By Dr. Mercola | Waking Times
If you’re like most people, chances are you’re consuming unhealthy amounts of sugar on a regular basis. Even if you’re not big on candy, most processed foods will provide you with an excessive amount of added sugars.
As noted in the BBC One report “The Truth About Sugar,” a serving of Pad Thai noodles contains 9.5 teaspoons of sugar and a package of sweet and sour chicken with rice contains 12.5 teaspoons, which is more than a can of soda.
A can of baked beans contains 6 teaspoons of sugar, which would ideally be your grand total for the day, so it’s important to realize that it’s not merely cakes, cookies, candy and ice cream that get people into trouble.
Even many baby foods contain shocking amounts of sugar, which can set your child on the path of lifelong sugar addiction and the health problems that go along with it. The idea that sugar is addictive is not new. A number of studies have shown it acts much like other addictive substances.
One of the latest studies looking at the addictive potential of sugar was published in the November 2019 issue of Scientific Reports, in which they point out that “Excessive sucrose consumption elicits addiction-like craving that may underpin the obesity epidemic.”
Sugar Alters Your Brain Chemistry
By using PET imaging along with beta-opioid and dopamine receptor agonists, the researchers were able to show how sucrose affects the brain chemistry in miniature pigs. The miniature pigs were chosen for the fact that they have well-defined subcortical and prefrontal cortical regions, which “enable a more direct translation to human brain function.” As explained by the authors:
“After 12 days of sucrose access, BPND [non-displaceable binding potentials] of both tracers had declined significantly in striatum, nucleus accumbens, thalamus, amygdala, cingulate cortex and prefrontal cortex, consistent with down-regulation of receptor densities … The lower availability of opioid and dopamine receptors may explain the addictive potential associated with intake of sucrose.”
Even a single exposure to sucrose produced as much as a 14% decrease in carfentanil (a beta-opioid receptor agonist) binding in the nucleus accumbens and cingulate cortex, which is consistent with opioid release.
In more layman terms, sugar consumption triggers the release of natural opioids and dopamine in your brain, thus lowering the availability of those receptors. Reduced receptor availability is a sign of overstimulation, as when your brain gets overstimulated, it downregulates the receptors in order to protect your brain from damage.
The drawback of this protective mechanism is that you now need a higher dose of the substance to get the same pleasure response, and this is a key mechanism by which addiction develops.
You can learn more about the mechanics of addiction in my interview with Dr. Pamela Peeke, author of “The Hunger Fix: The Three-Stage Detox and Recovery Plan for Overeating and Food Addiction.”
Sugar Affects Your Brain Like Other Addictive Drugs
Figure 4 from the Scientific Reports study shows how carfentanil binding potential changed from baseline levels over the course of 12 days. Figure 6 shows the change in raclopride, a selective antagonist on dopamine receptors.
Figure 4: Regional analysis of carfentanil bonding potential between baseline and after 12 days of sucrose water exposure.
Figure 6: Regional analysis of raclopride bonding potential between baseline and after 12 days of sucrose water exposure.
According to the authors, “The results clearly demonstrate that sucrose affects reward mechanisms in a manner similar to that of drugs of abuse.” In the discussion section of the paper, they further explain:
“The intake of sucrose as a palatable substance is known to release DA [dopamine] and induce dependency in rodents, with sucrose shown to be even more pleasurable than cocaine in rodents in certain contexts. Thus, rodents work more intensely to obtain sucrose than cocaine, even in the absence of food deprivation.
However, the effects of sucrose are regulated both by the homeostatic system and by hedonic reward circuits that may mediate the distinction between nutritional and hedonic aspects of sucrose action.