Tag Archives: leptin resistance

Food Pollution: Eating Disorders and Obesity

photo used under a creative commons license

In this week’s episode we discussed the effects of Food Pollution on Eating Disorders and Obesity.

Listen to internet radio with Eating Disorder Pro on Blog Talk Radio

In this episode we covered:

5:25 – The Systems Involved in Regulation of Appetite, Fat Storage, Weight Loss, Weight Gain, and Food Addiction
6:10 – What is Leptin?
6:24 – White Adipose Tissue (WAT) and Triglycerides
9:07 – The Effects of Food Pollution on the Weight Management System
10:57 – The Starvation Hormone – Leptin
11:40 – What drives Leptin Levels?
12:56 – Leptin Resistance
13:50 – Caller Question – How can I find out what my leptin levels are?
17:00 – Leptin Resistance
19:00 – The Effects of Food Additives and GMOs on Leptin
20:28 – Leptin and Anorexia
21:22 – The Effects of Anorexia and Obesity on the Endocrine System
22:46 – Cortisol
24:02 – Leptin and Anorexia
25:14 – Ghrelin: The Hunger Hormone
27:45 – Anorexia and Ghrelin – The Effects of High Ghrelin Levels on Treatment
30:44 – Bulimia and Ghrelin
32:10 – Obesity and Ghrelin
32:40 – Neuropeptide YY (PYY)
34:10 – Obesity and PYY
35:37 – PYY and Mood
35:55 – Regulating PYY through Diet and Exercise
38:55 – How to Regulate Leptin Levels

Links We Discussed
Peptide YY

Show Summary

The Weight Management System

In order to understand the role that food additives, genetically engineered organisms (GE’s), sweeteners, and neurotoxins play in the current epidemic of obesity and ED’s we must first understand the systems involved in appetite/hunger, fat storage, weight loss/gain and food addictions. There are three primary hormones involved in appetite/hunger regulation: Leptin, Ghrelin, Peptide YY.


Leptin, which is a peptide hormone, was discovered by scientists in 1994. It is found in gastric tissue and placenta but is most abundant in white adipose tissue (WAT) otherwise known as body fat. WAT is composed mainly of adipocytes (fat cells) that store energy in the form of triglycerides during times of nutritional abundance. During times of nutritional deprivation, fat cells release the triglycerides (fat) into the blood stream to provide energy for the body. If there is too much fat in the form of triglycerides, it is stored in different places, such as the hips or belly, in case it is needed later. It also accumulates in the arteries, causing coronary artery disease.

In general, the amount of WAT, or body fat, is determined by the balance between energy intake and energy output. While it is partly influenced by genetic factors, it is driven primarily by environmental factors, such as the amount and/or type of food eaten.

It is damaged by food additives that are neurotoxic or addictive and by environmental carcinogens and obesegens.
Under normal conditions, this system is carefully regulated so that WAT mass remains constant and close to a well defined ‘set point’ for each individual. The set point, which is designed to keep the body at a healthy weight, is part of a feedback loop that maintain homeostasis.

Disruptions of this steady state that are caused by damage to the systems involved, can lead to chronic decreases or increases in the quantity of WAT mass. Decreased amounts of WAT are associated with periods of dieting, malnutrition, as in the case of ED’s, Anorexia. During these periods, the healthy body sends a message to the brain to increase food intake and decrease energy output. Increased amounts of WAT are present with obesity. Under these conditions, leptin sends a message to the brain to inhibit food intake and increase energy expenditure. In this sense, leptin acts as a long-term regulator of optimal body weight. It has been dubbed the “starvation hormone” because it’s primary function is to keep us from eating too little or exerting too much, and thus avoid starving to death.

Leptin levels are driven by the amount of adipose tissue one has under normal conditions. While the system works well to keep weight at optimal levels, it becomes less and less effective the more (or in the case of Anorexia, the less) adipose tissue there is. In the case of excess weight, the farther one is from the optimum, or set point, the stronger the signal to decrease food intake and increase energy output.

However, there appears to be a threshold for leptin levels, such that when they get too high or remain too high for too long, the brain no longer registers or recognizes them. This is called Leptin resistance, and it’s very much like insulin resistance. When this happens, the brain no longer senses changes in leptin levels. Instead, it perceives, that the body is in a state of starvation.

As a result, the individual experiences the need to increase food intake and decrease energy expenditure, regardless of how much excess fat they actually have on board. This causes more weight gain, and more adipose tissue, which results in more Leptin resistance, which in turn results in more weight gain. This is an example of a classic vicious cycle.

In the case of Anorexia, leptin levels are too low, due to the lack of WAT or fat cells, so that the individual is leptin deficient. The message from the brain is the same as it was for the obese patient that was leptin resistant, eat more, exert less, but for a different reason. In this case, the individual actually is starving to death. Unfortunately, in the case of the Anorexic individual, whose fear of gaining weight is overwhelming, the response to feeling hungry is to eat even less, causing more weight loss, which triggers more hunger which leads to more fear, and we have another vicious cycle.

Fasting, food intake, exercising, awakening, and psychosocial stressors cause the body to release cortisol. Cortisol is released in a highly irregular manner with peak secretion in the early morning, which then tapers out in the late afternoon and evening. Energy regulation and mobilization are two critical functions of cortisol. Cortisol regulates energy by selecting the right type and amount of substrate (carbohydrate, fat or protein) that is needed by the body to meet the physiological demands that is placed upon it. Cortisol mobilizes energy by tapping into the body’s fat stores (in the form of triglycerides) and moving it from one location to another, or delivering it to hungry tissues such as working muscle. Under stressful conditions, cortisol can provide the body with protein for energy production through gluconeogenesis, the process of converting amino acids into useable carbohydrate (glucose) in the liver.

Additionally, it can move fat from storage depots and relocate it to fat cell deposits deep in the abdomen. Cortisol also aids adipocytes (baby fat cells) to grow up into mature fat cells. Finally, cortisol may act as an anti-inflammatory agent, suppressing the immune system during times of physical and psychological stress. The implications are that when you are stressed, you store more belly fat and are more susceptible to disease because your immune system is on vacation.

Leptin levels can also be high for individuals with anorexia. However, in this case it is because triglyceride levels are too high due to liver damage and/or anorexia-induced hormone disruptions.


Ghrelin, discovered in 1999 by scientists, is known as “the hunger hormone”. Produced in the stomach and pancreas, Ghrelin stimulates the appetite for the purpose of increasing the intake of food and promoting the storage of fat. When Ghrelin levels are high, we feel hungry. After we eat, Ghrelin levels fall and we feel satisfied.

Leptin and Ghrelin have a “teeter-totter” relationship. When leptin levels rise, ghrelin levels fall. Likewise, when ghrelin levels rise, leptin levels fall.

Whereas leptin acts as a long-term regulator of body weight, Ghrelin, on the other hand, is a fast-acting hormone that operates as a meal-initiation signal for short-term regulation of energy balance. There are distinct abnormalities in the production of Ghrelin among obese and eating disordered individuals. Part of the problem may be high levels of the stress hormone, cortisol, which is often seen with very low leptin levels. of Chronic stimulation is seen in clinical scenarios with chronic high cortisol levels and very low leptin levels. The more improper signaling that occurs, the more the incretin hormones agouti and ghrelin become disconnected from their master controller, leptin. The gasoline for this reaction is a chronic elevated cortisol. The longer it occurs, the more these abnormal signals are wired for in the person’s brain. This is what makes their treatment so difficult.

Those with anorexia tend to have high levels of ghrelin, which causes them to feel hungry. The sense of hunger is an extremely frightening feeling for most individuals suffering from Anorexia. So much so that they believe that they will never be able to relate normally to food, fearing that once they start eating they will never be able to stop. However, Grehlin levels normalize with weight restoration in individuals that refeed on a clean diet. For those that refeed using traditional refeeding protocols, Grehlin levels are likely to worsen as are Leptin levels. The result is increases hunger, increased fear and more restricting.

Among those with bulimia, Ghrelin does not respond as strongly when food is eaten, which could contribute to binge eating as the individual suffering from Bulimia does not “get full” even if they have overeaten. In the past, the assumption has been that there may be a predisposition in the Bulimic individual that “causes” this reactio and drives this disorder. However, it is possible that the toxins found in most of the foods in the U.S. may be changing brain chemistry in such a way that drives Bulimia.

Obese individuals tend to have low levels of Ghrelin, probably because they are Leptin Resistant, since Leptin and Ghrelin are inversely related. Research also shows that Ghrelin levels are higher after an individual loses weight, causing an increase in appetite, which may make it even more difficult to maintain weight loss for obese individuals.

Peptide YY (PYY)

PYY is a hormone that suppresses appetite. It was discovered to play a role in digestion in 1985. PYY regulates food intake, and is believed to improve leptin sensitivity. The amount of PYY released by our bodies is influenced by the number of calories we ingest; the more calories we ingest, the more PYY is released.

PYY levels are highest in individuals battling anorexia, followed by those individuals that are lean,which explains why both groups have less hunger and also may have more difficulty eating. PYY levels are lowest among obese and morbidly obese individuals. Individuals with bulimia also experience low levels of PYY, which helps to explain why all three groups feel more hunger. Research shows that the obese individual can decrease their PYY levels by 30% by reducing their body weight by 5.4%. PYY levels are not believed to be effected by weight restoration during recovery from anorexia. It is also important to note that high levels of PYY in anorexic individuals is associated with decreased bone mineral density (BMD).

Our mood also effects our PYY levels. Recent studies show that PYY levels are higher in those suffering from major depression. This explains why many people with major depression have a decreased appetite and experience weight loss.

PYY levels can be regulated through both diet and exercise. Diets high in quality protein tend to raise PYY levels highest, followed by diets high in healthy fats. High carbohydrate diets tend to raise PYY levels the least. Aerobic exercise has also been proven to raise PYY levels, whereas strength-training has no effect on PYY levels (although strength-training does lower ghrelin levels).

In conclusion, PYY regulates our appetite. The higher our PYY levels are, the more satiated we will feel. You can ensure your PYY levels are highest by eating a high protein diet and including aerobic exercise in our workout routine.

1. Eat a balanced diet. Be sure to eat foods that are high in protein, and remember to consume organic fruits vegetables. Even though you are resistant to leptin, you should still consume the proper nutrients.

2. Eat six time a day, on a schedule. If you have leptin resistance, you do not realize when you have eaten enough. To overcome this problem, create a set schedule of when to eat. It is best to have three meals each day. You should eat in the morning, the afternoon and the evening.

3. Create a food diary. In order to organize your schedule, create a food diary of the three meals and three snacks each day and the foods you will have during those meals. This method will help you to make sure that you are consuming a variety of foods. Also, by organizing your meals, you can make sure that you are not consuming an excess of food at a given meal.

4. Do not eat late at night. After you have your evening meal, do not eat anything else. If you eat before bedtime, you will feel uncomfortable, and any excess fat will have a less likely chance of being burned.

5. Exercise regularly. Exercise helps you to improve your metabolism, as well as increase your energy. To keep track of your exercise routine, write down the time of day that you will exercise on your schedule.

6. Understand the role of protein tyrosine phosphates 1B, or PTP 1B, in leptin resistance. When PTP 1B is expressed to a high extent, it blocks the signaling of leptin. A possible way to overcome leptin resistance is to inhibit the PTP 1B. Talk to your doctor about the progress of this research.

7. Learn what is happening in your body. If you are leptin resistant, your own body is essentially sabotaging your efforts at weight control. In the first place, your brain is not receiving signals to cease eating when fat stores accumulate, and you’ll find yourself hungry despite knowing rationally that you should be full. To balance your body’s chemistry, you’ll need to regulate yourself mentally since your body can’t do it for you. This will take consistent determination and will power.

8. Exercise even when your body tells you to quit. When the body becomes leptin resistant, it becomes accustomed to high levels of the chemical in the blood. A little weight loss can trigger a decrease in leptin, making your appetite larger and affecting your metabolism negatively. Even though the body has plenty of fat stores to burn, the muscles cease to do so in response to decreasing leptin. You may not see results quickly because of this, and you may find yourself particularly exhausted by exercise. Do it anyway, because you can’t correct leptin resistance without reaching a healthy weight.

9. Take irvingia gabonensis supplements. Irvingia gabonensis is a plant species whose fruit has been shown in medical studies to correct leptin resistance. In fact, one study showed that individuals taking 150 mg of the supplement twice a day showed marked improvements in body composition after just 10 weeks. This natural supplement is not thought to have any side effects, although longitudinal studies are ongoing.

10. Work with a trainer or accountability partner. The hardest part of overcoming leptin resistance is that you go through the rigors of exercise and the self-discipline of a healthy diet without any encouragement from your body. You’ll probably feel tired and hungry on a frustratingly frequent basis. Until you have reached and maintained a healthy weight, though, your body will never regain the ability to function properly with regard to body composition. Having a consistent ally in your pursuit will help you stay strong in the lowest points when your brain is receiving signals to eat more and exercise less in response to decreasing leptin in the blood. The fight will be hard, but overcoming these signals will help you live a longer, more fulfilling life.

Let’s Connect!

Like me on Facebook

Twitter @drrenae

Contact Dr Norton by phone 513-205-6543 or by form

Inquire about booking Dr Norton for a speaking engagement

Read About Dr Norton

View video about Dr Norton

Medical Advice Disclaimer: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her healthcare provider to determine the appropriateness of the information for their own situation or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

© 2012, Dr J Renae Norton. This information is intellectual property of Dr J Renae Norton. Reproduction and distribution for educational purposes is permissible. Please credit ‘© 2012, Dr J Renae Norton. //edpro.wpengine.com’

Appetite Hormones 101: Leptin

This series is designed to explain the role of hormones on both appetite and body weight goals, whether it’s weight loss or weight restoration. “Appetite Hormones 101” will be made up of three articles that describe the major appetite hormones: leptin, ghrelin, and peptide YY.


Leptin, discovered by scientists in 1994, is also known as the “starvation hormone”. According to leptin expert, Dr Robert Lustig, leptin sends a signal to our brains that fat cells have enough stored energy to engage in normal metabolic processes. Every individual has an optimal level of leptin, which is thought to be determined genetically. When leptin levels are below optimal levels, the brain receives a message to conserve energy because the body is in a state of deprivation. When this occurs, the brain sends a message to the body that it is hungry (in an attempt to get the individual to eat) so that leptin levels can be restored to an optimal level.

Leptin levels are typically high in obese individuals and low in severely underweight/malnourished individuals. When leptin levels are too high, the individual experiences leptin resistance.

When an individual becomes leptin resistant, the body prevents leptin from passing through the blood brain barrier, which also prevents the brain from receiving the signal that leptin levels are at an optimal level. Instead, the brain senses that the body is in a state of starvation, and the individual becomes hungry. Leptin levels go up as a result.

High triglyceride levels also contribute to the prevention of leptin passing through the blood brain barrier. Triglyceride levels are often high in obese individuals as a result of poor dietary choices. In the individual with anorexia, triglyceride levels are often high because of liver damage and anorexia-induced hormone disruption.

If you think that you may be suffering from Leptin Resistance, there are several things that you can do.

  • Get plenty of sleep. Lack of sleep disrupts many hormonal processes, including leptin levels.
  • Avoid non-fruit sources of fructose. Studies show that fructose raises triglyceride levels, blocking leptin from crossing the blood brain barrier.
  • Avoid lectins, (carbohydrate-binding proteins that are found in most plants, particularly seeds and tubers such as cereal crops, potatoes, and beans) especially those from cereal grains (rice, wheat, barley, corn and oats) as they tend to bind to leptin receptors, preventing leptin binding. This intensifies the affect of leptin resistance.
  • Cook and supplement with healthy fats, like coconut oil. Coconut oil lowers triglyceride levels, increases metabolism, and promotes healing in the gut (and liver for those recovering from anorexia).
  • Eat a high protein, low carb diet and stay active! Diet and exercise have the greatest effect on overcoming leptin resistance.


BMC Endocrine Disorders – “Agrarian diet and diseases of affluence – Do evolutionary novel dietary lectins cause leptin resistance?” (//www.biomedcentral.com/1472-6823/5/10)

Mark’s Daily Apple – “A Primal Primer: Leptin” (//www.marksdailyapple.com/LEPTIN/)

The Fat Resistance Diet – “Leptin Resistance”

Live Strong – “High Cholesterol Levels in Anorexia” (//www.livestrong.com/article/86767-high-cholesterol-levels-anorexia/)

Medical Advice Disclaimer: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her healthcare provider to determine the appropriateness of the information for their own situation or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

© 2011, Dr J Renae Norton. This information is intellectual property of Dr J Renae Norton. Reproduction and distribution for educational purposes is permissible.

Please credit ‘© 2011, Dr J Renae Norton.