Can sugar make you stupid? Studies point to yes.

Can sugar make you stupid?  

Oh dear.   

If the following study regarding the ingestion of sugar and cognition is true -- I should be gaining brains instead of losing them -- considering that I eat about 95% less of the sweet stuff since I had roux en y gastric bypass surgery.  

However as we all know, *MY brains are very special since I had weight loss surgery.   

The combination of a high-sugar intake and a lack of Omega-3 Fatty Acids caused brain fail in rats!  

What about... us?  What if poor diet causes brain issues that aren't reversible?  This intrigues me.

National Geographic -

 Sweet drinks scrambled the memories and stunted learning in lab rats in a new study—leading to "high concern" over what sugary diets may do to people, according to neuroscientist Fernando Gomez-Pinilla. (Read more about memory from National Geographic magazine.)

 For the study, Gomez-Pinilla's team first trained rats to successfully navigate a maze, giving them only water and standard rat chow for five days. During the following six weeks, the rats' water was replaced with syrups that were 15 percent fructose.

"Most sodas people consume are about 12 percent sugar, so imagine if you drank soda with sugar added instead of water," said Gomez-Pinilla, of the University of California, Los Angeles.m

During the six-week period, half the rodents were also given flaxseed oil and fish oil—both rich in omega-3 fatty acids. These antioxidants may protect against damage to chemical connections in the brain called synapses, past research suggests.

After six weeks of the fructose syrup, all the rats were slower at running the maze. However, those that had received omega-3s were slightly faster than their counterparts.

By studying the dissected brains of the study rats, the researchers determined that the high-fructose diets had sabotaged the ability of synapses to change, a key factor in learning. The sugary drinks had also disrupted the sugar-regulating protein insulin in a brain area called the hippocampus, which play a role in memory formation in both rats and humans.t

"I was very shocked to see how strong an effect these diets could have on the brain—I have high concern that the foods people eat can really affect mood and cognition," Gomez-Pinilla said.

Study Abstract -

We pursued studies to determine the effects of the metabolic syndrome (MetS) in brain, and the possibilities to modulate these effects by dietary interventions. In addition, we have assessed potential mechanisms by which brain metabolic disorders can impact synaptic plasticity and cognition.

We report that high-dietary fructose consumption leads to increase in insulin resistance index, insulin and triglyceride levels, which characterize MetS. Rats fed on an n-3 deficient diet showed memory deficits in Barnes Maze, which were further exacerbated by fructose intake.

In turn, n-3 deficient diet and fructose interventions disrupted insulin receptor signaling in hippocampus as evidenced by a decrease in phosphorylation of insulin receptor and its downstream effector Akt.

We found that high fructose consumption with n-3 deficient diet disrupts membrane homeostasis as evidenced by an increase in the ratio of n-6/n-3 fatty acids and levels of 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation.

Disturbances in brain energy metabolism due to n-3 deficiency and fructose treatments were evidenced by a significant decrease in AMPK phosphorylation and its upstream modulator LKB1 as well as a decrease in Sir2 levels. The decrease in phosphorylation of CREB, synapsin I and synaptophysin (SYP) levels by n-3 deficiency and fructose shows the impact of metabolic dysfunction on synaptic plasticity. All parameters of metabolic dysfunction related to the fructose treatment were ameliorated by the presence of dietary n-3 fatty acid.

Results showed that dietary n-3 fatty acid deficiency elevates the vulnerability to metabolic dysfunction and impaired cognitive functions by modulating insulin receptor signaling and synaptic plasticity.