Fasting – Ancestral Cure For Diabetes?

Today, we are bombarded with high-calorie foods; sweetened coffee, sugary drinks, processed snacks, and convenience food. This environment of caloric excess is at odds with our evolutionary past. In combination with our modern sedentary lifestyle, this sets us up for obesity, type II diabetes and other metabolic diseases. Our hunter-gatherer ancestors did not eat three meals a day, nor did they snack at regular intervals. Their eating patterns would regularly involve intermittent periods of reduced food (energy) intake.1

Now, some in the science community are saying that mimicking this intermittent fasting could be a simple, convenient, and cost-effective ancestral strategy for reversing type II diabetes.

Fasting is not a new dietary strategy. It became a spiritual practice, used widely amongst virtually all the major religions. At the turn of the 20th century, American physicians Frederick Allen and Elliott Joslin wrote extensively about fasting for diabetes management.2,3,4 This was before its use as a therapeutic tool fell out of favor during the pharmacological revolution of the 1950s.

Rates of diabetes are at an all-time high. One out of two Americans is pre-diabetic or diabetic, and insulin resistance has shown promise as a reliable predictor of age-related chronic diseases.5,6,7 Chronically elevated blood sugar and insulin levels are a hallmark of type II diabetes. Fasting (or intermittent fasting) has been shown to be effective in the short-term for reducing hyper-insulinemia, supporting weight loss, and improving metabolic markers associated with diabetes.8,9,10,11,12,13,14,15,16,17,18

 

Hyper-Insulinemia & Diabetes

In general terms, the more overweight or out of shape you are, the more insulin your cells require to accomplish the same task as a fit or lean person. Too many years of excessive caloric intake,  typically from too much sugar and calorie-dense processed foods, chronically stimulate the pancreas. The body responds to this exaggerated stimulus by dampening its response.  To appreciate the magnitude of the response, for every 1uU change in your insulin levels (not a dramatic shift,) you’ll experience approximately a 20% increase in insulin resistance.19 In essence, your cells refuse to take in more energy in a last-ditch attempt to save themselves.

The research supporting hyper-insulinemia as a cause of insulin resistance is sparse, but has considerable merit. Patients with pancreatic tumours that stimulate beta-cell activity (the insulin producing cells) to the greatest degree also have the greatest insulin resistance compared to less insulin resistance in the milder forms.20,21 In another study, researchers infused a constant physiologic dose of insulin into healthy, non-insulin resistant men whom all developed an artificial insulin resistance as a result.22 This artificial scenario actually sounds a lot like the standard American diet – a steady stream of sugar and calorically-dense (nutrient poor) foods eaten continuously throughout the day.

Most type II diabetic patients know that the insulin injections they use in their treatment leads to further weight gain (and thus the need for more insulin). Most diabetes doctors will tell you insulin injections make their patients more insulin resistant in the long run, worsening their condition, and thus increasing their need for insulin over time.23

 

Fasting & Diabetes

Your body’s physiology is naturally hard-wired to fast; a result of thousands of years of evolution. When fasting, blood sugar and insulin levels fall and your liver begins to breakdown glucose stored as glycogen to fuel your vital organs and brain.  

This is a very important because a liver overloaded with too much glucose will build up fat. Studies have shown that excess hepatic (liver) fat (independent of total and visceral fat) is associated with elevated blood sugar and hyper-insulinemia.24,25 It also leads to increased fat deposition to all areas of the body, including the pancreas, negatively affecting the beta cells that produce insulin.26

Insulin functions a lot like a fuel selector switch and as levels fall, the body shifts to primarily burning stored body-fat for fuel. Unfortunately, caloric excess is the norm today in Western countries, unlike the periods of food shortage our hunter-gatherer ancestors endured. The resulting of our Western dietary excesses is in chronic hyper-insulinemia and epidemic levels of diabetes across the globe.

 

The Research on Fasting

Unfortunately, the research on fasting is still very limited. However, there is increasing data on intermittent fasting (IF), alternate day fasting (ADF) and other forms of time-restricted feeding (TRF) to help provide a glimpse of potential benefits for type II diabetes.

A recent meta-analysis found intermittent fasting (IF) reduced fasting insulin levels 20-30% and blood sugar levels 3-6% in diabetics.27 The study authors concluded “…preliminary findings show promise for the use of IF and ADF as alternatives to caloric restriction for weight loss and type 2 diabetes risk reduction in overweight and obese populations…” while cautioning more research is needed.8 Intermittent fasting has also been shown to protect kidney function,which is  important for diabetics as diabetic nephropathy is common complication of the disease.28

Cardiovascular disease is another common risk in diabetes patients.7 Multiple studies have found time-restricted feeding (TRF) can lower body-weight, triglycerides and LDL cholesterol, while increasing HDL cholesterol, all reliable markers for reducing CVD risk.29,30

Inflammation and oxidative stress are also hallmarks of poor metabolic health and diabetes, and recent studies have shown potential benefit of fasting to fight inflammation and increase resistance to oxidative stress.31,32,33,34

Fasting (and its variety of forms) may be an effective nutritional strategy for correcting hyper-insulinemia, reversing diabetes, and improving cardio-metabolic complications associated with the disease. The benefits of fasting likely stem from a simple mechanism: it induces a caloric deficit. Fasting is simple, cost-effective, and it doesn’t matter what type of diet you’re currently following.  If you struggle with type II diabetes, look for qualified doctors, like diabetes expert Dr. Jason Fung MD who uses fasting extensively in his Intensive Dietary Management program for diabetic patients. Regardless whether you intermittently fast, simply “fast” between meals (by not snacking), or perform a therapeutic fast under medical supervision, build a habit out of your new nutritional strategy and you’ll discoverthe foundation for reversing hyper-insulinemia and diabetes.

 

References

1. Mattson, M. et al. Meal frequency and timing in health and disease. PNAS. Vol 111, no. 47, 16647-16653.
2. Joslin, Elliot. The Treatemnt of Diabetes Mellitus. Canadian Medical Association Journal 6, no 8 (1916):673-84.
3. Joslin, Ellot. The Treatment of Diabetes Mellitus. Philadelphia: Lea & Febiger, 1916).
4. Allen, Frederick. Prolonged Fasting in Diabetes. American Journal of Medical Sciences 150 (1915):480-5.
5. Manske, A. et al. Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-1029.
6. Fachini, F et al. Insulin resistance as a predictor of age-related diseases. J Clin Endocrinol Metab. 2001 Aug;86(8):3574-8.
7. Bonora E et al. HOMA-estimated insulin resistance is an independent predictor of cardiovascular disease in type 2 diabetic subjects: prospective data from the Verona Diabetes Complications Study. Diabetes Care. 2002 Jul;25(7):1135-41.
8. Varady K et al. Short-term modified alternate-day fasting: A novel dietary strategy for weight loss and cardioprotection in obese adults. Am. J. Clin. Nutr. 2009;90:1138–1143.
9. Bhutani S. et al. Improvements in coronary heart disease risk indicators by alternate-day fasting involve adipose tissue modulations. Obesity. 2010;18:2152–2159.
10. Bhutani S. et al. Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans. Obesity. 2013;21:1370–1379.
11. Klempel M.C. et al. Alternate day fasting (ADF) with a high-fat diet produces similar weight loss and cardio-protection as ADF with a low-fat diet. Metabolism. 2013;62:137–143.
12. Kroeger C.M. et al. Improvement in coronary heart disease risk factors during an intermittent fasting/calorie restriction regimen: Relationship to adipokine modulations. Nutr. Metab. 2012;9:98.
13. Varady K.A. et al. Improvements in LDL particle size and distribution by short-term alternate day modified fasting in obese adults. Br. J. Nutr. 2011;105:580–583.
14. Varady K. et al. Modified alternate-day fasting and cardioprotection: Relation to adipose tissue dynamics and dietary fat intake. Metabolism. 2009;58:803–811.
15. Ash S. et al. Effect of intensive dietetic interventions on weight and glycaemic control in overweight men with Type II diabetes: A randomised trial. Int. J. Obes. Relat. Metab. Disord. 2003;27:797–802.
16. Johnson J. 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;42:665–674.
17. Harvie M. et al. The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women. Br. J. Nutr. 2013;110:1534–1547.
18. Harvie M.N. 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. 2011;35:714–727.
19. Marchesini G et al. Association of nonalcoholic fatty liver disease with insulin resistance. The American journal of medicine 1999, 107:450-455.
20. Pontiroli et al.  Patients with insulinoma show insulin resistance in the absence of arterial hypertension. Diabetologia 1992, 35:294-295.
21. Pontiroli AE et al. The glucose clamp technique for the study of patients with hypoglycemia: insulin resistance as a feature of insulinoma.Journal of endocrinological investigation 1990, 13:241-245.
22. Del Prato S et al. Effect of sustained physiologic hyperinsulinaemia and hyperglycaemia on insulin secretion and insulin sensitivity in man. Diabetologia 1994, 37:1025-1035.
23. Henry RR et al. Intensive conventional insulin therapy for type II diabetes. Metabolic effects during a 6-mo outpatient trial. Diabetes care 1993, 16:21-31.
24. Cali A.M., de Oliveira A.M., Kim H., Chen S., Reyes-Mugica M., Escalera S., Dziura J., Taksali S.E., Kursawe R., Shaw M., et al. Glucose dysregulation and hepatic steatosis in obese adolescents: Is there a link? Hepatology. 2009;49:1896–1903.
25. D’Adamo E., Cali A.M., Weiss R., Santoro N., Pierpont B., Northrup V., Caprio S. Central role of fatty liver in the pathogenesis of insulin resistance in obese adolescents. Diabetes Care. 2010;33:1817–1822.
26. Al-Khalifa A., Mathew T.C., Al-Zaid N.S., Mathew E., Dashti H.M. Therapeutic role of low-carbohydrate ketogenic diet in diabetes. Nutrition. 2009;25:1177–1185.
27. Barnosky A, et al. Intermittent fasting vs daily calorie restriction for type 2 diabetes prevention: a review of human findings. Trans Res. Oct. 2014, vol 164, pg 302-311
28. Chung H, et al. Time-restricted feeding improves insulin resistance and hepatic steatosis in a mouse model of postmenopausal obesity. Metabolism. 2016 Dec;65(12):1743-1754.
29. Rothschild J, et al. Time-restricted feeding and risk of metabolic disease: a review of human and animal studies. Nutr Rev. 2014 May;72(5):308-18
30. Tinsely, G. La Bounty P. Effects of intermittent fasting on body composition and clinical health markers in humans. Nutr Rev. 2015 Oct;73(10):661-74.
31. Mattson M. Ruiquian. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. J Nutr Biochem, vol 16, iss3 March 2005, Pages 129–137
32. Aksungar F. et al. Interleukin-6, C-reactive protein and biochemical parameters during prolonged intermittent fasting. Ann Nutr Metab. 2007;51(1):88-95.
33. Johnson J. et al. Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radix Biol Med. 2007 Mar 1;42(5):665-74.
34. Faris, M. et al. Intermittent fasting during Ramadan attenuates proinflammatory cytokines and immune cells in healthy subjects. Nutr Res. 2012 Dec;32(12):947-55.

 

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“5” Comments

  1. It’s about carb acellularity.
    Kitavans and other cultures do quite well on tubers because they are cellular carbs. On the other hand, grains are acellular carbs that drive dysbiosis in the small intestine, leading to leptin and insulin resistance. This is one of the main drivers. When you have leaky gut and chronic endotoxemia, your body produces ROS to fight pathogens.
    Unfortunately, ROS overproduction leads to set off insulin resistance.
    Your body is fooled into thinking that you are in energy overload and your cells become insulin resistant.
    The main driver is chronic inflammation due to a messed up gut.
    Furthermore, gluten and ATIs are other powerful triggers of this nasty process.
    Rice is less harmful because its starch is organised in a less microbes-accessible configuration that triggers a weaker dysbiotic state.
    This is perfectly coherent with the reference you posted and it’s one of the main reasons why studying hunter gatherers it looks like that their health is mostly macronutrient independent.

  2. I’m very glad you didn’t mention the business biased research by dr.Longo with the fasting mimicking diet.
    He sells nasty pseudo vegan processed stuff with legumes and other amenities touting the alleged benefits of his approach with cherry picked circumstancial evidence.
    Please don’t do like some charismatic bloggers that endorse his business.

  3. I wonder if the consumption of tubers was higher in times of scaricty during the stone age, as is the case for the Hadza hunter gatherers today (https://www.ncbi.nlm.nih.gov/pubmed/19350623). I suspect a calorie restricted diet with tubers (or perhaps potatoes) could offer more benefits for diabetics.

    Evolutionary we should be well adapted to a diet with plenty of fruits and tubers, and if we have problems with carbohydrates, it may be more related to the type of carbs we eat today (grains, sucrose), than carbs per se.

    In a small study, native Hawaiians adopted their traditional diet for three weeks, composed mostly of tubers, with some fruits, vegetables and a small amount of chicken/fish. (https://www.ncbi.nlm.nih.gov/pubmed/2031501.) Blood sugar declined on average from 8.99 to 6.86, despite a carbohydrate intake of approx 300 grams/day. Caloric intake was however also spontaneously reduced from about 2600 kcal to 1600 kcal. But the very positive effects on numerous metrics seems to go much beyond the effect of calorie restriction. Also there were some experiments a hundred years ago (by Dr Mosse, published in the Irish journal of medicine, v1, 1903, p 42-44) showing less thirst, less sugar in the urine, lower blood sugar, and improved strength in diabetics when bread (300-500 gram) was replaced with potatoes (1-1.5 kg). This was attributed to the potash and the water content of potatoes.

    While potatoes isn´t «paleo», the nutritional composition is very similar as tubers. A characteristic of the tubers (and fruits) is among other things a very high potassium content, and a high potassium/phosphorus ratio compared to whole grains. It may be that potassium is a key nutrient needed to regulate blood sugar, as has been indicated already many decades ago (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3197792/), however potassium can be «wasted» if the diet is high in salt and phosphorus. There´s some evidence that added salt significantly increases the risk of diabetes, but potassium can likely counteract this.

    It may be that if one eat refined unsalted grains along with plenty of vegetables, this also can improve diabetes, as the overall nutritional composition then will be similar as these tubers. (Just as the combination of sucrose and vegetables will be similar as fruits.) Walter Kempner (1903-1997)´s rice diet indicated something like that; it was composed of white rice, sucrose, fruit, fruit juice, vitamins and iron, and was used for people with kidney disorders, hypertension, obesity, heart failure, and diabetes (https://www.ncbi.nlm.nih.gov/pubmed/13591100). Interestingly this diet was so unappealing that he had to whip some of his patients to make them eat it, because it lacked the salt and fat. This makes the point that overeating can be as much related to sugar and fat, as it is to refined carbohydrates. Or rather that it´s the combination of these things that´s the problem. However even potatoes with butter may not lead to overeating if it is not heavily salted and consumed alone: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1252113/pdf/biochemj01140-0284.pdf

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