The Importance of Diet in Diabetes

Article by Namrata Ashok

5-10 % of individuals with pre-diabetes become diabetic every year (1). In the UK, 90% of adults with diabetes have type 2 diabetes (2). Unfortunately, diabetes rates have increased almost 4-fold since 1980 globally, indicating the influence of lifestyle factors on the prevalence of diabetes (1). Diabetes stems from insulin-related dysfunction, yet, insulin has functions secondary to blood-glucose regulation, playing a role in muscle protein synthesis, bone formation, osteoporosis-related inflammation, the central nervous system, kidney function, and the blood vessel system (3). Therefore, diabetes systemically affects the body, making diet quality key to delaying or reversing its physiological effects.

Pre-diabetes vs diabetes

Diabetes is a condition that indicates abnormal blood sugar levels as a result of insulin dysfunction in the body. The primary function of insulin is blood-sugar regulation, whereby insulin is released by pancreatic cells to decrease blood sugar levels. Pre-diabetes occurs when cells in the body are beginning to become resistant to insulin. Blood glucose levels appear to be elevated, but not high enough to be diagnosed as Diabetes. Diabetes is classified into two types: type 1 diabetes (T1D) and type 2 diabetes (T2D).

Type 1 Diabetes

Type 1 diabetes is typically early onset, caused by genetic factors and environmental exposure, including early-life exposure to viruses, exhaustion of insulin-producing cells in the pancreas, early-life dietary behaviours and antibiotic exposure, birth delivery mode, gestational diabetes, and gut microbiota dysbiosis (4,5). Ultimately, T1D is an autoimmune condition whereby the body’s immune cells attack insulin-producing cells in the pancreas, inhibiting any production of insulin.

Type 2 Diabetes

On the other hand, Type 2 diabetes is typically late onset, diagnosed when cells are resistant to insulin or insufficient amounts of insulin are produced. Risk factors for type 2 diabetes include age, high cigarette smoking, high visceral fat, history of hypertension and diabetes mellitus, physical inactivity, and diet quality. A study of 8000 participants concluded that a family history of diabetes increased the risk of pre-diabetes by 26% (6). On the contrary, a research article suggested that changes to lifestyle, diet and physical activity specifically, “may decrease the risk of pre-diabetes progressing to diabetes for as long as 10 years. (7)” Ultimately, the goal of diabetes management revolves around increasing insulin sensitivity.

The influence of maternal history on diabetes

Pre-gestational hyperglycaemia is termed when type 1 or type 2 diabetes mellitus is diagnosed before pregnancy. Gestational diabetes is the development of diabetes during pregnancy, research has correlated prior diagnosis of gestational diabetes with a 10-fold increase in the risk of type 2 diabetes (8). A systematic review of 129 studies concluded that ⅓ of the women diagnosed with gestational diabetes was diagnosed with type 2 diabetes within 15 years (9). Despite maternal effects, predisposition to glucose intolerance in the offspring has been correlated with pre-gestational hyperglycaemia as a result of maternal environmental factors. These environmental factors include “in utero exposure, caring behaviours, milk composition and trans-generational inheritance,” which trigger aberrant mechanisms involved in insulin secretion (10).

Visceral fat & insulin resistance

Visceral fat is the fat surrounding abdominal organs and have been found to produce chronic pro-inflammatory proteins and hormones that threaten organ systems throughout the body. Higher amounts of visceral fat have been associated with increased risk of cardiovascular disease, type 2 diabetes, and mortality. Konieczna et al found that higher consumption of “ultra-processed foods and drinks was associated with greater age-related visceral and overall adiposity accumulation (11).” Several studies have suggested a significant relationship between systemic insulin resistance in the muscles and liver and visceral fat accumulation as a result of disrupted insulin-mediated signalling, although this relationship is non-causative (12,13). Interestingly, a 2011 study concluded that a 10g increase in soluble fibre consumption (fibre from vegetables, fruits, and beans) per day decreased visceral fat by 3.7% over 5 years (14).

Do I need to go low-carb?

Theoretically, a low carbohydrate diet would solve glucose intolerance issues and limit the need for insulin production. However, a 2016 literature review claimed that low-carbohydrate diets did not differ significantly from high-carbohydrate diets in improving blood sugar levels, especially with reported low adherence to low-carbohydrate diets (15,16). Moreover, the physical and emotional stress of “yo-yo” dieting has been associated with an increased risk of diabetes as chronic stress results in inefficient glucose uptake, increased fat accumulation in the liver, and suppression of insulin secretion (17,18). Research recommendations highlight significant improvements in type 2 diabetes and obesity upon the consumption of a diet rich in essential fatty acids and amino acids, as well as high fibre carbohydrates that include an abundance of phytochemicals and phytonutrients from leafy greens, cruciferous vegetables, low glycemic index fruits and vegetables, nuts, and seeds (19).

The glycemic index rates foods according to their effect on blood sugar levels when consumed in isolation. Significant improvements in blood sugar levels have been recorded when high glycemic foods were replaced with low glycemic index foods (20). Moreover, high fibre carbohydrates and whole grains have been shown to significantly reduce the risk of type 2 diabetes by reducing fasting blood glucose levels and insulin resistance (21). Dietary fibre slows down glucose absorption by decreasing intestinal permeability and delaying gastric emptying (22,23). Furthermore, dietary fibre has been associated with lower total cholesterol levels and reduced systemic inflammation (24). Therefore, targeting to increase fibre intake by 15g to 35g may be beneficial in reducing the “risk of premature mortality in adults with diabetes (25).”

What about keto?

The keto diet is a low carbohydrate high-fat diet, initially prescribed to manage epilepsy. As an alternative to glucose, ketones produced from stored fat are used for energy. Several studies found positive, but temporary correlations between the keto diet, type-2 diabetes management, and reduced antidiabetic medication (26). Nevertheless, long-term research shows “significant improvements in insulin sensitivity at 6 months, but not in a year.” Additionally, De Koning et al concluded that low carbohydrate diets high in animal proteins and fats increased type 2 diabetes risk by two-fold compared to low carbohydrate diets high in proteins and fats from plants (27). Therefore, approaching blood sugar regulation sustainably requires balanced and mixed meals with carbohydrates, fats, and protein. Recommendations advise consuming mixed meals containing the three macronutrients with findings that have depicted significantly decreased fluctuations in blood sugar levels (28).

Diabetes & gut health

The gut microbial environment in type 2 diabetic patients differs from that of healthy individuals with increased transport of sugars and amino acids, as well as decreased synthesis of butyrate (main fuel for cells that line the gut), structures that enable bacterial movement, and micronutrient metabolism. Ultimately, the environment in diabetic individuals is biased towards bacterial defence mechanisms against stress and inflammation, which simultaneously impairs insulin-stimulated glucose uptake and signalling (29).

Interestingly, studies have attributed altered gut microbiota with correlations between artificial sweeteners (saccharin, sucralose, aspartame) and glucose intolerance (30). Changes in the gut microbiota from the consumption of noncaloric artificial sweeteners appeared to have increased weight as well as fasting blood glucose levels in humans, independent of body mass index (31). Despite these findings, different artificial sweeteners presented different physiologic effects. For example, the consumption of sucralose increased absorption of glucose, yet the consumption of stevia significantly lowered insulin levels two hours post-meal compared to aspartame and sucrose (32). Therefore, the current body of research on the relationship between artificial sweeteners and glycemic regulation is contradictory and correlative.

In summary:

Lifestyle interventions, specifically diet and physical activity, can delay or reverse the progression of pre-diabetes and the risk of diabetes. A study that investigated the combination of high fibre diets with moderate intensity physical activity found a 58% reduction in the risk of diabetes (33).

Increased availability of ultra-processed foods and sedentary lifestyles have been associated with increased visceral fat, which has been linked with increased insulin resistance and type 2 diabetes risk.
Chronic stress suppresses insulin secretion and inflicts insulin resistance subsequently.
Mixed meals with dietary fibre have been associated with delayed gastric emptying, decreased intestinal permeability and decreased blood sugar fluctuations.
Keto diets can be advantageous for diabetes management, however, these findings are temporary.
Current research suggests associations between artificial sweeteners and glucose intolerance, however, further large-scale studies are required to substantiate this link.

This blog post was written by Namrata Ashok, a Sports Science and Nutrition BSc student at the University of Glasgow. Currently involved in two internships, work experience, podcasts, and further reading, alongside her studies, Namrata is enthusiastic about helping individuals heal and restore from the inside out, honing in on approaching the root cause. She is determined to explore the world of health, nutrition, and movement by combining research, theory, and practical experience.

References:

(1) https://pubmed.ncbi.nlm.nih.gov/17257284/

(2) https://www.nhs.uk/conditions/diabetes/

(3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8232639/#:~:text=Insulin%20regulates%20glucose%20levels%20in,resulting%20in%20overall%20weight%20gain.

(4) https://www.nature.com/articles/s41598-020-74678-6

(5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6306539/#:~:text=Women%20with%20GDM%20are%20predisposed,%25%20(3%2D15).

(6) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4116271/

(7) https://www.sciencedaily.com/releases/2013/08/130822091024.htm#:~:text=A%20study%20involving%20more%20than,prediabetes%20increase%20by%2026%20percent.&text=FULL%20STORY-,A%20study%20involving%20more%20than%208%2C000%20participants%20has%20shown%20that,of%20prediabetes%20increase%20by%2026%25.

(8) https://www.bmj.com/content/369/bmj.m1361

(9) https://www.diabetesresearchclinicalpractice.com/article/S0168-8227(20)30882-2/fulltext

(10) https://www.nature.com/articles/s41586-022-04756-4

(11) https://pubmed.ncbi.nlm.nih.gov/33610419/#:~:text=Background%20%26%20aims%3A%20Ultra%2Dprocessed,adiposity%2Dassociated%20adverse%20health%20outcomes.