Home

Type-2 diabetes affects over 400 million people globally, an astounding tenfold increase over the last 30 years.[1] Naturally, a generous amount of research is investigating the connection between the keto diet and diabetes. Findings thus far suggest that the keto diet may be a sensible treatment for type-2 diabetes.[2]

But there’s quite a bit more to the diabetes epidemic and the seemingly inexorable force that drives it…

We hear it on a monthly basis through mainstream news outlets that humans (especially those in the United States) are getting fatter and subsequently being diagnosed with type-2 diabetes. Chances are you don’t contemplate what that really means in the grand scheme of things; sadly, many of us are numb to it.

To put it bluntly: Obesity is killing us, and it won’t stop unless things change.

If you read this article (which you should), it behooves you to muse on the subject matter, particularly if you are planning on doing the keto diet to help treat type-2 diabetes and/or obesity. Even if you’re not obese or type-2 diabetic, you will hopefully walk away with a greater sense of urgency to incite positive change in those who need it most.

Table of Contents:

The Rise of Obesity and Type-2 Diabetes

Let’s start with a look at some of the (disconcerting) statistics showing just how prevalent obesity and type-2 diabetes have become.

The Center for Disease Control (CDC) has reported an astonishing threefold increase in childhood obesity rates (children and adolescents ages 2-19) in the United States over the past 30 years.[3] Projections are that obesity rates in children will double over the next decade. (To say that’s inauspicious is an understatement.)

How about adults, you ask?

Recent CDC data found that over 36% of adults in the U.S. are obese, with women being slightly more obese than men.[4] What’s most concerning is that the percentage of adults who are obese goes up nearly 5% every year.

Think about this for a minute: more than one in three adults in the U.S. are obese (and children are outpacing adults).

Bear in mind, this is only indicative of obese adults and doesn’t even include those who are overweight. If you include those who are overweight, that increases the prevalence to two in three U.S. adults.[5]

Essentially, if you’re in a healthy weight range you’re in the minority. Is that not bewildering?

In spite of all the advancements we’ve made with regards to our understanding of nutritional science and exercise physiology, we continue to get fatter? Moreover, since health foods and dietary supplements are booming industries, you would think we would be getting slimmer and the incidence of type-2 diabetes would be diminishing.

The Vicious Cycle of Obesity & Type-2 Diabetes

The epidemic of obesity and type-2 diabetes is one of the greatest plights mankind has ever faced. What makes this an uphill battle is that obesity and type-2 diabetes are vicious cycles driven by physiological and sociological factors.

Adults set the example for youth, and the way parents choose to feed their kids seems to be heavily influenced by how they feed themselves.

Thus, bad parental eating habits quickly grow on kids and it becomes a vicious cycle within the family, where being raised on poor dietary and lifestyle choices lead to obese children who grow old and give rise to the same unhealthy habits in their offspring.

To make matters worse, there is some evidence that adults who are obese with type-2 diabetes genetically predispose their progeny to diabetes.[6]

Not only are obesity and type-2 diabetes detrimental to health and longevity, but they can also put a dent in your bank account. It is estimated that the annual medical costs in the U.S. for people who are obese are roughly $2,000 higher than those in a healthy weight range.[7]

In the U.S. alone, that adds up to 100s of billions of dollars in extra medical expenses per year for treating conditions that are reversible through proper diet and exercise.

So, you can see the sociological aspect of this vicious cycle, but how about the physiological one?

Why Obesity Keeps You Fat

Once you’re obese, your body has a propensity to keep gaining body fat (this is especially true if you eat a lot of sugar and carbohydrates). As you continue to eat/drink sugary foods, your body produces more and more insulin to compensate for all the glucose in your bloodstream.

Eventually, your cells become resistant to the effects of insulin and your blood sugar levels remain chronically elevated.

When you’re insulin resistant, cells can’t effectively utilize the glucose in your bloodstream for energy. This is why pre-diabetics generally have high insulin levels (hyperinsulinemia) and high blood glucose levels (hyperglycemia), both of which are strongly correlated with abdominal fat gain.[8]

Keep this up for a while longer and your pancreas will start to produce less insulin. Soon enough, you’ll be obese and diabetic. If you don’t stop the habits that got you in this position, it will only get worse…

Obesity is a physiological vicious cycle because your body gets “comfortable” with being fat and insulin resistant. You essentially create new homeostasis.

In turn, your appetite and calorie intake remain high, your basal metabolic rate remains low (relative to your body weight), your energy and vitality are in the gutter, and your girth continues to expand.

Granted, there’s much more to the physiology of obesity and type-2 diabetes; this is just meant to illustrate the vicious cycle of it all.

You might notice how this all ties back into the keto diet, which is a very-low-carb diet (and thus, isn’t as insulinogenic as a conventional high-carb diet).

We will talk more about the efficacy of the keto diet for treating type-2 diabetes and obesity after taking a look at why obesity and type-2 diabetes typically occur simultaneously and how body fat impacts these conditions.

Why Obesity and Type-2 Diabetes Go Hand-in-Hand

While both subcutaneous fat and visceral fat are biologically necessary, having large amounts of visceral fat (also known as abdominal fat) is strongly correlated with conditions such as type-2 diabetes and cardiovascular disease.[9]

The term “beer belly” is a colloquial way of saying that someone has excessive visceral fat tissue; this is medically referred to as “central adiposity.”

Intuitively, obesity is indicative of central adiposity, both of which are comorbidities of type-2 diabetes.[10] 

In other words, central adiposity, obesity, and type-2 diabetes tend to occur simultaneously in many people. It’s almost as if they are all one and the same. Being obese and/or having a large amount of abdominal fat drastically increases the risk of developing type-2 diabetes and vice versa.

However, you can develop type-2 diabetes even if you’re a healthy weight and lean (though it’s not nearly as common).

“Good” Body Fat vs. “Bad” Body Fat

Just as with dietary fats, the stored fats in the human body are not all created equal. Body fat (adipose tissue) is mainly stored either below the skin (subcutaneous fat) or in the abdominal cavity, surrounding internal organs (visceral fat).

It’s important to note that adipose tissue and fat stores in the body aren’t inherently bad or unhealthy. Even skeletal muscle contains small amounts of lipid droplets (intramuscular triglycerides) which serve as a useful energy reservoir during exercise.[11]

In fact, body fat is a vital organ system and necessary for a myriad of bodily functions, including energy storage, heat production, insulation, and even hormone secretion. As with most things in life, consequences arise when we have excessive (or even too little) body fat, particularly white adipose tissue.

In adipose tissue, there are three distinct types of fat cells (that we know of): white fat cells, brown fat cells, and beige fat cells.

White fat cells in the human body secrete distinct cell-signaling proteins known as adipokines, such as adiponectin, leptin, and various inflammatory modulators. White fat also stores energy (in the form of lipids) and insulates/cushions the body. As such, having some white adipose tissue is necessary for health and longevity.

Brown fat cells, on the other hand, are rich in mitochondria that help increase metabolic rate and burn calories (thereby generating heat).[12] Naturally, brown adipose tissue tends to be more abundant in lean individuals while white adipose tissue predominates in those who are overweight or obese.

Beige fat cells are still relatively misunderstood but they are similar to brown fat cells in that they can metabolize lipids and glucose and dissipate the energy as heat. Some promising new research from the University of Pennsylvania School of Medicine suggests that a signaling pathway involving the mTOR protein complexes exists that effectively converts white fat cells into beige fat cells, and this could be a novel way to combat obesity and type-2 diabetes.[13]

As propitious as that sounds, the two best things you can do at this point in time to treat obesity and type-2 diabetes are eating healthier and exercising more. There is no way around this.

Your diet and activity level set the foundation for your health and longevity. Drugs may be useful in some situations, but obesity and type-2 diabetes are treatable without them in the vast majority of cases.

The Internal Health Risks of Excess Belly Fat (Central Adiposity)


We’ve analyzed the epidemiology of obesity, central adiposity, and type-2 diabetes quite a bit thus far, as well as the underlying role of body fat.

But what about the pathophysiology of these conditions?

For starters, the problem with having large amounts of belly fat (visceral fat) is that most of it is white adipose tissue. In addition to visceral/belly fat being an anatomical concern, it’s a metabolic and physiological one as well.

Excessive visceral fat in humans is strongly associated with elevated levels of blood triglycerides (i.e. hypertriglyceridemia), which is a major risk factor for cardiovascular disease – the leading cause of death in the U.S.[14]

Moreover, organ inflammation (especially in the pancreas and liver) and decreased levels of high-density lipoproteins (“healthy” cholesterol) with concomitant increases in very-low-density lipoproteins (“bad” cholesterol) have also been linked to obesity and excess visceral fat.[15]

The other systemic detriments that being obese presents are just as worrisome, including:[16],[17]

This is just the tip of the iceberg…

Central adiposity and obesity also greatly increase the risk of cancer, having a stroke, and of course, developing insulin resistance (which eventually can manifest into type-2 diabetes).[18]

Last but not least, being obese puts you at a much higher risk of all-cause mortality.[19]

In short, if your health and longevity mean much to you, then carrying a lot of visceral fat is the last thing you want. (If that doesn’t get you on the edge of your seat, nothing will.)

How Can Keto Treat Type-2 Diabetes and Obesity?

Arguably the three most relevant ways the keto diet can treat type-2 diabetes and obesity is by restoring a healthy gut microbiome, reducing insulin and blood sugar levels, and suppressing appetite (thereby helping control calorie intake).

Keto Diet for Restoring Healthy Gut Microbiota

Recent research found that slim people have a different array of microbes in their gut compared to overweight/obese people.[20] The bacteria that exist in our gastrointestinal tract are collectively referred to as gut microbiota (or the gut microbiome), and they appear to play a bigger role in body weight management than previously thought.

Essentially, what happens as we gain weight is our gut microbiome starts to lose healthy bacteria that help keep us healthy and slim. Specifically, research shows that overly fat individuals have significantly less Lactobacillus rhamnosus in their gut microbiome than slim people do. This bacterium, in particular, appears to be strongly correlated with body-weight and metabolism in humans.[21]

Lactobacillus Rhamnosus: A Key Bacterial Species for Fighting Obesity

What’s quite compelling about the research on obese individuals who supplement with certain strains of Lactobacillus rhamnosus is that their body weight decreased significantly without a reduction in calorie intake.[22]

Basically, obese individuals lose fat simply by increasing the amount of this specific bacterium in their body. With that being said, don’t rush to label this Lactobacillus rhamnosus probiotic as a “miracle pill” because it’s a bacterium that is supposed to be present naturally in our gut.

Evidence suggests that Lactobacillus rhamnosus strain PL60 works by increasing the production of a key fatty acid in humans called conjugated linoleic acid (CLA).[23] CLA is also found in grass-fed butter and grass-fed beef, which are becoming popular on the keto diet.[24]

CLA appears to works through several mechanisms that help reduce body fat. One way is by modulating the activity of an enzyme called lipoprotein lipase (LPL), thereby helping reduce fat storage and increasing the amount of existing fat that is burned for energy.[25] Thus, CLA helps prevent further fat storage while burning more of the body fat you already have.

In addition, CLA has been proposed to increase metabolic rate and even support lean body mass, both of which are favorable for enhancing body composition.[26]

In a recent meta-analysis that included 18 human studies, CLA supplementation was found to produce a modest loss in body fat over an extended period of time.[27]

Furthermore, another strain of Lactobacillus rhamnosus, known as Lactobacillus rhamnosus GG, has been shown to increase the expression of genes in the body that increase fat burning.[28] These genes work by activating specific enzymes in fat tissue that signal the body to liberate and burn stored body fat for energy.

Better yet, Lactobacillus rhamnosus GG also enhances insulin sensitivity. This is precisely what you want if you’re using the keto diet to treat type-2 diabetes and insulin resistance.

Probiotics & Prebiotics on Keto

So, this begs the question, “How do we restore a healthy gut microbiome balance for weight loss?”

There are two prudent options:

  • Supplementing with a probiotic that contains Lactobacillus rhamnosus GG and Lactobacillus rhamnosus PL60 (preferably at least 5 billion CFU of each)
  • Following the keto diet and incorporating a good amount of prebiotic fiber, such as inulin and acacia fiber

In short, probiotics are supplements containing “friendly” microorganisms that are believed to provide health benefits by balancing the gut microbiome (which affects virtually every bodily system).

As covered in the previous section, the evidence thus far suggests that Lactobacillus rhamnosus GG and Lactobacillus rhamnosus PL60 are two key probiotic strains for regulating body weight and metabolism.

This is not suggesting that other probiotics aren’t useful either since many strains exist and serve a myriad of beneficial purposes. By the same token, we stand to benefit by ingesting certain foods that feed healthy bacteria in our gut. These foods are often referred to as prebiotics, as they quite literally enable the growth and proliferation of healthy microorganisms in the body.

Dietary fiber, especially inulin and acacia fiber, are well-known to feed healthy gut microbes and help them grow/proliferate. In turn, these healthy microbes are able to “crowd out” the bad ones and restore a favorable gut microbiota balance.

Keto Diet for Reducing Blood Sugar and Insulin Levels

New studies investigating the benefits of the keto diet seem to pop up every day. A common recurring theme is that the keto diet helps lower blood glucose and insulin levels in those who are insulin resistant and/or type-2 diabetic.

Historically, low-carb diets were actually the first line of treatment for obesity as well as both type-1 and type-2 diabetes.[29] Once insulin was discovered, the way doctors treated diabetes changed drastically.

As counterintuitive as it seems, conventional treatment of type-2 diabetes includes a high-carb diet and use of drugs that sensitize cells to the effects of insulin (such as Metformin) or exogenous insulin to help reduce the amount of glucose in the bloodstream.

But there is growing evidence that doctors had it right from the get-go…

A recent meta-analysis of 11 clinical studies proposes that the keto diet is an effective alternative to treating type-2 diabetes by reducing both blood sugar and insulin levels without the need for medication or insulin.[30] In fact, it would be counterproductive to use exogenous insulin on the keto diet because the goal is to reduce insulin levels, not increase them.

Given the evidence, the research reviewers postulate that over the next five years guidelines for treating type-2 diabetes will shift back towards lowering carb intake and relying less on medication.

Keto Diet for Appetite Suppression

Regardless of what type of diet you follow, you will not lose weight if you constantly eat too much. There is an immense body of evidence that shows energy balance is the biggest factor in determining whether we lose weight, gain weight, or stay the same.[31]

Overcoming the unremitting food cravings is one of the biggest hurdles those with obesity and type-2 diabetes face, especially once they start reducing calorie intake. It’s only natural that your body will feel hungry as you begin losing weight and eating less.

For people with obesity and type-2 diabetes, the keto diet can be a godsend because fatty foods and protein tend to be more filling than carbohydrates and don’t produce the crazy mood/appetite swings that sugary foods often do.[32] In fact, one of the most patent symptoms of hyperglycemia is having the constant urge to eat.

Since the keto diet is extremely low in carbs while being higher in fat and protein, it can help you control blood glucose levels and avoid the hunger-inducing symptoms of hyperglycemia. In turn, this makes it easier for you to control calorie intake and encourage weight loss.

Moreover, ketone bodies (and ketosis) appear to suppress appetite by increasing the production of cholecystokinin (CCK) and reducing the production of ghrelin.[33],[34]

CCK is a hunger-suppressing neuropeptide made in the duodenum; it is typically lacking in obese individuals. Ghrelin, on the other hand, is a hunger-stimulating neuropeptide made primarily in the stomach and small intestine; it is generally overproduced in obese individuals.

As such, it may be beneficial for those have a hard time controlling their appetite to supplement with exogenous ketones. (This is especially useful if you’re new to the keto diet.)

Starting the Keto Diet

Both type-2 diabetes and obesity are classified as diseases and should be overseen by a licensed medical professional.

If this article has galvanized you into starting the keto diet and you’re a type-2 diabetic, be sure to consult with your primary care physician about your plans. While the Internet can be a great resource of information and educational, you shouldn’t take blog posts as medical advice (even if they are written by a medical doctor).

Should you decide to use the keto diet for treating type-2 diabetes and/or obesity, give our Keto Beginner’s Guide a read as it will get you up to speed on how keto works, what foods to eat, and what to expect.

References

    1. Zheng, Y., Ley, S. H., & Hu, F. B. (2018). Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nature Reviews Endocrinology, 14(2), 88. ↑
    1. Goday, A., Bellido, D., Sajoux, I., Crujeiras, A. B., Burguera, B., García-Luna, P. P., … & Casanueva, F. F. (2016). Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss program versus hypocaloric diet in patients with type 2 diabetes mellitus. Nutrition & diabetes, 6(9), e230. ↑
    1. “Obesity and Overweight for Professionals: Childhood | DNPAO | CDC.” Centers for Disease Control and Prevention. Web. 26 Nov. 2016. <http://www.cdc.gov/obesity/childhood/index.html> ↑
    1. Flegal, K. M., Kruszon-Moran, D., Carroll, M. D., Fryar, C. D., & Ogden, C. L. (2016). Trends in obesity among adults in the United States, 2005 to 2014. Jama, 315(21), 2284-2291. ↑
    1. Yang, L., & Colditz, G. A. (2015). Prevalence of overweight and obesity in the United States, 2007-2012. JAMA internal medicine, 175(8), 1412-1413. ↑
    1. Nilsson, E., & Ling, C. (2017). DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes. Clinical epigenetics, 9(1), 105. ↑
    1. Kim, D. D., & Basu, A. (2016). Estimating the medical care costs of obesity in the United States: systematic review, meta-analysis, and empirical analysis. Value in Health, 19(5), 602-613. ↑
    1. DeFronzo, R. A., & Ferrannini, E. (1991). Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes care, 14(3), 173-194. ↑
    1. Tchernof, A., & Després, J. P. (2013). Pathophysiology of human visceral obesity: an update. Physiological reviews, 93(1), 359-404. ↑
    1. Kahn, S. E., Hull, R. L., & Utzschneider, K. M. (2006). Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature, 444(7121), 840-846. ↑
    1. Bergman, B. C., Perreault, L., Strauss, A., Bacon, S., Kerege, A., Harrison, K., … & Bui, H. H. (2017). Intramuscular triglyceride synthesis: importance in muscle lipid partitioning in humans. American Journal of Physiology-Endocrinology and Metabolism, 314(2), E152-E164. ↑
    1. Saito, M., Okamatsu-Ogura, Y., Matsushita, M., Watanabe, K., Yoneshiro, T., Nio-Kobayashi, J., … & Tsujisaki, M. (2009). High incidence of metabolically active brown adipose tissue in healthy adult humans effects of cold exposure and adiposity. Diabetes, 58(7), 1526-1531. ↑
    1. Cassie M. Tran, Sarmistha Mukherjee, Lan Ye, David W. Frederick, Megan Kissig, James G. Davis, Dudley W. Lamming, Patrick Seale, Joseph A. Baur. Rapamycin blocks induction of the thermogenic program in white adipose tissue. Diabetes, 2016; db150502 ↑
    1. National Center for Health Statistics. Health, United States, 2015: With Special Feature on Racial and Ethnic Health Disparities. Hyattsville, MD. 2016. ↑
    1. Fontana, L., Eagon, J. C., Trujillo, M. E., Scherer, P. E., & Klein, S. (2007). Visceral fat adipokine secretion is associated with systemic inflammation in obese humans. Diabetes, 56(4), 1010-1013. ↑
    1. Seidell, J. C., Björntorp, P., Sjöström, L., Kvist, H., & Sannerstedt, R. (1990). Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels. Metabolism, 39(9), 897-901. ↑
    1. Mårin, P., Kvist, H., Lindstedt, G., Sjöström, L., & Björntorp, P. (1993). Low concentrations of insulin-like growth factor-I in abdominal obesity. International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity, 17(2), 83 ↑
    1. Azuma, K., Heilbronn, L. K., Albu, J. B., Smith, S. R., Ravussin, E., & Kelley, D. E. (2007). Adipose tissue distribution in relation to insulin resistance in type 2 diabetes mellitus. American Journal of Physiology-Endocrinology And Metabolism, 293(1), E435-E442. ↑
    1. Di Angelantonio, E., Bhupathiraju, S. N., Wormser, D., Gao, P., Kaptoge, S., de Gonzalez, A. B., … & Lewington, S. (2016). Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents. The Lancet, 388(10046), 776-786. ↑
    1. Million, M., Maraninchi, M., Henry, M., Armougom, F., Richet, H., Carrieri, P., … & Raoult, D. (2012). Obesity-associated gut microbiota is enriched in Lactobacillus reuteri and depleted in Bifidobacterium animalis and Methanobrevibacter smithii. International journal of obesity, 36(6), 817-825. ↑
    1. Sanchez, M., Darimont, C., Drapeau, V., Emady-Azar, S., Lepage, M., Rezzonico, E., … & Leone, P. (2014). Effect of Lactobacillus rhamnosus CGMCC1. 3724 supplementation on weight loss and maintenance in obese men and women. British Journal of Nutrition, 111(08), 1507-1519. ↑
    1. Gorbach, S., Doron, S., & Magro, F. (2017). Lactobacillus rhamnosus GG. In The Microbiota in Gastrointestinal Pathophysiology (pp. 79-88). ↑
    1. Lee, H. Y., Park, J. H., Seok, S. H., Baek, M. W., Kim, D. J., Lee, K. E., … & Park, J. H. (2006). Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1761(7), 736-744. ↑
    1. Hall, N., Schönfeldt, H. C., & Pretorius, B. (2016). Fatty acids in beef from grain-and grass-fed cattle: the unique South African scenario. South African Journal of Clinical Nutrition, 29(2), 55-62. ↑
    1. Ribeiro, A. S., Pina, F. L. C., Dodero, S. R., Silva, D. R., Schoenfeld, B. J., Sugihara, P., … & Tirapegui, J. (2016). Effect of conjugated linoleic acid associated with aerobic exercise on body fat and lipid profile in obese women: A randomized, double-blinded, and placebo-controlled trial. International journal of sport nutrition and exercise metabolism, 26(2), 135-144. ↑
    1. Kim, Y., Kim, J., Whang, K. Y., & Park, Y. (2016). Impact of conjugated linoleic acid (CLA) on skeletal muscle metabolism. Lipids, 51(2), 159-178. ↑
    1. Whigham, L., Watras, A. and Schoeller, D. (2007). ‘Efficacy of Conjugated Linoleic Acid for Reducing Fat Mass: A Meta-Analysis in Humans’, The American Journal of Clinical Nutrition, 85(5), 1203-1211. ↑
    1. Kim, S. W., Park, K. Y., Kim, B., Kim, E., & Hyun, C. K. (2013). Lactobacillus rhamnosus GG improves insulin sensitivity and reduces adiposity in high-fat diet-fed mice through enhancement of adiponectin production. Biochemical and biophysical research communications, 431(2), 258-263. ↑
    1. Morgan, W., Diabetes Mellitus its history, chemistry, anatomy, pathology, physiology and treatment and cases successfully treated, in Diabetes Mellitus its history, chemistry, anatomy, pathology, physiology and treatment and cases successfully treated. 1877, Sett Dey & Co. ↑
    1. Westman, E. C., Tondt, J., Maguire, E., & Yancy Jr, W. S. (2018). Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus. Expert review of endocrinology & metabolism, 13(5), 263-272. ↑
    1. Westerterp, K. R., Romieu, I., Dossus, L., & Willett, W. C. (2017). How are overall energy intake and expenditure related to obesity?. In Energy balance and obesity. World Health Organization. ↑
    1. Benelam, B., Satiation, satiety and their effects on eating behaviour. Nutrition Bulletin, 2009. 34(2): p. 126-173. ↑
    1. Stubbs, B. J., Cox, P. J., Evans, R. D., Cyranka, M., Clarke, K., & de Wet, H. (2018). A ketone ester drink lowers human ghrelin and appetite. Obesity, 26(2), 269-273. ↑
  1. Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2013). Ketosis and appetite-mediating nutrients and hormones after weight loss. European journal of clinical nutrition, 67(7), 759. ↑