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All You Need To Know About Intermittent Fasting 

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Posted: 26/09/2017

Updated: 12/01/2018

Intermittent fasting (IF) is a practice that involves abstaining from consumption of foods for a period of time, usually on consecutive days (daily) or alternative days (couple times a week).


Human beings have been fasting throughout history due to the lack of food available and also during religious practices like Ramadan.


So why should we practice intermittent fasting? Studies have proven that intermittent fasting not only can improve insulin resistance over time and can lead to a reduction in blood sugar levels (1), it can also help with weight loss, improve body composition and so much more. 

It is important to mention that fasting is distinct from starvation which is a nutritional insufficiency which can result in degeneration and death (2).

Why? -Possibilities


1. Lose weight

Intermittent fasting lowers insulin, raises growth hormone and noradrenaline levels. These hormones aid the breakdown of body fat and the body utilises these for energy resulting in weight loss. Noradrenaline also increases your metabolic rate to help you burn more calories (3).

2. Improve body composition

Moreover, it may improve your body composition as growth hormone also promotes muscle building. In one study, healthy subjects only ate once daily without reducing overall caloric intake. Weight remained the same but overall body composition improved as body fat decreased and lean weight increased (4).

3. Reduce cellular aging

Studies have shown to reduce cellular ageing in mammals via the increase in AMPK enzyme expression (5, 6, 7), cellular level repairs and metabolic rejuvenation (8).

4. Protection against type 2 diabetes

Changes in genes and molecules not only relate to longevity but also protection against disease. Intermittent fasting helps reducing insulin concentrations and improves insulin resistance which in turns, helps to reduce the risk of type 2 diabetes (9, 10).

5. Possible cancer prevention

Since insulin levels are lowered, it may help prevent cancer. Tumour cells have more insulin receptors than normal cells so high insulin levels can result in tumour growth.


Tumour cells also depend upon anaerobic metabolism of glucose for energy. During a fast, blood glucose concentrations are lowered and hence, these cells are starved of energy.

6. Other benefits?

Intermittent fasting has potential benefits for cognitive function, inflammation, hypertension and metabolic syndrome but not all studies have been conclusive (11).

Intermittent fasting may possibly help with weight loss, improvement in body composition, longevity and protection against type 2 diabetes and cancer.


*However, few randomised controlled trials (RCT) and observational studies support the health benefits from fasting, further research in humans is required.

Arguments against IF


1. Side effects

Fatigue, headaches, lack of concentration and poor mood may occur during the course of fasting. However, this may be temporary as your body adapts to the new changes.

2. May be harmful for some people

Children and pregnant women are susceptible to hypoglycaemia and are advised against this.


According to NHS choices, fasting may cause heartburn and is not advised for type 1 diabetic patients.

3. You have had or have an eating disorder (anorexia or bulimia)

Intermittent fasting may contribute to eating disorders or worsen them. It can create an unhealthy obsession with food (12).


Hyperphagia (overeating) may occur on non-restricted days (13) and may interfere with your psychological wellbeing (i.e. guilt or shaming yourself). Unhealthy obsessive-compulsive disorder (OCD) eating habits may develop if this worsens and intermittent fasting is not advised until a medical professional is consulted.

4. Underlying thyroid or adrenal issue

Individuals with an underlying thyroid or adrenal disease will have excessive cortisol concentrations in their systems.


Fasting is a state of stress which signals the body to secrete the stress hormone, cortisol into the system.


Elevated levels of cortisol stimulate gluconeogenesis (generation of glucose from substrates like protein from muscles) and liver and muscle glycogenolysis (breakdown of glycogen) meaning that you can have the effect of storing fat and breaking muscle tissue instead.

Intermittent fasting may be harmful for children, pregnant women, type 1 diabetics, those with eating disorders and those with thyroid and adrenal issues.

Body’s response to fasting


1. Fed state lasts for 3-5 hours depending on the amount and types of nutrients ingested

During meals, insulin levels are raised by the pancreatic beta cells.


Glucose is taken up by tissues such as the muscle or brain for direct use.


Excess glucose is stored as glycogen in the liver hepatocytes.

2. Fasting state or post-absorptive state occurs around 4 hours after last meal

Your body uses up most of the glucose from food and insulin levels fall.


Glycogenolysis (breakdown of glycogen) is stimulated by glucagon, a hormone that  releases glucose for energy which is to be used by the peripheral tissues and the brain. 

3. Gluconeogenic phase 

This phase occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise.


Gluconeogenic phase is important for maintaining blood glucose levels and the time when it occurs depends on how fast food is absorbed and how much liver glycogen is present.


After an overnight fast, the ability of the liver to carry out gluconeogenesis (production of glucose from other non-sugar compounds) is enhanced.


The release of gluconeogenic precursors from peripheral tissues and free fatty acids (FFA) from fat is increased due to low levels of insulin (14).


However, very little gluconeogenesis starts after 12 hours and glycogen still remains as the main source of energy.


After 24 hours, liver glycogen stores are depleted and gluconeogenesis becomes the prime source of energy for the next 24 hours (15).


Gluconeogenesis, the production of glucose from different non-sugar compounds, is stimulated by the increase in glucagon.


The liver manufactures glucose from amino acids, lactate, and glycerol.


  • Protein is broken down into amino acids in the liver (by-product urea)

  • Triglycerides (TAG) are broken down into fatty acids and glycerol




break down

break down




Fatty acids



Amino acids

via Transamination

  • synthesised into other compounds

  • stored as glycogen or fat

  • synthesised into cellular membrane

  • stored as triglyceride in fat cells

  • stored as glycogen or fat

  • made into new protein compounds

oxidised for energy

The body goes into a fed-fasting cycle and gluconeogenic phase. The fed state involves absorption and storage of nutrients. The fasting state is where the body utilises glycogen for energy and the gluconeogenic phase involves the breakdown of substrates for gluconeogenesis.

Hormones involved



Insulin has effects on both the synthetic (esterification) and breakdown (lipolysis) pathways of fats.


Its function is to inhibit lipolysis by blocking the enzyme, hormone-sensitive lipase (HSL), which is involved in the breakdown of stored fats. 


As fasting results in a drop in insulin, it removes the inhibitory effects on hormone-sensitive lipase (HSL) allowing it to mobilise the stored fats for energy (16).

Growth hormone

Growth hormone is released from the pituitary gland in the brain and regulated by the hypothalamus.


This hormone is stimulated by several factors such as oestrogen, testosterone, deep sleep and exercise.


This is an anabolic hormone that increases the development of bone, muscle tissue, protein synthesis and strengthens the immune system.


During a fast, growth hormones increase as much as 5-fold (17) and this facilitates fat burning and muscle gain.


Catecholamines are hormones produced by the adrenal glands situated on top of the kidneys.


The three catecholamines are adrenaline (epinephrine), noradrenaline (norepinephrine) and dopamine.

Noradrenaline and adrenaline can increase metabolic rate during a fast and utilises fat stores by activating hormone-sensitive lipase (HSL) in the adipose tissue.

With all these hormones, short-term fasting increases metabolic rate which helps to burn more calories resulting in weight loss.

Does it really work?


Won’t it make you lose muscle (burn protein)?

Although most people who lose weight will lose both muscle and fat, it has been claimed that intermittent fasting retains muscle mass (18). You will not start to lose muscle until 24 hours later after your meal depending on how much you eat.


Won’t it put you in starvation mode and lower your basal metabolism?

We should define these two terms now


  • Fasting: the body is consuming its reserves

  • Starving: all reserves have already been depleted and the body is living on vital tissue (muscle)


Short-term fasting can increase your metabolism. As mentioned, the secretion of adrenaline speeds up metabolism and thus increasing the ability to burn calories. Metabolism will not drop after around 72 hours of fast.


But I’ll be overwhelmed with hunger!

You may mistake your hunger for dehydration. Try drinking more water, tea or black coffee during your day and keep yourself immersed in activities as people tend to eat when they are bored.

Popular methods


The widely studied and popular approaches are the 16/8 method, alternate day fasting and the 5:2 diet. All of them can be effective and it all comes down to the individual.


You may drink water, black coffee and non-caloric beverages during the fast to reduce hunger levels.


Remember, this does not mean that you can eat anything you want (i.e. junk food, processed food, etc.). It is very important that you eat healthily and meet nutritional requirements!


16/8 method (Leangains protocol)


  • Skip breakfast, eat your first meal at noon and last meal at 8 pm. Fast during your sleep and repeat.

  • 16/8 for men and 14/10 for women


This easier method suggests that you should eat every day within an 8-hour window and fast for the other 16. For women, it's a 10-hour window and 14 hours fast.


Breakfast is skipped and eating is resumed in the early afternoon depending on your lifestyle (around 1-2pm). You then have 8 hours to meet your daily requirements and fast overnight during sleep.


This is the simplest way to include fasting into your life and more likely to commit to it.

Bulletproof coffee

You may incorporate bulletproof coffee into your mornings and continue to fast until the early afternoon. Bulletproof coffee contains healthy fats from grass-fat butter to control your hunger pangs. The presence of coconut oil can increase ketone production and boost metabolism. Evidence has shown to improve both physical and mental performance as well (19,20).

Eat-stop-eat (fasting for 24 hours)


This involves fasting for 24 hours on alternate days. This is an efficacious dietary method (21). Longer fasts may provide a deeper cellular cleaning (autophagy) but this may also be achieved with exercise.


As shown in a study, alternate day fasting resulted in fat oxidation and weight loss in obese patients (22). However, the downside is that after 16 hours for men and 14 hours for women, there is a possibility of losing muscle.


This method takes discipline and hard to follow. It is difficult to incorporate this into your daily plans and you will face difficulties during mealtimes. However, to begin with, you may build up slowly to 24 hours of having no food. Drinking plenty of liquids is vital but remember that you should not have any sugar in your drinks.

The 5:2 diet 

Eat 500-600 calories (a restriction which is 60%-70% below estimated requirements) on two non-consecutive days and eat normally for the remaining five days.


Fast on Mondays and Fridays (or any other day of your choice) with 2 or 3 small meals

There are different fasting methods and it depends on which one fits best into your schedule. Remember to have a well-balanced nutritious diet.


  • References
    Irritable bowel syndrome [Online] Available at: [Accessed: 22 June 2018]. Saha, L. (2014). Irritable bowel syndrome: Pathogenesis, diagnosis, treatment, and evidence-based medicine. World Journal of Gastroenterology, 20(22), p.6759. D. Cashman, M., K. Martin, D., Dhillon, S. and R. Puli, S. (2016). Irritable Bowel Syndrome: A Clinical Review. Current Rheumatology Reviews, 12(1), pp.13-26. Guidelines--Rome III Diagnostic Criteria for Functional Gastrointestinal Disorders. (2006). Journal of Gastrointestinal and Liver Diseases, 15(3), pp.307-12. Drossman, D. (2016). Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features, and Rome IV. Gastroenterology, 150(6), pp.1262-1279.e2. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Enck, P., Aziz, Q., Barbara, G., Farmer, A., Fukudo, S., Mayer, E., Niesler, B., Quigley, E., Rajilić-Stojanović, M., Schemann, M., Schwille-Kiuntke, J., Simren, M., Zipfel, S. and Spiller, R. (2016). Irritable bowel syndrome. Nature Reviews Disease Primers, 2, p.16014. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Hungin, A., Chang, L., Locke, G., Dennis, E. and Barghout, V. (2005). Irritable bowel syndrome in the United States: prevalence, symptom patterns and impact. Alimentary Pharmacology and Therapeutics, 21(11), pp.1365-1375. Gibson, P., Varney, J., Malakar, S. and Muir, J. (2015). Food Components and Irritable Bowel Syndrome. Gastroenterology, 148(6), pp.1158-1174.e4. Card, T., Canavan, C. and West, J. (2014). The epidemiology of irritable bowel syndrome. Clinical Epidemiology, p.71. Occhipinti, K. and Smith, J. (2012). Irritable Bowel Syndrome: A Review and Update. Clinics in Colon and Rectal Surgery, 25(01), pp.046-052. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Zhou, Q. and Verne, G. (2011). New insights into visceral hypersensitivity—clinical implications in IBS. Nature Reviews Gastroenterology & Hepatology, 8(6), pp.349-355. Ghoshal, U., Kumar, S., Mehrotra, M., Lakshmi, C. and Misra, A. (2010). Frequency of Small Intestinal Bacterial Overgrowth in Patients with Irritable Bowel Syndrome and Chronic Non-Specific Diarrhea. Journal of Neurogastroenterology and Motility, 16(1), pp.40-46. Ghoshal, U., Shukla, R. and Ghoshal, U. (2017). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy. Gut and Liver, 11(2), pp.196-208. Ghoshal, U. (2014). Irritable bowel syndrome and small intestinal bacterial overgrowth: Meaningful association or unnecessary hype. World Journal of Gastroenterology, 20(10), p.2482. Marshall, J., Thabane, M., Garg, A., Clark, W., Moayyedi, P. and Collins, S. (2010). Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut, 59(5), pp.605-611. Marshall, J., Thabane, M., Garg, A., Clark, W., Salvadori, M. and Collins, S. (2006). Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery. Gastroenterology, 131(2), pp.445-450. Spiller, R. and Campbell, E. (2006). Post-infectious irritable bowel syndrome. Current Opinion in Gastroenterology, 22(1), pp.13-17. Ericsson, C., Hatz, C. and DuPont, A. (2008). Postinfectious Irritable Bowel Syndrome. Clinical Infectious Diseases, 46(4), pp.594-599. Grenham, S., Clarke, G., Cryan, J. and Dinan, T. (2011). Brain?Gut?Microbe Communication in Health and Disease. Frontiers in Physiology, 2. The Brain-Gut Connection [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Fichna, J. and Storr, M. (2012). Brain-Gut Interactions in IBS. Frontiers in Pharmacology, 3. El-Salhy, M. and Gundersen, D. (2015). Diet in irritable bowel syndrome. Nutrition Journal, 14(1). Irritable Bowel Syndrome - National Library of Medicine - PubMed Health [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Rao, S., Yu, S. and Fedewa, A. (2015). Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome. Alimentary Pharmacology & Therapeutics, 41(12), pp.1256-1270. Moayyedi, P., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Ford, A. (2014). The Effect of Fiber Supplementation on Irritable Bowel Syndrome: A Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(9), pp.1367-1374. FRANCIS, C. (1994). Bran and irritable bowel syndrome: time for reappraisal. The Lancet, 344(8914), pp.39-40. Vazquez–Roque, M., Camilleri, M., Smyrk, T., Murray, J., Marietta, E., O'Neill, J., Carlson, P., Lamsam, J., Janzow, D., Eckert, D., Burton, D. and Zinsmeister, A. (2013). A Controlled Trial of Gluten-Free Diet in Patients With Irritable Bowel Syndrome-Diarrhea: Effects on Bowel Frequency and Intestinal Function. Gastroenterology, 144(5), pp.903-911.e3. Ford, A., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Moayyedi, P. (2014). Efficacy of Prebiotics, Probiotics and Synbiotics in Irritable Bowel Syndrome and Chronic Idiopathic Constipation: Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(10), pp.1547-1561. Basturk, A., Artan, R. and Yilmaz, A. (2016). Efficacy of synbiotic, probiotic, and prebiotic treatments for irritable bowel syndrome in children: A randomized controlled trial. The Turkish Journal of Gastroenterology, 27(5), pp.439-443. Zhang, Y., Li, L., Guo, C., Mu, D., Feng, B., Zuo, X. and Li, Y. (2016). Effects of probiotic type, dose and treatment duration on irritable bowel syndrome diagnosed by Rome III criteria: a meta-analysis. BMC Gastroenterology, 16(1). Guandalini, S., Magazzù, G., Chiaro, A., La Balestra, V., Di Nardo, G., Gopalan, S., Sibal, A., Romano, C., Canani, R., Lionetti, P. and Setty, M. (2010). VSL#3 Improves Symptoms in Children With Irritable Bowel Syndrome: A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Crossover Study. Journal of Pediatric Gastroenterology and Nutrition, 51(1), pp.24-30. Paineau, D., Payen, F., Panserieu, S., Coulombier, G., Sobaszek, A., Lartigau, I., Brabet, M., Galmiche, J., Tripodi, D., Sacher-Huvelin, S., Chapalain, V., Zourabichvili, O., Respondek, F., Wagner, A. and Bornet, F. (2007). The effects of regular consumption of short-chain fructo-oligosaccharides on digestive comfort of subjects with minor functional bowel disorders. British Journal of Nutrition, 99(02). Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. Peppermint Oil for IBS: Does it Work? [Online] Available at: [Accessed: 24 June 2018]. Grigoleit, H. and Grigoleit, P. (2005). Peppermint oil in irritable bowel syndrome. Phytomedicine, 12(8), pp.601-606. Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. IBS Diet: What to Do and What to Avoid [Online] Available at: [Accessed: 24 June 2018]. Johannesson, E., Simrén, M., Strid, H., Bajor, A. and Sadik, R. (2011). Physical Activity Improves Symptoms in Irritable Bowel Syndrome: A Randomized Controlled Trial. The American Journal of Gastroenterology, 106(5), pp.915-922.

Results vary with everyone in terms of fat loss, muscle gain, performance in sports and so on.


For individuals within normal weight ranges, it is unclear if intermittent fasting will bring you many benefits.


However, if you do want to try it out, remember to have a healthy diet and do not binge on junk food! Happy fasting everyone!

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