WHY SUGAR IS SO ADDICTIVE? – A NEUROLOGICAL ASPECT

WHY SUGAR IS SO ADDICTIVE?  – A NEUROLOGICAL ASPECT

        

Addiction is a kind of medical condition in which the person has unsustainable desire to consume a substance or engage in an activity, although knowing that it can cause various adverse effects. Taking that substance or engaging in that activity make the victim feel good. It case of sugar it is nearly the same. We Indians especially the Bengalis are very much addictive to sweets. The sweet item after a meal attracts maximum of us.

Sugar is used daily by most of the people. Modern food is very rich in sugar. This is one of the many cause behind the obesity epidemics.

Overconsumption of sugar can interact with different parts and substances of brain and changes their normal state and levels. Notably it affects the levels of Dopamine.

The most common form of sugar in our daily food is sucrose. When ingested this sugar is split in the digestive system into two constituents, glucose and fructose. Insulin and glucagon are two most important hormones that regulate the level of glucose in human body.

After ingestion and degradation of sugar, glucose molecules and absorbed and distributed to all organs and cells in our body. A group of proteins called GLUCs are responsible for transportation of glucose molecules to the brain. It mediates glucose uptake from ECF into astrocytes, oliogodendroglia and microglia but GLUT3 which has a much higher transport rate than GLUT1 facilitated neuronal glucose uptake. When glucose molecules reaches the destination cells, it not to go into the cell where it is consumed. There are different mechanisms behind thin. In some cells like RBCs use diffusion toget glucose from the blood plasma. Many other cell use active transport to transport glucose inside the cells. The main consumer of the total intake of the glucose is the brain. The human cortex along requires approx. 3x10²³ ATP/S/m³and energy expenditure to release one synaptic vesicle is roughly calculated to be 1.64x10⁵ molecules of ATP. The reason behind this that brain tissue or the neurons cannot store glucose thus it cannot use any glucose when the blood glucose level is low.

Neurological Aspect of Sugar Intake:

Figure 1: The neuronal network activated by sucrose intake. VII – facial nerve; IX –glossopharyngeal nerve; X – vagus nerve; Acb – nucleus accumbens; Amy – amygdala; ENP – enteric nervous plexus; LS – lateral septum; NTS – nucleus of the solitary tract; PB – parabrachial nucleus; PVT – paraventricular thalamic nucleus; T1R2/3 – sweet taste receptor subunits; VPM – ventral posteromedial nucleus of the thalamus; VTA – ventral tegmental area

Recent progress in molecular biology and genetics has revealed candidates for sweet perception, the members of T1Rfamily of receptors. More precisely, these studies showed that perception of sweetness in mammals depends on the expression of the receptor T1R3 that, at the apical membrane of the taste receptor cells, forms a complex with a related protein, T1R2. This T1R2-T1R3 heterodimer is a G-protein coupled receptor that binds with sugar and artificial sweeteners. Binding of sweet molecules to the T1R2-T1R3 receptor complex triggers a conformational change in the molecules of the complex. This change activates the G-protein, alpha-gustducin, which in turn activates adenylate cyclase and phospholipase C. Activation of these signaling molecules results in an increase in intracellular free calcium. The increase in calcium activates the transient receptor potential channel M5 (TRPM5), which causes release of the neurotransmitter and activation of the primary afferent neurons. Taste information ascends to the brain by the sensory fibers of the facial nerve (cranial nerve VII), which innervates the anterior tongue, and the glossopharyngeal nerve (cranial nerve IX) and the vagus nerve (cranial nerve X), which innervate the posterior tongue. Because the sweet taste buds are more concentrated at the anterior part of the tongue, the information about sweet taste enters the brain mostly by the facial nerve. Recent investigations suggest that the gastrointestinal tract may transfer to the brain information related to sweet molecules. The expression of all types’ ofT1Rs was found in the gastrointestinal tract, including the stomach, duodenum, jejunum, ileum, and colon. These taste receptors signal via the enteric nervous system to the brain.

 The enteric nervous system transfers guts sensory signals to the brain and can participate in forming long-term representations of gut sensations. These gut feelings, called ‘homeostatic emotions or even’ extended consciousness may affect our emotional state and underlie intuitive decision making. From the medullar NTS, the sensory information is directed to the parabrachial nucleus (PB; Figure 1) located in the pons. In addition to the main stream from the NTS to the PB, some NTS fibers run directly to the central amygdala, paraventricular thalamic (PVT), and paraventricular hypothalamic (PVH) nuclei. The brainstem gustatory centers may generate the mimetic response to the taste of sucrose in rats. The lesion of the PB impairs the increase in sucrose licking as a function of sucrose concentration seen in intact rats. Conversely, stimulation of the cannabinoid receptors CB1 in the PB selectively stimulates feeding of palatable foods in rats. From the PB, the gustatory pathway branches to densely innervate the medial hypothalamus, ventral tegmental area (VTA), and midline thalamic nuclei. From the parvocellular part of the ventral posterior thalamic nucleus (VPM), the gustatory information is directed to the primary gustatory insular cortex(Figure 1).

In the gustatory insular cortex, the neurons responsive to taste are located in the anterior, dysgranular region. Another thalamic gustatory related pathway travels from the PB to the PVT, and, after synapsing in the PVT, reaches the prefrontal cortex (Figure 1). The interconnecting loop formed by the prefrontal cortex, nucleus accumbens, lateral hypothalamus, and VTA is intimately related to the rewarding effects of sucrose. The taste of sucrose activates the dopaminergic neurons of the VTA and elevates dopamine levels in the nucleus accumbens. The dopamine levels increase in the accumbens in proportion to the sucrose concentration, and the neurons of the nucleus accumbens explicitly encode for the hedonic value of sucrose.

For us, Bengalis eating Rasgulla or Sandesh is one of the happiest moments of the life. And this phenomenon is totally normal. Sugar increases the release of neurotransmitter serotonin, which gives a person happy feeling. This also increases the release of insulin which eventually normalizes the blood sugar level, and when glucose is back to relatively low levels we will again strive to take sugar just to feel happy again. This leads to constantly eating sweets just to feel good. This results in overeating and possible addiction.

Another problem with sugar addiction is that the fact that human brain reacts differently to different trigger the impulses that tell us to stop eating. But for fructose this situation is rather different. Fructose amplifies the reward circuits much more than glucose, resulting affection of those foods containing fructose. Thus the human body needs much more fructose to suppress eating. Scientific studies have shown that glucose reduces the activity in hypothalamus, whereas fructose does not. The hypothalamus controls the hunger and thirst along with some metabolic functions.

Compared to glucose eating fructose also has been found to produce a smaller increase in satiety hormones. In a study on rats it has also being found that when fructose is delivered directly to brain the rats begins to eat, whereas glucose ingestion in the same way reduces their eating.

Recent studies show that after taking glucose those healthy non obese subjects show lower activity in the hypothalamus and the reward system and motivation. But fructose ingestion causes just the opposite, it also activates the nucleus accumbens which is a part of brain reward circuit resulting increased hunger and motivation compared to glucose.

The modern foods and drinks contain much more fructose and as the fructose is addictive this causes attraction of those foods and drinks. This proves the statistics that overweight and obese people globally increased from 857 million in 1980 to 2.1 billion in 2013 which is 1/3^rd of the world’s population.