The principle characteristic of obesity is excess adipose tissue. Currently, body mas index (BMI) is an accepted and widely used measure for obesity.
BMI= weight (kg)/Height (m2)
According to World Health Organization (WHO) BMI classification;
BMI (kg/m2) Thinness (stage) Reference Overweight Obesity (class)
30 <30 III
25 <25 ≥25
Above table shows obesity classes and thinness stages based on BMI distribution. BMI lower than 18.5 is considered as a stage thinness while BMI ≥30 is considered as obesity.
Limitations of BMI
There are certain limitations of BMI as a measure of obesity. The body weight parameter does not tell us the percentage of body fat mass and lean mass. The other limitation is the lack of information regarding body fat distribution. Fat distribution in the body could be around the trunk and upper body called the android. Android fat distribution is seen as more common in males. Body fat distribution is not in the center but rather on the bottom, hips, and thighs making a pear shape called a gynoid. Gynoid fat distribution is more common in females. Android fat distribution contributes to obesity-related clinical complications. Finally, regarding ethnic differences, at any given BMI Asian females have higher body fat by 5% compared to Caucasians.
Clinical complications of obesity
Medical complications associated with obesity are:
Obstructive sleep apnea
Nonalcoholic fatty liver disease
Gall bladder disease
Polycystic ovarian syndrome
Idiopathic intracranial hypertension
Coronary heart disease
Cardiac heart failure
Breast, colon, pancreases, uterus, cervix, esophagus, kidney, prostate
Benefits of 10% weight loss
A total of 10% weight loss will beneficially improve the following conditions affected by obesity:
Neural tube defects
Cancers of breasts, esophagus, stomach, colon, endometrium and kidney
Coronary artery disease
Carpal tunnel syndrome
Chronic venous insufficiency
Deep vein thrombosis (DVT)
Diabetes mellitus type II
Gall bladder disease
Impaired respiratory function
Infection following wounds
Low back pain
Urinary stress incontinence
Obesity and mortality
Obesity is related to mortality. A prospective study conducted suggested a high mortality rate in individuals with a BMI of 30 and above.
The lowest mortality rates are for those with BMI of 20-22.
Mortality begins to increase modestly with a BMI >25.
With a BMI of ≥30, mortality of all causes increased by 50-100%
What are the risks of disease development with BMI increase
Obesity and diabetes type II
Diabetes mellitus (DM) is a metabolic disorder that can alter the metabolism of carbohydrates, fat, and proteins. DM has been classified into two major types. DM type I and DM type II. DM type I is characterized by a deficiency of insulin in the blood due to the inability of β-Langerhans islet pancreatic cells to produce insulin. DM type II is the defect in peripheral tissue to uptake insulin called insulin resistance. Insulin reduces blood glucose by inducing glucose uptake in insulin-sensitive tissue such as skeletal muscle, fat and heart. Insulin also inhibits glucose production in the liver, kidney, and small intestine in the control of blood glucose. Insulin resistance occurs when the insulin-sensitive tissue loss response to insulin. The result of insulin resistance is high glucose in the blood, in an effort to store the excess glucose pancreas produces more insulin. This results into hyperinsulinemia and hyperglycemia.
Body mass index has a strong relationship to diabetes and insulin resistance. In obese individuals, the amount of nonesterified fatty acids, glycerol, hormones, cytokines, proinflammatory markers, and other substances that are involved in the development of insulin resistance, is increased. The pathogenesis in the development of diabetes is based on the fact that glucose is not taken by the insulin-sensitive tissue for proper storage, causing a lack of control of blood glucose. The development of diabetes becomes more inevitable if the failure of β-islet cells of the pancreas is accompanied by insulin resistance.
In obesity, there is a chronic and low-grade inflammation that is involved in the pathogenesis of several chronic diseases, such as type 2 diabetes, hypertension, atherosclerosis, fatty liver, cancer, asthma, and sleep apnea. The Association of obesity and inflammation has been reported more than 100 years ago. Inflammation is a physiological process characterized by an elevated number of white blood cells or increased levels of pro-inflammatory cytokines in the circulation or tissue. In general, inflammation is required for organ remodeling, tissue repairing, wound healing and immunity against infections. Inflammation is a protective reaction in the body to control harmful insults and to initiate the healing process. Overreaction of inflammatory response usually leads to multiple side effects such as tissue injury and organ dysfunction. Obesity-associated inflammation starts in adipose tissue and liver with elevated macrophage infiltration and expression of proinflammatory cytokines. The pro-inflammatory cytokines enter the bloodstream to cause systemic inflammation.
Weight gain and body mass are central to the formation and rising incidence of type 2 diabetes.
Congestive heart failure
Each unit increase in BMI increases the risk of congestive heart failure by 5% in men and 7% in women
Gallstone risk increases as BMI increases from 9% to 25% in women and 5% to 11% in men.
For each increase of 1 unit BMI hemorrhagic stroke increases by 6% and ischemic stroke increases by 4%.
In proportion to the increase in body weight; decreases total lung capacity (TLC), forced vital capacity (FVC), and maximum voluntary ventilation (MVV).
Increased risk of asthma has been reported in an individual with an increase in BMI.
Alzheimer’s and dementia
Obesity at older ages increases the risk of Alzheimer’s and dementia in women. In women for every 1 unit increase in BMI at age 70 increases the risk for Alzheimer’s and dementia by 36%. These associations are more prevalent in women compared to men.
Obstructive sleep apnea (OSA)
Obstructive sleep apnea occurs in 50% of severely obese. Most people with OSA have BMI > 30. OSA is present in 90% of obese subjects seek bariatric surgery. Potentially it is life-threatening condition. OSA can cause serious CV complications. OSA causes chronic structural changes in coronary arteries leading to a possible increase in myocardial ischemia, and an increase risk of rupture of artery plaque and thrombosis.
Non-alcohol fatty liver disease (NAFLD)
NAFLD occurs in more than 66% of obese subjects. Truncal obesity is risk for NAFLD development even with normal BMI.
Obesity and caners
35% of cancers are attributable to dietary factors. A wealth of epidemiological data connecting obesity and various malignancies has suggested; postmenopausal breast cancer, colon, pancreas, gallbladder and gastric cardia.
Management of obesity
obesity are high a priority area for primary care practitioners because they are associated with many comorbidities.
What is healthy nutrition during weight loss
Before starting a discussion of optimal diets for weight loss, a discussion of what nutrient inputs are needed for the body’s proper structure and function is appropriate. A balanced diet is one that meets all of the minimal requirements for essential nutrients, including amino acids, fatty acids, vitamins, minerals, and vitamin-like substances. Although minimal requirements are set by governmental advisors for the general population to prevent nutritional deficiencies, the nutritional requirements during weight loss are different from the nutritional needs of the otherwise healthy individual. An optimal diet during weight loss provides all of the nutrients in a way that maintains optimal health (which may include changes in body composition) during the adipose tissue loss process. Because carbohydrates are simply a source of energy, if energy needs are otherwise met, there is no dietary need for carbohydrate intake. Because certain amino acids in protein are not made by the human body, and dietary protein is used for structure (muscle, bone connective tissue) and provides more than just an energy source, this macronutrient is indispensable. Likewise, essential fatty acids are required for optimal health. It is very important to keep in mind that there may be differences in requirements based on individual variation.
Water has so many uses in the body and is so essential for human life that it must be consumed daily for optimal function. A few of the important functions that water performs are dissolving nutrients to make them accessible to cells, assisting in moving nutrients through cells, keeping mucous membranes moist, lubricating joints, evaporating for body temperature regulation, and removing waste from the body. For most people, the daily water losses are about six cups (1.5 L) of urine, two cups (0.5 L) of sweat, and one cup (0.25 L) from breathing. In sum, about nine cups (2.25 L) are required for most people each day, but the body has many regulatory systems to allow for a wide variation in water intake. Interestingly, about 20% of the water is obtained from the water in food and is generated from metabolic processes. For practical purposes, the general recommendation to “drink when you are thirsty” will suffice during the weight loss process.
List of essential human nutrition
• Vitamins: A, B1 (thiamine), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B7 (biotin), B9 (folic acid), B12 (cyanocobalamin), C (ascorbic acid), D, E, K • Minerals: calcium, phosphorus, magnesium, iron • Trace minerals: zinc, copper, manganese, iodine, selenium, molybdenum, chromium • Electrolytes: sodium, potassium, chloride • Amino acids: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine • Essential fatty acids: linoleic, α-linolenic.
Protein is the major structural component of the human body. Dietary protein is the source of amino acids to provide the “building blocks” to make the proteins, and when used for energy, burned in a bomb calorimeter, contains 4 kcal/g. Protein is required in the human diet because there are nine essential amino acids that the body cannot manufacture by itself (“essential” means that the body is unable to synthesize the nutrient). While maintenance dietary protein needs are estimated to be from 0.7 to 1.0 mg/kg/day, 1.2 to 1.5 g/kg lean body weight of the dietary protein is needed for the preservation of lean body mass and physical performance during weight loss. Picking the value of 1.5 g/kg/day, for adults with reference weights ranging from 60 to 80 kg, translates into total daily protein intakes 90 to 120 g/day. When expressed in the context of total daily energy expenditures of 2000 to 3000 kcal/day, about 15% of an individual’s daily energy expenditure (or intake if the diet is caloric) needs to be provided as protein. If calories are severely limited, then protein needs should be determined on a gram-per-kilogram basis. During weight loss, especially if strenuous exercise is a component of the process, more dietary protein may be advantageous.
Fat is a major component of cell structure and hormones and is the body’s primary source of energy containing 9 kcal/g when burned in a bomb calorimeter. Fat is required in the human diet because there are two essential fatty acids. A “tolerable upper limit intake level” is not set for total fat because there is no known level of fat at which an adverse effect occurs. Dietary fat may enhance fatty acid oxidation, and thus high-fat diets may be desirable to achieve the goal of dietary treatment of the obese individual. The optimal type of fat to eat during weight loss is not known, although recent evidence indicates that in the absence of carbohydrate intake (20 g or less/24 h) high-fat diets lead to lower levels of bloodstream saturates than in those eating a low-fat diet (11). (This may not be the case in calorie-restricted, low-fat diets.)
Carbohydrates are a source of energy containing 4 kcal/g when burned in a bomb calorimeter, and some single carbohydrates (monosaccharides) are used in physiologic compounds such as glycoproteins and mucopolysaccharides. While some dietary carbohydrates contain vitamins and minerals, there is no requirement for carbohydrates in the human diet because metabolic pathways exist within the body to make carbohydrates from dietary protein and fat. Dietary and endogenously created carbohydrate is stored as glycogen or converted to and stored as fat.
Source of Energy
To achieve lipolysis and increased fat oxidation in the dietary treatment of the obese individual, an important goal is to maximize fat as the major fuel source—fat from the diet and from adipose tissue stores. Carbohydrate then becomes a fuel source of much less importance because ketones (a metabolic product of lipolysis) can substitute for glucose in most tissues. Because carbohydrate used as a fuel is linked with lipogenesis, lipolysis and fat mobilization is reduced or halted when carbohydrate is a dominant fuel source. For optimal lipolysis and adipose tissue mobilization, keeping carbohydrates as an energy source to a minimum is preferable.
Essential Vitamins and Minerals
Dietary vitamins and minerals are required in small amounts and are found in food naturally. A few of the functions of vitamins include hormonal signaling and acting as mediators of cell signaling, regulators of cell and tissue growth and differentiation, precursors for enzymes, catalysts and coenzymes, and substrates in metabolism. Vitamins and minerals are now available in inexpensive pill and liquid form, and a “multivitamin” is recommended during weight loss, as a safety net.
Using nutritional ketosis as a diet therapy for obesity
The rationale of the dietary treatment of the obese individual is to alter the hormonal milieu to direct the body’s metabolism away from fat storage and toward fat mobilization and oxidation. Body systems can be directed toward fat oxidation in many ways, for example, through carbohydrate restriction or caloric restriction. Caloric restriction is usually achieved at least in part by carbohydrate restriction. Nutritional ketosis is a metabolic state in which fat and ketones are the major fuel sources to generate adenosine triphosphate (ATP) while glycolysis is minimized. Although often misconstrued as harmful or unhealthy, nutritional ketosis is not known to cause any short or long-term adverse consequences. In fact, many indigenous populations living on very low-carbohydrate diets were likely in chronic nutritional ketosis. Nutritional ketosis produces a relatively low level of ketone elevation above populations eating carbohydrate-containing diets but is not associated with a reduction in pH or a significant metabolic acidosis. Frequently, nutritional ketosis is confused with diabetic ketoacidosis—the metabolic state during which the absence of insulin leads to very high levels of ketones, elevated blood glucose, dehydration, and a low blood pH. When an individual is adapted to nutritional ketosis, fatty acids and ketones become the major energy sources. Fatty acids are an excellent fuel source and can be utilized for energy by most tissues, including cardiac and skeletal muscle. Ketone bodies (β-hydroxybutyrate and acetoacetate) contain 4 kcal/g (when burned in a bomb calorimeter) and can be utilized by all cells except those that do not have mitochondrial fat oxidation enzymes (erythrocytes, cornea, lens, retina) or sufficient oxygen to support oxidative metabolism (renal medulla). During nutritional ketosis, it is estimated that the daily glucose needed can be as low as 20 g/day because fatty acids and ketones are available for muscle and central nervous system use. Glucose becomes less important as a fuel source, with ketones substituting for glucose in most tissues that would otherwise use glucose. Glucose is manufactured through a process called gluconeogenesis, which occurs in both the liver and kidney. While the liver is the major gluconeogenic organ, capable of producing up to approximately 240 g of glucose per day when insulin levels are low, the kidneys may produce up to 20% of daily glucose needs. Precursors for gluconeogenesis come mainly from amino acids in the diet. As ketosis is desirable, some clinical programs use urinary ketone strips to verify adherence and the presence of the lipolytic state, colloquially known as “being in ketosis.” However, there can be significant subject-to-subject variability in urinary ketone response even when subjects eat uniform diets. Type 2 diabetes can also reduce the likelihood of urinary ketones. Most studies of the low-carbohydrate ketogenic diet (LCKD) have observed that the level of ketosis (urine and blood levels) decreases with time. It is unclear whether this effect is a result of increased efficiency at utilizing ketone bodies for energy or a decrease in the production of ketone bodies over time (presumably from adding carbohydrates back into the diet). However, this effect was also observed in one inpatient study that closely controlled carbohydrate intake at 21 g over two weeks and measured urine ketones on a daily basis
How to achieve nutritional ketosis
Dietary carbohydrate is the primary insulin secretagogue. Because pancreatic insulin secretion is stimulated by the glucose/amino acid ratio in the portal vein and in response to an increase in blood glucose, a powerful way to lower insulin levels is to reduce dietary carbohydrates. When the dietary intake of carbohydrates is reduced to less than 50 g/day, most individuals excrete ketones in the urine, leading to the descriptive name of “ketogenic diet.” Several popular diets have used the recommendation of very low levels of carbohydrates (<20 g/day) in the early stages of the diet to enhance lipolysis. The presence of urinary ketones is an indicator of an increase in fat oxidation. Several research groups have referred to this approach as a “very low-carbohydrate ketogenic diet” (VLCKD) or “low-carbohydrate ketogenic diet”. When dietary carbohydrate is low (20 g/day), insulin larger amounts of weight loss have been reported.
The ketogenic diet is a high-fat, moderate protein, and low carbohydrates (carbs) diet that offer many health benefits. The ketogenic diet involves the replacement of carbs with fats. This reduction in carbs puts your body into a metabolic state called ketosis. During ketosis, your body becomes incredibly efficient at burning fat for energy. The ketogenic diet has numerous benefits. The body uses ketones as a source of fuel during metabolism. This process lowers blood glucose and insulin levels.
Fats are the best and preferred fuel for the human body. Therefore, in the ketogenic diet, 75% of the calories should be consumed from fats. To maintain the body’s muscle mass 20% of protein should be consumed. The body requires micronutrients for most of the enzyme functions. These can be obtained from vegetables, but from only those vegetables which are low in Glycemic index (GI). Vegetables have some carbs. Therefore, only net carbs of 20g are permittable in a daily diet.
Health benefits of the ketogenic diet:
Different studies have shown that the keto diet has several health benefits for a wide variety of different clinical conditions. A few of them are heart diseases, cancers, Alzheimer’s disease, epilepsy, polycystic ovarian, and Parkinson’s disease.
The glycemic index (GI) is a measure of the blood glucose-raising potential of the carbohydrate content of a food compared to a reference food (generally pure glucose). Relative to pure glucose food is classified as a high (≥70), moderate (<70 and ≥55), and low (<55) glycemic index.
Consumption of high-GI food causes a sharp rise in blood glucose concentration and insulin spikes. Insulin spike (in response to high glucose) causes a decline in blood glucose level.
Measuring glycemic index of food;
The Glycemic index of a food is measured using a valid scientific method. These measured values of GI for different food is then published in different sources.
One of the established methods for measuring GI is feeding a certain number of people a portion of certain food containing 50 g of carbohydrates. Then their blood glucose is monitored for 2 hrs. The area under the curve (AUC) for their blood glucose over a period of two hrs for each individual is then measured. Similarly, the same individuals are fed with an equal carbohydrate portion of glucose called reference food and AUC is measured. The AUC for the test food is divided by the AUC of the reference food for each individual. This gives the GI. Averaging the GI of all the individuals gives the final GI for the test food.
Factors affecting GI:
There are several factors that affect the human blood glucose levels of the carbohydrate-containing food in question. In other words, how fast, a particular carbohydrate releases glucose in the blood. These factors include the physical form of the food, chemical composition, and structure of carbohydrates in food.
The physical form of food
A particular food can have different GI in two different physical forms. For example, raw carrots have a GI of 71 but cooked carrots have a GI of 85.
The physical form of carbohydrates:
One of the factors that affect the ability of carbohydrates to release glucose in the blood is its physical form. For example, wheat flour and bread have higher GL compared to whole wheat. The higher GI value of wheat flour is due to the fact that flour and bread have a bigger surface area for digestive enzymes to act and metabolize them.
Chemical composition of carbohydrates:
All carbohydrates are different in their chemical composition. Glucose is the simplest form of carbohydrate. It has a GL value of 100. Fructose is a type of carbohydrate that is found mostly in fruits. The body cannot metabolize fructose efficiently therefore it has a low GL value of 25. Similarly, fibers resist digestive enzymes and delay the metabolism of carbs. if the food is processed and natural fibers have been removed it will have a high GI. Therefore, most of the vegetables (that grow above the ground) contain fibers and have a comparatively low GI. On the other hand, white rice is mostly composed of carbohydrates and has a GL value of 74.
Body response to high verses low glycemic index;
By definition, the consumption of high-GI foods results in higher and more rapid increases in blood glucose concentrations than the consumption of low-GI foods. Rapid increases in blood glucose (resulting in hyperglycemia) are potent signals to the β-cells of the pancreas to increase insulin secretion. Over the next few hours, the increase in blood insulin concentration (hyperinsulinemia) induced by the consumption of high-GI foods may cause a sharp decrease in the concentration of glucose in blood (resulting in hypoglycemia). In contrast, the consumption of low-GI foods results in lower but more sustained increases in blood glucose and lower insulin demands on pancreatic β-cells.
An unpublished data has identified more physiological damage with sudden glucose spike and decline in blood compared to consistent high blood glucose concentration.
The glycemic load (GL) is the quality of carbohydrate in a given food (GI) multiplied by the amount of carbohydrate in a serving of that food. Lowering GL of the diet in type II diabetics might be the effective way to improve glycemic control.
The glycemic index indicates how rapidly a carbohydrate is digested and released as glucose (sugar) into the blood stream. In other words, how quickly foods break down into sugar in your bloodstream. A food with a high GI raises blood sugar more than a food with a medium to low GI.
A GL value for food <10 is considered as low GL food, 10-20 as moderate and >20 as high GL food. Low GI food has little impact on blood glucose, moderate has moderate while high GL food has high impact of blood glucose and cause glucose spikes in blood.
Food ranked high on the GI may represent a huge portion of a food because GI is not based on standard serving sizes. Basically, if a food is ranked high on the glycemic index it has readily available carbohydrate for quick absorption. However, the same food can have a low glycemic load because there may not actually be much total carbohydrate in a given serving of that food. A low GL is the better indicator that a food won’t have much impact on blood glucose levels.
For example: Watermelon has a high GI of 72, yet a low GL of 7.21. The high GI is based on 5 cups of watermelon, not an actual serving size of 1 cup. The low GL means one serving of watermelon doesn’t contain much carbohydrate, because it is actually mostly water. The low GL indicates that a serving of watermelon won’t have much impact on your blood sugar.
Glycemic load is dependent on the portion size. Sometimes it is difficult to consider the portion size while we are eating. It is highly likely that we might eat twice or even more of the permitted portion of a food that will account for low GL. Therefore, it is important to consider rather GI of the food as the indicator of blood glucose while making a healthier food choice.
Glycemic index verses glycemic load;
It is very important for diabetic people to know about the GL. As GL is dependent on the serving size. Therefore, Even a food with low GI can contribute to high blood sugar levels if serving size is not considered and it is consumed in large proportions. Different foods have different serving size. Next important thing for diabetic people is to have knowledge of serving size for their food of choice.
If you’re keen to learn about the GI and GL of your favorite foods, check out the University of Sydney’s glycemicindex.com website where you can put in almost any food and find out the values, depending on your serving size.