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Poor sleeping habits are associated with an increased risk of weight gain and obesity. Short sleepers (< 7 hours/night) and long sleepers (> 9 hours/night) are more likely to be obese. Other sleep characteristics associated with obesity include daytime napping, working night shifts, poor sleep quality and evening chronotype (being a “night person”). Individuals who tend to stay up late at night, and sleep during the morning hours, are more likely to have poor eating habits, engage in late-night snacking, have sleep apnea and higher levels of stress hormones. Night owls are also more likely to develop diabetes and metabolic conditions.  A study in the April 2017 issue of the American Journal of Clinical Nutrition evaluated sleep patterns in those with a genetic risk for obesity. Among individuals at risk for obesity, short sleepers and long sleepers had a greater body mass than normal sleepers, those who sleep between seven and nine hours per night. Sleep duration was not significantly associated with body weight in individuals with a low genetic risk for obesity. Sleep behaviors are more likely to affect individuals who are at risk for obesity based on their genes. This study sheds light on the interactions between our genes and our lifestyle. Sleeping behaviors influence our genes, and those at risk of obesity may be able to moderate weight gain by changing their sleeping habits. References
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There has been a dramatic increase in the incidence of type 1 diabetes in the past 30 years. Although there is no single cause of type 1 diabetes, a recently published article in The Lancet identifies the dietary and environmental triggers contributing to the development of this devastating disease (1).
In type 1 diabetes, the body does not make enough insulin. More than 18,000 youths diagnosed each year.
Interaction Between Genetics, Diet and the Environment
The main risk factor for type 1 diabetes is genetics, but an environmental trigger is necessary to initiate the disease process (2). The authors categorize risk factors based on childhood stage.
Viral infections, changes in the microbiota (the microorganisms in the gut), a lack of physical activity, rapid weight gain and psychological stress are also all risk factors. These factors can trigger the disease process in children who have a genetic risk for type 1 diabetes (1, 2). Environmental Risk Factors for Type 1 Diabetes Infographic
 Type 1 Diabetes - The Immune System Attacks The Pancreas
Type 1 diabetes is an autoimmune disease that typically develops during childhood and is characterized by high blood glucose (3). Glucose is a sugar that is the end product of starch digestion as seen in the diagram below. Glucose is also the main sugar in our bloodstream and main carbohydrate stored in our body.
Type 1 diabetes results when the immune system mistakenly identifies the beta cells in the pancreas as foreign invaders. The immune system attacks and destroys the insulin producing beta cells. Insulin is the hormone that moves glucose, our main energy source, from the bloodstream into our cells. Without insulin, not only does blood glucose rise to dangerous levels, the body’s cells are deprived of energy. An individual with type 1 diabetes must administer insulin daily (3).
Cause of Type 1 Diabetes is Unknown: Genes Play a Role HLA Gene Complex
The cause of type 1 diabetes is unknown (4) but it is generally accepted that multiple genes are involved in its development. In addition, many dietary and environmental risk factors have been identified. One important group of genes associated with type 1 diabetes is the human leukocyte antigen (HLA) gene complex (5). The HLA complex provides the body’s immune system with a set of tools to help it differentiate between our own proteins and proteins made by bacteria or viruses (5). Variations in this gene complex are linked to chronic diseases.
The Immune System - Identifying a Foreign Invader
Although our immune system is intended to attack viruses and bacteria, it is designed to respond specifically to proteins on the surface of these microorganisms, not the entire microorganism. Using the HLA complex, the immune system can distinguish between our own proteins (self) and proteins on the surface of microorganisms (foreign) (6). This allows the immune system to adapt to a variety of invaders, neutralizing and destroying foreign proteins on microorganisms, but ignoring the proteins that make up our organs. Variations in the HLA gene complex can create confusion for the body’s immune system, making it difficult to tell the difference between a foreign protein and a protein that is part of our own body.
The Immune System - Creating a Specialized Army
The immune system is designed to respond to foreign proteins that enter the body. Bacteria and viruses, common foreign invaders, have proteins on their surface which can be identified by our immune system. When presented with a foreign invader, the immune system launches its attack. The first line of defense attacks the foreign invaders, neutralizing or destroying them. But, these invaders usually attack again.
Fortunately, after the first strike a strategic mission is in the works by the immune system. Upon first exposure, the immune system sizes up the foreign invader and creates an antibody specifically designed to neutralize it. The immune system assesses the enemy and creates a small army of specialized soldiers ready to attack when the bacteria or virus invades again (6).
The Innocent Invader - Food Protein
When we consume protein, our digestive system breaks down the protein into individual amino acids as seen in the image to the right. The amino acids are then absorbed into our bloodstream and utilized by the body. Occasionally, a protein, or a protein fragment, escapes digestion and ends up in the bloodstream (7). Once in the bloodstream, the immune system might identify this food protein as a foreign invader and launch an attack. This is how a food protein, for example protein from peanuts, can result in an allergic reaction (8). With repeated exposures, the body will build up its specialized army, preparing itself for the next attack.
Mistaken Identity - If Food Protein Looks Like Body Protein
When protein sneaks across the intestines into the bloodstream, it can induce an immune response. This may initiate an allergic response or it may initiate an autoimmune response. In some cases, a section of a food protein is identical, or nearly identical, to a section of protein in an organ in our body. The body may mistakenly identify the protein in an organ, for example the pancreas, as a foreign invader.
The immune system rounds up its specialized antibodies. These specialized antibodies, created to attack the similar food protein, now attack the cells in the pancreas. It's a case of mistaken identity.
Milk Protein Mistaken for Beta Cells in the Pancreas Anatomy of the pancreas
A small section of a protein in cow’s milk appears just like a small section of protein in the beta cells (insulin-producing cells) of the pancreas (9). A study in the New England Journal of Medicine in 1992 tested 142 children with type 1 diabetes for antibodies to a protein in milk (bovine serum albumin) and compared the results to 79 healthy children without diabetes. All of the children with type 1 diabetes had the antibody to the specific milk protein, whereas only two of the healthy children had the antibody (9). This study demonstrates that the children with type 1 diabetes had exposure to cow’s milk. This exposure resulted in the creation of a specific antibody designed to neutralize and destroy the milk protein. The authors theorized that this anti-milk protein antibody mistakenly identified the pancreas as foreign and destroyed the beta cells. Not all studies have reproduced these results (10) and this theory of the role of cow’s milk as a causative agent in the development of type 1 diabetes remains controversial. Cow’s milk remains a risk factor, but not necessarily a cause of type 1 diabetes.
Environment and Diet Increase Risk For Type 1 Diabetes
The recent two-part article in The Lancet (1, 2) demonstrates the importance of understanding the interaction between diet, environment, and genetics. Although certain individuals may be genetically susceptible to type 1 diabetes, an environmental or dietary trigger is needed to initiate the disease process. The infographic above provides a visual representation of the dietary and environmental factors triggering the disease during various phases of childhood. Important dietary risk factors and dietary protective factors are summarized below (1).
Dietary Factors Influencing Development of Type 1 Diabetes
In Summary
The incidence of type 1 diabetes has increased over the past three decades. The exact cause of type 1 diabetes has not been identified because there are many factors influencing the development of the disease. Changes in our diet, our environment and our lifestyle over the past 30 years have contributed to the increase of this disease. In children who have a genetic risk for type 1 diabetes, the foods they eat, the amount of activity they engage in and the amount of weight they gain can trigger the onset of the disease. Children with a genetic risk have variations in their genes that increase the likelihood that the immune system will mistakenly identify the insulin producing cells in the pancreas as foreign invaders, destroying these cells slowly over time. Once destroyed, the cells in the pancreas can no longer produce insulin. This causes elevated blood sugar and type 1 diabetes results.
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Christine Dobrowolski is a nutritionist and whole-foods advocate. Categories
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