The Fasting Method – The Science2019-11-12T08:44:37-05:00

Fasting Science

Empowering you with knowledge to live healthier.

Fasting Science

Empowering you with knowledge to live healthier.

What is fasting?


Intermittent fasting? Isn’t that starvation…?

No. Fasting is different from starvation in one vital way: control.

Starvation means you don’t know when you will eat next.  It’s neither deliberate nor controlled.

Fasting, on the other hand, is entirely voluntarily done for spiritual, health or any other reason.

Food is available – you’re just choosing not to eat it. That can be for any length of time, hours to days. Or – with medical supervision – even weeks.  You can start or stop a fast for any reason, or no reason at all. Fasting has no standard duration.

Fasting may be the oldest and most powerful dietary intervention we know.

Consider the term “break fast.” It’s literally the meal that breaks our daily fast.  But to break a fast, me must be fasting.  So, fasting is not some cruel and unusual punishment, but merely a part of everyday life.  If you want to tip the balance towards weight loss, then you may increase the fasting portion of your day.

Benefits of Fasting


Weight loss is the most obvious health benefit. But, really, that’s just the start.

Other physical benefits of intermittent fasting include:

  • Weight and body fat loss5,6,8,9,11,12,37,38
  • Increased fat burning19
  • Lowered blood insulin and sugar levels20-22
  • Reduction in HbA1C23-25
  • Improved mental clarity and concentration13
  • Increased energy27-28
  • Increased growth hormone4,7,8
  • Activation of cellular cleansing by stimulating autophagy34-35
  • Reduction of inflammation36
  • Increased productivity (doesn’t take time and can be done anywhere)

Historically fasting periods were often called ‘cleanses,’ ‘detoxifications’ or ‘purifications.’ Whatever it was called, the idea was the same. Periodically abstaining from food helps clear toxins and rejuvenates the body.

Getting Started


Let’s keep it simple. Consider these steps:

  • Decide what type of fast you want to do
  • Decide upon the length of time you want to fast
  • Start fasting, and if you don’t feel well or have any concerns, stop
  • Continue all your usual activities outside of eating. Stay busy and live normally.
  • Break the fast gently
  • Repeat

Yes. It can be that simple.

What kinds of fasts should I consider?

Shorter fasts (less than 24 hours)

Intermittent fasting offers plenty of flexibility. You can fast for as long or short as you like, but fasts longer than a few days may require medical supervision. Here are some popular regimens you might consider. Generally, shorter fasts are done more frequently.


This way of doing intermittent fasting involves daily fasting for 16 hours – so, it’s 16 hours ‘off’ and 8 hours ‘on.’ Sometimes, the time you’re eating is referred to as the eight-hour eating ‘window.’ You eat all your meals within an eight-hour time period and fast for the remaining 16 hours. Generally, this is done daily or almost daily.

For example, you may eat all your meals between 11:00 am and 7:00 pm. Generally, that means skipping breakfast, but some prefer to skip dinner instead. You typically eat two or three meals within this eight-hour period.


This is a four-hour eating window and a 20-hour fast. For example, you might eat between 2:00 pm and 6:00 pm every day and fast for the other 20 hours. Generally, this would involve eating either one meal or two smaller meals in this period.

Longer fasts (more than 24 hours)

24-hour fast

This approach involves fasting from dinner to dinner (or lunch to lunch). If you eat dinner on day one, you would skip the next day’s breakfast and lunch and eat dinner again on day two. This means you’re still eating daily, but only once during the day. This would generally be done two to three times per week.

5:2 fast

This is the version of intermittent fasting that has the most scientific support, as most studies on intermittent fasting have focused on it.37-38 Dr. Michael Mosley popularized this variation of intermittent fasting in his book The Fast Diet.

5:2 involves five regular eating days and two fasting days. However, on these two fasting days you are allowed to eat 500 calories each day. These calories can be consumed at any time during the day, either spread throughout the day or as a single meal.

36-hour fast

This involves fasting for an entire day. So, for example, if you eat dinner on day one, you would fast for all of day two and not eat again until breakfast on day three. This generally works out to 36 hours of fasting. This might provide a more powerful weight loss benefit. The other great benefit is that it avoids the temptation to overeat dinner on day two.

Extended fasting

These sorts of fasts want to be carefully considered and planned for. For fasts greater than 48 hours, we recommend a general multivitamin to avoid micronutrient deficiency. The world record for fasting is 382 days, and going seven to 14 days may be possible for some people.39

Fasting for Health

Weight Loss


At its core, intermittent fasting is just allows the body to use stored energy – often, by burning excess body fat.

When we eat, we usually ingest more food energy than we can use at the time. So, some of that energy gets stored for later use. Body fat is just stored food energy.

How we store energy and create fat

How we store energy and create fat

Insulin is the hormone that regulates the storage of food energy. Insulin rises when we eat, helping to store the excess energy in one of two ways:

  • Carbohydrates are broken down into individual glucose (sugar) units, which can be linked into long chains to form glycogen, which is then stored in the liver or muscle. That’s the easy-to-access energy.
  • But, we have very limited storage space. Once we’re at capacity, the liver starts to turn that excess glucose into fat. This process is called de-novo lipogenesis (literally, “making new fat”). Some of this newly-created fat is stored in the liver, but most of it is exported to other fat deposits in the body. While it’s a more complicated process, there’s virtually no limit to the amount of fat that can be created.

So, two complementary food energy storage systems exist in our bodies. One is easily accessible but has limited storage space (glycogen). The other is more difficult to access but has almost unlimited storage space (body fat).

Using up that stored energy

Using up that stored energy

That process goes in reverse when we don’t eat (i.e. intermittent fasting). Insulin levels fall, signaling to the body that it’s time to start burning stored energy. Blood glucose falls, so the body has to pull glucose out of storage to burn for energy.

That glycogen in short-term storage is the most easily accessible. It’s broken down into glucose molecules to provide energy for the body’s other cells, and can generally provide enough energy to power much of the body’s needs for 24 to 36 hours.

After that, the body will start breaking down fat for energy.

So the body only really exists in two states: the fed (insulin high) state and the fasted (insulin low) state.

Either we’re storing food energy, or we’re burning stored energy. It’s one or the other. But, if eating and fasting are balanced, then there should be no net weight change. We’re in balance.

If we start eating the minute we roll out of bed and don’t stop until we go to sleep, we spend all our time in the fed state. Over time, we’ll likely gain weight because we’ve not allowed our body time to burn stored food energy.

To restore balance or to lose weight, we simply need to increase the amount of time spent burning food energy. That’s intermittent fasting.

Intermittent fasting allows the body to use its stored energy. After all, that’s what we stored it for.

If you’re eating every third hour, as is often recommended, your body will constantly use incoming food energy. It may never need to burn body fat.



It’s well known and accepted that type 2 diabetes (DMII) is a disease of insulin resistance.

One of insulin’s main jobs is to move glucose from the blood into the tissues, which can then use it as energy. But, when insulin resistance develops, the normal level of insulin is not able to move glucose into the cells.


Let’s consider an analogy. Imagine the cell to be a subway train. Glucose molecules are the passengers waiting to get onboard. Insulin gives the signal to open the train doors, and the passengers – glucose molecules – march in a nice, orderly manner into the empty subway train. Normally, it doesn’t really require much effort to get this glucose into the cell.

But what happens if the train’s not empty? What if it’s already full of passengers? Insulin gives the signal to open the door, but the passengers waiting on the platform can’t get on. From the outside, it appears that this train (cell) is now resisting taking on new passengers (insulin signals).

What can you do to pack more passengers into the train? One solution is to hire people to shove them into the trains. This was actually implemented in New York City in the 1920s and, while the practice has since died out in North America, subway pushers still exist in Japan, where they are euphemistically called “passenger arrangement staff.”

Insulin is the body’s subway pusher, shoving glucose into the cell, no matter the consequences. If the normal amount of insulin can’t get the glucose in, then the body calls for reinforcements: even more insulin. But the main cause of the insulin resistance is that the cell was already overflowing with glucose.

Because the cell is overfilled with glucose, the glucose spills out, leading to increased blood glucose levels. This leads to the diagnosis of type 2 diabetes. If you now give more insulin, or drugs that stimulate the production of insulin, then yes, temporarily, more glucose can be shoved into the cell. However, there is a natural limit. At a certain point, even extra insulin won’t be able to move more glucose into the cell.

This is exactly what happens in the typical course of type 2 diabetes. At first, the disease can be treated with a small dose of a single medication that stimulates the production of insulin. But, after a few years, this is no longer enough. So, the dosages increase.

More years pass and a second, then a third medication is added, all aimed at increasing the production of insulin. Finally, insulin itself is prescribed in higher and higher doses. The progression of treatment is clearly not helping the underlying problem: the type 2 diabetes is just getting worse. Medications only help control the blood sugar. They don’t address what’s causing type 2 diabetes.


If the core issue is glucose overfilling the cells, then the solution seems pretty obvious: get all that glucose out of the cell!

Pushing more in, as with insulin treatment, will only make things worse. So how do you get rid of excess glucose in the body? (Remember, it’s glucose in the tissue cells that’s the underlying problem. Without that, glucose in the bloodstream is no longer a problem.)

There are really only two ways of getting the toxic glucose overload out:

First, you need to stop putting glucose in. You can achieve this with very low carbohydrate or ketogenic diets. Indeed, many people have reversed diabetes by following such a diet. Fasting also eliminates carbohydrates – and all other foods, for that matter.

Second, your body needs to burn off the excess glucose. Fasting, again, is an obvious solution. Your body requires energy just to keep all the vital organs – such as the heart, lungs, liver and kidneys – working. Your brain, in particular, requires substantial energy to function properly, even during sleep periods. During fasting, no new glucose is coming in, so your body has no choice but to use up the stored glucose.

At its core, type 2 diabetes is a disease of excess glucose, both in our blood and also in our bodies. If you don’t eat, your blood sugar levels will come down. When your blood sugar levels are consistently in the normal range, you will no longer be considered diabetic. Diabetes reverse!



Fasting for Wellness and Autophagy

The most obvious benefits of fasting are that it helps with weight loss and type 2 diabetes. But there are many others – including autophagy (a cellular cleansing process), lipolysis (fat burning), as well as its anti-aging effects and neurological benefits.

In other words, fasting can benefit your brain and help your body stay younger!

Mammals generally respond to severe caloric deprivation by reducing organ size, but there are two prominent exceptions: the brain and (in males) the testicles. Reproductive function is preserved to propagate the species. But cognitive function is just as important and is highly preserved, even at the expense of every other organ.

That makes a lot of sense from an evolutionary standpoint. If food is scarce and difficult to find, a mental fog would make it that much harder. Our brain is one of the main advantages we have in the natural world.

During caloric deprivation, the brain maintains or even boosts its abilities. The best-selling novel Unbroken, by Lauren Hillenbrand, describes the experiences of American prisoners of war in Japan during World War 2. It outlines how, during extreme starvation, prisoners experienced a mental clarity that they themselves understood was due to starvation. One man described “reading” entire books from memory.

Humans, like all mammals, have increased mental activity when hungry, and decreased when satiated. We’ve all experienced a food coma – think about how you feel after a big Thanksgiving meal, complete with Turkey and pumpkin pie. Are you mentally sharp, or dull as a concrete block?

Despite popular belief, it’s not the tryptophan in the turkey causing that. In fact, turkey has about the same amount of tryptophan as other poultry. It’s just the sheer amount of food. The digestive system has to ramp up to handle all that turkey and pie, so less blood is available to go to the brain. About the only mental challenge we can handle after that enormous meal is sitting on the couch watching football.

What about the opposite? Think about a time that you were really, really hungry. Where you tired and sluggish? No. You were probably hyper alert, your senses sharp as a needle.

Animals that are cognitively sharp and physically agile during times of food scarcity have an advantage when it comes to survival. If missing a single meal reduces our energy and mental clarity, we would have even more trouble finding food – making it more likely that we would go hungry again. That’s a vicious cycle ending in death.

That’s not, of course, what happens. Our ancient ancestors grew more alert and active when hungry so that they could find their next meal – and the same thing still happens to us.

Even our language reflects the relationship between hunger and mental clarity. When we say we are hungry for something – like hungry for power or hungry for attention – it doesn’t mean we’re slothful and dull. It means we’re on our toes, alert and ready for action. Fasting and hunger energises us, despite popular misconceptions to the contrary.

In one study of mental acuity and fasting, none of the factors measured – including sustained attention, attentional focus, simple reaction time or immediate memory – was found to be impaired. Another study of two days of almost total caloric deprivation found no detrimental effect on cognitive performance or on sleep and mood.

But the neurological benefits of fasting aren’t limited to the times when we’re forgoing food. Animal studies show that fasting has remarkable promise as a therapeutic tool. Aging rats started on intermittent fasting regimens showed marked improvement in their motor coordination, cognition, learning and memory. Interestingly, there was even increased brain connectivity and new neuron growth from stem cells.

A protein called brain-derived neurotrophic factor (BDNF), which supports the growth of neurons and is important for long-term memory, is believed to be responsible for some of these benefits. In animals, both fasting and exercise significantly increase the beneficial BDNF effects in several parts of the brain. Compared to normal mice, mice on an intermittent fasting regimen showed less age-related deterioration of neurons and fewer symptoms of Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.

Human studies on caloric restriction find similar neurologic benefits – and, since fasting certainly restricts calories, this is one area where fasting and caloric reduction provide similar benefits. With a 30% reduction in calories consumed, memory significantly improved and the synaptic electrical activity in the brain increased.

In addition, insulin levels have an inverse correlation to memory – that is, the lower the insulin level, the more memory improves. On the flipside, a higher body mass index is linked to decline and mental abilities and decreased blood flow to those areas of the brain involved in attention, focus, reasoning and more complex, abstract thought. So, fasting provides neurological benefits two ways: it decreases insulin and leads to consistent, maintained weight loss.

When you buy a new car, everything works great. But, after a few years, it starts to get a little beat up and needs more maintenance. You need to replace the brake pads, then the battery, then more and more parts. Eventually, the car is breaking down all the time and costing thousands of dollars to maintain. Does it make sense to keep it around? Likely not. So, you get rid of it by buying a new car.

The cells in the body are like cars. As they age, subcellular parts need to be removed and replaced, and eventually, a cell gets too old to repair and needs to be destroyed to make way for a healthy new one.

In a process called apoptosis, also known as programmed cell death, cells that reach a certain age are programmed to commit suicide. While this may sound macabre at first, the process constantly renews cell populations, which is essential for good health. But when just some cellular components need to be replaced a processed called autophagy kicks in.

The word autophagy, coined by Nobel Prize-winning scientist Christian de Duve, derives from the Greek words auto (self) and phagein (to eat). So, the word literally means “to eat oneself.”

Autophagy is a form of cellular cleansing: it’s a regulated, orderly process of breaking down and recycling subcellular components when there’s no longer enough energy to sustain them. Once all the diseased or broken-down cellular parts have been cleansed, the body can start the process of renewal. New tissues and cells are built to replace those that were destroyed. In this way, the body renews itself. But it only works if the old parts are discarded first.

Our bodies are in a constant state of renewal. While we often focus on new cell growth, we sometimes forget that the first step in renewal is destroying the old, broken-down cellular machinery.

Apoptosis and autophagy are both necessary to keep our bodies running well. When these processes are hijacked, disease such as cancer occur, and the accumulation of older cellular components may be responsible for many of the effects of aging. These unwanted cellular components build up over time if autophagocytic processes are not routinely activated.

Increased levels of glucose, insulin and proteins all turn off autophagy. And it doesn’t take much. Even as little as three grams of amino acid leucine can stop it.

Here’s how it works: the mammalian target of rapamycin (mTOR) pathway is an important sensor of nutrient availability. When we eat carbohydrates and protein, insulin is secreted and the increased levels of insulin, or even just the amino acids from the breakdown of ingested protein, activate the mTOR pathway. The body senses that food is available and decides that, since there’s plenty of energy to go around, there’s no need to worry about the old subcellular machinery. The result is the suppression of autophagy. In other words, the constant intake of food, such as snacking throughout the day, suppresses autophagy.

Conversely, when mTOR is dormant – when it’s not being triggered by increase insulin levels or amino acids from ingested food – autophagy is promoted. As the body senses a temporary absence and nutrients, it must prioritise which cellular parts to keep. The oldest and most worn-out cellular parts get discarded, and amino acids from the breakdown cell are delivered to the liver, which uses them to create glucose during gluconeogenesis. They may also be incorporated into new proteins. It’s important to note that the dormancy of mTOR is only related to short to nutrient availability and not the presence of stored energy such as liver glycogen or body fat. Whether the body has stored energy is irrelevant for mTOR and autophagy.

Therefore, the strongest stimulus currently known to autophagy is fasting, and why fasting alone, unique among diets, simulates autophagy – simple caloric restriction isn’t enough. By eating constantly, from the time we wake up to the time we sleep, we prevent that activation of autophagy’s cleansing pathways. Simply put, fasting cleanses the body of unhealthy or unnecessary cellular debris. This is the reason longer fast are often called cleanses or detoxifications.

At the same time, fasting also stimulates growth hormone, which signals the production of some snazzy new cell parts, giving our bodies a complete renovation. Since it triggers both the breakdown of old cellular parts in the creation of new ones, Fasting may be considered one of the most potent anti-aging methods in existence.

Autophagy also plays an important role in the prevention of Alzheimer’s disease. Alzheimer’s is characterised by the abnormal accumulation of amyloid beta (AB) proteins in the brain, and it’s believed that these accumulations eventually destroy all the synaptic connections in the memory and cognition areas. Normally, clumps of AB protein are removed by autophagy: the brain cell activates the autophagosome, the cell’s internal garbage truck, which engulfs the AB protein targeted for removal and excretes it, so it can be removed by the blood and recycled into other protein or turned into glucose, depending on the body’s needs. But in Alzheimer’s disease, autophagy is impaired, and the AB protein remains inside the brain cell, where eventual buildup will result in the clinical syndromes of Alzheimer’s disease.

Cancer is yet another disease that may be a result of disordered autophagy. We’re learning that mTOR plays a role in cancer biology, and mTOR inhibitors have been approved by the US Food and Drug Administration for the treatment of various cancers. Fasting’s role in mTOR, thereby stimulating autophagy, provides an interesting opportunity to prevent the development of cancer. Dr. Thomas Seyfried, a professor of biology at Boston College, have proposed a yearly seven-day water-only fast for this very reason.

The Research

40-year-old male

20-year diabetes history

Alternating-day 24-hour fasts


HbA1c from 11%


down to 7.4%

0 lbs.
lost (12% of his bodyweight)
0 out of 4
diabetes meds deprescribed
0 days
to come off insulin
0 inches
lost from his waist (13% loss)

52-year-old male

25-year diabetes history

24-hour fasts, 3 times a week


HbA1c from 7.2%


down to 6.4%

0 lbs.
lost (17% of his bodyweight)
0 out of 1
diabetes med deprescribed
0 days
to come off insulin
0 inches
lost from his waist (20% loss)

67-year-old male

10-year diabetes history

Alternating-day 24-hour fasts


HbA1c from 6.3%


down to 6.2%

0 lbs.
lost (9% of his bodyweight)
0 out of 2
diabetes meds deprescribed
0 days
to come off insulin
0 inches
lost from his waist (13% loss)

Peer Reviewed Case Series1

Featured in the British Medical Journal


This case series documents three patients referred to the Intensive Dietary Management clinic in Toronto, Canada, for insulin-dependent type 2 diabetes. It demonstrates the effectiveness of therapeutic fasting to reverse their insulin resistance, resulting in cessation of insulin therapy while maintaining control of their blood sugars. In addition, these patients were also able to lose significant amounts of body weight, reduced their waist circumference and also reduce their glycated haemoglobin level. In our study, all three patients eliminated the need for insulin by initiating various intermittent fasting and time-restricted eating protocols. All three patients succeeded within a month and one in as little as five days. Further, all patients improved in multiple other clinically significant health outcome measures, such as HbA1C, body mass index and waist circumference.

Ongoing Research

In a joint collaboration with the Intensive Dietary Management Clinic in Toronto, The Fasting Method is currently collecting and analyzing their seven year data. The data collection primarily focuses on patients who have utilized therapeutic fasting strategies for: type 2 diabetes, obesity, polycystic ovarian syndrome (PCOS) and nonalcoholic fatty liver disease (NAFLD).

Case series’ on the following items are also being written up for peer review:
Post-menopausal women and fasting
Menopausal women and fasting
Menstruating women and fasting
Fasting and colitis reversal

  1. Furmli S, Elmasry R, Ramos M, Fung J. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Rep. 2018 Oct 9; 2018. pii: bcr-2017-221854. doi: 10.1136/bcr-2017-221854
  2. Zauner C, Schneeweiss B, Kranz A, et al. Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine. Am J Clin Nutr. 2000 Jun;71(6):1511-5.
  3. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8.
  4. Ho KY, Veldhuis JD, Johnson ML, et al. Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J Clin Invest. 1988 Apr;81(4):968-75.
  5. Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011 Oct 27;365(17):1597-604. doi: 10.1056/NEJMoa1105816.
  6. Espelund U, Hansen TK, Højlund K, et al. Fasting unmasks a strong inverse association between ghrelin and cortisol in serum: studies in obese and normal-weight subjects. J Clin Endocrinol Metab. 2005 Feb;90(2):741-6. Epub 2004 Nov 2.
  7. Heilbronn LK, Smith SR, Martin CK, Anton SD, Ravussin E. Alternate-day fasting in nonobese subjects: effects on body weight, body composition, and energy metabolism. Am J Clin Nutr. 2005 Jan;81(1):69-73.
  8. Catenacci VA, Pan Z, Ostendorf D, et al. 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.
  9. Natalucci G, Riedl S, Gleiss A, Zidek T, Frisch H. Spontaneous 24-h ghrelin secretion pattern in fasting subjects: maintenance of a meal-related pattern. Eur J Endocrinol. 2005 Jun;152(6):845-50.
  10. Bhutani S, Klempel MC, Berger RA, Varady KA. Improvements in coronary heart disease risk indicators by alternate-day fasting involve adipose tissue modulations. Obesity (Silver Spring). 2010 Nov;18(11):2152-9. doi: 10.1038/oby.2010.54. Epub 2010 Mar 18.
  11. Gilliland IC. Total fasting in the treatment of obesity. Postgrad Med J. 1968 Jan;44(507):58-61.
  12. Trepanowski JF, Kroeger CM, Barnosky A, et al. Effect of Alternate-Day Fasting on Weight Loss, Weight Maintenance, and Cardioprotection Among Metabolically Healthy Obese Adults: A Randomized Clinical Trial. JAMA Intern Med. 2017 Jul 1;177(7):930-938. doi: 10.1001/jamainternmed.2017.0936.
  13. Persynaki A, Karras S, Pichard C. Unraveling the metabolic health benefits of fasting related to religious beliefs: A narrative review. Nutrition. 2017 Mar;35:14-20. doi: 10.1016/j.nut.2016.10.005. Epub 2016 Oct 14.
  14. Sievert K, Hussain SM, Page MJ, et al. Effect of breakfast on weight and energy intake: systematic review and meta-analysis of randomised controlled trials. BMJ 2019; 364 :l42
  15. Varady KA. Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? 2011.
  16. Harvie MN, Pegington M, Mattson MP, et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond). 2010;35(5):714–727. doi:10.1038/ijo.2010.171
  17. Catenacci VA, Pan Z, Ostendorf D. 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.
  18. Ganesan K, Habboush Y, Sultan S. Intermittent Fasting: The Choice for a Healthier Lifestyle. Cureus. 2018;10(7):e2947. 2018 Jul. doi:10.7759/cureus.2947
  19. Moro T, Tinsley G, Bianco A, et al. 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;14(1):290. 2016 Oct. doi:10.1186/s12967-016-1044-0
  20. Rothschild J, Hoddy KK, Jambazian P, Varady K. Time-restricted feeding and risk of metabolic disease: a review of human and animal studies. Nutrition Reviews. 2014; 72(5):308-318.
  21. Shariatpanahi ZV, Shariatpanahi MV, Shahbazi S, Hossaini A, Abadi A. Effect of Ramadan fasting on some indices of insulin resistance and components of the metabolic syndrome in healthy male adults. Br J Nutr. 2008 Jul;100(1):147-51. Epub 2007 Dec 6.
  22. Munsters MJ, Saris WH. Effects of meal frequency on metabolic profiles and substrate partitioning in lean healthy males. PLoS One. 2012;7(6):e38632. doi: 10.1371/journal.pone.0038632. Epub 2012 Jun 13.
  23. Furmli S, Elmasry R, Ramos M, Fung J. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Rep. 2018;2018:bcr2017221854. Published 2018 Oct 9. doi:10.1136/bcr-2017-221854
  24. Carter S, Clifton PM, Keogh JB. Effect of Intermittent Compared With Continuous Energy Restricted Diet on Glycemic Control in Patients With Type 2 Diabetes: A Randomized Noninferiority Trial. JAMA Netw Open. 2018 Jul 6;1(3):e180756. doi: 10.1001/jamanetworkopen.2018.0756.
  25. Carter S, Clifton PM, Keogh JB.The effects of intermittent compared to continuous energy restriction on glycaemic control in type 2 diabetes; a pragmatic pilot trial. Diabetes Res Clin Pract. 2016 Dec;122:106-112. doi: 10.1016/j.diabres.2016.10.010. Epub 2016 Oct 19.
  26. Mattson MP, Moehl K, Ghena N, Schmaedick M, Cheng A. Intermittent metabolic switching, neuroplasticity and brain health. Nat Rev Neurosci. 2018;19(2):63–80. doi:10.1038/nrn.2017.156
  27. Hussin NM, Shahar S, Teng NI, Ngah WZ, Das SK. Efficacy of fasting and calorie restriction (FCR) on mood and depression among ageing men. J Nutr Health Aging. 2013;17(8):674-80. doi: 10.1007/s12603-013-0344-9.
  28. Persynaki A, Karras S, Pichard C. Unraveling the metabolic health benefits of fasting related to religious beliefs: A narrative review. Nutrition. 2017 Mar;35:14-20. doi: 10.1016/j.nut.2016.10.005. Epub 2016 Oct 14.
  29. Horne BD, Muhlestein JB, Lappé DL, et al. Randomized cross-over trial of short-term water-only fasting: metabolic and cardiovascular consequences. Nutr Metab Cardiovasc Dis. 2013 Nov;23(11):1050-7. doi: 10.1016/j.numecd.2012.09.007. Epub 2012 Dec 7.
  30. Ganesan K, Habboush Y, Sultan S. Intermittent Fasting: The Choice for a Healthier Lifestyle. Cureus. 2018;10(7):e2947. Published 2018 Jul 9. doi:10.7759/cureus.2947
  31. Varady KA, Dam VT, Klempel MC, et al. Effects of weight loss via high fat vs. low fat alternate day fasting diets on free fatty acid profiles. Sci Rep. 2015 Jan 5;5:7561. doi: 10.1038/srep07561.
  32. Mattson MP. Lifelong brain health is a lifelong challenge: from evolutionary principles to empirical evidence. Ageing Res Rev. 2015 Mar;20:37-45. doi: 10.1016/j.arr.2014.12.011. Epub 2015 Jan 7.
  33. Longo VD. Programmed longevity, youthspan, and juventology. Aging Cell. 2019 Feb;18(1):e12843. doi: 10.1111/acel.12843. Epub 2018 Oct 17.
  34. Mattson MP, Longo VD, Harvie M. Impact of intermittent fasting on health and disease processes. Ageing Res Rev. 2017 Oct;39:46-58. doi: 10.1016/j.arr.2016.10.005. Epub 2016 Oct 31.
  35. Longo VD, Mattson MP. Fasting: molecular mechanisms and clinical applications. Cell Metab. 2014 Feb 4;19(2):181-92. doi: 10.1016/j.cmet.2013.12.008. Epub 2014 Jan 16.
  36. Johnson JB, Summer W, Cutler RG, et al. Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radic Biol Med. 2007 Mar 1;42(5):665-74. Epub 2006 Dec 14.
  37. Harris L, Hamilton S, Azevedo LB, et al. Intermittent fasting interventions for treatment of overweight and obesity in adults: a systematic review and meta-analysis. JBI Data of Syst Rev and Imp Rep: 2018;16(2):507–547. doi: 10.11124/JBISRIR-2016-003248
  38. Harris L, McGarty A, Hutchison L, Ells L, Hankey C. Shortterm intermittent energy restriction interventions for weight management: a systematic review and metaanalysis. Obesity Reviews. 2017.
  39. Stewart WK, Fleming LW. Features of a successful therapeutic fast of 382 days’ duration. Postgrad Med J. 1973;49(569):203–209.