Health

Schizophrenia Around the World

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Mental illnesses, such as schizophrenia, are not always well understood. Records of people with episodes and symptoms similar to schizophrenia date back to Egyptian times. However, there seems to be no difference in prevalence across races, or cultures. The origin or cause of schizophrenia is not known, although a strong genetic component is likely.

Although the word schizophrenia literally means split mind, but it is more like a split from reality. The positive or heightened effects often associated with schizophrenia are hallucinations, delusions and disorganized speech and behavior. It also has negative or under represented effects such as reduced expressions, speaking, and pleasure.

The onset of schizophrenia peaks at age 15-25 however in males the mean age is 31 and in females is 41. This gender difference may be due estrogen levels in females which may act as an endogenous antipsychotic.

Diagnosis and perception of the disease has more of a cultural connotation. Whether or not we see the symptoms of hallucinations or delusions as threatening or not depends on culture. In the US people are more likely to be described as mentally ill or schizophrenic compared to other cultures who see value in hallucinations. Some cultures see mental illness, such as schizophrenia, as a connection or communication with a super natural force.

The delusions of schizophrenic patients tend to reflect the culture form which they come. For example, someone in America is often paranoid about things such as technology or surveillance. In communities such as Ireland with a strong religious history tend to have visions of angels and a higher being and are seen as saint-like. In places such as Nigeria in which mental illness is seen as evil done by evil spirits people often have delusions of ghosts or witches.

While mental illnesses are difficult to treat, it is possible to help manage symptoms. Because mental illness varies from person to person it is important to find the right combination of drugs, therapy, and support to aid in combating schizophrenia. Interestingly, in developed nations, the fast-paced life may impede healing processes of schizophrenics because any minor disturbance can cause stress.

Antipsychotic drugs basically block dopamine receptors to help regulate abnormal dopamine levels seen in schizophrenics. However, many antipsychotics have many side effects that require monitoring. Therapy can be offered along with this to help control schizophrenic tendencies and avoiding substance abuse. Familial support is also very helpful through this process. Schizophrenia is often found in conjunction with some sort of substance abuse. Because the pathways that are affected by schizophrenia also play a role in substance abuse it can heighten the effects of that substance.

For more information please see:

https://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

http://www.mentalhealthamerica.net/conditions/schizophrenia

http://www.pbs.org/wnet/brain/episode3/cultures/

 
 
 

Disease/Health/Hot topics

Do Concussions Cause Schizophrenia?

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Short answer: no.  Long answer: yes.  Welcome to the complex world of gene-environment interactions.  
Concussions are not safe by any means; they might put you at risk for memory problems or an earlier onset of dementia.  The good news is that if your genes are healthy, a concussion probably won’t spontaneously give you schizophrenia.  The bad news is some people have hidden risk factors for the disease that can come out if conditions are right.  
Schizophrenia and autism are both spectrum disorders.  Autism can range from the mild awkwardness of Asperger’s (think Sheldon Cooper) to an inability to speak.  Like autism, schizophrenia is a little different for everyone.  Some may have negative symptoms like low IQ, memory loss, or lack of emotion.  Others have more positive symptoms like hallucinations or delusions.  
Where do these differences come from?  Schizophrenia is not a simple disease like diabetes or cystic fibrosis, where one gene is defective.  It seems like schizophrenia comes from a combination of many different gene mutations.  Obviously, having more mutations is worse, but some mutations are worse than others.  One schizophrenic patient might have a half-dozen small mutations adding up, while another patient has one or two extremely destructive mutations.  So the different combinations of risk factors explains some of the differences in severity as well as symptoms.  

Image result for fugue
Not that kind of fugue

Stay with me while I throw one more thing into the mix: life experiences.  Remember Walter White’s “fugue state”?  He woke up with no memory of why he was standing naked in the produce aisle.  Supposedly, the stress of having terminal cancer, a disabled son, and a newborn daughter (not to mention a drug empire) was enough to drive him temporarily insane.  Walt was faking of course, but trauma can have real lasting effects on a person’s mental health.  
Imagine a freshman on the football field.  He has two mutations affecting his neurons.  Maybe a protein is slightly out of shape, or he’s overproducing some neurotransmitter.  But it’s nothing his brain can’t handle.  Then along comes a fifth-year senior with a full beard, and he’s on the ground tasting the color purple.  That hit was enough to push him over the threshold into full-blown schizophrenia.  Like many others, he starts developing symptoms at around age 20, with his high school concussion long forgotten.  
Denmark to the rescue!  Using their obsessive record keeping,  a study in 2014 had access to 100,000 participants with head trauma.  That huge sample size makes the study very reliable.  The study found that head trauma increased the risk of schizophrenia by 65%.  Other studies (here and here) have shown that a family history of schizophrenia increases the risk even more.  
 
Trauma, whether psychological or physical, has frightening power to reveal and magnify hidden disorders.  At this point in modern medicine, there’s still no way of knowing for sure who is at risk.  For now, please wear a helmet.

 

Disease/Health

Overprescribed and Undermedicated

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A recent segment from the liberal-leaning news source Vox was titled “Do I have ADHD?”. A female in her twenties believed she indeed had the disorder, but had never been diagnosed. In truth, there is no concrete answer to the question. While the DSM-5 lists criteria to diagnose the disorder, there is question as to whether the list is accurate. Current academia leans to one of two sides, that Americans are either overdiagnosed or underdiagnosed.
Of course, there are arguments to both, otherwise we’d have little debate. In one sense, the amount of drug companies offering ADHD medication increased just before the rise in diagnoses, prompting experts to create a Big Pharma conspiracy around “selling the ill, to sell the pill”. In another sense, however, studies repeatedly show that young children treated for the disorder drastically improve their learning abilities, and that the more cases found, the better our education.
But the fact of the matter remains, we can never know for sure whether someone has a mental disorder.
A blog post on Adderall addiction a few months back got me wondering, “How badly can access to psychiatric medication change someone’s life?”. Within the post a young woman candidly exposed how easy it was for her to fake a psychiatric exam to receive the drug, when she had personally never struggled with the symptoms of ADHD. She had already become addicted thanks to a friend’s stash, and had finally decided to get herself a prescription for the medication.
While there is no doubt that ADHD prescription medications have helped thousands, have they perhaps hurt just as many in the process? Even outside of the abuse that is rampant among American college students, how many children were wrongly diagnosed for simply being a hyperactive child? I remember those days. No kid wants to sit in school, church, or really sit anywhere. Children are by their nature curious beings, and they will always become distracted by the slightest piece of new information.
I am not here to say that diagnoses are all false, but statistics proves to us that misdiagnoses happen. Whether we are giving drugs to kids without a disorder, or giving the wrong drugs to kids if they have a different disorder, we are not providing them with the free life they deserve. One way or another, if the child was misdiagnosed, administration of drugs will change their lives forever.

Switching over to another psychiatric disorder, schizophrenia, there is a large push to notice symptoms, or even precursors of symptoms in children. Because schizophrenia usually does not show signs until late adolescence, it is very hard to treat in its early stage. The disorder is a result of improper brain cell growth and differentiation, and one hypothesis places the blame on low levels of a protein called beta-catenin. If recognized in childhood, could administration of this protein, or inhibition of its breakdown, help brains grow normally? But once again, how does one morally administer medication to a child without knowing for sure if they have the disorder?
While the question remains unanswered, prescription medication for schizophrenia can only be administered after symptoms show up. And if the beta-catenin hypothesis is indeed correct, by then the damage is already done. The only purpose of the medication is to treat the symptoms, not the cause, and of course it would seem improbable to add beta-catenin after the brain has finished developing.
Antipsychotics are the main treatment option for schizophrenics. These drugs are dopamine-receptor blockers (sometimes serotonin-receptor blockers) and work by “slowing down” the parts of the brain that overstimulate themselves to create the hallucinations so commonly received by schizophrenics.
But schizophrenia has other detriments. Most notably, social isolation and depression. The antipsychotics are only focused on the so-called “positive” symptoms of the disorder, and do nothing to treat these other symptoms. Even further, they unselectively block dopamine receptors, even in pathways of the brain that are undamaged from schizophrenia, leading to numerous adverse effects.
Because of all of this, schizophrenics often refuse to take medication for their disorder, and I do not blame them. As stated, the damage to the brain is already done, terrible side-effects occur, and the drug does not even treat half of the symptoms.
_________________________________________________________________________________
I am led now to my conclusion (and the title of this article): Americans seem to be overprescribed and undermedicated. We may have doctors willing to give us all sorts of drugs that promise to improve our lives, but in the end the drugs cannot solve the issue at hand. In one case, we create a situation where abuse is rampant and misdiagnoses can alter one’s future forever, and in another we simply don’t have the science to fix the problem at hand.
While I am not against prescription drugs, and agree they do much good in the world, it is our duty to exhaust all efforts to mediate problems by non-prescription means first. Many schizophrenics learn how to live with their disorder with behavioral therapy. In other words, they know how to recognize and cope with the symptoms. But of course, cases ensue where prescription is indeed the best option. The same is with ADHD, and even other disorders. Many behavior therapies can be implemented that mediate the symptoms, and when those fail, perhaps then prescription medication should be used.

Disease/Health

Cancer and Schizophrenia: The Thin Line

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    The majority of people, including myself would never believe there existed a link between cancer and schizophrenia. With respect to cancer, we have uncontrolled cell growth and impairment of bodily functions. A disease that appears quite physical in nature. Schizophrenia on the other hand is one of the oldest and well documented mental disorders that exists in our society, and it crosses all borders and cultures. The physical manifestations of schizophrenia seem to be an extension of the broken mind. However, in my neurochemistry class this week we discussed an overlap between these two diseases that appear to be polar opposites. For those of you who aren’t well rehearsed in biochemistry, I’ll pretend to know what I’m talking about and explain it to you. Essentially the accumulation of a protein called beta catenin within brain cells results in cell growth. This is a necessary process for brain cells to properly operate. If this process goes unchecked though, we get cancer (which is bad). Our bodies are aware of this, and in some cases they can get over zealous. A protein that counters the beta catenin pathway is called GSK3. Basically GSK3 tags the beta catenin floating around for destruction. This is great because if beta catenin was always signaling the cell to grow we would all get brain cancer. But, the opposite side of the coin is that if GSK3 never allows beta catenin to signal, our cells are rigid and unable to move. Neuroscientist are hypothesizing that the suppression of beta catenin signaling is playing a roll in schizophrenia. This is exciting news, but we must remember that schizophrenia has a large number of causes ranging from genetic issues to infections, and we will not be able to understand it by mapping out a single pathway.

What we should take away from this is that two seemingly opposite diseases can be related in some ways. The unchecked over signaling of one pathway can result in a vastly different disease when compared to its suppression.

‘Quite frankly Mr. Cartwright, I think this disease is all in your head.’
Disease/Health/Hot topics/Uncategorized

Your Brain Is Giving Itself the Munchies

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You may have heard from a friend of a friend that THC, the main ingredient in cannabis, causes the munchies.  That’s because it’s a turbocharged version of a brain original: endocannabinoids.
The brain has its own versions of a lot of addictive drugs.  Neurotransmitters like dopamine and endorphins are similar to drugs like meth and heroin.  
Technically, it’s cannabis plants that create chemicals to mimic the brain, not the other way around.  Endocannabinoids (eCB’s) naturally make us hungry and reward us for eating.  Humans have bred cannabis to activate this system.

Food addiction

Image result for homer dreaming of donuts
The product of eons of evolution

Dopamine is the “feel good hormone.”  The reward pathway is how dopamine gets dumped into the brain, and eCB’s turn on the reward pathway when we eat.  When rats have their eCB receptors taken out, they don’t get as addicted to drugs.  That basically means all addictive drugs use the eCB system to go through the reward pathway.
So if eCB’s make drugs addictive, and they also make you want to eat food… can they make food addictive?  
Yes.  Cravings make sense when food is scarce.  We are made to crave food because it helped us survive in caveman days.  But when we can eat as much as we want, food cravings can lead to the deadly problem of food addiction.  In the same way that we develop tolerance to drugs, it takes more and more calorie-rich food to satisfy our cravings.  
 

Parts of the eCB system

  • The eCB molecules
  • Receptors that eCB’s attach to (these are the on switches for the effects of eCB’s)
  • Enzymes that make eCB’s
  • Enzymes that destroy eCB’s

Controlling hunger with science

Want to speed up or slow down the eCB system? Make a drug that attaches to one of those receptors or enzymes.  To activate the system you could increase the enzyme that makes eCB’s, and slow down the one that breaks them apart.  One strategy for stopping the effects of eCB’s is to turn off receptors.
That’s what the drug rimonabant did.  A decade ago, rimonabant was a breakthrough drug for obesity.  It worked by attaching to eCB receptors and shutting them down.  But it did the same thing to opioid receptors, causing depression.  The drug stopped cravings so well that people could no longer feel pleasure.  
You’ve probably heard that it takes 20 minutes for the “feel full” signal to get to your brain.  That signal is a hormone called leptin.  It breaks down eCB’s.  Mice that can’t make leptin have a lot of eCB’s in their brains.  The brain wrongly thinks the body is starving, causing overeating.  Something a little different happens to overweight people: leptin resistance.  Besides short-term appetite, leptin also regulates fat storage because it is made by fat cells.  It decreases during famine and increases when we’ve stored up enough fat for winter.  But with so many fat cells in an obese patient, their brains readjust to a baseline of massive amounts of leptin.  Losing weight, then, is like trying to quit a drug, because the brain still thinks the old level of leptin is normal.  Drugs that increase leptin sensitivity are at the cutting edge of obesity treatment, but they may only be able to delay a crisis.  

Related image
Guess which one can’t make leptin

 
Endocannabinoids are central to a startling number of brain functions.  They are necessary for everything from energy balance and appetite to addiction and reward.  Malnutrition still kills millions of people every year, but most of those people are not starving to death.  The meaning of malnutrition has expanded to over-nutrition.  Solving that problem will be a lot more complicated than airdropping rice, and to do it we’ll need to understand endocannabinoids.

 
 

Disease/Health

Should We Find a Pill to Cure Obesity?

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Nowadays, pharmaceutical companies often try to develop specialized drugs for all kinds of diseases and addictions. In most cases I would say that this is a good idea—if there is a pill that can cure cancer or Alzheimer’s, by all means give it to me. But when it comes to diseases like obesity, I’m not quite sure that taking a simple pill would be the best approach to cure it.
mcd_obesity
We have a system in our bodies called the endocannabinoid system (ECS). And yes, as it sounds, cannabis led to its discovery. The ECS impacts many areas of the body , mostly leading to an overall balance in the body. There are two signaling molecules, called endocannabinoids (eCBs) that have a huge impact on what and when we eat. eCBs activate a hormone which tells you that you’re hungry, and then stimulates food intake. In healthy people, eCB levels are highest without food intake, and lowest with food intake—so the lack of eCBs can tell you that you’re not hungry.
From an evolutionary perspective, the body views some fat as good. Fat stores energy when food isn’t available, so it’s good to have a small store built up. This is why eCBs in the stomach can stimulate fatty food intake.
But for most people in America, food is always available. So an intake of too much fat (AKA a high fat diet) can be detrimental. eCBs become overactive with high fat diets, and so it keeps telling you that you’re hungry.
To add to this effect, eCBs affect our internal reward system—they can increase things like dopamine (the happy compound) whenever you eat. You like to be happy, so the hormones that tell you that you’re full get dampened, and you keep eating. This can lead to an addiction to food.
Food addiction is just one component of obesity. There are many other factors which can lead to obesity. One factor is our culture; we no longer eat just when we’re hungry—we eat when we’re bored or sad, or just because it’s lunch or dinner time.
Stood up for the prom.
Back to the main question—should we find a pill to cure obesity, or rather, food addiction?
Should we really be targeting the systems in the body like the ECS? A mechanism which can impact many other parts of our lives? We don’t want to stop feeling happy about eating food (or in the case of anorexic individuals, activate the reward mechanism that makes one feel happy about not eating food). It makes more sense to target the real source of this addiction—lifestyle choices.
obesity
We don’t make time to exercise or cook anymore. In our overly corporate culture, we place more importance on work and making money than health. Maybe we should take a step back and look at our lifestyle choices instead of trying to create a pill to cure everything.

Health

Why Is Cake So Good?

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If there was a pill you could take that would stop you from gaining weight, would you take it? Imagine a world where you won’t have to worry about what you’re eating and how it will impact your health. You won’t have to turn to food for comfort when upset or anxious. Taxpayers will save money with obesity being less of a burden on our healthcare system. Sounds great, right?

Too bad there is a catch.
Sure, you won’t be turning to high-fat and sugar foods for comfort, but that is because you will no longer get that happy feeling that comes from eating some of our favorite, and least healthy, foods. In fact, you won’t want to eat them at all. Ever.
Our brains are wired to seek out food that will give us long-term energy. Before we had access to food we didn’t have to hunt for, we expended a lot of energy just finding our food. Now that we’re able to buy whatever food we want with very little energy, we take in much more than we could ever use. We still crave these calorie-dense foods because our brains don’t know if the food will suddenly run out.

Our brains not only trick us into thinking we want high-fat, high-sugar foods but it rewards us for it too. Endocannabinoids, a class of chemicals produced by the brain that are responsible for many pleasurable sensations, are in part, synthesized when we ingest high fat and high sugar foods. In fact, in obese patients it has been demonstrated that endocannabinoids are over-active in their brains. But it isn’t just our brains, our fat tissue, and perhaps liver and pancreas are actually able to produce endocannabinoids. These endocannabinoids work to reward us for eating foods high in sugar and fat, which in turn generate more endocannabinoids, and reinforce the behavior even further. The other “happy chemicals” in the brain, dopamine and opioids, are also active in our brains when we eat these foods.

Endocannabinoids aren’t only active when we eat. These compounds have long been implicated in drug and alcohol addictions. They are responsible for the “high” users feel and are the compounds that make treatment extremely difficult. It is logical then to acknowledge a different kind of addiction, one to food. Food addictions are very real and very difficult to treat. The same things are going on in the brains of food addicts as in the brains of drug addicts. However, unlike drug use, we need food to live, you can’t simply take away the drug in the case of food addiction, or give a pill that would take away the urge. Researchers, dieticians, and physicians will need to devote more time to studying the mechanisms of food addiction to try to combat it and stop it before it starts.
As far as a magic diet pill goes? It is more complicated than that. Maybe we might have to train our brains to not crave high fat and high sugar food. The secret might just be to consume in moderation, exercise more, and eat your veggies.

Health

How Is Your Brain Stomach?

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Why and how your brain gets hungry
What is your brain stomach?
Well, there is not a tiny little stomach sitting in your brain. That would be uncomfortable, but there is the endocannabinoid system. Endocannabinoid; endo meaning from inside, cannabinoid meaning like cannabis (commonly known as weed). Basically scientists asked the question why does weed do funny stuff. That lead to the discovery of this group of molecules naturally found inside the body that reacts with the same receptor as weed, hence the name.
What does it do?
The endocannabinoids, lets call them eCB for short, are one of the main ways that your brain deals with food. They have two major roles the brain related to food. First are in charge of stimulating eating and getting the body prepared to store food. They do this by interacting with a receptor we call CB1. When they bind to CB1 your brain tells your body that it is time to eat. Your body also has chemicals that signal that you are not hungry. These are blocked by some of the eCB’s so that you feel hungry longer and eat more.
The second way it works it by signaling pleasure while eating food. Food is nessiesary for your body. So your body likes it when you eat food. This happens because nerve cells (neurons) in your brain release dopamine. Dopamine signals your brain that what you are doing is pleasurable. This only happens in short blips because other neurons stop the release of dopamine. That is where eCBs come in. ECBs stop the stopping neurons. This means your body releases more dopamine and you feel even better.
So how do we ever stop eating if eCBs are telling us to eat and dopamine is telling us it is fun? Well after eating enough your body releases the hormone Leptin. It stops the eCBs from signaling and sets the body back into balance. It also lets your neurons stop producing dopamine by removing the eCBs. This process is healthy. Your body needs to eat when it needs food and stop when it is full.
When it goes wrong
The eCB system is very complex. It depends on a lot of things to be balanced. One of the most important things is diet. This is because eCB are made from the tiny amounts of fat that we naturally have in our cells. When we eat very high fat diets there are more fats to convert to eCBs. This leads to large amounts of dopamine in your brain. This release of dopamine in the brain can make people addicted to food. They experience the desire to eat even if their body is not actually hungry. This is why people have so hard a time going on diets. Their brain wants fatty foods and lots of it. In severe cases this can lead to extreme obesity and many other health problems.

What does this mean
It means that it really is harder to make the healthy choice when it comes to food. But good news. The healthier we eat the more our eCB will be balanced and the easier it will be to eat healthier foods.

Disease/Health

Can Obesity Cause Cognitive Disfunction?

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The paper that I read for this week argued that obesity, along with genetic and socioeconomic factors, could be a result of an addictive lifestyle based on the reward system in the brain that signals the body to continue to eat high calorie foods that tend to be extremely palatable to humans. Similar to drug addiction, someone who consumes high calorie foods can experience pleasure, making people over consume these nutrient poor food types that result in an addiction-like pleasure from food. Some individuals use food consumption of high calorie substances to subdue feelings of anxiety, depression and mental fatigue, resulting in an addictive form of eating. These individuals have also reported withdrawal like symptoms when their normal compulsive eating behaviors were delayed. Overall, obesity could be part of an addictive cycle of compulsive food consumption, regulated by the pleasure centers in the brain.
Along with additive behavior, I found further information that obesity has also been linked to cognitive impairments, which could further alter a person’s ability to make healthy food choices and perform normal eating habits. Type II diabetes, the form of diabetes that is resistant to the effects of insulin, has been associated with people who are overweight or obese. When insulin isn’t functioning properly in this type of diabetes, there is an excess of sugar in the blood, known as hyperglycemia. It is hypothesized that improper control of blood sugar in diabetic patients is associated with cognitive impairment in some of the following ways:

  • While there is not a defined mechanism for cognitive impairment in diabetes, patients with type II diabetes were determined to have cognitive impairments including decreases in attention, processing, memory, and recall of information.
  • It has also been determined that people with type II diabetes have an increased risk for Alzheimer’s disease.
  • Furthering the problem with diabetes, improper control of blood sugar in diabetic patients may alter neurotransmitter function. Important neurotransmitters such as acetylcholine, norepinephrine, and dopamine were found to have decreased levels in animal models with diabetes. These neurotransmitters are important for sending messages and signals from the brain to the rest of the body for proper bodily functions.
  • High body fat is associated with inflammation of the brain, further impacting cognitive function.

The clinical significance of diabetes associated cognitive impairment has not been defined, as there are not routine cognitive tests in the clinical setting. However, this cognitive impairment caused by the combination of diabetes and obesity could be contributing to overeating by decreasing memory function and compromising decision-making when a person chooses to eat.
Overall, obesity is a complex problem that likely has contributing factors from many different mechanisms in the brain. The cause of obesity varies from person to person such that genetic, socioeconomic, addiction, and induced cognitive impairment are likely only a few of the causal reasons for a person who is obese. With more evidence of the brain’s role in obesity, understanding of reward pathways and cognitive function should be further assessed for possible viable treatments of obesity.
 

Health

Why We Can’t Stop Eating?

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There’s no denying that Americans’ collective waistband is growing tighter. According to the CDC, around 36% of adults and 17% of children are now considered obese – the highest it’s ever been. And not only did this epidemic cost US taxpayers a paltry $147 billion in 2008, but it also contributes to a plethora of other diseases including heart disease, cancer, and diabetes (1). Despite what many daytime TV ads try to tell us, dietitians and doctors say that the best way to combat obesity is through healthy diet and exercise.
Which bring up the question: what’s going on in our brains that make it so hard to eat healthy?
The answer that neuroscientists point to is our endocannabinoid system. While there are several other functions of the endocannabinoid system the main role it plays in our body is regulating our appetite. Namely, when endocannabinoid receptors like CB1 are activated by neurotransmitters such as AEA to produce feelings of hunger. However this obviously isn’t the whole story. Here are some ways that the endocannabinoid system influence our eating habits on a larger scale:
Endocannabinoids increase our sensitivity to sweetness and high-calorie foods
It’s no secret that we as humans love foods that are sweet and high in calories, and there is science behind the reason why. Generally, foods that are sweet are also high in calories and our endocannabinoid system rewards us when we continually eat sweet food. CB1 receptors found on the tongue were also found to react more strongly to high-fat foods. One experiment even found that ingestion of high-fat foods caused dopamine outflow in the ventral striatum, an important mechanism for reward (2).
Looking at food increases endocannabinoid levels
For most of us, even the sight of food elicits an emotional response. This is no accident. Endocannabinoid receptors are even localized on the retina and are important in mediating palatable memory by activating the endocannabinoid system found in the brain. Thus, our food preferences are strengthen by these implicit food memories (3).
Food and substance addiction work the same way
Food and illegal substances (meth, cocaine, marijuana etc.) all use a similar pathway to promote addiction. More specifically, food and substance addiction both activate the brain reward dopaminergic and opioid systems. When it comes to food addiction, some studies have found that there is compromised dopaminergic signaling and downregulated dopamine receptors in obese patients. Another study found that subjects that were considered obese had increased dopamine release in respond to food cues (4).
Sources:

  1. https://www.cdc.gov/obesity/data/adult.html
  2. https://www.ncbi.nlm.nih.gov/pubmed/22561130
  3. Bouchard, J.-F., Casanova, C., Cécyre, B., & Redmond, W. J. (2016). Expression and Function of the Endocannabinoid System in the Retina and the Visual Brain. Neural Plasticity, 2016, 9247057. http://doi.org/10.1155/2016/9247057 ▲
  4. . DʼAddario C, Micioni Di Bonaventura MV, Pucci M, Romano A, Gaetani S, Ciccocioppo R, et al. (2014): Endocannabinoid signaling and food addiction. Neuroscience Biobehavior Reviews 47:203–224.

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