Diet For Obesity: Diagnosis And Selection Of Nutrition

Alexander Bruni
Author: Alexander Bruni Time for reading: ~16 minutes Last Updated: August 08, 2022
Diet For Obesity: Diagnosis And Selection Of Nutrition

Obesity is one of the most common pathologies of the 21st century and a real scourge of modern society. This is a widespread problem in all countries - from highly developed (for example, in the UK, the percentage of overweight patients has long exceeded 20) to less industrial ones.

In the article we will tell:

  1. Causes of obesity
  2. Adipose tissue as an endocrine organ
  3. obesity disorders
  4. fatty liver
  5. Nutrition for obesity
  6. Prohibited Products
  7. childhood obesity
  8. Nutrition Strategies for Children
  9. Diagnosis of obesity
  10. Pregnancy and obesity

Obesity is one of the most common pathologies of the 21st century and a real scourge of modern society. This is a widespread problem in all countries - from highly developed (for example, in the UK, the percentage of overweight patients has long exceeded 20) to less industrial ones. According to WHO estimates, in 2004 alone, the number of obese people exceeded 1.4 billion - what can we say now, 12 years later?

This is not only a decisive factor and trigger for most cardiovascular diseases, metabolic disorders, but also a disease that significantly reduces the standard of living.

Causes of obesity

Genetics, of course, plays a significant role at all levels of the functioning of the body and makes a significant contribution, in particular, to the constitutional features of the structure. However, the decisive word remains precisely with external factors and the conditions that surrounded the child from the cradle: after all, even the healthiest baby, with the wrong approach of parents, threatens not only to gain extra pounds and centimeters of subcutaneous folds, but also to develop persistent, eating habits, which in an adult age will invariably become an obstacle to the right way of life.

Among the main causes of overweight are the following:

  1. Energy imbalance - in other words, we consume more than we are able to spend.

    Our body is an ingenious system that in any situation - in the conditions of peaceful coexistence of all residents inhabiting it, both cellular and non-cellular, or during civil wars in the form of autoimmune diseases, when foreign pathogenic agents invade its territory - it bakes mainly about one goal: how to maintain balance is the key to normal functioning, first of all, of enzymes.

     

    Most of the reactions that take place in the human body are energy-consuming. The transfer of glucose, the transport of ions, the activation of signaling pathways all require a kind of currency in the form of ATP molecules. So, the entire excess of substances that come with food is simply unprofitable to remove in transit through the intestines: you never know when that very rainy day will come.

    Thus, adipose tissue, at one time, ensured survival: our ancestors did not manage to kill mammoths and saber-toothed tigers every day.

     

  2. Violation of the hypothalamus - the main conductor of energy metabolism. It is in this, one of the key structures of the brain, that the centers of “hunger” and “satiation” are located, and a number of protein and polypeptide molecules involved in appetite control are also produced.

  3. Endocrine - a decrease in thyroid function (hypothyroidism), a decrease in the production of adrenal hormones and somatotropin by the adenohypophysis.

  4. Sleep disorders: The synthesis of hormones responsible for hunger and satiety (ghrelin and leptin) is associated with sleep-wake cycles.

  5. Long-term use of certain drugs - in particular, glucocorticoids.

Adipose tissue as an endocrine organ

Adipose tissue is a source of many biologically active substances and hormones that exhibit both central and peripheral effects.

First of all, leptin is produced here - a satiety hormone, which, passing freely through the customs border of the blood-brain barrier (with the help of a special transport system) that separates the nervous tissue from the circulating blood, affects the receptors of the hypothalamus - the key structure of the brain, where it reduces the production of the one responsible for hunger. neuropeptide Y. There comes a feeling of satiety.

Interestingly, the level of this hormone is significantly different in men and women - in the former it is much lower, which is associated with higher concentrations of testosterone in the blood.

An increase in the amount of adipose tissue is invariably accompanied by an increase in the production of leptin, which entails a natural decrease in the sensitivity of cell receptors to it - leptin resistance develops.

Study: Obesity

Such disorders affect not only the dysregulation of appetite: leptin is also involved in the functioning of the reproductive system. So, many researchers note the cyclicity of leptin levels associated with the successive change of conductors in the body of a woman - sex hormones. In particular, its concentration reached a maximum in the luteal phase, when this protein hormone actively stimulated the self-programmed death of corpus luteum cells - their apoptosis - in the absence of pregnancy.

Study: The Hormone Leptin and Reproductive Problems

 

Another equally important hormone produced by fat cells - adiponectin - also has, like leptin, a protein nature. Activation of signaling pathways leads to:

  • Increased utilization of glucose by skeletal muscles.

  • Relaxation of smooth muscles and, as a result, a decrease in blood pressure. This effect is mediated by stimulation of endothelial cells, the inner lining of blood vessels, to the production of a relaxation factor - nitric oxide.

  • It prevents the division and calcification of smooth myocytes of the vascular wall, thus providing an anti-atherogenic effect. In addition, it inhibits the capture of cholesterol and its esters by cleaning cells - macrophages - which, despite the wide range of enzymes they contain, are incapable of splitting this organic compound and only accumulate it, turning over time into the so-called "foamy" cells. .

  • Suppression of glucose synthesis from non-carbohydrate components - inhibition of gluconeogenesis in the liver.

Study: Metabolic Effects of Adiponectin

obesity disorders

  1. Hypertension is associated primarily with direct stimulation of insulin, the concentration of which in the blood is many times higher than normal in overweight people, the sympathetic nervous system (its mediators, as you know, interacting with the corresponding receptors on myocardial cells, increase the frequency and strength of contractions , and also have a direct effect on smooth myocytes of the vascular wall).

    In addition, insulin also acts on the kidneys: it contributes to the retention of sodium, which pulls water along with a trailer - the volume of circulating blood increases.

    With obesity, the production of angiotensinogen by adipocytes also increases - its subsequent conversion to angiotensin 2 stimulates the secretion of aldosterone by the adrenal cortex, a mineralocorticoid that causes reverse absorption in the renal tubules of sodium and secretion of potassium.

    In addition to this, the right atrium reduces the synthesis and release of natriuretic hormone, which helps to reduce the concentration of sodium in the blood by excreting it in the urine - edema develops.

    Study: Obesity-Related Hypertension: Pathogenesis, Cardiovascular Risk, and Treatment

     

  2. With the deposition of fat in the chest and abdominal cavity, the mobility of the diaphragm - the main respiratory muscle - and the ribs is limited, which leads to impaired ventilation of the lung parenchyma. In such patients, there is a decrease in the vital capacity of the lungs, as well as a decrease in forced expiratory volume.

    In addition, obesity suppresses the synthesis of the pro-inflammatory hormone adiponectin, which increases the risk of bronchial asthma.

     

  3. Carbohydrate metabolism disorders, in particular, the development of insulin resistance, are a decisive step in the pathogenesis of type 2 diabetes mellitus. So, for example, in the liver, free fatty acids prevent insulin from binding to hepatocytes, and also suppress the inhibitory effect of this hormone on gluconeogenesis (synthesis of glucose from non-carbohydrate components).

    In addition, free fatty acids are toxic to insulin-producing pancreatic beta cells and impair glucose uptake and further utilization by skeletal muscle.

     

Study: Obesity and Insulin Resistance

fatty liver

Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases in gastroenterology, which is characterized by fouling, in the literal sense of the word, of hepatocytes with fat cells - the liver turns into goose foie gras.

Fatty liver, as a rule, is associated with excessive intake of carbohydrates: when all the energy needs of the cells are satisfied, some of the excess will be prudently stored in the pantries of the liver in the form of glycogen - an energy reserve for a rainy day. However, given the limited space allotted for storing jars of jam, what could not be transformed into glycogen will turn into lipids in the process of biochemical reactions.

So, do not be afraid of fats in the diet: they get better just because of the uncontrolled intake of sugars, which initially seem useful and harmless. “Everything is poison and everything is medicine,” Paracelsus correctly stated.

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Obesity activates a signaling pathway in hepatocytes that is invariably associated with chronic inflammation and increased levels of lipid metabolites such as diacylglycerol. The latter, by preventing phosphorylation of the insulin receptor, directly contributes to the development of insulin resistance.

In addition, an increase in the concentration of free fatty acids contributes to the disruption of their oxidation in our power plants - mitochondria - and leads to an increase in the production of free radicals located in the respiratory chains located in them. Oxidative stress develops, which further damages the parenchyma of the organ and stimulates the progression of fibrosis - the replacement of liver cells with connective tissue.

 

Most patients with NAFLD do not show clinical symptoms, or they are not specific enough:

  • dull pain in the right hypochondrium;

  • fatigue;

  • dyspepsia;

  • hepatosplenomegaly - an increase in the size of the liver and spleen.

Laboratory indicators also do not always reflect the picture: for example, the levels of ALT and AST (alanine aminotransferase and aspartate aminotransferase) may be slightly elevated or even remain within the normal range - which is why it is undesirable to focus solely on their concentration when making a diagnosis.

It is much better to measure uric acid (more than 20% of overweight people have hyperuricemia), C-reactive protein, and serum ferritin, both of which are characteristic and highly sensitive markers of inflammation and are elevated in fatty liver. In addition, it is necessary to control the level of insulin, glucose and C-peptide, as well as the lipid profile.

Study: Non-alcoholic fatty liver disease and obesity: Biochemical, metabolic and clinical presentations

Nutrition for obesity

Patients with obesity, in addition to moderate physical activity, need in tandem with a nutritionist to create the right diet that satisfies all the necessary needs of the body. First of all, the main rule for them can be formulated as follows: spend more than receive.

Severe calorie restriction is a direct road to a breakdown and subsequent depressive states and self-flagellation. Yes, reducing your calorie intake makes sense - but only in cases where it is adequate and gradual.

 

In general, in the absence of adrenal exhaustion, three meals a day remains the universal type of food for most people. Compliance with “hungry” intervals by eliminating all snacks between main meals helps to establish carbohydrate metabolism and increase the sensitivity of cell receptors to insulin.

In addition, it is advisable to adhere to intermittent fasting - its easiest variation to start with is 12/12 - in other words, for 12 hours you eat (2 or 3 meals are just ideal), in the remaining 12 ( including sleep) - drink only water, herbal teas or coffee without milk and sugar.

 

Over time, you can “lengthen” the hunger window and move on to, for example, practicing 14/10, 16/8 and 20/4 - any of these methods is an effective way to gently, smoothly reduce weight, and then maintain it at a normal level.

Also, overweight patients should exclude fast carbohydrates - sweets, dried fruits, honey, which contribute to a rapid increase in glucose levels and the same sharp decline. Considering that in the mechanisms of development of insulin resistance, one of the key roles belongs to fructose, which subtly bypasses all the paths of saturation, strict control over the consumption of fruits and their restriction are mandatory.

It is recommended to consume at least 30 grams of fiber - this is not only a powerful stimulant of intestinal motility, but also a kind of broom that clears its lumen. It can be used as a source of psyllium powder or apple pectin, washed down with water or added (as a binder) to the dough. However, given that dietary fiber also acts as a sorbent, they must be taken separately from other dietary supplements.

Prohibited Products

If you are overweight, it is strictly necessary to limit the use of:

  • sweets, ice cream, marshmallows, marmalade and other sources of refined sugars;

  • sweet fruits: mango, banana, persimmon;

  • freshly squeezed juices and smoothies - this is a real sugar bomb under the guise of a healthy product;

  • ready-made sauces: they are not only sources of glutamates that excite the nervous system, but also extra calories and hidden sugar;

  • fast food and semi-finished products;

  • bakery products, instant cereals;

  • dairy products: they increase plasma levels of insulin and insulin-like factor-1, and also contribute to an increase in androgen production;

  • carbonated and alcoholic drinks.

childhood obesity

Childhood obesity, one of the most pressing problems of the modern world, is the result of a long-term energy imbalance, when the amount of energy consumed is many times greater than the needs of the body.

Despite a certain role of genetics, the increase in the number of obese children is primarily associated with a low level of physical activity and the predominance of food waste rich in sugars and trans fats in the diet.

Neuroendocrine disorders, congenital anomalies and chromosomal mutations fade into the background - their role in gaining excess body weight against the background of the influence of environmental factors becomes more and more insignificant.

So, in the UK in 2008 alone, according to statistics, 16.8% of boys and 15.2% of girls aged 2 to 15 had problems with overweight - you can imagine how these figures have changed now, 12 years later.

 

Obesity is associated with the development of insulin resistance, impaired glucose tolerance and increased blood pressure, all of which contribute directly or indirectly to the development of chronic diseases. Similarly with an adult organism, in a child's body there are also:

  • sleep apnea;

  • cardiovascular pathologies;

  • osteoarthritis;

  • hypertension;

  • depression, low self-esteem and poor quality of life.

Study: Obesity in children

Nutrition Strategies for Children

Age

calories

Fluid intake

1 year

900 kcal/day

1100-1200 ml/day

2-3 years

1000 kcal/day

1300 ml/day

4-8 years old

1200 kcal/day for girls

 

1400 kcal/day for boys

1600 ml/day

9-13 years old

1600 kcal/day for girls

 

1800 kcal/day for boys

1900 ml/day for girls

 

2100 ml/day for boys

14-18 years old

1800 kcal/day for girls

 

2200 kcal/day for boys

2000 ml/day for girls;

 

2600 ml/day for boys

Age

Number of fruits

Number of vegetables

1 year

1 cup per day (250 ml)

¾ cup per day

2-3 years

1 cup

1 cup

4-8 years old

1.5 cups

1 cup for girls;

 

1.5 cups for boys;

9-13 years old

1.5 cups

2 cups for girls;

 

2.5 cups for boys;

14-18 years old

1.5 cups for girls;

 

2 cups for boys;

2.5 cups for girls;

 

3 cups for boys;

Diagnosis of obesity

Obesity is one of the main components that make up the metabolic syndrome. This is a whole complex of pathologies, which includes:

  • insulin resistance;

  • type 2 diabetes mellitus;

  • arterial hypertension;

  • tendency to thrombosis;

  • dyslipidemia;

  • visceral obesity.

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According to the WHO criteria for 2002, the following laboratory parameters are taken into account when making a diagnosis:

BMI

over 30

Fasting plasma glucose

more than 6.1 mmol/l

Triglyceride level

more than 1.7 mmol/l

HDL content

for men - less than 0.9 mmol / l;

for women - less than 1 mmol / l.

Waist to hip ratio

(indicator of visceral obesity)

For men > 0.9

For women > 0.85

Arterial pressure

≥140/90 mmHg

Study: Diagnostic Criteria for Metabolic Syndrome

Pregnancy and obesity

Pregnancy is a unique period in the life of every woman, which is characterized by a number of quantitative and qualitative changes aimed at creating the most favorable conditions for the growth and development of a new organism.

There is an intensive development of adipose tissue - that metabolic safety cushion that will provide the fetus with the necessary substrates for energy. We have already talked about the hormonal function of this tissue: here, due to the rather high activity of the aromatase enzyme, androgens are transformed into estrogens, primarily into estradiol, thus mediating the extraovarian synthesis of sex hormones.

However, excess body weight is accompanied not only by a more enhanced function of the previously mentioned enzyme: there are changes in the composition of estrogens themselves - in particular, the number of their active forms exceeds inactive ones. To this should be added the direct production of estrogens by the placenta - thus, the arithmetic summation reflects the development of hyperestrogenemia.

 

During the gestation period, the production of progesterone, a direct competitor of glucocorticoids for receptors in fat cells, also increases, by binding to them, it makes it impossible for the hormones of the adrenal cortex to activate lipolysis, the process of burning fat.

Starting from the 6th week, placental trophoblasts actively synthesize leptin, which stimulates hematopoiesis in the fetus and is involved in the regulation of growth and development processes. So, pregnancy is characterized by a whole orchestra of hormonal changes, however, a positive energy balance still plays a decisive role in the mechanisms of obesity.

There are certain recommendations for weight gain during pregnancy, developed by the Institute of Medicine of the American Academy of Sciences and based on baseline body mass index. We remind you that BMI = weight (kg) : height² (m²)

BMI before pregnancy

Weight gain throughout pregnancy (kg)

Weight gain per week (kg)

Low body weight (BMI < 20)

12.5-18

0.5

normal body weight

(BMI = 20-25)

11.5-16

0.4

Overweight

(BMI=25-30)

7-11.5

0.3

Obesity (BMI > 30)

< 7

0.2

Complications associated with overweight during gestation are observed in 85% of patients and are accompanied by:

  1. Pathologies from the side of the cardiovascular.

  2. Disorders of carbohydrate metabolism - normally, physiological insulin resistance develops, in which the sensitivity of peripheral tissues to this protein hormone of the pancreas somewhat decreases, which is necessary, first of all, to provide the developing fetus with energy.

Visceral obesity, in itself, is accompanied by an excess concentration of insulin in the blood. Hyperinsulinemia occurs due to a compensatory increase in the production of the hormone by the islets of Langerhans in response to a decrease in the sensitivity of cellular receptors to it, and, therefore, the inability of glucose to properly enter the cells from the bloodstream. The risk of gestational diabetes increases from 2% (as it is presented in patients with normal carbohydrate metabolism) to 17% - more than 8 times.

All this cannot but affect the health of the child - the nature of the pathologies varies widely depending on how long hyperglycemia developed in the mother. Thus, it is noted:

  • defects of the central nervous system;

  • hyperplasia of pancreatic cells;

  • malformations of the heart and gastrointestinal tract;

  • intrauterine fetal death.

Newborns of obese mothers are most likely to have an increased risk of macrosomia, characterized by a body weight of more than 4000 g. These babies also tend to have higher levels of leptin and pro-inflammatory interleukin-6.

In addition to all of the above, obesity is an independent risk factor for miscarriage and its termination, observed in conditions of excessive concentrations of androgens and insulin.

Research: Obesity and pregnancy: mechanisms of short term and long term adverse consequences for mother and child

The material is based on research:
  • Obesity

  • The hormone leptin and reproductive problems

  • Metabolic effects of adiponectin

  • Obesity-Related Hypertension: Pathogenesis, Cardiovascular Risk, and Treatment

  • Obesity and insulin resistance

  • Non-alcoholic fatty liver disease and obesity: Biochemical, metabolic and clinical presentations

  • Obesity in children

  • Diagnostic criteria for metabolic syndrome

  • Pregnancy and obesity

  • Obesity and pregnancy: mechanisms of short term and long term adverse consequences for mother and child

 

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