Nutritional Therapy for Type II Diabetes Mellitus

There is plenty of evidence in the scientific literature of subjects using lifestyle and nutritional interventions to reduce or come off diabetic medication and attain normal control of blood glucose. So if you’re seeing a consultant of any kind who says this is not possible – it’s time to find a different consultant.


It is likely you are already aware that there is a connection between T2DM and nutrition. However, information around nutrition is confusing with a huge divergence of opinions from experts on the cause of T2DM and what dietary habits may be best.

Whether you have been diagnosed with Type II Diabetes Mellitus (T2DM) or pre-diabetes or believe you may be at risk, this post aims to give you some perspective on what you can do and how nutritional therapy may help.

Before we dive in, it is worth mentioning now that there is a lot you can do to manage and even in some cases reverse the T2DM (dependent on length since diagnosis amongst other variables) which can lead to an overall improvement in quality of life and mitigation of other associated conditions.

You don’t need to take our word for this, there is plenty of evidence in the scientific literature of subjects using lifestyle and nutritional interventions to reduce or come off diabetic medication and attain normal control of blood glucose. So if you’re seeing a consultant of any kind who says this is not possible – it’s time to find a different consultant (1–4).

It is important to note that there is no blame to be apportioned here to those who have T2DM or other metabolic disease. Many people watch what they eat, follow government guidelines, portion control and exercise and still end up with metabolic conditions.

So why would this be? Some like to point to genetics, and it’s true there are certain individuals and ethnicities that are more likely to get diabetes. This doesn’t give the full answer though, we had the same genetics 200 years ago and diabetes, obesity and related conditions are exponentially higher than they are now. What is happening now that wasn’t the case then? This article will try and find some resolution for this question (5–8).


How Do You Get T2DM?

The development of any disease may be very different in any given individual, meaning even though the disease outcome can be the same – the root cause is not. However, there are some general rules that are likely to apply to anyone diagnosed with T2DM.

By the time you are diagnosed with T2DM, blood sugar is elevated as shown by above range fasting blood glucose blood test (>7.0 mmol/L) and above range HbA1c blood test (>6.5%) conducted by your physician (HbA1c is effectively a measure of 3 month average blood glucose). As such the T2DM is defined as a blood glucose disease and all medications prescribed to T2 diabetics are dedicated to reducing blood sugar to keep it within the normal range (9).

Unfortunately this is a very simplistic view of the mechanisms involved within T2DM and tells us nothing of how an individual got to this place. No one wakes up one day with high blood sugar for no reason. This is a process that can take years, possibly decades. Understanding this process goes some way to understanding the root cause.

The blood glucose centred view of T2DM has led to the development of drug therapy, such as Metformin (which inhibits blood sugar production from the liver which is the cause elevated blood sugar in T2DM) or extra injected insulin (the hormone that lowers blood glucose) which is required when blood sugar lowering drugs are no longer effective.

When considering nutritional therapy and lifestyle interventions, instead of looking at this from a blood glucose perspective, it’s more helpful to look at this from an insulin perspective.

Insulin is a hormone secreted from an organ known as the pancreas in response to elevation in blood glucose. Insulin has several functions but the main ones relevant to T2DM is telling the liver to stop producing glucose and telling the body’s cells to allow glucose in to be stored or used as energy. When functioning normally you eat, your blood glucose rises from the food consumed and insulin is released which tells your liver cells to stop making glucose and your muscle cells (and other body cells) to take up glucose. This drops your blood glucose back to the normal range within about 1-2 hours following consumption of food (10–12).

The patho-physiology of T2DM starts with something known as insulin resistance (IR). IR refers to a process where the body’s cells, most specifically liver and muscle cells, stop listening to the signal of insulin. This means in-spite of insulin secretion, there isn’t the same suppressive response upon glucose production in the liver and uptake of glucose by the other cells is impaired (12,13).

IR isn’t a disease as such; it is just descriptive of a process that exists on a sliding scale between insulin sensitivity (IS) and IR which changes dependent on the context of your life. For example we know most people are more IS in the mornings than in the evenings, a bad night’s sleep can make you more IR or an infection can make you more IR. There are even some situations where the body may choose to be IR when there is limited energy availability, such as with fasting, so that glucose is spared for use by the brain (14–16).

The problem arises when IR is chronic. This can occur over years with many variables contributing including; dietary choices, muscle loss, chronic stress, chronically insufficient sleep, chronic inflammation, autoimmunity and many other causes and combinations of factors. What all of the factors have in common is that they get cells to stop ‘listening’ to the signal of insulin which means the pancreas has to create a ‘louder’ signal to control blood glucose (12).

By the time T2DM is diagnosed, it is usually following a prolonged period with elevated insulin or hyper-insulinimia (which in itself has several effects in the body including hypertension, cholesterol dysregulation and increased abdominal fat), until the demand for insulin outstrips the maximum supply and then blood glucose starts to creep up out of normal range. At this point it is common for insulin production to drop; no one understands this fully though there are several theories including visceral fat accumulation in the pancreas and β-cell dysregulation caused by excessive demand. At this point it is very difficult to control blood glucose when continuing on the same path (13,17,18).









Figure 1: How the development of Type 2 Diabetes relates to insulin production, insulin sensitivity and blood sugar control (18)



What can be done to support Type 2 Diabetes?

So we know T2DM is a condition of insulin dysregulation and control of blood glucose is only as a result of this, what can be done?

This is a complicated question. As stated previously – the root cause in any given individual maybe different. This means the interventions that may be most effective in one person may not be the same in another.

However, there are some very general principals anyone could follow that we believe, from the scientific evidence and clinical experience could go a long way in improving and in some cases, reversing T2DM.

All the interventions involve lifestyle change, as the Henry Ford saying goes ‘if you’ve always do what you’ve always done, you’ll always get what you’ve always gotten’. This is to say, if you have T2DM, pre-diabetes, metabolic syndrome; something in your life is not agreeing with your biology, living a life or following a diet that does suit your biology is necessary to exact change (19).

Overall – this is about quality of life, we aim to allow anyone, no matter who they are or what stage of life they are at, to experience the best quality of life they can. Whether this is performing in a sport you love, spending more time with children/grandchildren or just having more energy, we’re confident with the right interventions all this is achievable and the label of T2DM needn’t define how you live.



This is probably where you can affect the biggest change in T2DM or any related metabolic condition.

The modern food system is excellent in producing calories to the extent that we’ve solved famine and starvation in developed countries.  Unfortunately in doing this we’ve created food products devoid of nutrition and in some cases inappropriate for human biology (20,21).

Food guidelines are often tied to what is supplied by agri-business and not necessarily to what is optimal for our health. Often people who diligently follow recommendations can end up with metabolic issues.

There is disagreement within nutrition over what nutritionally may be the causative factor in metabolic disease and consequently, a lot of conflicting advice over what you should be eating with dietary trends and fads coming and going. Some dietary trends are more prevalent than others but that may have more to do with money driving these trends than the actual efficacy. So how is someone to choose how to eat?

It is extremely unlikely that one single food type, macronutrient or lifestyle trend is the cause of T2DM, looking at it like this is extremely reductionist. Our blood sugar control exists in a complex system that can be influenced by numerous variables so there is no one causative factor but more likely a combination of many factors have that have driven the rise in prevalence of these conditions (22).

Its true there is a lot of individuality when selecting a diet depending on the individuals context and goals. In fact numerous different diet types that create consistent calorie restriction have been shown to be beneficial for T2DM when adhered to (2,3,23–25).

Though calorie restriction will benefit T2DM, how it’s achieved is likely to determine long term success.  Thinking of metabolic disease in terms of calories is not helpful as your calorie balance is not constant and there are things you can do to eat more and remain healthy or eat less and be unhealthy. This nutritional advice focuses very generally on what is likely to be effective in T2DM.


There are no magic foods in nutrition but protein is damn near close as it gets.

Calories from protein are not the same as calories from carbohydrate or fat – the body utilises carbohydrate and fat primarily as sources of energy. Protein can be used as energy but contributes so many other functions that energy production from protein is very inefficient.

As this is the case protein benefits of protein when compared to carbohydrate and fat can be summarised as follows;

  • Protein is the most satiating macronutrient meaning you are fuller for longer
  • Protein has a higher thermic effect than carbohydrate or fat meaning it causes your metabolic rate to increase
  • Protein stimulates muscle growth which also increases the metabolic rate
  • High protein diets have been shown to reverse:
    • Non-alcoholic fatty liver disease (associated with insulin resistance)
    • Cause greater weight loss when compared with other diets even when calories are equated
    • Be beneficial for cardiovascular risk factors
    • Beneficial for T2DM by contributing to balanced blood glucose (27–32).

Aiming for a protein intake of 25-40% of total daily calories consumed is likely to yield the best results. Getting 40% of calories from protein is not easy but is a decent target to aim for though most will do well to hit 25-35%. To do this you will require a good serving of protein at every meal. Following this advice is likely to result in less hunger between meals and more consistent energy (30).

Best sources of protein are meat, fish and eggs. Animal proteins contain all the essential amino acids and have been shown to be superior to plant proteins when it comes to absorption so these are the best focus for protein within the diet (33).

There is a trend for plant-based diets recently which has been proposed as an intervention for T2DM. A very well controlled metabolic ward study (highest level of evidence possible) compared a plant-based to an animal-based diet for glycemic control and found the animal-based diet to be significantly better despite eating more calories. A plant based diet may be superior to a standard western diet but we would see its use for T2DM as limiting in terms of protein consumption and not necessarily optimal for glycemic control (34).

Once protein intake is fixed, how much carbohydrate or fat makes up the rest of your diet can be down to preference. Though reducing carbohydrates has been shown to be beneficial for glycemic control, the type of carbohydrates may be more important than how much – this will be dealt with further on in this segment.

Vegetable Oils

By vegetable oils we mean sunflower oil, rapeseed oil, peanut oil, basically if it’s a seed or a nut. Olive oil is not a vegetable oil as it’s a fruit, this goes for avocado oil which are both fine to consume.

Vegetable oils were originally used as lubrication for machines until it was discovered in the early 1900s that they could make a cheap ingredient to add to food (35).

This is a great example of a resolution to the calorie problem whilst adding no nutrition to the human diet. As well as being calorie-dense and nutrient-poor they are composed of a polyunsaturated fat known as omega 6 or linoleic acid (36).

Linoleic acid is actually essential in our diets in very small amounts and needs to be balanced with the consumption of an equal amount of omega 3 polyunsaturated fat. We find that ancestral populations consume omega 6 to omega 3 in a ratio of about 2:1 or even 1:1 in some cases (37–39).

These fats actually get incorporated into our cell membranes where they affect the communication and messaging of our cells. In balance, they produce normal amounts of inflammation and anti-inflammation as both processes are necessary for health.

When we have an excess of omega 6 we find that the balance of inflammation is dysregulated and tends towards more inflammation. Inflammation is implicit in T2DM and it is hypothesised that an inflammatory state may be a cause for insulin resistance in the first place (37,40,41).

Modern humans are consuming composed of 10-20% polyunsaturated fat of which about 95% is omega 6. Compare this to those living ancestral lifestyles (and have extremely low rates of chronic disease) where around 2% of their diet is made up from a balance of omega 6/omega 3 fats (39).

These oils are not really human food, they are highly processed and heat-treated to extract the oil which frequently makes the oils oxidised and rancid. Consuming vegetable oil increases the inflammation and may contribute to insulin resistance, these are frequently found in processed food and there is no reason to eat them. They are best avoided for T2DM (36,42,43).


This is controversial as though it is generally agreed refined grains such as flour are off the menu for diabetics, whole grains are frequently touted as something that should make up most of your diet.

The issue with this is; clinically – we just don’t see a benefit to grain consumption. If you have T2DM or are concerned about insulin resistance, you can test this for yourself. Eat a bunch of eggs for breakfast and test your blood sugar before and after. Now do the same with oats, you could even weigh and measure the foods to ensure they are of equal calories – the results will speak for themselves (34).

Though carbohydrates are not bad in and of themselves, grains are a much denser source of carbohydrates than other foods such as root vegetables. Though some may be able to re-introduce these foods on occasion when they have improved their glycemic control, eating this when diabetic will lead to blood sugar fluctuations that may result in energy crashes and the need to consume more food between meals (34,44).

Grains include oats, rice (white and brown), wheat, barley, rye and other agricultural plants.

Processed Foods

These foods are multi-ingredient low protein, high carbohydrate, high fat. They tend to be made of sugar, refined grain and vegetable fat. They are the perfect storm for dysregulated blood sugar, provide a load of calories, no nutrition and make you want to eat more.

An extremely well controlled and conducted metabolic ward study showed people would eat 500 calories more a day on processed foods compared to whole food (45).

To be clear we are talking about biscuits, cakes, pastries, chocolate bars, sweets, ice cream. This stuff is trash, it shouldn’t be in anyone’s diet regularly especially not someone with T2DM.



If you think the key to T2DM is ‘eating less and moving more, you may think that a long steady-state cardio exercise like running or cycling is best.

Though long-distance cardio is certainly going to burn the most calories, it comes a close second to sitting on the couch and eating processed food in terms of the worst thing you can do for T2DM.

Long steady state chronic cardio sends a message of adaptation for your body to be efficient, to conserve energy. This is exactly the opposite of what you want in T2DM, you want to be inefficient with energy, you want your body to burn through energy at a faster rate so that your demand for glucose is increased and this way you won’t have too much in your blood.

Think about this for a second, you go running 3-4 times a week which tells your body you want it to be efficient. Your body listens, adapts, and reduces your metabolic rate. Then you go and live a sedentary lifestyle (as most people do) the rest of the time with your efficient metabolism whilst surrounded by an abundance of food. This is a recipe for disaster, you want a faster metabolism not a slower one (46,47).

One of the ways running reduces your metabolism is by reducing muscle mass. Muscle is expensive tissue that takes energy to build and maintain, if your body wants to be efficient this is one of the first things to go. The two biggest glucose sinks in your body are your liver and your muscles – increase muscle mass increases insulin sensitivity. Unless we do something about it muscle mass starts reducing when we get to 30. It is actually a major reason for people becoming more insulin resistant and even diabetic. As we lose muscle, there is fewer places to put blood sugar so it rises.

The best way to increase muscle mass is resistance training. Anyone can resistance train, anyone has the ability to put on muscle – if you are alive you can adapt to stimulus. The beauty of resistance training is how scalable it is, whether you are 90 or 25 there is a level of resistance that you can do that is appropriate that will help you increase strength and muscle mass (48).

Nutritional therapists at Biospan are familiar with prescribing appropriately scaled resistance training programs. The other option would be to find a good trainer who is experienced with T2DM.



There are many wonderful things about modern life that make things more convenient. Unfortunately convenient doesn’t always mean better. Our modern lives are in no way representative of the environment we evolved in and doesn’t always match well with our biology. Many of the differences between our evolved and modern environment can be perceived as stressful by our bodies.

If things are so easy why is this? We are built pretty well to deal and adapt to acute stress – in fact acute stress has been shown to be healthy (resistance training for example). However, we are not very well placed to handle low levels of ongoing chronic stress. Things like work stress, family stress, arguments, money worries, scrolling social media, eating processed food, high blood sugar, low blood sugar and health worries are all low levels stressors that affect our stress hormone production but don’t necessarily ever go away like an acute stressor (49).

This effect on hormones can change our biochemistry. For example one of the master stress hormones, cortisol, instructs the liver to produce blood glucose to deal with stress. We often find that stress is related to T2DM and it may be to do with this mechanism (50–52).

So what can be done as it’s not possible, realistic or necessarily desirable to eliminate most of these stressors.

The solution is to change your perception of stress. This is not something that happens by magic, but something that can actually be practiced. Just like a muscle, your mind can be trained. Proven methods for stress management are meditation, yoga and gratitude journaling. Meditation has actually been shown to shrink the amygdala (the fight or flight part of the brain) over time. Which you do will be down to preference and what you can be consistent with – this isn’t a quick fix, but over time you may find that you are more resilient to stress (53–57).

Headspace is a good place to start for meditation, there are a plethora of online courses for yoga and information for gratitude journaling.



Really this is related to stress as if you improve sleep you will improve stress and vice versa (58).

Sleep is crucial for so many functions in the body, but specific to T2DM, lack of sleep results in insulin resistance and is perceived as a stress by the body. There is no question that improving sleep will improve outcomes in any condition (14).

Having a regular wake up time is crucially important. This is where you set your body clock, whether you’ve had 8 hours or none, get up at the same time every day and ideally get sun on your eyes when it comes up. Once you’ve done this you set yourself up for a good sleep.

Practicing ‘sleep hygiene’ can also increase the quality of your sleep. This means; having a regular bed time. Making sure you start to wind down 2 hours before bed, (have calm conversation, doing something non-stimulating). Make sure your room is dark and look at no screens within an hour of bed (ideally 2 hours). Make sure your room is cold, ideally between 16-18 degrees centigrade (our bodies need to cool down at night to be able to get to sleep). All of these practices have been shown to reduce time to fall asleep, increase sleep quality and reduce waking up in the middle of the night (59).

Following this advice will set up your circadian rhythm to maximise the chance of good sleep.



Someone who consumes a grain free, high protein diet with no processed food, resistance train, manages stress and sleep is likely to greatly improve their glycemic control.

For some people, this advice alone will be enough for them to achieve their goals. For others it may get them some of the way or just lead to more questions than answers.

That’s where Biospan can help. With our functionally trained nutritionists we can unravel your health history and use testing to identify what your root cause(s) may be and design a suitable intervention that you can work with.

If you found this article interesting but want to know more, please get in touch and we will be happy to help.



  1. Roberts CK, Barnard RJ. Effects of exercise and diet on chronic disease. Journal of Applied Physiology. 2005.
  2. Hallberg SJ, Gershuni VM, Athinarayanan SJ. Reversing type 2 diabetes: A narrative review of the evidence. Nutrients. 2019;
  3. Taylor R. Reversing type 2 diabetes. Pract Diabetes. 2011;
  4. Westman EC, Yancy WS, Mavropoulos JC, Marquart M, McDuffie JR. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab. 2008;
  5. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: Underlying causes and modification by exercise training. Compr Physiol. 2013;
  6. Mendrick DL, Diehl AM, Topor LS, Dietert RR, Will Y, La Merrill MA, et al. Metabolic Syndrome and Associated Diseases: From the Bench to the Clinic. Toxicological sciences : an official journal of the Society of Toxicology. 2018.
  7. Shai I, Jiang R, Manson JE, Stampfer MJ, Willett WC, Colditz GA, et al. Ethnicity, obesity, and risk of type 2 diabetes in women: A 20-year follow-up study. Diabetes Care. 2006;
  8. Xiang L, Wu H, Pan A, Patel B, Xiang G, Qi L, et al. FTO genotype and weight loss in diet and lifestyle interventions: A systematic review and meta-analysis. Am J Clin Nutr. 2016;
  9. Of D, Mellitus D. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014;
  10. Stumvoll M, Tataranni PA, Stefan N, Vozarova B, Bogardus C. Glucose allostasis. Diabetes. 2003;
  11. McGuckin E, Cade JE, Hanison J. The pancreas. Anaesthesia and Intensive Care Medicine. 2020.
  12. Petersen MC, Shulman GI. Mechanisms of insulin action and insulin resistance. Physiological Reviews. 2018.
  13. McArdle MA, Finucane OM, Connaughton RM, McMorrow AM, Roche HM. Mechanisms of obesity-induced inflammation and insulin resistance: Insights into the emerging role of nutritional strategies. Frontiers in Endocrinology. 2013.
  14. Stenvers DJ, Scheer FAJL, Schrauwen P, la Fleur SE, Kalsbeek A. Circadian clocks and insulin resistance. Nature Reviews Endocrinology. 2019.
  15. Fernández-Real JM, Pickup JC. Innate immunity, insulin resistance and type 2 diabetes. Trends Endocrinol Metab. 2008;
  16. Bak AM, Vendelbo MH, Christensen B, Viggers R, Bibby BM, Rungby J, et al. Prolonged fasting-induced metabolic signatures in human skeletal muscle of lean and obese men. PLoS One. 2018;
  17. Samuel VT, Shulman GI. The pathogenesis of insulin resistance: Integrating signaling pathways and substrate flux. Journal of Clinical Investigation. 2016.
  18. Ramlo-Halsted BA, Edelman S V. The Natural History of Type 2 Diabetes: Practical Points to Consider in Developing Prevention and Treatment Strategies. Clin Diabetes. 2000;
  19. Hunter DJ. Gene-environment interactions in human diseases. Nature Reviews Genetics. 2005.
  20. r H, Wood BM, Raichlen DA. Hunter-gatherers as models in public health. Obesity Reviews. 2018.
  21. Tuso P. Prediabetes and lifestyle modification: time to prevent a preventable disease. Perm J. 2014;
  22. O’Neill S, O’Driscoll L. Metabolic syndrome: A closer look at the growing epidemic and its associated pathologies. Obes Rev. 2015;
  23. Larson-Meyer DE, Heilbronn LK, Redman LM, Newcomer BR, Frisard MI, Anton S, et al. Effect of calorie restriction with or without exercise on insulin sensitivity, ??-cell function, fat cell size, and ectopic lipid in overweight subjects. Diabetes Care. 2006;
  24. Zeevi D, Korem T, Zmora N, Israeli D, Rothschild D, Weinberger A, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015;
  25. Kelly T, Unwin D, Finucane F. Low-carbohydrate diets in the management of obesity and type 2 diabetes: A review from clinicians using the approach in practice. International Journal of Environmental Research and Public Health. 2020.
  26. Petracci M, Soglia F, Leroy F. Rabbit meat in need of a hat-trick: from tradition to innovation (and back). Meat Science. 2018.
  27. Cordain L, Eaton SB, Miller JB, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: Meat-based, yet non-atherogenic. Eur J Clin Nutr. 2002;
  28. Santesso N, Akl EA, Bianchi M, Mente A, Mustafa R, Heels-Ansdell D, et al. Effects of higher-versus lower-protein diets on health outcomes: A systematic review and meta-analysis. European Journal of Clinical Nutrition. 2012.
  29. Phillips SM, Chevalier S, Leidy HJ. Protein “requirements” beyond the RDA: implications for optimizing health. Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2016.
  30. Cuenca-Sanchez M, Navas-Carrillo D, Orenes-Pinero E. Controversies Surrounding High-Protein Diet Intake: Satiating Effect and Kidney and Bone Health. Adv Nutr An Int Rev J. 2015;
  31. Duarte SMB, Faintuch J, Stefano JT, de Oliveira MBS, Mazo DF de C, Rabelo F, et al. Hypocaloric high-protein diet improves clinical and biochemical markers in patients with Nonalcoholic Fatty Liver Disease (NAFLD). Nutr Hosp. 2014;
  32. Antonio J, Peacock CA, Ellerbroek A, Fromhoff B, Silver T. The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. J Int Soc Sports Nutr. 2014;
  33. Berrazaga I, Micard V, Gueugneau M, Walrand S. The role of the anabolic properties of plant-versus animal-based protein sources in supporting muscle mass maintenance: a critical review. Nutrients. 2019.
  34. Hall KD, Guo J, Courville AB, Boring J, Brychta R, Chen KY, et al. Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake. Nat Med. 2021;
  35. Garcés R, Martínez-Force E, Salas JJ. Vegetable oil basestocks for lubricants. Grasas y Aceites. 2011;
  36. Orsavova J, Misurcova L, Vavra Ambrozova J, Vicha R, Mlcek J. Fatty acids composition of vegetable oils and its contribution to dietary energy intake and dependence of cardiovascular mortality on dietary intake of fatty acids. Int J Mol Sci. 2015;
  37. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;
  38. Calder PC. Omega-3 polyunsaturated fatty acids and inflammatory processes: Nutrition or pharmacology? Br J Clin Pharmacol. 2013;
  39. Simopoulos AP. Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases. Biomed Pharmacother. 2006;
  40. Fontes JD, Rahman F, Lacey S, Larson MG, Vasan RS, Benjamin EJ, et al. Red blood cell fatty acids and biomarkers of inflammation: A cross-sectional study in a community-based cohort. Atherosclerosis. 2015;
  41. Nicolaou A. Eicosanoids in skin inflammation. Prostaglandins Leukot Essent Fat Acids. 2013;
  42. Sears B, Perry M. The role of fatty acids in insulin resistance. Lipids in Health and Disease. 2015.
  43. Erhan SZ, Sharma BK, Perez JM. Oxidation and low temperature stability of vegetable oil-based lubricants. Ind Crops Prod. 2006;
  44. Manheimer EW, Van Zuuren EJ, Fedorowicz Z, Pijl H. Paleolithic nutrition for metabolic syndrome: Systematic review and meta-analysis. Am J Clin Nutr. 2015;
  45. Hall KD, Ayuketah A, Brychta R, Cai H, Cassimatis T, Chen KY, et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 2019;
  46. Melby C, Scholl C, Edwards G, Bullough R. Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate. J Appl Physiol. 1993;
  47. Smith RL, Soeters MR, Wüst RCI, Houtkooper RH. Metabolic flexibility as an adaptation to energy resources and requirements in health and disease. Endocrine Reviews. 2018.
  48. Van Der Heijden GJ, Wang ZJ, Chu Z, Toffolo G, Manesso E, Sauer PJJ, et al. Strength exercise improves muscle mass and hepatic insulin sensitivity in obese youth. Med Sci Sports Exerc. 2010;
  49. McEwen BS. Neurobiological and Systemic Effects of Chronic Stress. Chronic Stress. 2017;
  50. Paredes S, Ribeiro L. Cortisol: The villain in metabolic syndrome? Rev Assoc Med Bras. 2014;
  51. Joseph JJ, Golden SH. Cortisol dysregulation: the bidirectional link between stress, depression, and type 2 diabetes mellitus. Annals of the New York Academy of Sciences. 2017.
  52. Cohen S, Janicki-Deverts D, Doyle WJ, Miller GE, Frank E, Rabin BS, et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc Natl Acad Sci U S A. 2012;
  53. Sharma M, Rush SE. Mindfulness-Based Stress Reduction as a Stress Management Intervention for Healthy Individuals: A Systematic Review. J Evidence-Based Complement Altern Med. 2014;
  54. Brown RP, Gerbarg PL. Yoga breathing, meditation, and longevity. In: Annals of the New York Academy of Sciences. 2009.
  55. Chlebak CM, James S, Westwood MJ, Gockel A, Zumbo BD, Shapiro SL. Mindfulness meditation & gratitude journalling: The experiences of graduate counselling psychology students. Couns Spiritual / Couns spiritualité. 2013;
  56. Kral TRA, Schuyler BS, Mumford JA, Rosenkranz MA, Lutz A, Davidson RJ. Impact of short- and long-term mindfulness meditation training on amygdala reactivity to emotional stimuli. Neuroimage. 2018;
  57. Li AW, Goldsmith CAW. The effects of yoga on anxiety and stress. Alternative Medicine Review. 2012.
  58. Kolb H, Martin S. Environmental/lifestyle factors in the pathogenesis and prevention of type 2 diabetes. BMC Medicine. 2017.