The fastest growing lifestyle-induced chronic disease

Diabetes mellitus (commonly referred to as diabetes) represents a number of diseases that involve problems associated with the hormone insulin. Normally, the pancreas releases insulin into the blood to help store and metabolize sugar and fat released from food ingested. Diabetes occurs when:

• The pancreas does not produce any insulin
• The pancreas does not produce enough insulin
• The body does not respond appropriately to insulin, a condition called “insulin resistance”

Diabetes represents a chronic, lifelong disease, afflicting approximately 18.2 million Americans. (See below for more statistics.) Almost one third, or approximately 5.2 million people, are unaware they have diabetes. Additionally, 41 million people have prediabetes, a condition that matures into the full disease.
 

 

History

Diabetes was first described in about 1500 BCE in ancient Egypt as “too great emptying of the urine.” Indian physicians, around the same time, identified the condition as madhumeha or “honey urine,” noting that the urine of diabetics would attract ants.

The term “diabetes” or “to pass through” was first used in 250 BCE by the Greek Apollonius of Memphis. Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in about 400-500 BCE with type 1 associated with youth and type 2 with obesity. The term “mellitus” or “from honey” was added by Thomas Willis (1621-75), a British physician in the late 1600s, to separate the condition from diabetes insipidus, which also associates with frequent urination but isn’t related to diabetes, the condition.

Diabetes appears to have been a death sentence in the ancient era. Hippocrates (c. 460 BCE–c. 370 BCE) makes no mention of it, and Galen (129 AD–c. 200-16 AD) commented that he had only seen two cases during his career.

Pathogenesis of diabetes has only been understood experimentally since about 1900. The discovery of a role for the pancreas in diabetes generally ascribes to Joseph von Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards.

In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical normally produced by the pancreas. He proposed calling this substance insulin, from the Latin insula, meaning island, in reference to the insulin-producing islets of Langerhans in the pancreas. The islets of Langerhans was discovered in 1869 by the anatomist Paul Langerhans (a German pathologist and biologist). He identified the key cells in the pancreas that produced insulin.

Effective treatment for diabetes was developed in 1921-22 when Canadians Frederick Banting and Charles Best demonstrated they could reverse induced diabetes in dogs by giving them an extract of insulin from healthy dogs.

Type 1 vs. type 2 diabetes

In general, people with diabetes either have a total lack of insulin production (type 1 diabetes) or they have too little insulin or cannot use insulin effectively (type 2 diabetes).

Both types of diabetes greatly increase the risk for a range of serious complications. Diabetes remains the leading cause of blindness and kidney failure. It also continues to be a critical risk factor for heart disease, stroke, and foot or leg amputations.

Type 1 diabetes: Formerly called juvenile-onset or insulin-dependent diabetes. The body’s immune system destroys the cells that release insulin, stopping insulin production. Without insulin, cells cannot absorb sugar (glucose) to produce energy. Accounts for 5-10 out of 100 people.

Type 2 diabetes: Formerly called adult-onset or non-insulin-dependent diabetes. Develops at any age, but most common during adulthood. The body isn’t able to use insulin correctly. This is called insulin resistance. As it gets worse, the pancreas may make less and less insulin. This is called insulin deficiency. Type 2 diabetes accounts for the majority of people who have diabetes.

Symptoms

Type 2 diabetes develops slowly, and symptoms may be mild and easy to dismiss at first.

As the disease progresses, symptoms become more severe and potentially dangerous.

Diabetes also has a powerful effect on the heart. Women with diabetes are twice as likely to have another heart attack after the first one. They’re at quadruple the risk of heart failure when compared to women without diabetes. Diabetes can also lead to complications during pregnancy.

Early diabetes symptoms

Advanced diabetes symptoms

If you have two or more of these symptoms, see your doctor. Without treatment, diabetes becomes life-threatening.

Diabetes statistics: It’s not a pretty picture

• More than 9.3 percent of the world’s population has diabetes.
• More than 18.2 million people in the U.S. have diabetes.
• One in four people have no idea they have diabetes.
• More than one in three adults have prediabetes, and 15-30 percent of them will develop type 2 diabetes within five years.
• Non-Hispanic black, Hispanic, and American Indian adults, including Alaska Native adults are about twice as likely to have diabetes as non-Hispanic white adults.
• In 2015, diabetes cost the United States in excess of $250 billion in direct medical costs and reduced productivity.
• The average medical expenses for people with diabetes are about 2.3 times higher than they would be in the absence of diabetes.
• Diabetes is the seventh leading cause of death in the United States, either as the underlying cause of death or as a contributing factor.
• Half of the people with diabetes die of cardiovascular disease, including heart disease and stroke.
• Diabetes is the leading cause of kidney failure.

Causes

The pancreas produces insulin and releases it when you eat. It helps transport sugar from your blood to cells, mostly muscle, throughout your body, where it’s used for energy.

In type 2 diabetes, the body becomes resistant to insulin and it no longer is able to transport sugar into cells. In response, the pancreas works harder to make more insulin. Eventually, the pancreas becomes fatigued and/or damaged and may become unable to produce any insulin.

If you don’t produce enough insulin, or if your body doesn’t use it efficiently, sugar builds up in the bloodstream. This leaves the body’s cells starved for energy. Currently we do not know exactly what triggers this series of events, but we are getting closer to definitive answers as research expands. Some researchers think it has to do with cell dysfunction in the pancreas, or with cell signaling and regulation. There may be a genetic predisposition to developing type 2 diabetes, as well. Excess body weight and fat has been shown to increase risk of insulin resistance and diabetes. There could also be an environmental trigger that includes foods consumed over time, lack of physical activity, increased stress, social isolation, and even exposure to chemical pollution. Most likely, it’s a combination of factors that increases the risk of type 2 diabetes.

Plant-based diets and exercise may prevent or even reverse type 2 diabetes

Although controversial and not yet accepted by many medical and pharmaceutical “experts,” there is a growing body of scientific literature showing that individuals following a plant-based and vegetarian diet, and who engage in regular daily physical activity, can improve their blood sugar control via improved insulin sensitivity, and thus reduce or eliminate type 2 diabetes.

Research shows that plant-based diets associate with significant clinical improvements in diabetes indices, as indicated by reductions in A1C, body weight, plasma lipid concentrations, and urinary albumin excretion, in as little as six weeks. These results compare favorably with those observed in people taking oral diabetes drugs, without any residual drug side effects.

A low-fat, plant-based diet influences nutrient intake and body composition in several ways that affect insulin sensitivity. Because low-fat, plant-based diets are low in fat and high in fiber, they typically result in reductions in total calorie intake. This results in a consistent weight-reducing effect that has been shown to affect sugar control. Also, a reduction in total fat intake (particularly the proportion of dietary saturated-to-unsaturated fat) and intake of low-glycemic index and high-fiber foods has been shown to increase insulin sensitivity. Finally, plant-based, low-fat diets associate with reductions in iron stores that also increase insulin sensitivity.

In a study published by the American Diabetes Association, people who ate the most animal protein were the most likely to develop diabetes. In this study, researchers showed participants who consumed the most animal protein were 22 percent more likely to develop diabetes, compared with those who ate the least. For every additional 10 grams (0.35 oz.) of animal protein, the risk for developing diabetes went up by 6 percent!

Other studies also have found increased diabetes risk associated with high intakes of animal protein. For example, eating a diet high in animal protein leads to an earlier death compared with people who consume less, according to a study analyzing data from 6,381 American adults, aged 50 and older. Participants who ate the most animal protein had a five-fold increased risk of death related to diabetes. Those younger than 65 who ate the most animal protein had a 74 percent increased risk of death from any cause, and a four-fold increase in death related to cancer, during a follow-up of 18 years. Risks for death were diminished or absent when protein sources were plant-derived.

Finally, according to a study published in Nutrition & Diabetes, a low-fat, plant-based diet reduced pain associated with diabetic neuropathy. In this randomized controlled trial, 35 individuals with type 2 diabetes and painful diabetic neuropathy were assigned to either a low-fat vegan diet for 20 weeks or to a control group who consumed their “normal” diet. At the end of 20 weeks, the individuals in the vegan diet group lost an average of 14 pounds and showed greater improvements in pain measures, as compared with the control group, indicating potential for a plant-based diet in the treatment of diabetic neuropathy.
 
 
References

• American Diabetes Association. 2003. “Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications” (Position Statement). Diabetes Care; 26 (Suppl. 1):S51.
• Barnard, N.D., et al. 2005. “The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity.” American Journal of Medicine; 118:991. Bunner, A.E., et al. 2015. “A dietary intervention for chronic diabetic neuropathy pain: A randomized controlled pilot study.” Nutrition & Diabetes; 5:e158. doi: 10.1038/nutd.2015.8.
• Chiu, T.H.T., et al. “Taiwanese vegetarians and omnivores: Dietary composition, prevalence of diabetes, and IFG.” PLOS One. Online Feb. 11, 2014. Fraser, G.E., 2003. “Vegetarianism and obesity, hypertension, diabetes, and arthritis.” Diet, Life Expectancy, and Chronic Disease. Oxford, U.K., Oxford University Press; p. 129.
• Goff, L.M., et al. 2005. “Veganism and its relationship with insulin resistance and intramyocellular lipid.” European Journal of Clinical Nutrition; 59:291. Hua, N.W., et al. 2001. “Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians.” British Journal of Nutrition; 86:515.
• Harland J., Garton L. “An update of the evidence relating to plant-based diets and cardiovascular disease, type 2 diabetes, and overweight.” Nutrition Bulletin. 2016; 41:323-338
• Jenkins, D.J., et al. 1987. “Low-glycemic index diet in hyperlipidemia: Use of traditional starchy foods.” American Journal of Clinical Nutrition; 46:66. Jenkins, D.J., et al. 2003. “Type 2 diabetes and the vegetarian diet.” American Journal of Clinical Nutrition; 78: 610S.
• Kendall, A., et al. 1991. “Weight loss on a low-fat diet: Consequence of the imprecision of the control of food intake in humans.” American Journal of Clinical Nutrition; 53:1124.
• Laitinen, J.H., et al. 1993. “Impact of intensified dietary therapy on energy and nutrient intakes and fatty acid composition of serum lipids in patients with recently diagnosed non-insulin-dependent diabetes mellitus.” Journal of the American Dietary Assn.; 93:276.
• Levine, M.E., et al. 2014. “Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population.” Cell Metabolism; 19:407.
• Nicholson, A.S., et al. 1999. “Toward improved management of NIDDM: A randomized, controlled, pilot intervention using a low-fat, vegetarian diet.” Preventive Medicine; 29:87. Petersen, K.F., et al. 2004. “Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.” New England Journal of Medicine; 350:664.
• Van Nielen, M., et al. 2014. “Dietary protein intake and incidence of type 2 diabetes in Europe: The EPIC-INTERACT case-cohort study.” Diabetes Care. Published ahead of print April 10, 2014.