New Insights on Addiction, Mood, Memory, and Cognitive Ability

An array of new science is painting not only a clear picture of addiction but of how the same brain issues relate to poor memory, poor mood, and poor cognitive function.  While we can think of addiction in terms of a clinical problem like drug or alcohol abuse, the same issues are involved with eating and other behavior patterns that are either a waste of your time (like too much WEB surfing or video games) or detrimental to your life (like gambling or using credit cards beyond your means).  One common thread is a lack of BDNF.

Glutamate is needed for normal nerve transmission.  Scientists have just discovered that the glial cells in your brain control and manage glutamate availability, a finding that in itself is a major discovery.  Since glial cells are "wound up" by stress, chemical exposure, leptin resistance, and other health problems, it can create a situation of glutamate-driven excitotoxic nerve stress.  This wound up excitotoxic stress depletes dopamine and BDNF, leaving a person with a poor mood and a desire for a fix that feels good - opening the door to addiction of any kind.

One new study shows that raising BDNF levels in cocaine-addicted mice causes glutamate levels to return to normal and addictive behavior to stop (within three weeks). 

It is normal, but not healthy, that BDNF production declines with age.  Aerobic exercise and various nutrients can improve BDNF levels (pantethine, acetyl-l-carnitine, blueberries, fish oil, curcumin, and likely many others).

It is interesting that the generally inflammatory gene signal, NF-kappaB, is activated in early life to facilitate the process of rapid nerve cell development in an infant.

It is also interesting that BDNF levels are also stimulated by brain injury, our body's strategy to make new brain cells in a time of need.  In this case the BDNF production once again NF-kappaB in order to activate the BDNF-driven growth of new brain cells.  Researchers went on to show that it is the mechanism of NF-kappaB activation that determines if BDNF helps form new brain cells or if the formation of new brain cells is actually blocked. 

For example, if NF-kappaB is activated by the inflammatory stimulant TNFa, then BDNF's ability to generate new brain cells is blocked.  Excess TNFa comes from being overweight or other inflammatory health problems of an ongoing nature, which now explains why these problems are associated with cognitive decline.

It is also noteworthy that optimal thyroid function is required for BDNF repair function following brain injury.  It is often the case that an injury knocks thyroid function for a loop, which would then impair the ability of nerve cells to recover from an accident.  Optimizing thyroid function may be a key to optimal BDNF levels - and at this time that has been demonstrated for injury recovery.

Additive tendencies on any subject, whether small or large, are a red flag telling you that your brain in low in BDNF and headed in the wrong direction.  Reducing excitotoxic nerve damage by having adequate antioxidants in your brain and by building BDNF is the path to better brain function, better memory, better cognitive ability, and being more in control of your subconscious impulses.  There is a path out - all one has to do is follow it and over time your nerves can make better connections and your future will be brighter.