Can intermittent fasting cause diabetes

Science News. Fasting every other day to lose weight impairs the action of sugar-regulating hormone, insulin, which may increase diabetes risk. ScienceDaily, 20 May European Society of Endocrinology. Could intermittent fasting diets increase diabetes risk? Retrieved November 12, from www. Yet finding the most effective way to lose weight and keep it off can be a challenge, especially for mothers with a However, it is not superior to conventional calorie restriction diets, scientists have found out in the largest investigation on A new article reports on a randomized clinical trial ScienceDaily shares links with sites in the TrendMD network and earns revenue from third-party advertisers, where indicated.

Print Email Share. For starters, skipping whole meals can result in poorer blood glucose control, not to mention issues such as fatigue and reduced energy—and, thus, an increased risk of injury.

Skipping meals may also cause people to make poor diet choices, which can have the opposite effect on their waistline and blood sugar. Your dietitian and diabetes care and education specialist can help guide and support you through this process.

While losing weight can be beneficial for people with diabetes, because it increases insulin sensitivity, putting weight back on can have the opposite effect, increasing the risk for diabetes complications.

Another risk of IF for people with diabetes is hypoglycemia , or low blood sugar. A study published in February in the journal Diabetic Medicine found that IF doubles the risk for hypoglycemia in people with type 2 diabetes. People who are on specific diabetes medications — sulfonylureas and insulin, in particular — may be at increased risk of this complication, which can be life threatening.

Certain people, such as those who are pregnant or breastfeeding or have an underlying disease or medical condition, should also avoid IF, Pupo says. When that happens, your liver responds by producing too many ketones , which can build up in the body and damage the kidneys as well as cause brain swelling, Pupo says. DKA may even lead to a diabetic coma or death, she adds. A few case studies, such as a study published in October in the Journal of the Endocrine Society , and another published in November in American Journal of Case Reports have shown that there may be a link between IF, used in conjunction with a keto diet, and DKA.

For anyone, regardless of whether you have diabetes, cutting out meals and restricting entire food groups can cause nutritional deficiencies. Talk to your doctor.

Before starting IF, talk to your doctor to come up with a safe approach and adjust any of your medication doses as needed. If left untreated in people with diabetes, low blood sugar hypoglycemia can be fatal, the American Diabetes Association reports. Find a plan that works for you. Plans for IF vary. Although the ADA and EASD describe the goal of treatment as being aimed at preventing or delaying the complications of this disease, the goal of this review is to take a closer look at the possibility of using intermittent fasting as a non-medicinal option for the treatment of type 2 diabetes through improved insulin sensitivity.

When considering the therapeutic role of intermittent fasting in patients with diabetes, there are three hormones that likely play a significant role. These include insulin, as well as the adipokines leptin and adiponectin. Figures 1 , 2 and 3 describe the effects of these hormones on various tissues. It is the purpose of this review to provide insight into the influence of these hormones on the development of insulin resistance and type 2 diabetes, as well as the beneficial effects of intermittent fasting on these metabolic markers.

Moving forward, we hope this review is a summary of the current literature on the use and efficacy of intermittent fasting in the clinic. We also hope this review serves as a catalyst for physicians to publish case reports and partake in controlled studies regarding intermittent fasting and diabetes. Effects of Insulin on Various Tissues [ 7 , 8 ]. Effects of Leptin [ 9 , 10 ]. Effects of Adiponectin [ 10 ]. A literature review was performed for articles related to the impact of intermittent fasting on type 2 diabetes mellitus.

Searches through the references of retrieved articles was also performed. Finally, the websites of professional organizations such as the American Diabetes Association and European Association for the Study of Diabetes were searched for specific guidelines and recommendations.

Trials were included if the study design involved one of the three most commonly reported intermittent fasting regimens: alternate day fasting, periodic fasting, or time-restricted feeding. Finally, studies were included if the outcome measures included measurement for fasting glucose, HbA1C, fasting insulin, leptin, or adiponectin both in patients with and without a history of diabetes.

Exclusion criteria consisted of duplicates, abstracts, non-English articles, articles that did not include human subjects, those that did not report outcome measures for any of the previously described variables, and works that were unpublished or unrelated to the topic of interest. Our initial search returned studies. Two reviewers independently reviewed abstracts to determine whether studies met our inclusion criteria. Studies that met criteria were then further reviewed to determine whether they would be included in our review.

After careful review, a total of 17 articles were ultimately chosen and are available for review in Tables 1 and 2. Intermittent fasting has recently gained popularity as a means of improving body composition and metabolic health [ 28 , 29 ]. There are several different regimens of intermittent fasting.

One such regimen is alternate day fasting, in which days of fasting are separated by days of ad libitum food consumption [ 29 ]. See Fig. Obesity is known to be a major risk factor for the development of type 2 DM.

There are a number of mechanisms believed to contribute to the development of insulin-resistance in obese patients. These include, but are not limited to, systemic chronic inflammation and ectopic lipid deposition [ 7 , 9 , 30 , 31 ].

Visceral adipose tissue is known to function as both a paracrine and endocrine organ through the secretion of adipokines [ 10 ]. These adipokines are either proinflammatory leading to chronic low-level inflammation, such as leptin, or anti-inflammatory such as adiponectin [ 10 ].

Leptin is known to play a role in the regulation of body weight through signaling to the hypothalamus and other brain regions to suppress food intake and increase energy expenditure [ 9 ]. The inflammatory effects of leptin are likely due to its role in the production of IL-6, which induces the synthesis of C-reactive protein in the liver as well as upregulation of the pro-inflammatory cytokine TNF-alpha [ 10 ]. Interestingly, patients with higher levels of BMI and insulin resistance were found to have increased leptin levels, possibly signifying that patients with obesity and insulin resistance are developing leptin resistance as well [ 10 ].

On the contrary, adiponectin is known to have antidiabetic and anti-inflammatory effects. Adiponectin acts on various receptors that results in an increase in skeletal muscle and hepatic fatty acid oxidation, reduced hepatic gluconeogenesis, and increased glucose uptake [ 10 ]. It also exerts anti-inflammatory effects through direct action on inflammatory cells, action of NF-kB, and interactions with TNF-alpha [ 10 ]. Adiponectin levels decrease with accumulation of visceral fat [ 10 ].

They found that in patients with the metabolic syndrome, which includes obesity and insulin resistance, an imbalance in levels of leptin and adiponectin appeared to play a role in metabolic alteration that increased the risk of type 2 diabetes [ 10 ]. Interestingly, several studies have demonstrated that intermittent fasting, even in the absence of fat loss, has resulted in a reduction of leptin levels and an increase of adiponectin, which results in improvements of insulin resistance [ 32 ].

It has long been known that restricting calories can reduce body weight and increase metabolic health [ 33 ]. A study by Larson-Meyer et al. However, several obesity trials have demonstrated that humans have significant difficulty sustaining daily calorie restriction for extended periods of time [ 28 ].

On the other hand, intermittent fasting has higher compliance and has shown promise in the improvement of metabolic risk factors, body composition, and weight loss in obese individuals [ 28 , 35 , 36 ]. During this transition the body begins to switch from the synthesis and storage of lipids to mobilization of fat in the form of ketone bodies and free fatty acids [ 28 ].

This transition of fuel source, or metabolic reprogramming, has been highlighted as a potential mechanism for many of the beneficial effects of intermittent fasting. Lastly, intermittent fasting has been shown to reduce adiposity, particularly visceral fat and truncal fat, largely due to mild energy deficits [ 12 , 17 ].

Insulin plays a significant role in glucose homeostasis due to its influence in promoting the storage and utilization of glucose. However, the effects of insulin are not limited to glucose homeostasis. Insulin also plays a role in the stimulation of DNA synthesis, RNA synthesis, cell growth and differentiation, amino acid influx, protein synthesis, inhibition of protein degradation, and most importantly, the stimulation of lipogenesis and inhibition of lipolysis [ 8 ].

It is the development of insulin resistance, which is defined as the necessity of higher circulating insulin levels in order to produce a glucose lowering response, that is thought to be responsible for the development of type 2 diabetes [ 7 ].

In order to promote regulation of glucose homeostasis, insulin works primarily on receptors in skeletal muscle, liver, and white adipose tissue [ 7 ]. In short, there are several proposed mechanisms regarding the development of insulin resistance. One of the more prominent theories describes the association of increased adiposity and the subsequent chronic inflammation that leads to the development of insulin resistance in tissues [ 7 ].

Intermittent fasting, as described previously, may reduce adiposity and subsequently insulin resistance via reduction of caloric intake as well as due to metabolic reprogramming. The role of AMPK at a biochemical level is outside of the scope of this review, however activation of AMPK through a low energy state has been shown to initiate physiologic responses that promote healthy aging [ 37 ]. Increased levels of insulin, whether through increased energy intake or insulin resistance, leads to the activation of downstream mediators that ultimately inhibit AMPK.

The role of AMPK in improved insulin sensitivity is most evident via the positive effects of the commonly prescribed biguanide, metformin.

Metformin is known to promote the activation of AMPK, and has been shown to be very effective in the treatment of type 2 diabetes as well as in the mitigation of a number of chronic disease states [ 37 ]. In theory, decreased energy intake, such as that is achieved through intermittent fasting, will lead to prolonged decreased levels of insulin production and increased levels of AMPK, which likely plays a role in the improvements in insulin sensitivity and glucose homeostasis.

Several studies have shown promise for the use of intermittent fasting protocols as a potential treatment for diabetes. Tables 1 and 2 illustrate the findings of several recent studies regarding intermittent fasting and its effect on measures including body weight, fasting glucose, fasting insulin, adiponectin, and leptin.

In a systematic review and meta-analysis by Cho et al. Lastly, when comparing leptin and adiponectin levels between the intermittent fasting subjects and the control subjects in all studies, the reviewers found increased adiponectin levels A case series by Furmli et al. Over the course of the study, all patients had significant reductions in HbA1C, weight loss, and all of the patients were able to stop their insulin therapy within 1 month [ 26 ].

Interestingly, the three patients in this case series all reported tolerating fasting very well, and no patient stopped the intervention at any point out of choice [ 26 ]. This suggests that intermittent fasting may not only be successful as a non-medicinal treatment option for patients with type 2 diabetes, but supports the notion that this intervention is tolerable as well.

Carter et al. Finally, a similar clinical trial by Gabel et al. In America, we often eat 3 meals per day in addition to frequent snacking. Furthermore, in American culture most social engagements involve food. Asking patients to eliminate these experiences from their day to day lives may become burdensome, and thus hinder patient compliance. Therefore, it would be more appropriate to gradually introduce intermittent fasting in the form of time restricted feeding.

This allows the patient some daily flexibility in choosing when to consume calories, thus increasing the likelihood of compliance. Lastly, patients who have become adapted to time restricted feeding may choose to switch to alternate day or periodic fasting with the supervision and guidance of a registered dietician.

When considering the use of fasting in patients with diabetes, a number of points should be weighed. First, it is important to discuss potential safety risks associated with fasting. Patients taking insulin or sulfonylurea medications should be closely monitored by their healthcare provider in order to prevent hypoglycemic events [ 39 ]. Because studies are demonstrating a decreased need for insulin in patients who follow intermittent fasting protocols, blood glucose levels and medication titration should be observed closely by the physician.

Physicians should help patients make appropriate adjustments to their medications, especially on days of fasting. Physicians may choose to have patients keep daily blood sugar and weight logs and send them weekly or biweekly via electronic message in order to assist providers in medication titration over time.

Of note, while the goal of adapting this pattern of eating is to reduce or eliminate the need for medications, including insulin, there are situations in which insulin may be necessary, such as severe hyperglycemia. Failure to do so may result in significant consequences, such as the development of hyperosmolar hyperglycemic syndrome.