Obesity is a significant cause of morbidity and mortality worldwide. There has been a significant worsening of the obesity epidemic due to a symphony of factors that control hunger, fullness, and ultimately your weight. Did you know that sleep and the things you see online can greatly affect your eating patterns or behavior? Also involved in these complex processes are hormones, specifically leptin and ghrelin.
Ideally, these two hunger hormones work together to help keep you maintain a healthy weight. Unfortunately, most of us end up being overweight or obese. In fact, more than 1.9 billion adults were overweight and over 650 million were obese in 2016 (1). Who’s to blame? Is it our hormones? If yes, can you keep them in check?
To answer these questions, you first have to know how your hormones work.
What Is Ghrelin?
Ghrelin is produced in the gut. Most of us know it as the hunger hormone, but it is also sometimes referred to as lenomorelin. It stimulates hunger by traveling through your bloodstream and entering the brain to act on the neurons in your hypothalamus.
Its main function is to increase appetite. It prompts the brain 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. The higher your levels, the hungrier you get. It makes you eat more food, consume more calories and store fat (2, 3). It also affects your sleep-wake cycle, reward-seeking behavior, taste sensation, and carb metabolism (4, 5).
What Increases Ghrelin Levels?
Ghrelin levels normally increase before meals, during an empty stomach. Then they decrease shortly after, once you become full (6). You might think that obese people have higher ghrelin levels, but that isn’t always the case. They may just be more sensitive to the hormone’s effects. In fact, some studies show that their levels can be lower than in lean people (7, 8, 9). Other evidence even suggests that obese people have more active ghrelin receptors, GHS-R, which causes leads to increased calorie intake (10, 2).
But regardless of how much body fat you have, ghrelin levels will increase and make you feel hungry as soon as you start fasting. This is a natural body response that tries to protect you from starvation. During fasting, your “fullness hormone” called leptin decreases. Your metabolic rate also shoots down significantly, especially when devoid of calories for long periods of time (11, 12).
These adaptations aren’t easy, making it difficult to lose weight and keep it off. Your hormones and metabolism will always try to adjust to make up for all the weight you lost. What can be done then? Is there a way for you to lower your ghrelin levels?
How Can You Keep A Healthy Ghrelin Level?
Ghrelin cannot be controlled with medications, diets, or supplements. But there are things you can do to help keep a healthy level.
- Do Not Go to Extremes. It is not just obesity that alters ghrelin levels, anorexia too (13, 14)!
- Sleep Well. Lack of sleep can increase your ghrelin levels. It has been linked to increased hunger and weight gain (15, 16).
- Build More Muscles. Higher amounts of fat-free mass are associated with lower ghrelin levels (17, 18, 19).
- Consume More Protein. A high-protein diet can increase feelings of fullness. One reason behind this is the reduction in ghrelin levels (20).
- Keep A Stable Weight. Drastic weight changes and yo-yo dieting will disrupt key hormones like ghrelin (21).
- Cycle Your Calories. Periods of higher calorie intake can decrease hunger hormones and boost leptin levels. A 29-45% increase in your calorie intake for 2 weeks can help decrease ghrelin amounts by as much as 18% (22).
What Is Leptin?
Leptin is secreted mainly by white adipose tissue, and levels are positively correlated with the amount of body fat. Like many other hormones, leptin is secreted in a pulsatile fashion and has a significant diurnal variation with higher levels in the evening and early morning hours (23).
Leptin mediates its effects by binding to specific leptin receptors, ObRs, present in the brain as well as in peripheral tissues. The binding of leptin to the receptors activates several signal pathways that are important for the regulation of energy homeostasis, food intake, and glucose homeostasis (23). It also has many other functions related to fertility, immunity and brain function (25).
When you eat, your body fat goes up, leading your leptin levels to go up. Thus, you eat less and burn more. Conversely, when you don’t eat, your body fat goes down, leading your leptin levels to drop. At that point, you eat more and burn less.
This kind of system is known as a negative feedback loop and similar to the control mechanisms for many different physiological functions, such as breathing, body temperature, and blood pressure. It should keep you from starving or overeating. However, something is broken in the mechanism that is supposed to prevent us from overeating.
What is Leptin Resistance?
People who are overweight or obese have a lot of body fat in their fat cells. And since fat cells produce leptin in proportion to their sizes, obese patients are expected to have very high levels of leptin (26).
Given the way leptin is supposed to work, obese people should naturally be able to limit their food intake. Their brains should recognize that they have plenty of energy stored. However, in some people, leptin signaling does not work. While copious leptin is present, the brain doesn’t see it (27). This condition is known as leptin resistance, which is now believed to one of the main contributors to obesity (28).
When your brain doesn’t receive the leptin signal, it erroneously thinks that you are starving even if you have more than enough energy stored. This makes your brain change its behavior in order to regain body fat (29, 30, 31). Your brain then encourages you to eat more and reduce your energy expenditure by burning fewer calories at rest.
For most people who struggle with leptin resistance, willing yourself to overcome the leptin-driven starvation signal is next to impossible.
What Causes Leptin Resistance?
Several possible mechanisms have been identified (32, 33):
- Inflammation. Inflammatory signals in your brain, specifically in the hypothalamus, is an important cause of leptin resistance, both in animals and humans.
- Free Fatty Acids. High levels of free fatty acids in your bloodstream may increase fat metabolites in your brain and interfere with leptin signaling.
- High Leptin Levels. Elevated leptin levels in the first place seems to cause resistance.
Many of these factors are amplified by obesity. That means you can get trapped in a vicious cycle of gaining weight and becoming more resistant to leptin over time.
Can You Reverse Leptin Resistance?
If you have a lot of body fat, specifically in the belly area, you are most likely resistant to leptin. It is not entirely clear how resistance can be reversed, but some experts think that reducing diet-induced inflammation can be helpful. Focusing on an overall healthy lifestyle is also an effective strategy.
You can do the following:
- Avoid Processed Foods. Highly processed foods may compromise the health of your gut and induce inflammation (34).
- Eat Soluble Fiber. Consuming soluble fiber can help improve your gut health and prevent obesity (35).
- Be Active. Physical activity can help reverse leptin resistance (36).
- Sleep and Rest Well. Poor sleep is implicated in issues with leptin (37).
- Decrease Your Triglyceride Levels. High triglycerides can prevent the transportation of leptin from the circulation to your brain. You can decrease your triglyceride levels by decreasing your carb intake (38, 39).
- Consume More Protein. Eating more protein can cause automatic weight loss, which may result from an improvement in leptin sensitivity (40).
There isn’t a simple way to reverse leptin resistance. All you can do is make long-term lifestyle changes that will help improve the quality of your life overall.
What Are the Other Hormones That May Affect Your Weight?
1. Insulin
Who doesn’t know insulin? For sure, you have heard of it at least once, in relation to diabetes. This hormone is produced by the beta cells in the pancreas and is secreted in small amounts during the day and in larger amounts after eating.
Insulin allows your cells to take in blood sugar for energy or storage, depending on what you need. It is also the main fat storage hormone in the body. It tells fat cells to store fat and prevents stored fat from being broken down.
If your cells are insulin resistant, which is a common diagnosis, both blood sugar and insulin levels increase significantly. Chronically elevated insulin levels, a condition known as hyperinsulinemia, may cause several health problems, including obesity and metabolic syndrome (41, 42, 43).
Eating more sweets, which contain refined sugar, and processed foods like fast-food chains may drive insulin resistance and increase insulin levels (44, 45, 46).
Here’s how you can normalize your insulin levels and improve insulin sensitivity:
- Avoid or minimize sugar intake as fructose and sucrose increase insulin levels and promote insulin resistance
- Reduce your carb intake
- Fill up on protein to lose belly fat and eventually insulin resistance
- Eat healthy fats, specifically omega-3s, which are abundant in fish
- Exercise regularly
- Get enough magnesium through supplements to improve insulin sensitivity
- Drink green tea
2. Cortisol
The adrenal glands release more cortisol when your body senses stress. While this hormone is vital for survival, excessively high amounts of cortisol can cause overeating and weight gain (47).
A strict diet can also increase cortisol levels. Evidence showed that those who had low-calorie diets had greater amounts of cortisol levels as they seem to be more stressed than those who are eating normally (48).
There are ways to reduce your cortisol level:
- Follow a balanced diet
- Never cut calories to extremely low levels
- Relax by practicing yoga and meditation
- Listen to feel-good music
- Sleep more
3. Estrogen
Women know estrogen by heart. This hormone is mainly produced by the ovaries and is involved in regulating the female reproductive system and menstruation.
Did you know that both extremely high and low levels of estrogen can cause weight gain? This depends on your age, overall state of health, and the action of other hormones.
Estrogen starts promoting fat storage at puberty, in an attempt to maintain fertility during your childbearing years (49). Also, it can stimulate fat gain at the start of pregnancy.
Obese women have higher levels of estrogen levels than those with normal weight due to environmental influences (50).
At menopause, when estrogen levels start to drop because less is being produced in the ovaries, the site for fat storage shifts from the hips and thighs to the abdomen. This will promote insulin resistance and increase disease risks (51, 52).
To help you manage your estrogen levels, follow these nutrition and lifestyle strategies:
- Eat more fiber to reduce estrogen levels
- Consume more cruciferous vegetables
- Take flax seeds, which are known to have beneficial effects on estrogen in many women (53, 54)
- Exercise regularly because physical activity is known to be helpful normalize estrogen levels in both premenopausal and postmenopausal women (55, 56)
4. Neuropeptide Y (NPY)
Neuropeptide Y (NPY) is a hormone produced by cells in the brain and nervous system. It stimulates appetite, especially for carbs, and is highest during periods of fasting or food deprivation (57, 58, 59).
Levels of NPY may also increase during of stress, which can lead to overeating and abdominal fat gain (60, 61, 62).
You can follow these recommendations to lower your NPY levels:
- Eat enough protein
- Don’t fast for too long because very long fasts, such as over 24 hours, can dramatically increase NPY levels (63, 64).
- Eat more soluble fiber to feed the friendly gut bacteria and help reduce NPY levels
5. Glucagon-Like Peptide-1 (GLP-1)
Glucagon-like peptide-1 (GLP-1) is a hormone produced in your gut in response to meal intake. The main actions of GLP-1 are to stimulate insulin secretion and inhibit glucagon secretion, thus playing a huge role in keeping blood sugar levels stable. It also makes you feel full.
Evidence showed that the decrease in appetite that occurs immediately after a weight loss surgery is also brought about by the increased production of GLP-1 (65). Another study showed that taking a GLP-1 solution with breakfast can make you feel more satisfied and eat 12% fewer calories at lunch (66).
Here are a few suggestions on how you can increase your GLP-1 levels:
- Eat high-protein foods like fish, whey protein and yogurt
- Consume anti-inflammatory foods
- Leafy greens like spinach and kale can help you increase your GLP-1 levels and lose more weight
- Take probiotics, which can help reduce your food intake
6. Cholecystokinin (CCK)
Cholecystokinin (CCK) is a peptide hormone linked to the gastrointestinal (GI) system. The receptors are expressed in the central nervous system, specifically in the hippocampus, cerebral cortex, and striatum. Levels of CCK-producing neurons in the brain are low at birth but steadily increase into adulthood. Like GLP-1, cholecystokinin (CCK) is also a satiety hormone (67).
Higher amounts of CCK have been shown to reduce food intake in both lean and obese people (68, 69, 70).
You can increase your CCK levels by:
- Eat plenty of protein and fiber at every meal
- Consuming more fat to trigger the release of CCK
7. Peptide YY (PYY)
The gut hormone peptide YY (PYY) is an amino acid peptide that is produced from specialized L-cells found predominantly within the distal GI tract. It is released from the gut into the circulation in a nutrient-dependent manner. It can control appetite. It is believed to play a major role in reducing food intake and decreasing your risk of obesity (71, 72).
To increase your PYY levels, you should:
- Eat a low-carb diet as elevated blood sugar may impair PYY’s effects (73, 74)
- Consume more protein from either animal or plant sources
- Take plenty of fiber
Key Takeaway
Your hormones are designed to work together to help increase or decrease your appetite and fat storage. Unfortunately, if the system does not work well, you may find yourself struggling with weight problems long-term.
Luckily, diet and lifestyle changes have powerful effects on our hormones. Keep in mind the above-mentioned tips to maintain a healthy weight.
References:
(1) https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
(2) https://www.ncbi.nlm.nih.gov/pubmed/17212793
(3) https://www.ncbi.nlm.nih.gov/pubmed/26042199
(4) https://www.ncbi.nlm.nih.gov/pubmed/17212793
(5) https://www.ncbi.nlm.nih.gov/pubmed/26042199
(6) https://www.ncbi.nlm.nih.gov/pubmed/11473029
(7) https://www.ncbi.nlm.nih.gov/pubmed/12625808
(8) https://www.ncbi.nlm.nih.gov/pubmed/15768041
(9) https://www.ncbi.nlm.nih.gov/pubmed/11289032
(10) https://www.ncbi.nlm.nih.gov/pubmed/15917842
(11) https://www.ncbi.nlm.nih.gov/pubmed/11126336
(12) https://www.ncbi.nlm.nih.gov/pubmed/9024254
(13) https://www.ncbi.nlm.nih.gov/pubmed/21453750
(14) http://europepmc.org/article/med/15771315
(15) https://www.ncbi.nlm.nih.gov/pubmed/15602591
(16) https://www.ncbi.nlm.nih.gov/pubmed/15583226
(17) https://www.ncbi.nlm.nih.gov/pubmed/12466337
(18) https://www.ncbi.nlm.nih.gov/pubmed/12519848
(19) https://www.ncbi.nlm.nih.gov/pubmed/16819531
(20) https://www.ncbi.nlm.nih.gov/pubmed/22178258
(21) https://www.ncbi.nlm.nih.gov/pubmed/20417876
(22) https://www.ncbi.nlm.nih.gov/pubmed/15079159
(23) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829242/
(24) http://joe.endocrinology-journals.org/content/223/1/T25.long
(25) https://www.sciencedirect.com/science/article/pii/S1550413113002003
(26) https://www.ncbi.nlm.nih.gov/pubmed/8532024/
(27) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3281561/
(28) https://www.ncbi.nlm.nih.gov/pubmed/23359004
(29) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104762/
(30) https://www.ncbi.nlm.nih.gov/pubmed/10215564
(31) https://onlinelibrary.wiley.com/doi/10.1046/j.1365-2281.1998.00129.x/full
(32) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248304/
(33) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319208/
(34) https://www.ncbi.nlm.nih.gov/pubmed/19755625
(35) https://www.ncbi.nlm.nih.gov/pubmed/18031592
(36) https://www.ncbi.nlm.nih.gov/pubmed/18031592
(37) https://www.ncbi.nlm.nih.gov/pubmed/15531540
(38) https://www.ncbi.nlm.nih.gov/pubmed/15111494
(39) http://www.nejm.org/doi/full/10.1056/NEJMoa022637
(40) https://www.ncbi.nlm.nih.gov/pubmed/16002798
(41) https://www.ncbi.nlm.nih.gov/pubmed/15314628
(42) http://diabesity.ejournals.ca/index.php/diabesity/article/viewFile/19/61
(43) https://www.ncbi.nlm.nih.gov/pubmed/18227495
(44) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2707514/
(45) https://www.ncbi.nlm.nih.gov/pubmed/16166564
(46) https://www.ncbi.nlm.nih.gov/pubmed/20547978
(47) https://www.ncbi.nlm.nih.gov/pubmed/11070333
(48) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895000/
(49) https://www.ncbi.nlm.nih.gov/pubmed/15070958
(50) https://www.ncbi.nlm.nih.gov/pubmed/24915457
(51) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964739/
(52) https://www.ncbi.nlm.nih.gov/pubmed/9929857
(53) https://www.ncbi.nlm.nih.gov/pubmed/14749240
(54) https://www.ncbi.nlm.nih.gov/pubmed/20347861
(55) https://www.ncbi.nlm.nih.gov/pubmed/21903887
(56) https://www.ncbi.nlm.nih.gov/pubmed/22614972
(57) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1642692/
(58) https://www.ncbi.nlm.nih.gov/pubmed/21439311
(59) https://www.ncbi.nlm.nih.gov/pubmed/19515905
(60) https://www.ncbi.nlm.nih.gov/pubmed/19515905
(61) https://www.ncbi.nlm.nih.gov/pubmed/17603492
(62) https://www.ncbi.nlm.nih.gov/pubmed/25061562
(63) https://www.ncbi.nlm.nih.gov/pubmed/10102700
(64) https://www.ncbi.nlm.nih.gov/pubmed/7683962
(65) https://www.ncbi.nlm.nih.gov/pubmed/25673670
(66) https://www.ncbi.nlm.nih.gov/pubmed/9449682
(67) https://www.ncbi.nlm.nih.gov/pubmed/16246215
(68) https://www.ncbi.nlm.nih.gov/pubmed/6294699
(69) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382399/
(70) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302146/
(71) https://www.ncbi.nlm.nih.gov/pubmed/22375166
(72) https://www.ncbi.nlm.nih.gov/pubmed/19064614
(73) https://www.ncbi.nlm.nih.gov/pubmed/25661189
(74) https://www.ncbi.nlm.nih.gov/pubmed/24302008