What happens to apetite hormones like ghrelin and leptin when a person in coma?

What happens to apetite hormones like ghrelin and leptin when a person in coma?

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Don't coma individuals feel hungry? If so, how does the brain senses this condition (as coma is caused by neural death or damage) and switches off gene expression of ghrelin and leptin.

Is there any research done on revealing the mechanism by which apetite hormones expression are shut down during brain death???


Why Does Weed Make You Hungry?

Have you ever mixed Cheetos and Sour Straws? Have you ever covered spicy pickles with whipped cream for an afternoon treat? Have you ever emptied the contents of your refrigerator into the kitchen sink and eaten it with a large spoon?

If you can answer yes to any of these questions, you’ve experienced (maybe “enjoyed” is a better word) the munchies. Having the munchies is an integral part of the marijuana experience, and every cannasseur has their own hilarious story to tell (peanut butter/marshmallow fluff/caramel corn sandwich, anyone?).

But why does weed make you hungry? What’s going on in your body that makes any and every combination of food sound like the best thing ever? The experts at Honest Marijuana are here to peel back the foil, remove the plastic, and pop the top, if you will, to reveal the chemistry and biology that causes you to become ravenous after toking a doobie.

Before we get to that, it’s essential that you understand the natural feeling of hunger (without the influence of weed). That’s what we’ll focus on in the next section.

The Biology of . . . Appetite

For most of us, snacking is a bad habit. For Melissa Moss, a Californian with a rare genetic disorder, it's a matter of life and death. A chromosomal abnormality known as Prader-Willi syndrome has cursed her with both an insatiable appetite and a metabolism so slow that she gains weight eating just 1,600 calories a day.

Moss, an articulate 28-year-old, used to steal leftovers from cafeteria trays when she was in elementary school, or even pick scraps off the floor. Now that she's an adult, food is never far from her mind. She spends hours every day counting calories, weighing and reweighing foods, and figuring out, down to the last half pretzel, how much she can eat. Her 1,300-calorie-a-day diet of yogurt, fruit, fat-free turkey sandwiches, and diet TV dinners is spartan and monotonous, but it has kept her slender, and alive. Untreated, most people with the syndrome become obese by their teenage years and are dead by adulthood, killed by heart disease, diabetes, or other conditions. Some have died from gorging until their stomachs actually burst.

Cruel as it is, Prader-Willi could prove to be important to scientists trying to understand the complex biology of appetite. Researchers are trying to determine exactly how the syndrome's genetic abnormalities spur the appetite. If they succeed, they could not only help treat the roughly 20,000 Americans afflicted with the syndrome but also help explain how the rest of us eat—and why so many of us eat too much.

Eating may seem basic, but the whole process, from feeling hungry to finally pushing away from the table, is controlled by elaborate and largely mysterious circuitry between brain and gut. Scientists have identified more than 250 genes and at least 40 neurochemicals that regulate metabolism and appetite, but it's clear that in humans, social cues are at least as powerful as biological signals. The study of metabolism and appetite, one appetite researcher wrote, is like "a few small islands of scientific understanding surrounded by a vast sea of uncertain phenomena."

The neurobiology of eating, according to one model, begins when positive signals flow from the mouth through the cranial nerves to the brain. Dopamine and opioids are then released that create a sense of pleasure. At the same time, hormones are released that begin to curb the appetite. As more food goes down the hatch, the belly begins to expand. That triggers messages back to the brain to slow down eating. The small intestine also provides feedback as specific nutrients set off neurological and hormonal signals that say "I'm full."

So where, exactly, does hunger come from? The obvious answer is that the brain initiates the sensation to get more energy and nutrients. But Ralph Norgren, a behavioral scientist at Pennsylvania State University, says researchers can't find a day-to-day correlation between how much we eat and how much energy we expend. It's only when the numbers are tracked over the course of a week that a strong relationship becomes clear. "It doesn't happen in an individual meal or during a day, but it does happen, and it's very precise," he says. Increase the time frame even further to an evolutionary scale and the relationship grows more obvious. William Zipf, a pediatric endocrinologist and Prader-Willi expert at Ohio State University, says, "All our traits were designed to find food, take in food, store food. That's what we needed to survive 30,000 years ago." Inside every thin person, in other words, is someone who feels he's more likely to survive if he eats more.

Prader-Willi could prove a guide to this uncertain terrain because its origins are so specific. Unlike most genetic diseases, the syndrome is rarely inherited. Instead, it is caused by a random accident during egg, sperm, or embryonic formation that either deletes or muffles dozens of genes along a stretch of chromosome 15. Ten of the genes, when disrupted, have been linked to the characteristics of Prader-Willi. In addition to ravenous appetites, Prader-Willi patients have weak muscles, slow metabolisms, small hands, feet, and genitals, and a distinctive triangular mouth. They are often short and very fair, and they tend to have significant learning disabilities. Compulsive behaviors—skin picking, repetitive questioning, and a need to collect and rearrange objects—are common. They can also be very stubborn. (Melissa, luckily, has milder symptoms than most.) Many also have remarkably good memories, and some have an unusual talent with jigsaw puzzles.

Scientists now believe that the same genes that are disrupted in patients with those symptoms are also involved in the function of the hypothalamus, one of the most ancient parts of the brain. The hypothalamus mediates hormonal responses and controls metabolic systems such as heart rate, body temperature, and growth. It has also been fingered, by appetite researchers, as the central switching station for the neural circuitry that controls eating. The overeating, however, does not begin at birth. "It's almost as if [in Prader-Willi patients] this part of the brain that controls eating is turned off in the first couple of years," says Merlin Butler, a cytogeneticist and pediatrician at Children's Mercy Hospital in Kansas City. "And then once it's turned on, it never gets turned off again."

But are people with the syndrome always hungry, or do they simply never feel full? William Zipf has seen a child eat more than 25 chicken salad sandwiches during an hour-long study and then ask for lunch, suggesting that those with the syndrome never feel satiated. Other scientists say the problem lies with a hyperactive appetite. But Moss says that she doesn't always feel hungry. "I don't know if I ever really feel full, though," she adds.

Meanwhile, researchers are taking a closer look at the neurochemicals associated with appetite and metabolism. At the University of Florida College of Medicine in Jacksonville, pediatric geneticist Daniel Driscoll recently launched a project to look for abnormal levels of leptin, ghrelin, and neuropeptide Y in the blood and cerebrospinal fluid of Prader-Willi patients and other obese children. Leptin and ghrelin are both hormones that have powerful systemic effects on eating and metabolism. When injected into the hypothalamus of a rat, neuropeptide Y has been shown to induce overeating immediately.

A good deal of recent appetite research has also focused on the role of the brain's pleasure centers. Some of the same neurochemicals involved in eating seem to underlie drug addiction, says Norgren. Cocaine and heroin, for instance, increase dopamine levels in the brain. "Eating preferred foods does exactly the same thing," Norgren says, "from the same parts of the brain." Travis Thompson, director of the Institute for Child Development at the University of Kansas Medical Center, believes that the neurotransmitter gamma-aminobutyric acid is somehow involved in producing the obsessive-compulsive behaviors. Several genes involved in manufacturing one of the receptors for the neurotransmitter lie on the chromosome that is altered in Prader-Willi patients. More telling, Thompson has found that Prader-Willi patients have three times as much of the neurotransmitter in their blood as those without the syndrome.

Given that this neurotransmitter inhibits dopamine in the brain, it's possible that people are simply chasing the pleasure of a full stomach. "Clearly, in Prader-Willi, some switch that's on goes off, or one that is off goes on," Driscoll says. "Nobody knows. That's the Holy Grail. You find that out, and it gives you a window right into the house of obesity—a view right into the dining room itself."

What happens in anorexia nervosa?

Anorexia nervosa significantly impacts both the body and the mind. The low weight state leads to a variety of medical consequences, including bone loss (osteopenia) and the loss of one’s menstrual period (amenorrhea). Many of these symptoms can be explained by the way hormones respond to the signals that we send our body when we restrict food intake for an extended period.

  • Amenorrhea: Anorexia nervosa is associated with profound decreases in reproductive hormones (e.g. LH, FSH, and estrogen). The mechanism may be related to leptin levels, which are lower than expected based on height and weight, and seem to send the signal that energy availability is low, and our bodies aren’t ready for reproduction.
  • Osteoporosis: Poor bone health is possibly one of the most compelling consequences as people who develop anorexia nervosa at a young age and may never reach peak bone mass. Severe complications, like bone fractures, can occur even as late as 40 years after diagnosis. The combination of low leptin and sex-hormone levels, high cortisol levels and poor nutrition can explain this feature.
  • Thyroid levels: It is not uncommon for T3 levels to be low in people with anorexia nervosa. This manifests as bradycardia (slow heart rate) and hypothermia (low body temperature)—features that serve to preserve energy.
  • Behavioral/psychological symptoms (e.g., anxiety, hyperactivity, impulsivity): Hormones that activate our fight-or-flight response (i.e. cortisol) are typically elevated in anorexia nervosa. This could have something to do with behavioral features of the illness that promote quick decisions and a high state of alert.

Perhaps the most fundamental question about hormones and anorexia nervosa of interest to researchers is about the impact of physiology in the development of the disorder. Is there a hormonal perturbation that promotes a low-weight state or predisposes one to the illness? Studies have looked at hormones like PYY that may predispose patients to reduce food intake, but in general, there is no evidence to conclude that this is the case. However, the hormonal irregularities experienced by individuals with anorexia nervosa are what one would expect in those who are starved. The question then becomes—what causes individuals with anorexia nervosa to overcome such a strong biological drive to regain lost weight? Whether it has to do with delaying reward, habit formation or differences in taste preference or something else we haven’t thought of yet, is a big focus of research today and is crucial to fully understand the illness.

Hormones in the blood

Let’s take a closer look at how each of these blood-circulating hormones work.

Ghrelin is made in the stomach. It stimulates hunger by entering the brain and acting on the neurons in the hypothalamus to increase the activity of the hunger-causing nerve cells and reducing the activity of hunger-inhibiting cells. As the stomach empties, the release of ghrelin increases. As soon as the stomach is filled, it decreases.

Insulin-like peptide 5 (ILP-5) was found to stimulate hunger in 2014. It is the second circulating hormone to have this effect and is mainly produced in the colon. But we still don’t know its physiological role.

Cholecystokinin (CCK) is produced in the upper small bowel in response to food and gives a feeling of fullness. It is released soon after food reaches the small bowel. Researchers have found CCK can stop a mouse from eating as soon as it’s injected into the brain.

Peptide YY, glucagon-like peptide 1 (GLP-1), oxyntomodulin and uroguanilin are all made from the last part of the small bowel and make us feel full. They are released in response to food in the gut.

Leptin is the most powerful appetite-suppressing hormone and is made in fat cells. It was discovered in 1994. The more fat cells we have, the more leptin the body produces.

Amylin, insulin and pancreatic polypeptide are made in the pancreas. Studies in the United States have shown that when insulin enters the brain it inhibits hunger, telling the brain “there is enough energy in the body, take a rest”.

Amylin, discovered in 1981, is made in the same cells that make insulin (the beta cells). It has been shown to inhibit food intake.

The exact role of pancreatic polypeptide is not yet known, but there is evidence that it inhibits hunger.

The hypothalamus also receives signals from pleasure pathways that use dopamine, endocannabinoids and serotonin as messengers, which influence eating behaviour.

Once full, the stomach reduces the desire to eat both by lowering ghrelin production and by sending a message to the hypothalamus. Ghrelin levels reach a low around 30 to 60 minutes after eating.

Levels of hormones that make us feel full – CCK, PYY, GLP-1, amylin and insulin – all increase following a meal to reach a peak about 30 to 60 minutes later.

All the hormones then gradually return to their fasting levels three to four hours after a meal.

Sleep Well and Let the Brain Work

When you sleep after a tiresome day, your work shift is over. However, for your brain, the work never ends as the nervous system performs essential maintenance and repair work while we sleep.

Therefore, sleeping well is vital to maintaining physical and mental health. It keeps your body healthy and functioning like clockwork. If you cannot sleep or rest long enough, you may experience side effects such as mood swings, poor memory, difficulty concentrating, and even weakened immunity.

If the steps above don’t solve your sleeping problems, talk to a doctor or sleep specialist. Your brain needs this daily period to take care of your physical or mental health, and skipping this step can bring severe problems in the future.

How To Decrease Your Appetite Permanently?

How to suppress your appetite mainly depends on the hormones which are communicating your need to eat to the brain. These include ghrelin that actually makes you feel hungry, and neuropeptide Y that particularly stimulates cravings for carbohydrates (9, 22). Since i t may be impossible to control these hormone levels, it’s equally important to keep in mind that losing your hunger cues completely may not be a good idea as it may deprive you of the nutrients you need for your body to work well. You should try healthy ways to reduce your appetite which is a way to concentrate on reducing them to avoid overeating.

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Inquire into many a health-minded person’s diet, whether a trainer, a professional athlete, or even Beyoncé, and you’ll find that many will say that they take a day off from being regimented about what they put into their bodies. What that looks like may differ from person to person, whether it’s allowing themselves a glass of wine at dinner, a big meal on Friday night, or a hall pass come Sunday. But what actually happens to your body when you, so to speak, cheat?

For people getting enough daily calories (versus someone who is restricting), a little cheating shouldn’t really throw you out of whack, in terms of your appetite-regulating hormones. “Since hormones like leptin and ghrelin exist to prevent starvation, nothing significant would happen to someone who is already getting enough calories on a daily basis,” says Ryan Andrews, a coach with Precision Nutrition. “If someone is consuming an appropriate amount of energy for their body each day, and then they eat slightly more, the body will likely adjust, and nothing remarkable will really happen.”

The needle on the scale should likely stay put, too. "The body seems to have a little bit of wiggle room, calorically speaking,” says Andrews. “And if someone eats a bit below their needs or a bit above their needs, the body compensates and keeps things stable to prevent weight gain or loss. If someone eats a bit too much day after day after day, though, then it can lead to weight gain.”

Which makes a case for a regularly scheduled cheat meal instead of a full-fledged cheat day. “I'm a fan of whatever can help someone eat in a way that allows them control their overall intake,” says Andrews. “If this means they look forward to a larger meal on Sunday or a dessert on Friday—great. I would just challenge people to think about the difference between eating a bit more than usual on Saturday night versus an all-out cheat day with forced overeating. It's when one meal becomes a day that things often spiral out of control."

Another potential downside skews more psychological: You might be stripping all of the enjoyment out of eating a healthy, well-balanced diet. If Sunday becomes fun day, Monday through Saturday becomes food purgatory. “Oftentimes when we restrict a food, we increase its desirability,” he says. “So if someone says I can only have potato chips on my cheat day, that might just fuel the idea of overeating the potato chips because they know they can't eat them for another six days. What if instead they had a reasonable amount of potato chips throughout the week? Might that work better?"

How Does Sleep Work?

Every person has an internal timekeeping system known informally as the "circadian clock," which is located in the hypothalamus near the front of the brain. The circadian clock is programmed to reset, or "entrain," every 24 hours. This 24-hour cycle, the circadian rhythm, is guided by natural light and plays a major role in hormone production, as well as mood, appetite and digestion, body temperature, and other bodily functions.

This clock consists of roughly 20,000 nuclei clustered together to form a structure called the suprachiasmatic nucleus (SCN). During the day, the retinas in your eyes perceive natural sunlight and transmit signals through a nerve tract that leads directly to the SCN. These signals inform the brain whether it is day or night.

In the evening as natural light begins to disappear, the pineal gland in your brain will produce melatonin, a natural hormone that induces feelings of relaxation and sleepiness. When you wake up in the morning and your eyes perceive natural light, the body will produce another hormone, cortisol, that promotes alertness and wakefulness. The brain stem also communicates with the hypothalamus to produce GABA, a hormone that decreases arousals and helps the body wind down.

In addition to circadian rhythm, your sleep is also regulated by a process called sleep-wake homeostasis. Also known as your sleep drive, this mechanism regulates feelings of tiredness and wakefulness. For every hour you're awake, your sleep drive will become stronger, and these feelings will culminate right before you go to bed.

Your circadian rhythm and sleep-wake homeostasis do not exist in a vacuum. Circadian rhythm disorders can cause you to feel tired and alert at times of the day that do not align with natural light cycles. Examples range from mild conditions such as jet lag to more serious conditions such as advanced or delayed sleep-wake phase disorder, irregular sleep-wake rhythm disorder, and shift work disorder. Factors that can affect or alter your sleep-wake homeostasis include light exposure, diet, stress, medical conditions, and your sleep environment.

What Are the Stages of Sleep?

The term sleep architecture refers to the physical structure of your sleep cycle. The sleep cycle of a healthy adult consists of four distinct stages. The first three stages are considered non-rapid eye movement (NREM) sleep, and the last stage is considered rapid eye movement (REM) sleep.

  • NREM 1: The first stage signifies the transition between wakefulness and sleep. NREM consists of light sleep characterized by a gradual reduction to your heartbeat, breathing rate, eye movements, and brain wave activity. The muscles will also begin to relax, though they may twitch – movements known as hypnic jerks or sleep starts. This stage usually lasts several minutes.
  • NREM 2: The second stage also consists of light sleep, though your heartbeat, breathing rate, eye movements, and brain wave activity will drop to lower levels than during NREM 1. Your body temperature will also decrease significantly and eye movements will completely cease. NREM 2 is the longest of the four sleep stages.
  • NREM 3: This stage marks the beginning of slow-wave, or deep, sleep. Heartbeat, breathing rates, and brain wave activity will decrease to their lowest possible levels and the muscles will completely relax. NREM 3 is a longer stage when you first fall asleep but it will gradually shorten throughout the night. Historically, sleep experts believed the sleep cycle also included a second slow-wave stage known as NREM 4, but current nomenclature combines the two slow-wave stages into a single stage (NREM 3).
  • REM: The final stage of your sleep cycle will first occur about an hour and a half after you nod off. As the name suggests, your eyes will move erratically beneath your eyelids, and your brain waves will become more active. Breathing rates also increase, and your heart rate and blood pressure elevate to levels that are closer to those during wakeful periods. Dreaming primarily takes place during this stage, as well, and your muscles will be temporarily paralyzed this bodily mechanism prevents you from physically responding to dreams.

Overall, each sleep cycle usually lasts between 90 and 120 minutes. The duration of each stage largely depends on your age, since people spend less time in REM sleep as they get older.

How Much Sleep Does a Person Need?

The average adult should receive at least seven hours of sleep for every 24-hour cycle. Sleeping less than seven hours can leave you more vulnerable to different diseases and medical conditions, and also affect your ability to concentrate and increase your risk of errors and accidents. That said, the sufficient amount of sleep for a given individual depends on their age.

Sleeper Group Age Range Recommended Daily Sleep
Infant 4-12 months 12-16 hours (including naps)
Toddler 1-2 years 11-14 hours (including naps)
Preschool 3-5 years 10-13 hours (including naps)
School age 6-12 years 9-12 hours
Teen 13-18 years 8-10 hours
Adult 18+ 7-9 hours

Insufficient sleep creates a problem known as sleep debt. Let's say you are an adult 18 years or older who receives six hours of sleep every night. Just one week of inadequate rest produces seven hours of sleep debt. Napping can provide a quick pick-me-up, but it does not deliver the same restorative functions of nightly sleep. As a result, chronic sleep deprivation can lead to serious health problems down the road.

Q. Does leptin affect other parts of the body?

Leptin appears to have many functions that scientists are still exploring. "It didn't work as a weight loss agent, but there's now starting to be some other things that are really interesting about it," Atkinson says.

The hormone plays a role in heart and bone health, Lustig says. "We know that leptin is very important in keeping the immune system happy and that chronic inflammation occurs in the face of inadequate leptin signaling, and that's part of cardiovascular disease."

"We also know that leptin has direct effects on bone to increase bone health and bone mineral density, so when your leptin's working right, your bones are healthier and they accrue more calcium," he says.

Scientists are also finding some associations between leptin and certain cancers, Atkinson says. For example, some recent research suggests that leptin can promote the growth of melanoma, a type of skin cancer.

According to Atkinson, leptin may even affect women's fertility. "If the brain doesn't sense leptin, you won't be fertile. If you think back to our caveman days, when there were lots of famines, if you didn't have enough fat to survive a pregnancy, then you're better off not getting pregnant in the first place. Some people have thought that the leptin feeds back on the hypothalamus to keep the reproductive hormones working well, too."


Richard Atkinson, MD, clinical professor of pathology, Virginia Commonwealth University.

Robert H. Lustig, MD, professor of pediatrics, University of California, San Francisco member, Endocrine Society's Obesity Task Force.


  1. Diandre

    Let's live.

  2. Louden

    I think this is a great idea

  3. Derwent

    Of course. And I ran into this.

  4. Denys

    I accept it with pleasure.

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