Summary: Ketamine is an anesthetic and can also reduce pain sensation. However, its use to treat depression is new. Studies show that few ketamine infusions can provide prolonged relief from depression. However, some doctors have raised concerns regarding the risk of ketamine abuse. Fortunately, a new study in rodents shows that ketamine is not addictive. It does cause an increase in dopamine. However, any such upsurge is short-lived and thus does not appear enough to cause addiction.

Ketamine is an anesthetic, and it is also known to help with pain. However, its use in managing depression is new. There is significant interest in ketamine treatment for depression as the studies show that it may help provide prolonged relief, unlike traditional antidepressants.

However, conversely, it is no secret that ketamine is also a club drug, a substance of abuse. It causes euphoria at higher dosages. Therefore, doctors worry that its frequent use may put their patients at risk, and many might become addicted to it. 

But some experts think that though it is psychotropic, it does not appear addictive. After all, it has been available for a long time, and there are not many people addicted to ketamine. Now, a new study shows that though it may stimulate the reward pathway, it also affects some other brain pathways that help prevent ketamine abuse.

Addiction vs. Dependence

Before discussing the risk of addiction further, it is vital to understand that addiction and dependence are two different things. Addiction is when one seeks a substance despite its negative health consequences. Addiction is a kind of behavioral disorder. For instance, opioid addiction treatment is carried out when abuse of opioids begins to produce negative effects on the body.  

Dependence, on the other hand, causes withdrawal syndrome on discontinuation of the use of the substance. In addition, dependence often causes severe physical signs. Drugs that cause dependence may affect most people who use them regularly.

Although most people may become dependent on some substances after their prolonged use, the same is not true for addiction. Studies show that only some people become addicted. Moreover, addiction only affects a small number of people.

For example, studies show that only one-fifth of cocaine users are really addicted to it. And for opiates, this rate is about 30%. In a recent study, researchers tried to understand the risk of addiction to ketamine.

Ketamine has a short-lived impact on the reward pathway

Generally, people get addicted to substances as they increase the levels of the pleasure molecule dopamine. For example, cocaine can boost the brain’s dopamine level for a long time. However, after some time, it would start falling, and thus a person would seek the drug to increase dopamine level again.

In the new study, researchers used a special device that allowed mice to self-administer ketamine. They found that it increased dopamine levels in mice, so they repeated the self-administration. However, they found dopamine levels elevated due to ketamine also falling quite quickly, unlike many other drugs of abuse.

Ketamine also seems to have the effect that prevents reward pathway stimulation

Researchers wanted to know why, unlike other drugs of abuse, ketamine treatment for depression causes such a short-lived increase in dopamine levels. They found that ketamine increased dopamine by inhibiting NMDA receptors. However, it also modulated other receptors, called the D2 receptors, that act as a brake on the rapidly increasing dopamine. 

Hence, they found that it is this dual mechanism that helps prevent permanent changes in the brain, unlike other drugs. Therefore, ketamine does not cause long-term behavioral changes. The increase in dopamine levels is for such a short time that it is not enough to cause addiction. The researchers concluded that there is almost zero addiction risk of ketamine in rodents.

Of course, these are still early findings. Nonetheless, it provides the basis for further studies. There is a need to find out if this is also true for humans. Considering that quite often, what works in rodents also works in humans, it is likely that it does not cause addiction. Even if it does cause, any such effect is probably quite low.

Summary: Exercise can help boost brain health in multiple ways. It may help by improving metabolic health and thus indirectly slowing down neurodegeneration. However, a new study now suggests that exercise can directly impact the brain as it can significantly boost neurotransmitters and growth factors. Thus, the study found that 30 days of workout can boost dopamine levels by 40% and BDNF levels by 60%. It means that training has immediate, mid-term, and long-term benefits for brain health. It can help prevent and manage neurodegenerative disorders more effectively than thought earlier.

A new study suggests that exercise could be the most effective way to prevent neurodegeneration. They found that exercise may boost many bioactive compounds in the brain and even boost neurotransmitters’ levels.

Experts have long believed that the rise of neurodegenerative diseases in the last few decades has a lot to do with lifestyle. After all, genetics cannot change in a few decades. Infectious diseases have also become less common. It appears that nutrition status has also improved over the decades.

So, what could be the cause of an increase in neurodegenerative diseases? It could be a rising concentration of environmental toxins, and some lifestyle issues like obesity, high-calorie intake, unbalanced diet, and lack of physical activity

The more researchers study the role of exercises in wellness, the more they are surprised. It appears that a high level of physical activity may be the best way to boost physical and mental health. The benefits of regular physical activity are innumerable.

Exercise may help in neurodegeneration in multiple ways

Experts have long known how exercise may help prevent neurodegeneration disease symptoms by boosting metabolism, improving energy metabolism, preventing mitochondrial dysfunction, lowering insulin resistance, and more.

However, new studies confirm that regular exercise can boost the level of specific bioactive compounds that help prevent neurodegeneration. Thus, the study found that just about 30 days of exercise, that is, voluntary wheel running by mice, could boost the levels of dopamine and BDNF (brain-derived neurotrophic factor).

Researchers were amazed to see that regular exercise could boost dopamine levels by as much as 40%. Which is more than many drugs can do. It means exercise may have greater benefit for mental health than certain pharmacological drugs in conditions like Parkinson’s. In fact, regular exercising along with expert guidance through telehealth can also help in addiction recovery eliminating the chances of relapse.

Earlier studies have proven that exercise can benefit significantly in Parkinson’s. However, those studies could not demonstrate how exercise helps and to what degree. It now appears that exercise has a more favorable impact on brain health than imagined earlier.

Moreover, this study found that the impact on exercise is felt several days after discontinuing it.

The same study found that 30 days of the exercise was enough to boost BDNF levels by 60%, which is significant. There are no known pharmacological drugs that can boost the level of this growth factor so much.

Researchers think that increased dopamine levels in the brain have short and mid-term benefits in Parkinson’s, while an increase in BDNF has long-term benefits. An increase in BDNF may help prevent further neurodegeneration and even boost regenerative processes.

Although this particular study focused on the benefits of Parkinson’s, researchers think that regular exercise may help in many neuropsychiatric disorders. For example, regular workout could be a perfect way to overcome anxiety and depression.

Since exercise can not only boost the levels of various neurotransmitters but can also enhance the concentration of growth factors, it is pretty likely that regular workout may significantly reduce the risk of other neurodegenerative disorders like age-related cognitive decline and dementia.