Dieting alone is ineffective for most overweight adults, and even those who successfully lose weight often gain it back soon afterward. The snacking impulse is a common source of weight-loss sabotage.
Scientists have discovered that the inability to lose weight often stems from the powerful effects of emotional stress and depression on the brain. This chemically triggers strong cravings for comfort foods and snacks. If this is your problem, you may be suffering from an abnormal increased appetite for consumption of food known as reactional hyperphagia. Simply put, emotional stress causes brain-chemical and hormonal changes that decrease feelings of satiety (fullness) and promote—and "reward"—the compulsion to snack, especially on comfort foods.
In this article, you will learn how a saffron extract targets appetite dysregulation at the neurotransmitter level, inhibiting the compulsion-reward cycle and reducing the snacking impulse.
In one small 4-week study, a decrease in between-meal snacking was reported by women taking a proprietary extract of saffron!1 And in another human study using the same extract, the overall number of snacking episodes was reduced within 8 weeks—by 55%!2
The restrictions of dieting often generate stress, anxiety, and depression. In some people, the resultant changes in neurotransmitters and hormones create an overwhelming impulse to seek out what scientists call "highly palatable," or comfort, foods.3-12
Surrendering to this impulse then triggers brain activity associated with reward, which temporarily alleviates stress, anxiety, and depression. This off-diet eating may result in weight gain, guilt, and renewed dieting—all stressors that perpetuate the cycle.3-10,13
If this sounds like your dieting pattern, your brain and hormones may be sabotaging your weight-loss attempts, and leaving you with undeserved guilt and frustration.
You may have stress-induced reactional hyperphagia, which is defined as the abnormal increased appetite for consumption of food.8,13,14
Many people who are not dieting still experience emotional stress from other sources and experience the same compulsive-addictive form of emotion-based overeating. This "stress-snacking" feedback cycle can eventually lead to weight gain and more stress. It is no coincidence that high obesity rates have become an escalating health concern during this era of chronically high stress levels.3-14
To maintain a healthy weight comfortably, it is important to interrupt and block this sabotaging hyperphagic cycle.
The good news is that scientists have developed a botanical formulation that helps break this pattern.
Saffron is a spice that is constituted from the red stigmas of Crocus sativus L. In randomized, placebo-controlled research on humans, a standardized and proprietary extract of saffron reduced the desire to snack, diminished the craving for comfort foods, produced satiety, and facilitated weight loss—without any stimulant effect, side effect risk, or unrealistic level of continuous willpower.
The 'Feed-Feedback' Cycle
Many weight-loss drugs that are meant to reduce appetite are dangerous. For example, phenylpropanolamine is associated with hemorrhagic stroke.17
However, a particular extract of saffron appears to be unique in its ability to target the neurochemical pathways underlying the craving for comfort foods and the compulsion to eat between meals (reactional hyperphagia).
Growing research has been shedding light on these pathways of compulsive snacking, and how they set up a feed-feedback cycle that is essentially stress, stress-relief, stress, stress-relief, and so on.
Early research showed that the food restrictions of weight-loss diets are major sources of stress and anxiety. Some people respond to this greater stress by developing cravings for specific (comfort) foods associated with stress relief, making them more susceptible to obesity than others.3-6
In 2004, a rodent study demonstrated that during chronic stress, glucocorticoids—hormones that are generated by the hypothalamus-pituitary-adrenal (HPA) axis and that predominantly affect metabolism—often stimulate activities in the brain that induce a preference for comfort food. Rats under stress consumed no more calories than the placebo group, but showed a distinct desire for getting a greater proportion of their calories from comfort food. Ingestion of comfort food diminished the signs of stress, creating a reward feedback—completing the feed-feedback cycle.7
A study in 2007 reviewed earlier research on both animals and humans, and proposed a theory termed Reward Based Stress Eating. Evidence indicated that during stress, cortisol (a glucocorticoid), together with the body's reward circuitry, causes dysregulation of the finely tuned balance of appetite control. Cravings increase stress, which triggers an increase in the reward value of highly palatable (comfort) food. The result is an increased intake of high-calorie snack food, and a greater accumulation of visceral fat.8
Then, in 2009, researchers found that—in response to glucocorticoid-induced increases in comfort food intake—circulating insulin levels rise. These increases, as well as greater deposition of abdominal fat, are directly and specifically linked to higher consumption of comfort-foods—rather than to higher consumption of calories from any source. These insulin effects appeared to dampen the response to stress, thus providing reward feedback (stress relief) for eating comfort foods.9
In a landmark study published in 2010, researchers found that the dysregulated brain reward pathways that trigger drug and alcohol addiction are identical to the biomolecular mechanisms behind comfort-food cravings.10
In a 2011 study, scientists discussed the circular relationship between hyperphagia (increased appetite), comfort food intake, and obesity. They suggested that in some individuals, the presence of this feed-feedback cycle at an early age may lead directly to obesity later in life. They further suggested that obesity itself may increase signaling along inflammatory, oxidative, and mitochondrial stress pathways—altering normal reward functions and promoting compulsive snacking.18
On the heels of these findings, and with obesity at epidemic levels, scientists searched in earnest for a way to safely break the feed-feedback cycle.
Targeting the Biochemistry of Appetite
In the quest for a novel intervention to block reactional hyperphagia and the cycle of compulsive snacking, attention quickly turned to the active components in saffron—and for a number of good reasons.
First, now that dieting and stress had been found to increase the reward value of comfort food for many people,8 it was natural to examine agents believed to modulate stress in order to identify those that might beneficially affect the appetite and snacking impulse. In ancient medical systems, saffron has traditionally been used to reduce anxiety, relieve stress, and enhance mood.19
Second, no effective FDA-approved drug is available that can regulate the neurochemistry of appetite without substantially dangerous side effects,20 which have been found to include pulmonary hypertension and heart valve disease.21 Scientists realized that—if verified to be effective in inhibiting the snacking compulsion in placebo-controlled studies on humans— saffron would constitute a safe and natural alternative.
Third, neurotransmitter imbalance, particularly low levels of serotonin, has been shown to increase vulnerability to overeating, food cravings, and depression.22 A number of journal-published studies had shown that safranal and crocin, active constituents of saffron, have demonstrated effects comparable to prescription medications in mitigating the symptoms of depression.23-25 One of the most commonly prescribed group of anti-depressant medications are the selective serotonin reuptake inhibitors (SSRI), which are well known to produce a number of adverse side effects, including sedation, weight gain, sexual dysfunction, and suicidal thoughts.26-28 This improved serotonin-enhancing activity suggested that saffron may be a safe and potent weapon to break the feed-feedback cycle and inhibit reactional hyperphagia—for several reasons:
- Stress increases levels of cortisol, which can cause dysregulation of appetite—serotonin, through serotonergic neurons, regulates appetite.12
- Stress activates the entire HPA axis, which is involved in the feed-feedback cycle—and serotonin regulates and normalizes HPA activity.29
- Compulsive snacking and reactional hyperphagia are strongly related to depression, anxiety, and mood—and serotonin can improve all of these snacking-related emotional states.30
- Stress increases levels of glucocorticoids, which can diminish the transport efficiency of serotonin, in turn lowering serotonin activity and negatively affecting both mood and appetite31—promoting serotonin activity would be a natural way to counter this transport effect and favorably modulate both mood and appetite.
In subsequent animal and human studies, saffron extracts proved highly effective in safely managing depression and anxiety32-35—the same emotional disorders that trigger reactional hyperphagia.
However, this constituted only an indirect link between saffron and modulation of the snacking compulsion. Scientists still needed to prove that saffron's powerful ability to modulate stress would in turn translate into a significant reduction in hyperphagic snacking, both in terms of desire and behavior.
For the gold standard in scientific proof, this would demand investigating the effects of saffron extract—specifically on snacking desire and frequency—by conducting randomized, placebo-controlled, double-blind studies on humans.