effects. However, whenever a review makes a factual claim, such as “robust effects” on GLP-1 activity, it’s crucial to investigate the original studies, the so-called primary literature.

For instance, here’s the segment concerning soy: researchers illustrated that soybeans can stabilize blood sugars by prompting GLP-1 release. The dietary intake of soybean protein incites GLP-1, and notably, soybean protein elevates GLP-1 expression and secretion. “This combined evidence strongly implies that soybean protein influences GLP-1 secretion.” Sounds promising! Yet if you examine these three sources, that was derived from studies on mice, rats, and in vitro experiments.

Gardenia-derived options similarly supposedly enhance GLP-1 secretion based on cellular and rodent studies—but, when actually evaluated in humans, those in the gardenia cohort experienced a decline in GLP-1.

Evidence also implies that ginseng augments GLP-1 release, yet again, this is merely evidence from rats and test tubes.

What’s the situation with that red-wine component, resveratrol? It’s effective in diabetic rats, but not in diabetic humans.

Green tea is claimed to elevate GLP-1 levels in real patients, actual human subjects! However, in reality, the increase over placebo did not achieve statistical significance.

Olive oil is posited to generate higher GLP-1 concentrations compared to butter, but the referenced study showed no significant difference. This was conducted with healthy subjects, though. A comparable investigation involving individuals with diabetes did reveal a greater GLP-1 response, albeit only by about 15 percent.

Avocados offer abundant monounsaturated fats as well. Online, you may encounter supposed experts asserting that consuming avocados can be as effective as receiving weight-loss injections, claiming it works “just like the miraculous weight-loss shot Ozempic”—and that’s coming from a nutritionist!

Guaca-mo-zempic may show effects if you’re a rat, but in humans, GLP-1 was found to be significantly lower in the avocado-enriched meal.

Regarding online assumptions, what do we understand about berberine, the supplement labeled “nature’s Ozempic”—a component of barberries, which I’ve previously highlighted as a treatment for acne? Well, berberine enhances GLP-1 secretion in rats and petri dishes, yet no GLP-1 studies involving humans have been conducted thus far. What truly matters, though, is weight loss, and there have been multiple investigations on the impact of berberine and barberries on body weight. No positive outcomes were observed, either for berberine supplements or barberries alone.

This is all rather disappointing. A compound found in the spice fenugreek appeared to enhance GLP-1 signaling in a laboratory setting, but no human studies exist, and it didn’t even succeed in mice. Consequently, fenugreek fell short, but there are some spices that can authentically elevate GLP-1 in humans.

If individuals consume the same dish, but chew each bite either 15 times or 40 times, the blood levels of the appetite-suppressing hormone GLP-1 in the bloodstream are elevated after 40 chews compared to 15. Those who chewed 40 times ended up ingesting approximately 75 fewer calories than the 15-time chewers. The researchers propose that increased chewing may assist individuals in maintaining their weight. However, who would want to sit down and count their chews? What if you simply consume chewier foods?

What if individuals eat shredded cabbage, which necessitates more chewing, versus an equal quantity of pureed cabbage: identical food but requiring different degrees of chewing? GLP-1 blood levels were greater in the shredded cabbage cohort.

group than the pureed-cabbage-non-chewing one, at 45, 60, and 90 minutes, at least initially. The investigators were diligent in ensuring that both groups consumed food at the same pace, since devouring even identical meals at a slower speed can lead to an increased GLP-1 response.

The researchers had participants consume an equal quantity of ice cream over either a five-minute or a 30-minute interval. Those who ingested the identical amount of food at a slower rate exhibited a notable elevation in GLP-1 levels in their bloodstream for hours post-meal—approximately a 30 percent increase overall.

On average, the individuals involved were overweight, yet considerably leaner than a typical American. What if we, in essence, conducted a similar study, but with obese participants who could greatly benefit from the additional GLP-1 surge? And, here we go.

As indicated in the title, the researchers discovered differing outcomes when comparing obese adolescents to obese adults. With the obese teenagers, the researchers observed the same result as with the overweight adults—a markedly elevated GLP-1 response following slower consumption. However, the eating pace seemed inconsequential among obese adults. The same held true for satiety. Obese adolescents reported feeling fuller and more satisfied for extended periods when eating at a slower pace, but eating speed didn’t appear to make a difference for the adults suffering from obesity.

Yet for some individuals, increased chewing and slower eating may elevate GLP-1 levels regardless of what is consumed. Are there particular foods that specifically enhance GLP-1? In my previous video, I examined a variety of foods, drinks, and supplements that don’t seem effective, but a few spices might have an impact.

Participants were provided with rice-and-vegetable curry prepared with three distinct spice dosages. The bland control meal contained no spices whatsoever, just tomato puree with eggplant. The low-spice meal incorporated a tablespoon of curry spices alongside onions, garlic, and ginger, while the third variation, the high-spice curry, had two tablespoons—double the spices. The spices included turmeric, coriander seeds, cumin seeds, dried Indian gooseberry powder (known as amla), cayenne pepper, cinnamon, and cloves, mixed in the ratio of 8:4:4:4:2:1:1, respectively. The average increases in GLP-1 blood concentration for those consuming the low-spice and high-spice meals were 17 percent and 32 percent, respectively, compared to the bland control meal without spices. The caloric and macronutrient content was about the same, yet the spicier meals significantly enhanced GLP-1 levels.

But which spice was responsible? Ginger compounds elevated GLP-1 in mice, but not rats or humans; we appeared to be more like the rats: no impact. For many of the remaining spices, there is not even in vitro data to support their efficacy, only in silico information, meaning just some form of computer modeling that did not actually assess anything in a biological context. However, we do possess data regarding curcumin, the yellow compound present in turmeric.

This research utilized 180 mg of curcumin, which is the equivalent of about a single teaspoon of turmeric. The investigators also trialed fish oil supplements; however, while the fish oil was ineffective, the curcumin reduced the blood sugar spike after consumption, a function that both GLP-1 and GLP-1 medications can achieve, although GLP-1 levels were not directly analyzed. The researchers propose it may be a GLP-1 effect, given that curcumin stimulates GLP-1 in rodents, as well as in cultured cells, yet no human study had occurred…until now. Six months of curcumin supplementation resulted in a fourfold increase in GLP-1 levels in comparison to placebo. Hence, turmeric may indeed provide benefits.

What of cinnamon? Scandinavian investigators provided participants rice pudding with and without one or three grams of cinnamon, which equates to roughly a third of a teaspoon or a full teaspoon. Those receiving the full teaspoon of cinnamon more than doubled the GLP-1 increase from baseline when compared to the control pudding lacking cinnamon. Therefore, this is another spice that may be effective, although individuals did not report feeling any more satiated eating the cinnamon-laden pudding versus the plain version.

Lastly, the third spice identified to elevate GLP-1 in humans? Cayenne pepper. What transpired when about half a teaspoon of cayenne pepper was incorporated into a meal? Within a brief time frame—15 minutes—a single spicy meal significantly amplified blood levels of GLP-1, although, akin to the cinnamon study, this did not appear to translate into an increased sense of fullness. However, the researchers did not assess subsequent food intake.

Most toxins encountered by humans derive from bitter plants—for instance, strychnine and hemlock. Simultaneously, several of the most favored beverages globally are bitter, as are numerous nutritious foods.

Bitter taste receptors exist not only on our tongues but also throughout much of our digestive system, on the very same cells lining our gut that produce the appetite-suppressing hormone GLP-1. Indeed, several bitter compounds have been shown to effectively stimulate the release of hormones like GLP-1 in laboratory experiments and animal studies. What about humans? Beer is one of those widely enjoyed bitter drinks, thanks to hops.

Considering that bitter herbs have evidently been utilized in periods of scarcity to diminish hunger, researchers examined low-and-high doses of hop extracts on participants enduring a 24-hour fast, discovering that both doses appeared to reduce hunger sensations more effectively than placebo. Could this be a GLP-1 effect? Let’s discover.

Administering a hops extract prior to a meal, in either immediate or delayed-release capsules, resulted in significantly more GLP-1 release compared to a placebo. Moreover, more crucially, when study participants were provided endless ham sandwiches a few hours later, they consumed markedly less. They did not experience significant shifts in hunger or feelings of fullness, but overall, still ate approximately 200 calories less.

Thus, a bitter hops extract substantially reduced caloric consumption while enhancing appetite-suppressing hormones like GLP-1. These alterations occurred without participants feeling any different regarding their appetites or disliking the sandwiches. However, the extract did induce feelings of nausea, bloating, and discomfort, but possibly this provides further evidence that it may function through GLP-1, as these are common adverse effects of GLP-1 mimicking medications, such as Ozempic. Well, wait. No wonder they

consumed less, yet clearly the level of digestive discomfort did not correspond to the amount they reduced their intake.

The primary reason I’d advise caution concerning hops is due to a substance found in hops known as 8-PN, which I’ve previously discussed in a two-part video series.

What about quinine, possibly the most acclaimed bitter compound in human history? Sourced from the bark of the cinchona tree, quinine was not solely the first successful treatment for malaria 400 years ago, but astonishingly remains a widely-used and effective remedy to this day. Administering 275 mg of it prompts GLP-1 secretion. Is that sufficient to genuinely suppress appetite and body weight? Dietary Quinine Minimizes Body Weight and Food Consumption, in rats…But what about in humans? “Intragastric quinine delivery diminishes hedonic eating,” which refers to consuming food for pleasure even when not genuinely hungry––for instance, a chocolate milkshake.

And if you’re assuming that, naturally, they’d consume less milkshake if they just ingested something extremely bitter, think again. The quinine was introduced directly into their stomach via a tube; thus, it evaded the bitter taste buds in their mouth. Nonetheless, those bitter receptors persist in the gut, which we may not even consciously perceive. The researchers also conducted brain imaging and concluded that being inadvertently given around 200 mg of quinine not only influenced how much the study participants felt inclined to eat, but it also affected their actual consumption by disrupting reward-related brain pathways.

And you don’t even need to scrape some tree bark to obtain it. It’s readily available in every grocery store as tonic water. A liter of tonic water contains approximately 60 to 70 mg of quinine, while bitter lemon, another favored cocktail component, has about half of that amount. However, acquiring 200 mg of quinine would still equate to consuming three quarts of tonic water. Could we manage with less? Indeed. In this research, individuals received just 18 mg of quinine or a placebo, and then, an hour later, everyone was offered an all-you-can-eat supply of ham-and-cheese sandwiches. Remarkably, caloric consumption was notably lower following the quinine than the placebo by around 14 percent. Thus, drinking a third of a liter of tonic water prior to a meal could decrease your caloric intake by 82 calories. But a third of a liter of tonic water contains…over a hundred calories; thus, it wouldn’t provide much help.

Tonic water is basically carbonated sugar water infused with quinine. Currently, there are sugar-free options—or, you could opt for the raw material. What if you obtained approximately the same quantity of quinine using powdered bark? “The impacts of administering approximately a third of a teaspoon daily of powdered cinchona bark on satiety, weight loss, and body composition in a group of overweight adults.” There was significantly greater weight reduction, notable waist reduction, and even slimmer hips in the bark group compared to placebo. Moreover, the weight loss was attributed to fat mass, with superior preservation of lean mass relative to placebo.

Therefore, in humans, quinine may elevate GLP-1, reduce hedonic appetite, lower hunger, diminish caloric intake, and lessen body fat. What are the drawbacks?

In my previous video, I mentioned how quinine in a third of a liter of tonic water can suppress appetite and promote weight loss, but there are “hazards associated with quinine consumption.” Quinine is a medication and may indeed be one of the most frequent causes of severe drug-induced complications.

The levels of quinine present in tonic water can instigate potentially lethal immunologically-mediated hypersensitivity reactions, similar to allergic responses, where it interacts with antibodies triggering autoimmune reactions that might include chills, fever, lowered blood pressure, painful blueish discoloration of extremities, and clotting within your blood vessels. It can also damage your red blood cells, leading to anemia, affect your platelets, resulting in bruising and bleeding, and harm your white blood cells, resulting in immune dysfunction, alongside acute kidney injury, breakdown of your muscles, liver damage, heart issues, respiratory failure, low blood sugar, blindness, and toxic epidermal necrolysis, which can lead to genital blistering, sloughed penile erosion, or an eroded scrotum.

Even minimal exposure to quinine in everyday beverages can trigger severe adverse effects involving multiple organ systems. Thus, the “moral of the story” is that a relaxing gin and tonic may contribute to life-threatening illnesses. Now, while these are rare, idiosyncratic reactions, just because peanuts can pose a deadly risk to someone with a peanut allergy doesn’t imply that everyone must steer clear of peanuts. However, there are non-hypersensitivity adverse effects as well. For instance, when quinine isn’t damaging scrotums, it could still be diminishing them. Researchers discovered quinine to be so harmful to the testicles of rats that they proposed it should be investigated as a male contraceptive.

Quinine is an extremely toxic substance in case of overdose, with vision impairment as a frequent consequence. The reason individuals might have quinine pills at home is that some utilize them for nocturnal leg cramps. The U.S. Food and Drug Administration determined that this practice was unsafe; thus, it prohibited quinine’s usage for this reason, in both over-the-counter and prescription solutions, after receiving hundreds of reports concerning severe adverse events linked to quinine usage, including 93 fatalities.

It remains accessible through prescription as a malaria treatment, though, which doctors were prescribing for leg cramps, circumventing FDA recommendations, but given its rare yet severe allergic reactions, and the threat of overdosing on quinine pills, that’s likely not advisable. Thankfully, following warnings from the FDA, the use of quinine for treating muscle cramps has dramatically decreased.

Certainly, while the FDA may have banned it from one section of the pharmacy, it could still be found in another, in the guise of tonic water. But can the lower concentrations of the drug found in beverages still lead to issues? Yes, an overdose could result in blindness, impacting not only the retina at the back of your eye but also your iris at the front, resulting in oval pupils. How strange is that?

Alright, but what if you don’t overdose? Can quinine still influence your eyesight? After the Armed Forces Institute of Pathology detected quinine in autopsy samples from military aviation fatalities, scientists had participants consume tonic water for a fortnight, and were indeed able to reveal some irregularities. Even momentary blurriness of vision can be catastrophic if experienced by any individual operating heavy machinery at elevated speeds. Hence, due to the worry that tonic water intake may have played a part in aviation mishaps, the consumption of tonic water by pilots is actually prohibited three days prior to flying—I wasn’t aware of that!

So, how much is excessive? There was an instance reported involving a 46-year-old male experiencing progressive visual decline and trouble with nighttime driving over three months, during which he had been consuming a gallon of tonic water daily. Alright, a gallon might be too much. This individual was consuming a liter of tonic water before the emergence of his “Quinine water-triggered heart arrhythmia.” His physicians believe the general public is simply unaware of the dangers linked to excessive intake of tonic water, but how many individuals are consuming nearly a quart each day?

The “no-adverse-effect” threshold in humans has been approximated to be 52.5 mg of quinine per day, which corresponds to about two and a half cups (590 ml) of tonic water. Based on ototoxicity, impairment to our hearing, perhaps we ought not to consume significantly more than two cups (470 ml) a day. However, these levels are derived from attempts to extrapolate from animal studies.

Since quinine was so frequently prescribed for leg cramps, can’t we examine large groups of individuals and check if any adverse outcomes occurred? Yes, indeed, we can, and those who received quinine prescriptions faced a 27 percent higher likelihood of acute kidney injury, which is not as severe as death: “Association Between Long-term Quinine Exposure and All-Cause Mortality.” Monitoring 175,000 individuals for approximately six years, researchers discovered that those ingesting around 200 mg of quinine daily had a 25 percent increased risk of mortality. Those on about 300 mg faced an 83 percent greater risk of death, and individuals taking 400 mg or more seemed to double their mortality risk. Therefore, I would advise steering clear of quinine.

Although the FDA has established that carbonated drinks may safely contain up to 83 mg of quinine per liter, bottles of fizzy beverages generally do not specify the amount contained, and some well-known brands do not list it as an ingredient at all. How can you determine if your drink contains quinine or not? Shine a black light on it, and see if it glows with an iridescent blue hue. Quinine is the secret element for creating fluorescent Jell-O shots.

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