11 Powerful Hormones for Effective Weight Loss

Weight Loss | Hormones | Insulin | Glucagon | Ghrelin | Leptin | Cortisol

They regulate metabolism, appetite, and fat storage. Yet, hormones don’t play a minor role in weight loss in today’s conventional fitness industry.

Learn why hormones induce weight loss and how your lifestyle can balance them naturally.

How Do Hormones Affect Weight Loss?

If you put too many pounds on the scales, you overeat and do not exercise enough. Surprisingly, this is still the general view on weight gain today.

But are we just too lazy? After all, people have never been so obsessed with living as healthy as they are today.

Do we move too little on average today to lose weight, as most family doctors would have us believe?

Do billions of people voluntarily decide to overeat every day?

If people answer these questions with yes, they probably did their math without the hormones involved in weight loss.

Can Hormones Prevent Weight Loss?

Hormones are chemical messengers that give crucial signals for regulating hunger, satiety, thirst, body temperature, or even weight (Starka et al. 2020¹).

With the help of the hypothalamus, a control center in your brain, the hormone balance is significantly involved in keeping bodily functions in a healthy equilibrium.

This principle of homeostasis also applies to essential metabolic processes. Hence, losing weight is hard once your hormones are out of balance.

Hormones decide whether you store or use energy, whether you are hungry or satiated, and how fat or muscle mass is distributed around the body.

It’s not due to a mere lack of willpower that more than 75% of adults in the U.S. are already overweight or obese (CDC 2012²).

If your hormonal balance is set incorrectly, you will not lose weight no matter how much you restrain yourself from eating or exercising several times a week.

Therefore, pediatric endocrinologist Dr. Robert Lustig concludes that the obesity epidemic is due to a hormonal imbalance, not a caloric one.

The hormonal system has the primary role in developing obesity, even though the cultural changes of the last half-century initiated it (Lustig 2001³).

And this Western lifestyle has long ceased to be a purely American issue but rather a global one.

Why Calorie Counting Does Not Work

Hormones are the missing piece of why eating less and exercising more has not inevitably led to success.

Because of the varying impact of foods on hormone balance, a calorie is not always a calorie.

Hence, according to a British study, 99.5% of 99,791 overweight women and 76,704 overweight men could not lose weight successfully through a classic calorie deficit (Fildes et al. 2015⁴).

Our body is not a combustion engine that runs equally well on any fuel source, no matter how dirty. Instead, its life expectancy depends on the quality of food.

So why is calorie counting still the standard of the fitness industry?

Because this allows industrially produced foods such as protein bars or vegan butter to sell first-class. Moreover, this fake food is shelf-stable for almost forever.

The ongoing obesity pandemic is a composition of increasingly stressful lives and the industrialization of food.

Eating less and exercising more is not a good recipe for this toxic lifestyle. You may lose weight with it in the short term, but whether it is body fat that you are losing is determined by your hormones.

A study conducted on participants in the weight-loss TV series The Biggest Loser shows that people cannot lose weight sustainably with calorie reduction and exercise if hormones are left out of the equation.

Thus, the participants who lost the most weight through calorie restriction still suffered from an overwhelmingly reduced basal metabolic rate six years later (Fothergill et al. 2016⁵).

Because of this yo-yo effect, conventional dieting does not work. The reason is the hormones involved in weight loss, first and foremost, our fat-storage hormone.

When small meals stimulate insulin, you can’t break down body fat, and the body burns lean mass instead. Let’s have a look at how this hormone works.

How to Balance Your Weight Loss Hormones

Here are the 11 most important hormones that can help you lose weight. I’ve derived simple but science-backed tips to help you get these hormones back in check.

1. Insulin

The most important hormone when it comes to weight loss is insulin. Most people have heard of insulin and immediately associate it with diabetes.

That’s because regulating blood glucose levels is a crucial job of this hormone. After an excess of sugar molecules in the blood is harmful, the body strives to control the amount of sugar (glucose).

The fastest way to rid the blood of glucose is to transport it into the cells, which are used as energy or stored as fat.

And it is precisely this regulation of glucose amount in the blood that insulin is responsible for at any given time.

Accordingly, insulin plays an essential role in supplying energy to cells. On the other hand, it is also our primary storage hormone.

Finally, insulin also signals fat cells to take up excess energy.

In addition, the fat-storage hormone has a so-called antilipolytic effect (Jensen et al. 1989⁶).

Hence, it prevents fat breakdown by enzymes (lipolysis) and, in return, promotes fat build-up (Meijssen et al. 2001⁷).

In short, high insulin levels prevent fat burning.

Since insulin regulates blood glucose, it is only legitimate that its presence blocks energy use from fat stores.

Accordingly, when you supply adequate glucose by eating carbohydrates, insulin does a first-rate job of consuming that energy.

However, if too much glucose enters the bloodstream due to high carbohydrate consumption, insulin ensures that the excess energy is stored in fat cells (Muretta et al. 2009⁸).

How to Lower Insulin Levels

Low-Carb: The main trigger for insulin production is a high blood glucose level. Therefore, reducing carbohydrates is the most obvious way to keep insulin levels low (Gower et al. 2015⁹).

Fructose: A randomized controlled trial from Switzerland shows that even small amounts of the sweet molecule in sugar cause insulin resistance and fat production in the liver of healthy young men (Aeberli et la. 2013¹⁰).

Healthy fats: Unlike carbohydrates and proteins, healthy fats do not significantly increase insulin levels (Nuttall et al. 1991¹¹). In addition, research shows that omega-3 fatty acids can improve insulin sensitivity. As a result, blood glucose can be broken down more efficiently (Ramel et al. 2008¹²). Therefore, a low-carb, high-fat (LCHF) diet such as the keto diet is ideal for lowering insulin levels.

Fasting: The most effective way to reduce high levels of insulin is to refrain from food. In addition, intermittent fasting can burn visceral (organ) fat even more effectively than low-carb diets (Catenacci et al. 2016¹³).

Exercise: Last but not least, physical activity helps lower blood glucose. Exercise helps improve insulin action and, thus, glucose consumption (Richter et al. 2013¹⁴). When blood glucose levels drop, insulin levels can also recover.

2. Glucagon

In the context of blood glucose, there exists another player besides insulin that you need to get to know. In short, glucagon is the antagonist of insulin.

While insulin is released by increasing blood sugar, your body releases glucagon when the blood sugar gets too low.

Therefore, glucagon pursues the same goal as insulin: it wants to keep blood sugar in balance. Both hormones thus target what is known as blood glucose homeostasis.

Consequently, it is hardly surprising that glucagon is also produced in the pancreas. In contrast to insulin, secretion occurs through alpha instead of beta cells.

Unlike insulin, which lowers a high blood glucose level, glucagon raises a low blood glucose level (Keller et al. 1983¹⁵).

For this purpose, two mechanisms exist in the body:

• On the one hand, glucagon can stimulate the liver to break down glucose from carbohydrate stores (glycogen).
• On the other hand, glucagon can signal fat cells to release stored fat.

In summary, glucagon is a hormone that mobilizes stored energy and stimulates sugar and fat burning. On the other hand, its counterpart, insulin, stores energy, and blocks fat burning.

How to Increase Glucagon

Fasting: While insulin levels decreased, in one study, glucagon levels doubled on the third day of fasting and slowly fell over the following six weeks, always remaining above baseline (Marliss et al. 1970¹⁶).

Low-carb: While high-carbohydrate foods elevate insulin levels, a low-carbohydrate diet can lower them and boost glucagon release.

Protein: Both animal and plant protein sources have been shown to boost glucagon production and lower the ratio of insulin to glucagon (Claessens et al. 2008¹⁷).

3. Ghrelin

After the hormone that stores energy in your body and its counterpart, we now turn to the one that initiates energy intake.

Consequently, ghrelin is better known as the hunger hormone. Moreover, ghrelin is the only messenger outside the central nervous system that triggers appetite.

The body releases ghrelin in response to an empty stomach to tell you to eat again in a short time (Klok et al. 2007¹⁸).

For this reason, also the reward center in the brain is stimulated to make food more interesting to you (Müller et al. 2015¹⁹).

After a meal, on the other hand, ghrelin levels are low. After the stomach is full, there is no more purpose for food intake.

Studies show that ghrelin levels do not always decrease as they should after a meal in overweight people. Because they continue to feel hungry, these people risk overeating (Klok et al. 2007²⁰).

Consequently, dysfunction of ghrelin balance can lead to weight gain. Conversely, ghrelin production must be functioning for you to lose weight.

How to Regulate Your Ghrelin Balance

Protein: according to an Oxford study that compared eating a high-protein meal with a high-carbohydrate meal, protein consumption can significantly lower ghrelin levels in the body (Blom et al. 2006²¹).

Fructose: The fruit sugar is often marketed as healthy, which it is not. Fructose is the sweet molecule besides glucose in conventional sugar. Metabolic researchers have found that diets high in fructose can increase ghrelin levels and cause obesity (Teff et al. 2004²²).

Medication: Although ghrelin makes you hungry, you should not consider taking ghrelin blockers. Ghrelin is also crucial for learning, memory, gastric acid secretion, sleep-wake rhythm, or reward behavior and should not be artificially affected (Müller et al. 2015²³).

4. Leptin

Leptin is the counterpart of the hunger hormone ghrelin. Accordingly, it is also known as the satiety hormone.

Like insulin and glucagon, which regulate their build-up and breakdown, leptin also has to do with fat cells.

However, in the case of leptin, it is the fat cells that secret the hormone and help you lose weight.

When you eat, and your fat cells determine that enough energy has been supplied, they release leptin as a signal to your brain to stop eating.

If your leptin levels are low, on the other hand, your brain receives the message that fat stores are empty, which in turn triggers feelings of hunger (Friedman et al. 1998²⁴).

Consequently, leptin is responsible for regulating the total amount of stored energy in the body.

When signaling to regulate body fat ceases to function correctly, the condition is leptin resistance.

In essence, leptin resistance develops similarly to insulin resistance, which is why these metabolic disorders often occur together (Martin et al. 2008²⁵).

Dr. Robert Lustig further concludes hyperinsulinemia is the indirect cause of leptin resistance (Lustig et al. 2004²⁶).

When the body is constantly flooded with vast hormone amounts, sensitivity to the hormonal signal decreases.

In short, with leptin resistance, your brain takes longer to realize that you are already full.

The result can be overeating, weight gain, obesity, and other metabolic disorders (Myers et al. 2010²⁷).

The more you eat the wrong foods, the worse leptin resistance (and insulin resistance) can become.

So here are the most effective tips to achieve healthy leptin levels.

How to Regulate Your Leptin Balance

Low-carb: Carbohydrates – especially refined carbohydrates like sugar – can turn off leptin receptors in the brain, so you need longer or higher levels of leptin to feel full (Shapiro et al. 2008²⁸).

Healthy fats: In contrast to the excessive consumption of carbohydrates, studies have shown that fat does not lead to leptin resistance (Dirlewanger et al. 2000²⁹). Since fat increases satiety but not insulin levels, a low-carb, high-fat diet such as the keto diet is ideal for weight loss.

Fructose: Fructose is not only a liver toxin like alcohol but also more dangerous than other carbohydrates in developing leptin resistance and obesity (Shapiro et al. 2008³⁰). Therefore, it is advisable to avoid high-fructose corn syrup, agave syrup, and large amounts of fruit sugar in general.

Sleep: If you’ve ever heard that sleep is essential for losing weight, here comes the scientific confirmation. Researchers have shown that shorter sleep results in lower levels of the satiety hormone in the body (Spiegel et al. 2004³¹).

Exercise: Although the effect of exercise on weight loss tends to be overestimated, it can help increase leptin sensitivity (and insulin sensitivity) and thereby increase the perception of satiety (Kang et al. 2013³²).

5. Cholecystokinin (CCK)

The next in a series of satiety hormones is cholecystokinin (CCK). It is secreted by cells in the intestine in response to a meal.

CCK is the first gut hormone known to affect appetite (Gibbs et al. 1973³³). In this regard, it is closely related to the primary satiety hormone leptin.

On the one hand, CCK promotes leptin secretion (Konturek et al. 2001³⁴). On the other hand, leptin enhances CCK-induced satiety (Peters et al. 2006³⁵).

An elevated level of CCK can be detected in the human body approximately 15 minutes after eating (Liddle et al. 1985³⁶)

In addition to satiety, cholecystokinin also plays an essential role in the following processes in the body (Okonkwo et al. 2021³⁷):

• Inhibition of gastric acid secretion and release of digestive enzymes
• Contraction of the gallbladder and regulation of bile acid
• Regulation of gastric emptying
• Energy production, protein synthesis, and cell growth

Our bodies produce CCK when we consume protein or fat (Dockray et al. 2012³⁸). As a result, food intake and, in particular, our cravings for sugar and carbohydrates are reduced (Lieverse et al. 1995³⁹).

Recent research suggests that obese people develop a type of CCK resistance. Reduced sensitivity to the hormone makes them more likely to overeat, which may contribute to the progression of CCK resistance (Cawthon et al. 2021⁴⁰).

How to Promote Satiety Through Healthy CCK Levels

Healthy fats: Consuming natural fats in the form of pastured butter, extra virgin olive oil, or fattier cuts of meat supports CCK production, keeping you fuller longer (Dockray et al. 2012⁴¹).

Protein: One study found that a high-protein diet, as opposed to a high-carbohydrate diet, can help increase CCK levels and thus satiety (Chungchunlam et al. 2015⁴²).

Exercise: Although research is severely limited, there is evidence that high-intensity interval training (HIIT) or the combination of aerobic and strength training may increase CCK levels (Zouhal et al. 2019⁴³).

6. Glucagon-Like Peptide-1 (GLP-1).

The incretin and satiety hormone glucagon-like peptide-1 (GLP-1) is also secreted in the gut in response to nutrient absorption.

Its main functions are to keep blood glucose levels stable and produce a feeling of satiety (Müller et al. 2019⁴⁴).

This hormone could also help weight loss reduce body mass index (BMI) and waist circumference in overweight adults (Zhang et al. 2015⁴⁵).

Moreover, researchers explain the reduced hunger and increased satiety after gastric bypass surgery by an increased GLP-1 response to food intake (Morinigo et al. 2006⁴⁶).

The beneficial effects of GLP-1 make this hormone an exciting candidate for the treatment of obesity, diabetes, and neurodegenerative diseases (Müller et al. 2019⁴⁷).

Research suggests that people with obesity may experience problems with GLP-1 signaling (Anandhakrishnan et al. 2016⁴⁸).

As with the other hormones for weight loss, this suggests a possible type of GLP-1 resistance. This decreasing GLP-1 sensitivity may also explain the elevated fasted plasma GLP-1 levels in obese children and adults (Stinson et al. 2021⁴⁹).

How to Balance GLP-1 Levels Naturally

Healthy fats: In numerous studies in humans and animals, the monounsaturated fatty acids from virgin olive oil were able to increase both GLP-1 levels and insulin sensitivity (Bodnaruc et al. 2016⁵⁰). This combined hormone effect is ideal for weight loss.

Protein: Protein-rich foods increase GLP-1 levels (Gillespie et al. 2015⁵¹). In particular, collagen, the essential protein for skin, hair, bones, and joints, has increased satiety via GLP-1 (Rubio et al. 200852).

Inflammation: Eat more anti-inflammatory foods and avoid consuming pro-inflammatory foods, such as refined carbohydrates and industrial seed oils. Inflammation, which often accompanies obesity, inhibits the release of GLP-1 in the body (Gagnon et al. 2015⁵³).

7. Peptide YY (PYY)

Along with GLP-1, peptide YY (PYY) is produced in the gut after eating. Here, the amount secreted is proportional to the fat ingested with food (Pironi et al. 1993⁵⁴).

It enters the hypothalamus in the brain via the bloodstream, reducing appetite (Wu et al. 2019⁵⁵).

According to studies, individuals with obesity exhibited attenuated peptide YY responses after eating, leading to uncontrolled overeating (Zwirska-Korczala et al. 2007⁵⁶).

Therefore, adequate levels are thought to play an essential role in reducing increased food intake, especially after extensive exercise (Zouhal et al. 2019⁵⁷).

In addition, researchers at Oxford have found that obese individuals do not have elevated fasting PYY levels, but chronic overeating does.

Hence, this again suggests a protective mechanism against excessive food intake and other weight loss hormones (Cahill et al. 2011⁵⁸).

How to Promote a Vital PYY Response

Protein: According to studies, high-protein meals initiate the most significant increase in PYY, followed by high-fat meals (Lomenick et al. 2009⁵⁹).

Low-carb: Not only do high-carbohydrate meals stimulate PYY the least, but PYY levels decrease more rapidly after high-carbohydrate meals, whereas PYY continues to rise for hours after high-fat and high-protein meals (Lomenick et al. 2009⁶⁰). That could be one reason for not staying full for long after a high-carbohydrate meal.

Healthy fats: PYY release increases proportionally with the number of fatty acids ingested with food (Pironi et al. 1993⁶¹). Therefore, a ketogenic diet rich in healthy fats is also promising regarding PYY balance.

Exercise: According to studies, training has limited positive effects on PYY production. While individuals with average weight can increase their PYY levels with exercise, overweight individuals achieved this result only with long-term training for at least 32 weeks (Jones et al. 2009⁶²).

8. Neuropeptide Y (NPY)

Neuropeptide Y or NPY is the most abundant peptide in the central nervous system. It is primarily found in the brain (hypothalamus) and is both a hormone and a neurotransmitter.

NPY and PYY are important brain-gut peptides. Therefore, their actions are closely related to appetite regulation and the development of obesity (Wu et al. 2019⁶³).

Moreover, NPY is considered the most potent appetite-stimulating compound in the human body.

Every other hunger or satiety hormone regulates food intake by acting on NPY in the hypothalamus. While leptin suppresses NPY activity, ghrelin stimulates it.

Accordingly, elevated NPY increases food cravings, predominantly carbohydrates (Beck 2006⁶⁴).

In addition to hunger, NPY stimulates fat storage and weight gain via the central nervous system while decreasing sex drive, locomotion, energy expenditure, and body temperature (Minor et al. 2009⁶⁵).

In addition, stress leads to increased NPY levels in fat cells, which contributes to abdominal fat storage in particular (Kuo et al. 2007⁶⁶).

However, elevated NPY levels make sense as a stress response because NPY has stress-reducing, anxiety-relieving, and neuroprotective properties, according to researchers at the University of Graz, Austria (Reichmann et al. 2016⁶⁷).

You may have also heard that researchers have found that a wide variety of living things can live at least 33% longer if they eat less (McDonald et al. 2010⁶⁸).

Because NPY acts as the primary hunger signal in this context, researchers now suspect it plays an essential role in extending lifespan (Minor et al. 2009⁶⁹).

How to Curb Cravings Through NPY

Healthy fats: Although NPY makes you hungrier for carbohydrates, eating fats more strongly inhibits NPY activity, reducing this appetite more effectively (Beck 2006⁷⁰).

Proteins: Researchers at Oxford found in animal studies that reducing protein in the diet caused a more significant release of NPY and more body fat (White et al. 1994⁷¹).

Exercise: Recent studies suggest that NPY balance cannot be affected by intense training to the extent that weight loss may result (Khajehnasiri et al. 2019⁷²; Benite-Ribeiro et al. 2016⁷³). Therefore, the effects of exercise on this hormone for weight loss are again minimal.

9. Cortisol

The adrenal glands secrete cortisol in response to stress. Accordingly, cortisol is considered a stress hormone.

Cortisol is essential to prepare the body for fight or flight.

Therefore, the standard repertoire of physiological responses to stressful situations that cortisol initiates is called the fight-or-flight response.

After cortisol is released, it immediately increases blood sugar. For this reason, stress can trigger cravings for sweets  (Epel et al. 2001⁷⁴).

The mobilized energy aims to strengthen muscles and eventually escape the stressor and survive (Owen et. al 1973⁷⁵).

This response to acute stress was essential for survival during evolution. However, with chronic stress, cortisol can have instead harmful effects.

Due to psychological stress, blood glucose levels can remain high for months, stimulating insulin release. Accordingly, studies show that persistently high cortisol levels lead to significantly elevated insulin levels (Whitworth et al. 1994⁷⁶).

And the storage hormone is known to be a primary contributor to obesity. Thus, psychological stress increases body mass index and abdominal fat in the long run (Rosmond et al. 1998⁷⁷).

In addition, researchers have found that an enzyme that can reactivate inactive cortisol (cortisone) is increased in the abdominal fat of obese individuals (Ayachi et al. 2006⁷⁸).

As a result of cortisol reactivation, BMI, obesity around the middle, and associated disease risks increase (Rask et al 2002⁷⁹).

If you can keep stress responses in check, cortisol balance will be as well. However, this is not an easy procedure in everyday life. Ultimately, you cannot avoid all the stress factors.

Therefore, specific methods have evolved to help manage stress better.

How to Lower Cortisol Levels

Sleep: Deep, healthy sleep for just one or two nights can better affect cortisol levels than months of stress management seminars. One night without sleep is enough to double your cortisol levels (Joo et al. 2012⁸⁰).

Exercise: Movement can improve the whole body’s response to stress in the long run. Because it can lower cortisol levels, blood pressure, and blood sugar, yoga is an effective stress reduction exercise (Pascoe et al. 2017⁸¹).

Meditation: In addition to yoga, meditation is another mindfulness-based stress management strategy that can benefit severely stressed individuals in particular (Klimes-Dougan et al. 2019⁸²).

10. Estrogen

Estrogen is the primary sex hormone in women. Nevertheless, estrogen is also naturally present in male bodies, but not in high amounts.

In addition to its primary function in reproduction in the female body and regulating sex drive in both sexes, the hormone also plays a role in fat distribution.

However, the reduction of estrogen levels does not lead to weight loss. Menopausal women gain abdominal fat despite lower estrogen levels (Lovejoy 1998⁸³).

For this reason, estrogen levels are a sensitive issue. They must be regulated carefully since neither too high nor too low will help you lose weight.

In addition to hormonal changes during the life cycle, lifestyle factors can help keep estrogen levels balanced.

How to Balance Estrogen Levels Naturally:

Low-Carb: Our high-carbohydrate Western diet drives insulin levels, which lowers sex hormone-binding globulin (SHBG), another hormone (Daka et al. 2013⁸⁴). SHBG binds estrogen in the blood, keeping it in balance.

Sports: The right balance is also crucial when exercising. Too much exercise can cause a drop in estrogen, leading to the absence of the menstrual cycle. On the other hand, appropriate exercise can lower elevated estrogen levels enough to positively affect women at risk for breast cancer (Kossman et al. 2011⁸⁵).

Personal care: Many personal care products contain xenoestrogens, chemicals that can mimic estrogen in your body. They can bind to estrogen receptors and activate them, upsetting the hormonal system (Singleton et al. 2003⁸⁶).

Plastic: Chemicals in plastic containers have estrogen-like effects on the body. Therefore, it is vital to avoid plastic to keep your estrogen levels in check (Yang et al. 2011⁸⁷).

11. Testosterone

Many think estrogen and testosterone are mortal enemies, constantly waging a fierce hormone war.

Some women even fear that weight training and eating meat could cause increased testosterone levels and result in an overly masculine appearance.

On the other hand, few people know that testosterone also performs essential tasks in the female body. For example, testosterone is instrumental in estrogen production, which is why a deficiency affects it.

Consequently, a certain hormonal balance of testosterone is essential for both men and women, even if it does not occur to the same extent in the sexes.

A healthy testosterone level positively contributes significantly to the following aspects of the human body (Tyagi et al. 2017⁸⁸):

• Mood
• Libido
• Muscle mass
• Bone density
• Body fat distribution

Accordingly, testosterone is a hormone that plays an essential role in weight loss. Therefore, it is also referred to as a fat-reducing hormone (De Pergola 2000⁸⁹).

However, compared to women, the consequences of impaired testosterone balance can be more severe in men.

Therefore, researchers even conclude that increased testosterone in men results in abdominal fat loss (Rebuffe-Scrive et al. 1991⁹⁰).

If testosterone levels drop significantly in men, estrogen balance is compromised. As a result, fatty tissue may grow on the chest (Swerdloff et al. 2019⁹¹).

How to Balance Testosterone Levels Naturally

Fasting: A study of 42 men found a significant increase in testosterone levels and reduced body fat after only eight weeks of 16/8 intermittent fasting (Moro et al. 2016⁹²).

Low-Carb: A high-carbohydrate diet decreases insulin sensitivity and testosterone release (Pitteloud et al. 2005⁹³). Simple glucose consumption lowers testosterone levels in men by about 25% over several hours (Caronia et al. 2013⁹⁴).

Fructose: Fructose (e.g., from sugar, smoothies, juices) is converted to fat by the liver, which lowers sex hormone-binding globulin (SHBG) in the blood, which keeps testosterone (and estrogen) at healthy levels (CFRI 2007⁹⁵).

Exercise: While intense endurance training lowers testosterone levels, weight training helps increase them significantly (Anderson et al. 2016⁹⁶; Timon Andrada et al. 2007⁹⁷).

Sleep: Even a single week of inadequate sleep (less than 5 hours) can decrease testosterone production by more than 10% (Leproult et al. 2011⁹⁸).

Balance Hormones for Weight Loss Through Diet

Hormones are the key to sustainable weight loss. Fortunately, a simple lifestyle can balance them naturally.

For example, intermittent fasting combined with low-carb is the most effective to minimize fat storage and maximize fat burning (Catenacci et al. 2016⁹⁹).

In my new book, Intermittent Fasting 101: The Science-Backed Beginner’s Guide to Lose Weight Without Dieting and Working Out, you can learn how this works.

On the other hand, healthy fats and proteins help your hormones stimulate satiety and curb appetite in the long term (Lomenick et al. 2009¹⁰⁰).

However, you should avoid one substance, mainly because it fuels cravings. We are talking about fructose, the supposedly healthy fruit sugar.

Fructose is not only the sweet molecule in table sugar but also a liver toxin like alcohol, causing the same adverse health effects (Lustig 2013¹⁰¹).

Because fructose promotes leptin and insulin resistance, it sets in motion a vicious cycle that ultimately paves the way to type 2 diabetes via fatty liver (Tappy and Lê 2010¹⁰²).

In short, fructose makes obese individuals feel like they are starving while carrying hundreds of thousands of calories of energy reserves.

While training can positively impact some hormonal balances, compensatory appetite often overshadows these benefits (Zouhal et al. 2019¹⁰³).

Thus, exercise is not the Swiss Army knife of weight loss marketed to us.

Last but not least, lack of sleep and psychological stress are other lifestyle factors that can prevent (abdominal) weight loss via hormones (Rosmond et al. 1998¹⁰⁴).

In summary, a ketogenic diet low in carbohydrates and high in healthy fats is ideal for setting hormone balance up for fat burning and satiety (Nuttall et al. 2016¹⁰⁵).

The pleasant side effect prevents modern diseases such as diabetes and cancer (Orgel et al. 2014¹⁰⁶).

Learn how to balance weight loss hormones naturally in my new book: Intermittent Fasting 16/8 for Women: Achieve Hormone Harmony to Lose Weight Fast Without Losing Your Mind – Incl. 30-Day Fasting Challenge and Meal Plan.

How to Balance Weight Loss Hormones FAQ

Which hormone helps you lose weight?

The most critical hormones in weight loss are insulin and leptin. While leptin helps you lose weight by promoting satiety, insulin promotes fat storage instead.

How do I balance my hormones to lose weight?

You can best balance hormones naturally for weight loss through intermittent fasting and a ketogenic diet.

What hormones can cause weight loss?

Storage, satiety, stress, and sex hormones affect weight loss. While leptin, glucagon, CCK, and peptide YY support weight loss, insulin, ghrelin, and neuropeptide Y can prevent weight loss.

What are the 6 fat burning hormones?

Insulin, leptin, ghrelin, glucagon, cortisol, and cholecystokinin are the six critical hormones in fat burning. While leptin, glucagon, and CCK help burn fat, insulin, ghrelin, and cortisol prevent weight loss.

Studies click to expand!

#1-7

¹Stárka L, Dušková M. What is a hormone?. Physiol Res. 2020 Sep 30;69(Suppl 2):S183-S185. doi: 10.33549/physiolres.934509. Review. PubMed PMID: 33094616; PubMed Central PMCID: PMC8603735.

²CDC. Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1960–1962 Through 2009–2010. Atlanta, GA: Centers for Disease Control and Prevention, 2012.

³Lustig RH. The neuroendocrinology of childhood obesity. Pediatr Clin North Am. 2001 Aug;48(4):909-30. doi: 10.1016/s0031-3955(05)70348-5. Review. PubMed PMID: 11494643.

⁴Fildes A, Charlton J, Rudisill C, Littlejohns P, Prevost AT, Gulliford MC. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015 Sep;105(9):e54-9. doi: 10.2105/AJPH.2015.302773. Epub 2015 Jul 16. PubMed PMID: 26180980; PubMed Central PMCID: PMC4539812.

⁵Fothergill E, Guo J, Howard L, Kerns JC, Knuth ND, Brychta R, Chen KY, Skarulis MC, Walter M, Walter PJ, Hall KD. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity (Silver Spring). 2016 Aug;24(8):1612-9. doi: 10.1002/oby.21538. Epub 2016 May 2. PubMed PMID: 27136388; PubMed Central PMCID: PMC4989512.

⁶Jensen MD, Caruso M, Heiling V, Miles JM. Insulin regulation of lipolysis in nondiabetic and IDDM subjects. Diabetes. 1989 Dec;38(12):1595-601. doi: 10.2337/diab.38.12.1595. PubMed PMID: 2573554.

⁷Meijssen S, Cabezas MC, Ballieux CG, Derksen RJ, Bilecen S, Erkelens DW. Insulin mediated inhibition of hormone sensitive lipase activity in vivo in relation to endogenous catecholamines in healthy subjects. J Clin Endocrinol Metab. 2001 Sep;86(9):4193-7. doi: 10.1210/jcem.86.9.7794. PubMed PMID: 11549649.

#8-14

⁸Muretta JM, Mastick CC. How insulin regulates glucose transport in adipocytes. Vitam Horm. 2009;80:245-86. doi: 10.1016/S0083-6729(08)00610-9. Review. PubMed PMID: 19251041.

⁹Gower BA, Goss AM. A lower-carbohydrate, higher-fat diet reduces abdominal and intermuscular fat and increases insulin sensitivity in adults at risk of type 2 diabetes. J Nutr. 2015 Jan;145(1):177S-83S. doi: 10.3945/jn.114.195065. Epub 2014 Dec 3. PubMed PMID: 25527677; PubMed Central PMCID: PMC4264021.

¹⁰Aeberli I, Hochuli M, Gerber PA, Sze L, Murer SB, Tappy L, Spinas GA, Berneis K. Moderate amounts of fructose consumption impair insulin sensitivity in healthy young men: a randomized controlled trial. Diabetes Care. 2013 Jan;36(1):150-6. doi: 10.2337/dc12-0540. Epub 2012 Aug 28. PubMed PMID: 22933433; PubMed Central PMCID: PMC3526231.

¹¹Nuttall FQ, Gannon MC. Plasma glucose and insulin response to macronutrients in nondiabetic and NIDDM subjects. Diabetes Care. 1991 Sep;14(9):824-38. doi: 10.2337/diacare.14.9.824. Review. PubMed PMID: 1959475.

¹²Ramel A, Martinéz A, Kiely M, Morais G, Bandarra NM, Thorsdottir I. Beneficial effects of long-chain n-3 fatty acids included in an energy-restricted diet on insulin resistance in overweight and obese European young adults. Diabetologia. 2008 Jul;51(7):1261-8. doi: 10.1007/s00125-008-1035-7. Epub 2008 May 20. PubMed PMID: 18491071.

¹³Catenacci VA, Pan Z, Ostendorf D, Brannon S, Gozansky WS, Mattson MP, Martin B, MacLean PS, Melanson EL, Troy Donahoo W. A randomized pilot study comparing zero-calorie alternate-day fasting to daily caloric restriction in adults with obesity. Obesity (Silver Spring). 2016 Sep;24(9):1874-83. doi: 10.1002/oby.21581. PubMed PMID: 27569118; PubMed Central PMCID: PMC5042570.

¹⁴Richter EA, Hargreaves M. Exercise, GLUT4, and skeletal muscle glucose uptake. Physiol Rev. 2013 Jul;93(3):993-1017. doi: 10.1152/physrev.00038.2012. Review. PubMed PMID: 23899560.

#15-19

¹⁵Keller U, Schnell H, Sonnenberg GE, Gerber PP, Stauffacher W. Role of glucagon in enhancing ketone body production in ketotic diabetic man. Diabetes. 1983 May;32(5):387-91. doi: 10.2337/diab.32.5.387. PubMed PMID: 6132846.

¹⁶Marliss EB, Aoki TT, Unger RH, Soeldner JS, Cahill GF Jr. Glucagon levels and metabolic effects in fasting man. J Clin Invest. 1970 Dec;49(12):2256-70. doi: 10.1172/JCI106445. PubMed PMID: 5480852; PubMed Central PMCID: PMC322727.

¹⁷Claessens M, Saris WH, van Baak MA. Glucagon and insulin responses after ingestion of different amounts of intact and hydrolysed proteins. Br J Nutr. 2008 Jul;100(1):61-9. doi: 10.1017/S0007114507886314. Epub 2008 Jan 2. PubMed PMID: 18167171.

¹⁸Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34. doi: 10.1111/j.1467-789X.2006.00270.x. Review. PubMed PMID: 17212793.

¹⁹Müller TD, Nogueiras R, Andermann ML, Andrews ZB, Anker SD, Argente J, Batterham RL, Benoit SC, Bowers CY, Broglio F, Casanueva FF, D’Alessio D, Depoortere I, Geliebter A, Ghigo E, Cole PA, Cowley M, Cummings DE, Dagher A, Diano S, Dickson SL, Diéguez C, Granata R, Grill HJ, Grove K, Habegger KM, Heppner K, Heiman ML, Holsen L, Holst B, Inui A, Jansson JO, Kirchner H, Korbonits M, Laferrère B, LeRoux CW, Lopez M, Morin S, Nakazato M, Nass R, Perez-Tilve D, Pfluger PT, Schwartz TW, Seeley RJ, Sleeman M, Sun Y, Sussel L, Tong J, Thorner MO, van der Lely AJ, van der Ploeg LH, Zigman JM, Kojima M, Kangawa K, Smith RG, Horvath T, Tschöp MH. Ghrelin. Mol Metab. 2015 Jun;4(6):437-60. doi: 10.1016/j.molmet.2015.03.005. eCollection 2015 Jun. Review. PubMed PMID: 26042199; PubMed Central PMCID: PMC4443295.

#20-24

²⁰Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34. doi: 10.1111/j.1467-789X.2006.00270.x. Review. PubMed PMID: 17212793.

²¹Blom WA, Lluch A, Stafleu A, Vinoy S, Holst JJ, Schaafsma G, Hendriks HF. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr. 2006 Feb;83(2):211-20. doi: 10.1093/ajcn/83.2.211. PubMed PMID: 16469977.

²²Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. doi: 10.1210/jc.2003-031855. PubMed PMID: 15181085.

²³Müller TD, Nogueiras R, Andermann ML, Andrews ZB, Anker SD, Argente J, Batterham RL, Benoit SC, Bowers CY, Broglio F, Casanueva FF, D’Alessio D, Depoortere I, Geliebter A, Ghigo E, Cole PA, Cowley M, Cummings DE, Dagher A, Diano S, Dickson SL, Diéguez C, Granata R, Grill HJ, Grove K, Habegger KM, Heppner K, Heiman ML, Holsen L, Holst B, Inui A, Jansson JO, Kirchner H, Korbonits M, Laferrère B, LeRoux CW, Lopez M, Morin S, Nakazato M, Nass R, Perez-Tilve D, Pfluger PT, Schwartz TW, Seeley RJ, Sleeman M, Sun Y, Sussel L, Tong J, Thorner MO, van der Lely AJ, van der Ploeg LH, Zigman JM, Kojima M, Kangawa K, Smith RG, Horvath T, Tschöp MH. Ghrelin. Mol Metab. 2015 Jun;4(6):437-60. doi: 10.1016/j.molmet.2015.03.005. eCollection 2015 Jun. Review. PubMed PMID: 26042199; PubMed Central PMCID: PMC4443295.

²⁴Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature. 1998 Oct 22;395(6704):763-70. doi: 10.1038/27376. Review. PubMed PMID: 9796811.

#25-29

²⁵Martin SS, Qasim A, Reilly MP. Leptin resistance: a possible interface of inflammation and metabolism in obesity-related cardiovascular disease. J Am Coll Cardiol. 2008 Oct 7;52(15):1201-10. doi: 10.1016/j.jacc.2008.05.060. Review. PubMed PMID: 18926322; PubMed Central PMCID: PMC4556270.

²⁶Lustig RH, Sen S, Soberman JE, Velasquez-Mieyer PA. Obesity, leptin resistance, and the effects of insulin reduction. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1344-8. doi: 10.1038/sj.ijo.0802753. PubMed PMID: 15314628.

²⁷Myers MG Jr, Leibel RL, Seeley RJ, Schwartz MW. Obesity and leptin resistance: distinguishing cause from effect. Trends Endocrinol Metab. 2010 Nov;21(11):643-51. doi: 10.1016/j.tem.2010.08.002. Epub 2010 Sep 16. Review. PubMed PMID: 20846876; PubMed Central PMCID: PMC2967652.

²⁸Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. doi: 10.1152/ajpregu.00195.2008. Epub 2008 Aug 13. PubMed PMID: 18703413; PubMed Central PMCID: PMC2584858.

²⁹Dirlewanger M, di Vetta V, Guenat E, Battilana P, Seematter G, Schneiter P, Jéquier E, Tappy L. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000 Nov;24(11):1413-8. doi: 10.1038/sj.ijo.0801395. PubMed PMID: 11126336.

#30-36

³⁰Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. doi: 10.1152/ajpregu.00195.2008. Epub 2008 Aug 13. PubMed PMID: 18703413; PubMed Central PMCID: PMC2584858.

³¹Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004 Nov;89(11):5762-71. doi: 10.1210/jc.2004-1003. PubMed PMID: 15531540.

³²Kang S, Kim KB, Shin KO. Exercise training improves leptin sensitivity in peripheral tissue of obese rats. Biochem Biophys Res Commun. 2013 Jun 7;435(3):454-9. doi: 10.1016/j.bbrc.2013.05.007. Epub 2013 May 11. PubMed PMID: 23669042.

³³Gibbs J, Young RC, Smith GP. Cholecystokinin elicits satiety in rats with open gastric fistulas. Nature. 1973 Oct 12;245(5424):323-5. doi: 10.1038/245323a0. PubMed PMID: 4586439.

³⁴Konturek JW, Konturek SJ, Kwiecień N, Bielański W, Pawlik T, Rembiasz K, Domschke W. Leptin in the control of gastric secretion and gut hormones in humans infected with Helicobacter pylori. Scand J Gastroenterol. 2001 Nov;36(11):1148-54. doi: 10.1080/00365520152584761. PubMed PMID: 11686213.

³⁵Peters JH, Simasko SM, Ritter RC. Modulation of vagal afferent excitation and reduction of food intake by leptin and cholecystokinin. Physiol Behav. 2006 Nov 30;89(4):477-85. doi: 10.1016/j.physbeh.2006.06.017. Epub 2006 Jul 26. Review. PubMed PMID: 16872644.

³⁶Liddle RA, Goldfine ID, Rosen MS, Taplitz RA, Williams JA. Cholecystokinin bioactivity in human plasma. Molecular forms, responses to feeding, and relationship to gallbladder contraction. J Clin Invest. 1985 Apr;75(4):1144-52. doi: 10.1172/JCI111809. PubMed PMID: 2580857; PubMed Central PMCID: PMC425438.

#37-43

³⁷Okonkwo O, Zezoff D, Adeyinka A. Biochemistry, Cholecystokinin. [Updated 2021 May 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534204/

³⁸Dockray GJ. Cholecystokinin. Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):8-12. doi: 10.1097/MED.0b013e32834eb77d. Review. PubMed PMID: 22157397.

³⁹Lieverse RJ, Jansen JB, Masclee AA, Lamers CB. Satiety effects of a physiological dose of cholecystokinin in humans. Gut. 1995 Feb;36(2):176-9. doi: 10.1136/gut.36.2.176. PubMed PMID: 7883212; PubMed Central PMCID: PMC1382399.

⁴⁰Cawthon CR, de La Serre CB. The critical role of CCK in the regulation of food intake and diet-induced obesity. Peptides. 2021 Apr;138:170492. doi: 10.1016/j.peptides.2020.170492. Epub 2021 Jan 8. Review. PubMed PMID: 33422646.

⁴¹Dockray GJ. Cholecystokinin. Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):8-12. doi: 10.1097/MED.0b013e32834eb77d. Review. PubMed PMID: 22157397.

⁴²Chungchunlam SM, Henare SJ, Ganesh S, Moughan PJ. Dietary whey protein influences plasma satiety-related hormones and plasma amino acids in normal-weight adult women. Eur J Clin Nutr. 2015 Feb;69(2):179-86. doi: 10.1038/ejcn.2014.266. Epub 2015 Jan 7. PubMed PMID: 25563737.

⁴³Zouhal H, Sellami M, Saeidi A, Slimani M, Abbassi-Daloii A, Khodamoradi A, El Hage R, Hackney AC, Ben Abderrahman A. Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses. Nutr Rev. 2019 Jul 1;77(7):455-477. doi: 10.1093/nutrit/nuz005. Review. PubMed PMID: 31125091.

#44-48

⁴⁴Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ, Stemmer K, Tang-Christensen M, Woods SC, DiMarchi RD, Tschöp MH. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019 Dec;30:72-130. doi: 10.1016/j.molmet.2019.09.010. Epub 2019 Sep 30. Review. PubMed PMID: 31767182; PubMed Central PMCID: PMC6812410.

⁴⁵Zhang F, Tong Y, Su N, Li Y, Tang L, Huang L, Tong N. Weight loss effect of glucagon-like peptide-1 mimetics on obese/overweight adults without diabetes: A systematic review and meta-analysis of randomized controlled trials. J Diabetes. 2015 May;7(3):329-39. doi: 10.1111/1753-0407.12198. Epub 2014 Sep 10. Review. PubMed PMID: 25043423.

⁴⁶Morínigo R, Moizé V, Musri M, Lacy AM, Navarro S, Marín JL, Delgado S, Casamitjana R, Vidal J. Glucagon-like peptide-1, peptide YY, hunger, and satiety after gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab. 2006 May;91(5):1735-40. doi: 10.1210/jc.2005-0904. Epub 2006 Feb 14. PubMed PMID: 16478824.

⁴⁷Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ, Stemmer K, Tang-Christensen M, Woods SC, DiMarchi RD, Tschöp MH. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019 Dec;30:72-130. doi: 10.1016/j.molmet.2019.09.010. Epub 2019 Sep 30. Review. PubMed PMID: 31767182; PubMed Central PMCID: PMC6812410.

⁴⁸Anandhakrishnan A, Korbonits M. Glucagon-like peptide 1 in the pathophysiology and pharmacotherapy of clinical obesity. World J Diabetes. 2016 Dec 15;7(20):572-598. doi: 10.4239/wjd.v7.i20.572. Review. PubMed PMID: 28031776; PubMed Central PMCID: PMC5155232.

#49-54

⁴⁹Stinson SE, Jonsson AE, Lund MAV, Frithioff-Bøjsøe C, Aas Holm L, Pedersen O, Ängquist L, Sørensen TIA, Holst JJ, Christiansen M, Holm JC, Hartmann B, Hansen T. Fasting Plasma GLP-1 Is Associated With Overweight/Obesity and Cardiometabolic Risk Factors in Children and Adolescents. J Clin Endocrinol Metab. 2021 May 13;106(6):1718-1727. doi: 10.1210/clinem/dgab098. PubMed PMID: 33596309; PubMed Central PMCID: PMC8118577.

⁵⁰Bodnaruc AM, Prud’homme D, Blanchet R, Giroux I. Nutritional modulation of endogenous glucagon-like peptide-1 secretion: a review. Nutr Metab (Lond). 2016;13:92. doi: 10.1186/s12986-016-0153-3. eCollection 2016. Review. PubMed PMID: 27990172; PubMed Central PMCID: PMC5148911.

⁵¹Gillespie AL, Calderwood D, Hobson L, Green BD. Whey proteins have beneficial effects on intestinal enteroendocrine cells stimulating cell growth and increasing the production and secretion of incretin hormones. Food Chem. 2015 Dec 15;189:120-8. doi: 10.1016/j.foodchem.2015.02.022. Epub 2015 Feb 18. PubMed PMID: 26190610.

⁵²Rubio IG, Castro G, Zanini AC, Medeiros-Neto G. Oral ingestion of a hydrolyzed gelatin meal in subjects with normal weight and in obese patients: Postprandial effect on circulating gut peptides, glucose and insulin. Eat Weight Disord. 2008 Mar;13(1):48-53. doi: 10.1007/BF03327784. PubMed PMID: 18319637.

⁵³Gagnon J, Sauvé M, Zhao W, Stacey HM, Wiber SC, Bolz SS, Brubaker PL. Chronic Exposure to TNFα Impairs Secretion of Glucagon-Like Peptide-1. Endocrinology. 2015 Nov;156(11):3950-60. doi: 10.1210/en.2015-1361. Epub 2015 Aug 13. PubMed PMID: 26270730.

⁵⁴Pironi L, Stanghellini V, Miglioli M, Corinaldesi R, De Giorgio R, Ruggeri E, Tosetti C, Poggioli G, Morselli Labate AM, Monetti N. Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY. Gastroenterology. 1993 Sep;105(3):733-9. doi: 10.1016/0016-5085(93)90890-o. PubMed PMID: 8359644.

#55-59

⁵⁵Wu Y, He H, Cheng Z, Bai Y, Ma X. The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis. Curr Protein Pept Sci. 2019;20(7):750-758. doi: 10.2174/1389203720666190125105401. Review. PubMed PMID: 30678628.

⁵⁶Zwirska-Korczala K, Konturek SJ, Sodowski M, Wylezol M, Kuka D, Sowa P, Adamczyk-Sowa M, Kukla M, Berdowska A, Rehfeld JF, Bielanski W, Brzozowski T. Basal and postprandial plasma levels of PYY, ghrelin, cholecystokinin, gastrin and insulin in women with moderate and morbid obesity and metabolic syndrome. J Physiol Pharmacol. 2007 Mar;58 Suppl 1:13-35. PubMed PMID: 17443025.

⁵⁷Zouhal H, Sellami M, Saeidi A, Slimani M, Abbassi-Daloii A, Khodamoradi A, El Hage R, Hackney AC, Ben Abderrahman A. Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses. Nutr Rev. 2019 Jul 1;77(7):455-477. doi: 10.1093/nutrit/nuz005. Review. PubMed PMID: 31125091.

⁵⁸Cahill F, Shea JL, Randell E, Vasdev S, Sun G. Serum peptide YY in response to short-term overfeeding in young men. Am J Clin Nutr. 2011 Apr;93(4):741-7. doi: 10.3945/ajcn.110.003624. Epub 2011 Feb 2. PubMed PMID: 21289220.

⁵⁹Lomenick JP, Melguizo MS, Mitchell SL, Summar ML, Anderson JW. Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. 2009 Nov;94(11):4463-71. doi: 10.1210/jc.2009-0949. Epub 2009 Oct 9. PubMed PMID: 19820013; PubMed Central PMCID: PMC2775646.

#60-65

⁶⁰Lomenick JP, Melguizo MS, Mitchell SL, Summar ML, Anderson JW. Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. 2009 Nov;94(11):4463-71. doi: 10.1210/jc.2009-0949. Epub 2009 Oct 9. PubMed PMID: 19820013; PubMed Central PMCID: PMC2775646.

⁶¹Pironi L, Stanghellini V, Miglioli M, Corinaldesi R, De Giorgio R, Ruggeri E, Tosetti C, Poggioli G, Morselli Labate AM, Monetti N. Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY. Gastroenterology. 1993 Sep;105(3):733-9. doi: 10.1016/0016-5085(93)90890-o. PubMed PMID: 8359644.

⁶²Jones TE, Basilio JL, Brophy PM, McCammon MR, Hickner RC. Long-term exercise training in overweight adolescents improves plasma peptide YY and resistin. Obesity (Silver Spring). 2009 Jun;17(6):1189-95. doi: 10.1038/oby.2009.11. Epub 2009 Feb 26. PubMed PMID: 19247279; PubMed Central PMCID: PMC3845441.

⁶³Wu Y, He H, Cheng Z, Bai Y, Ma X. The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis. Curr Protein Pept Sci. 2019;20(7):750-758. doi: 10.2174/1389203720666190125105401. Review. PubMed PMID: 30678628.

⁶⁴Beck B. Neuropeptide Y in normal eating and in genetic and dietary-induced obesity. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1159-85. doi: 10.1098/rstb.2006.1855. Review. PubMed PMID: 16874931; PubMed Central PMCID: PMC1642692.

⁶⁵Minor RK, Chang JW, de Cabo R. Hungry for life: How the arcuate nucleus and neuropeptide Y may play a critical role in mediating the benefits of calorie restriction. Mol Cell Endocrinol. 2009 Feb 5;299(1):79-88. doi: 10.1016/j.mce.2008.10.044. Epub 2008 Nov 11. Review. PubMed PMID: 19041366; PubMed Central PMCID: PMC2668104.

#66-72

⁶⁶Kuo LE, Kitlinska JB, Tilan JU, Li L, Baker SB, Johnson MD, Lee EW, Burnett MS, Fricke ST, Kvetnansky R, Herzog H, Zukowska Z. Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome. Nat Med. 2007 Jul;13(7):803-11. doi: 10.1038/nm1611. Epub 2007 Jul 1. PubMed PMID: 17603492.

⁶⁷Reichmann F, Holzer P. Neuropeptide Y: A stressful review. Neuropeptides. 2016 Feb;55:99-109. doi: 10.1016/j.npep.2015.09.008. Epub 2015 Sep 30. Review. PubMed PMID: 26441327; PubMed Central PMCID: PMC4830398.

⁶⁸McDonald RB, Ramsey JJ. Honoring Clive McCay and 75 years of calorie restriction research. J Nutr. 2010 Jul;140(7):1205-10. doi: 10.3945/jn.110.122804. Epub 2010 May 19. PubMed PMID: 20484554; PubMed Central PMCID: PMC2884327.

⁶⁹Minor RK, Chang JW, de Cabo R. Hungry for life: How the arcuate nucleus and neuropeptide Y may play a critical role in mediating the benefits of calorie restriction. Mol Cell Endocrinol. 2009 Feb 5;299(1):79-88. doi: 10.1016/j.mce.2008.10.044. Epub 2008 Nov 11. Review. PubMed PMID: 19041366; PubMed Central PMCID: PMC2668104.

⁷⁰Beck B. Neuropeptide Y in normal eating and in genetic and dietary-induced obesity. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1159-85. doi: 10.1098/rstb.2006.1855. Review. PubMed PMID: 16874931; PubMed Central PMCID: PMC1642692.

⁷¹White BD, He B, Dean RG, Martin RJ. Low protein diets increase neuropeptide Y gene expression in the basomedial hypothalamus of rats. J Nutr. 1994 Aug;124(8):1152-60. doi: 10.1093/jn/124.8.1152. PubMed PMID: 8064364.

⁷²Khajehnasiri N, Khazali H, Sheikhzadeh F, Ghowsi M. One-month of high-intensity exercise did not change the food intake and the hypothalamic arcuate nucleus proopiomelanocortin and neuropeptide Y expression levels in male Wistar rats. Endocr Regul. 2019 Jan 1;53(1):8-13. doi: 10.2478/enr-2019-0002. PubMed PMID: 31517616.

#73-79

⁷³Benite-Ribeiro SA, Putt DA, Santos JM. The effect of physical exercise on orexigenic and anorexigenic peptides and its role on long-term feeding control. Med Hypotheses. 2016 Aug;93:30-3. doi: 10.1016/j.mehy.2016.05.005. Epub 2016 May 11. PubMed PMID: 27372853.

⁷⁴Epel E, Lapidus R, McEwen B, Brownell K. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology. 2001 Jan;26(1):37-49. doi: 10.1016/s0306-4530(00)00035-4. PubMed PMID: 11070333.

⁷⁵Owen OE, Cahill GF Jr. Metabolic effects of exogenous glucocorticoids in fasted man. J Clin Invest. 1973 Oct;52(10):2596-605. doi: 10.1172/JCI107452. PubMed PMID: 4729053; PubMed Central PMCID: PMC302520.

⁷⁶Whitworth JA, Williamson PM, Brown MA, Colman P. Hyperinsulinemia is not a cause of cortisol-induced hypertension. Am J Hypertens. 1994 Jun;7(6):562-5. doi: 10.1093/ajh/7.6.562. PubMed PMID: 7917157.

⁷⁷Rosmond R, Dallman MF, Björntorp P. Stress-related cortisol secretion in men: relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. J Clin Endocrinol Metab. 1998 Jun;83(6):1853-9. doi: 10.1210/jcem.83.6.4843. PubMed PMID: 9626108.

⁷⁸Ayachi SE, Paulmyer-Lacroix O, Verdier M, Alessi MC, Dutour A, Grino M. 11beta-Hydroxysteroid dehydrogenase type 1-driven cortisone reactivation regulates plasminogen activator inhibitor type 1 in adipose tissue of obese women. J Thromb Haemost. 2006 Mar;4(3):621-7. doi: 10.1111/j.1538-7836.2006.01811.x. PubMed PMID: 16460444.

⁷⁹Rask E, Walker BR, Söderberg S, Livingstone DE, Eliasson M, Johnson O, Andrew R, Olsson T. Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity. J Clin Endocrinol Metab. 2002 Jul;87(7):3330-6. doi: 10.1210/jcem.87.7.8661. PubMed PMID: 12107245.

#80-87

⁸⁰Joo EY, Yoon CW, Koo DL, Kim D, Hong SB. Adverse effects of 24 hours of sleep deprivation on cognition and stress hormones. J Clin Neurol. 2012 Jun;8(2):146-50. doi: 10.3988/jcn.2012.8.2.146. Epub 2012 Jun 29. PubMed PMID: 22787499; PubMed Central PMCID: PMC3391620.

⁸¹Pascoe MC, Thompson DR, Ski CF. Yoga, mindfulness-based stress reduction and stress-related physiological measures: A meta-analysis. Psychoneuroendocrinology. 2017 Dec;86:152-168. doi: 10.1016/j.psyneuen.2017.08.008. Epub 2017 Aug 30. PubMed PMID: 28963884.

⁸²Klimes-Dougan B, Chong LS, Samikoglu A, Thai M, Amatya P, Cullen KR, Lim KO. Transcendental meditation and hypothalamic-pituitary-adrenal axis functioning: a pilot, randomized controlled trial with young adults. Stress. 2020 Jan;23(1):105-115. doi: 10.1080/10253890.2019.1656714. Epub 2019 Sep 11. PubMed PMID: 31418329.

⁸³Lovejoy JC. The influence of sex hormones on obesity across the female life span. J Womens Health. 1998 Dec;7(10):1247-56. doi: 10.1089/jwh.1998.7.1247. Review. PubMed PMID: 9929857.

⁸⁴Daka B, Rosen T, Jansson PA, Råstam L, Larsson CA, Lindblad U. Inverse association between serum insulin and sex hormone-binding globulin in a population survey in Sweden. Endocr Connect. 2013 Mar 1;2(1):18-22. doi: 10.1530/EC-12-0057. Print 2013 Mar 1. PubMed PMID: 23781314; PubMed Central PMCID: PMC3680959.

⁸⁵Kossman DA, Williams NI, Domchek SM, Kurzer MS, Stopfer JE, Schmitz KH. Exercise lowers estrogen and progesterone levels in premenopausal women at high risk of breast cancer. J Appl Physiol (1985). 2011 Dec;111(6):1687-93. doi: 10.1152/japplphysiol.00319.2011. Epub 2011 Sep 8. PubMed PMID: 21903887; PubMed Central PMCID: PMC4116411.

⁸⁶Singleton DW, Khan SA. Xenoestrogen exposure and mechanisms of endocrine disruption. Front Biosci. 2003 Jan 1;8:s110-8. doi: 10.2741/1010. Review. PubMed PMID: 12456297.

⁸⁷Yang CZ, Yaniger SI, Jordan VC, Klein DJ, Bittner GD. Most plastic products release estrogenic chemicals: a potential health problem that can be solved. Environ Health Perspect. 2011 Jul;119(7):989-96. doi: 10.1289/ehp.1003220. Epub 2011 Mar 2. PubMed PMID: 21367689; PubMed Central PMCID: PMC3222987.

#88-94

⁸⁸Tyagi V, Scordo M, Yoon RS, Liporace FA, Greene LW. Revisiting the role of testosterone: Are we missing something?. Rev Urol. 2017;19(1):16-24. doi: 10.3909/riu0716. PubMed PMID: 28522926; PubMed Central PMCID: PMC5434832.

⁸⁹De Pergola G. The adipose tissue metabolism: role of testosterone and dehydroepiandrosterone. Int J Obes Relat Metab Disord. 2000 Jun;24 Suppl 2:S59-63. doi: 10.1038/sj.ijo.0801280. Review. PubMed PMID: 10997611.

⁹⁰Rebuffé-Scrive M, Mårin P, Björntorp P. Effect of testosterone on abdominal adipose tissue in men. Int J Obes. 1991 Nov;15(11):791-5. PubMed PMID: 1778664.

⁹¹Swerdloff RS, Ng CM. Gynecomastia: Etiology, Diagnosis, and Treatment. [Updated 2019 Jul 7]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279105/

⁹²Moro T, Tinsley G, Bianco A, Marcolin G, Pacelli QF, Battaglia G, Palma A, Gentil P, Neri M, Paoli A. Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. J Transl Med. 2016 Oct 13;14(1):290. doi: 10.1186/s12967-016-1044-0. PubMed PMID: 27737674; PubMed Central PMCID: PMC5064803.

⁹³Pitteloud N, Hardin M, Dwyer AA, Valassi E, Yialamas M, Elahi D, Hayes FJ. Increasing insulin resistance is associated with a decrease in Leydig cell testosterone secretion in men. J Clin Endocrinol Metab. 2005 May;90(5):2636-41. doi: 10.1210/jc.2004-2190. Epub 2005 Feb 15. PubMed PMID: 15713702.

⁹⁴Caronia LM, Dwyer AA, Hayden D, Amati F, Pitteloud N, Hayes FJ. Abrupt decrease in serum testosterone levels after an oral glucose load in men: implications for screening for hypogonadism. Clin Endocrinol (Oxf). 2013 Feb;78(2):291-6. doi: 10.1111/j.1365-2265.2012.04486.x. PubMed PMID: 22804876.

#95-101

⁹⁵Child & Family Research Institute. Too Much Sugar Turns Off Gene That Controls Effects Of Sex Steroids. [Updated 2007 Nov 21]. In: ScienceDaily. Retrieved February 13, 2022 from www.sciencedaily.com/releases/2007/11/071109171610.htm

⁹⁶Anderson T, Lane AR, Hackney AC. Cortisol and testosterone dynamics following exhaustive endurance exercise. Eur J Appl Physiol. 2016 Aug;116(8):1503-9. doi: 10.1007/s00421-016-3406-y. Epub 2016 Jun 4. PubMed PMID: 27262888.

⁹⁷Timón Andrada R, Maynar Mariño M, Muñoz Marín D, Olcina Camacho GJ, Caballero MJ, Maynar Mariño JI. Variations in urine excretion of steroid hormones after an acute session and after a 4-week programme of strength training. Eur J Appl Physiol. 2007 Jan;99(1):65-71. doi: 10.1007/s00421-006-0319-1. Epub 2006 Oct 19. PubMed PMID: 17051372.

⁹⁸Leproult R, Van Cauter E. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA. 2011 Jun 1;305(21):2173-4. doi: 10.1001/jama.2011.710. PubMed PMID: 21632481; PubMed Central PMCID: PMC4445839.

⁹⁹Catenacci VA, Pan Z, Ostendorf D, Brannon S, Gozansky WS, Mattson MP, Martin B, MacLean PS, Melanson EL, Troy Donahoo W. A randomized pilot study comparing zero-calorie alternate-day fasting to daily caloric restriction in adults with obesity. Obesity (Silver Spring). 2016 Sep;24(9):1874-83. doi: 10.1002/oby.21581. PubMed PMID: 27569118; PubMed Central PMCID: PMC5042570.

¹⁰⁰Lomenick JP, Melguizo MS, Mitchell SL, Summar ML, Anderson JW. Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. 2009 Nov;94(11):4463-71. doi: 10.1210/jc.2009-0949. Epub 2009 Oct 9. PubMed PMID: 19820013; PubMed Central PMCID: PMC2775646.

¹⁰¹Lustig RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013 Mar 1;4(2):226-35. doi: 10.3945/an.112.002998. PubMed PMID: 23493539; PubMed Central PMCID: PMC3649103.

#102-106

¹⁰²Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23-46. doi: 10.1152/physrev.00019.2009. Review. PubMed PMID: 20086073.

¹⁰³Zouhal H, Sellami M, Saeidi A, Slimani M, Abbassi-Daloii A, Khodamoradi A, El Hage R, Hackney AC, Ben Abderrahman A. Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses. Nutr Rev. 2019 Jul 1;77(7):455-477. doi: 10.1093/nutrit/nuz005. Review. PubMed PMID: 31125091.

¹⁰⁴Rosmond R, Dallman MF, Björntorp P. Stress-related cortisol secretion in men: relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. J Clin Endocrinol Metab. 1998 Jun;83(6):1853-9. doi: 10.1210/jcem.83.6.4843. PubMed PMID: 9626108.

¹⁰⁵Nuttall FQ, Almokayyad RM, Gannon MC. The ghrelin and leptin responses to short-term starvation vs a carbohydrate-free diet in men with type 2 diabetes; a controlled, cross-over design study. Nutr Metab (Lond). 2016;13:47. doi: 10.1186/s12986-016-0106-x. eCollection 2016. PubMed PMID: 27453716; PubMed Central PMCID: PMC4957917.

¹⁰⁶Orgel E, Mittelman SD. The links between insulin resistance, diabetes, and cancer. Curr Diab Rep. 2013 Apr;13(2):213-22. doi: 10.1007/s11892-012-0356-6. Review. PubMed PMID: 23271574; PubMed Central PMCID: PMC3595327.