A little hormone called leptin may be the reason for those insatiable sugar cravings.
As you may have expected, overeating may be a form of addiction.
Researchers now suspect that leptin may play a crucial role in food addition along with other neurotransmitters such as dopamine. Together these hormones regulate our cravings for highly “rewarding” food – typically high in sugar, salt, and fat (3; 4).
How Does Leptin Work?
Leptin levels initially act to monitor fat mass, help reduce appetite and ultimately control weight (5).
When the body becomes resistant to leptin, other hormones are ultimately thrown out of balance.
Diverse Functions of Leptin
- Independent of food intake, leptin along with the affect of other hormones, may alter the metabolism of fatty acids by its action on the hypothalamus (14).
- Leptin imbalance may damage liver cells (15; 16), as well as the pancreas, platelets, blood vessels and heart muscle (17).
- Leptin release may contribute to susceptibility to autoimmune disease due to affect on immune tolerance and responsiveness (18)
- May be implicated in chronic kidney disease (19; 20)
- Leptin may play mediating role in innate immune responses and allergic responses. (21), and also inflammation (22).
- May play modulating role in rheumatic diseases (rheumatoid arthritis), including cartilage, synovium, bone and immune cells (23).
- Higher concentrations of leptin may possibly stimulate tumor growth and contribute to “metabolic burden” (24; 25)
- Leptin deficiency may cause obesity, diabetes, and other endocrine problems (26)
- Leptin may also promote coronary artery disease, hypertension, & thrombosis (27; 28) and has been linked to levels of C-reactive protein, a well-studied marker of inflammation related to cardiovascular disease (29).
- Leptin may have modulating effect on bone (30; 31).
- Leptin may help restore hypothalamic-pituitary axes including gonadal, thyroid, growth hormone, and to a lesser extent adrenal axes (32).
Similar to insulin resistance, leptin resistance can occur when receptors become unresponsive to increasing levels of leptin hormone, commonly found in states of obesity & related complications such as non-alcoholic fatty liver disease.
There generally seems to be a push-pull relationship between obesity and leptin resistance with confusion over whether one causes the other (33).
What is Leptin Resistance?
1.) Elevated triglycerides seem to be an important mediator for leptin in both obese and starvation states (34; 35), may account for the inflammation and immune activation that may link obesity with leptin resistance (36), and can be an early sign of insulin resistance and poor sugar management.
2.) Leptin resistance may be caused by altered leptin transport past the blood brain barrier and malfunctioning of leptin receptors due to cellular stress common in states of obesity and insulin resistance (37).
3.) Healthy digestive and gut function may also be linked to leptin resistance
a. External toxins and inflammatory food proteins such as dietary lectins found in cereal grains (wheat, rice, corn, etc) may disrupt the blood brain barrier, potentially linking gut health with leptin insensitivity.
b. Lipopolysaccharides (LPS) are internal toxins generated from imbalance of healthy bacteria in the gut and are also associated with the development of leptin resistance (38)
c. Short chain fatty acids (byproducts of fermentation from healthy bacteria in the colon) can promote leptin levels to induce satiety and may also have anti-inflammatory effects (39)
Some individuals may be more or less susceptible to leptin resistance due to slight differences in gene expression.
For instance, slight differences in leptin and leptin receptor genes known as “polymorphisms” may account for why anti-depressant medications may be linked to risk of obesity in some people, and have no association for others (45).
Ancestral genes underlying some of these mechanisms may have developed over millions of years which were critical to survival in times of scarce food.
Unfortunately, now these same genes may now be a trigger for obesity and related “modern” diseases (46).
“Insufficient adaptation” to new environmental factors such as an increased consumption of cereal grains from wheat, rice and corn, may partly account for leptin resistance (47).
Medical Approach to Leptin Resistance
1.) Bariatric surgery most effective for pediatric obesity possibly through an effect on leptin and eating behavior, yet comes with potential risks and reserved for most significant complications of obesity (40)
2.) Statins have been shown to modulate leptin activity (41), but an earlier meta-analysis of randomized controlled trials published in The Lancet indicated a 9% increase in diabetes incidence for those taking statins over a four year period (42). There is a call for more research to clarify the role of statins in carbohydrate metabolism
3.) In studies of rats, Metformin may help restore leptin sensitivity, and may be a useful alongside leptin in treatment of obesity (43)
In my opinion, obesity medications are largely unproven, and mostly target the effects of obesity such as hypertension.
Medications may offer assistance in combination with other approaches, but I feel that they can shift focus away from ubiquitous lifestyle factors such as:
- high availability of foods high in sugar, fat and salt
- incidence of food marketing (especially that which targets children)
- possible sensual cues like sight, and smell that may also trigger overeating behavior.
My opinion aside, it is important to work with a health professional to prioritize an approach that is right for you.
Food can be highly addictive, affecting the same brain pathways as opiate drugs!
Our food environment now contains food that is cheap, highly palatable, widely available, and increasingly accepted as addictive.
In an article published February 1st, 2012 in Nature – one of the most highly respected journals on the globe, concludes:
“Added sweeteners pose dangers to health that justify controlling them like alcohol…” (44)
Mark my words:
This may turn out to be one of the most important journal articles published in our lifetimes. We may look back at this article as one of the most important developments in the fight against obesity and related problems.
I recommend following Marion Nestle, PhD, a leading resource in Food Politics who has been covering the politics of obesity, food marketing to children, and the sugar debate.
She’s also covering the news regarding sugar toxicity in depth.