Diabetes – a group of metabolic diseases characterized by hyperglycemia (elevated blood glucose) resulting from a defect in the production or action of insulin secreted by pancreatic beta cells. Chronic hyperglycemia is associated with damage, dysfunction and failure of various organs, especially eyes, kidneys, nerves, heart and blood vessels. Due to the cause and course of the disease, we can distinguish: type 1 diabetes, type 2 diabetes, pregnant diabetes and other, less common types.

The most common form of diabetes is type 2 diabetes, which consists in reduced sensitivity of tissues to insulin (insulin resistance). This condition requires the production of an excessive amount of insulin, which in the further course of the disease exceeds the secretory capacity of the pancreas. In type 2 diabetes, there is damage to the beta cells in the pancreatic islets and impaired, and then the cessation of insulin secretion.

Type 1 diabetes is based on primary, insufficient insulin secretion, while maintaining normal tissue sensitivity to this hormone. Gestational diabetes is the result of hormonal changes related to pregnancy.

Types 1 and 2 are polygenic, i.e. they are the result of mutations in many genes, unlike monogenic ones, e.g. of the MODY type.

The principle of modern diabetes therapy is the treatment of all disorders accompanying the disease, and not just the control of carbohydrate metabolism. The pursuit of normalization of body mass, increase in physical activity, proper diet, treatment of lipid disorders, hypertension and other cardiovascular diseases in diabetes, and maintenance of glycemia in the range closest to the non-diabetic (normoglycemia) reduces the risk of developing complications.

Diabetes – a group of metabolic diseases characterized by hyperglycemia (elevated blood glucose) resulting from a defect in the production or action of insulin secreted by pancreatic beta cells. Chronic hyperglycemia is associated with damage, dysfunction and failure of various organs, especially eyes, kidneys, nerves, heart and blood vessels. Due to the cause and course of the disease, we can distinguish: type 1 diabetes, type 2 diabetes, pregnant diabetes and other, less common types.

Gestational diabetes

Gestational diabetes – a transient disorder diagnosed based on elevated blood glucose (which may be accompanied by the presence of glucose in the urine), which appears in healthy women until the end of pregnancy. However, it is a threat to the fetus and a woman, and 30-50% of women who have gestational diabetes have developed type 2 diabetes over the next 15 years. It is thought that pregnancy-related changes are physiological changes related to pregnancy: insulin resistance caused by placental hormones (lactogen, growth hormone), disorders of insulin secretion and increased secretion of glucose by the liver. In 3-8% of women, the pancreas can not satisfy the increased insulin requirement. Gestational diabetes is mainly manifested in the 3rd trimester when these hormones are the strongest.

Threats to a woman: Premature birth, pre-eclampsia, increased probability of Caesarean section.

Threats to the fetus: fetal macrosomes – glucose and amino acids penetrating the placental barrier stimulate pancreatic islet hyperplasia, which leads to increased secretion of insulin acting anabolically. The result is an excessive use of substrates for the construction of own tissues and a large birth weight. Excess urine excreted by the fetus causes polyhydramnios that can lead to premature birth. Significant mother hyperglycemia may lead to fetal acidosis, intrauterine death or congenital malformations neural tube and heart (cardiomyopathy).

Treatment – diet, in the event of insulin failure.

Diabetes of known cause (secondary diabetes)

Many diseases and some medications may contribute to the development of hyperglycaemia. The most common of these diseases are: a group of diseases of the pancreas (mainly the exocrine part), endocrinopathy (diseases of the endocrine system), liver disease and long-lasting systemic steroids.

Diabetes of known cause includes:

– disorders of β cells genetically determined (MODY type diabetes describes mutations of 8 different genes (MODY1-8), mutations of mitochondrial genes)
– genetically determined defects of insulin action
–  neonatal diabetes – caused by the defect of the Kir 6.2 subunit of the potassium channel in β cells; is usually seen in infancy, can be effectively treated by the use of oral sulfonylureas
– LADA – an autoimmune form of diabetes similar to type 1 diabetes that manifests itself in adulthood
– diseases of the endocrine part of the pancreas (eg in the course of cystic fibrosis, inflammation, tumors, hemochromatosis)
– endocrinopathies (eg Cushing’s disease, overactive thyroid gland, pheochromocytoma, glucagonoma, somatostatinoma, acromegaly)
– diabetes caused by drugs or other chemicals (eg glucocorticoids, thyroid hormones, dilantine, α-interferon, aspartame)
– rare forms of immunologically-mediated diabetes
– diabetes caused by infection (eg congenital rubella, cytomegalovirus)
– other genetic syndromes that may progress with diabetes (Down’s syndrome, Klinefelter syndrome, Turner syndrome, Prader-Willi syndrome, Wolfram syndrome, Friedreich’s ataxia, Huntington’s chorea, porphyry)

Predisposing factors

Susceptibility to type 1 and type 2 diabetes is hereditary. It seems, however, that even those who inherit a tendency to type 1 diabetes will need an environmental factor. Type 1 is caused by certain infections (mainly viral) or (in a smaller group of patients), stress or environmental exposure (including drugs and some chemical compounds). As possible environmental factors, viruses or cows’ milk proteins were suspected. There are individual genetic susceptibilities to certain factors that can cause diabetes, which has been linked to specific HLA genotypes. Probably susceptibility is responsible for many genes. Previously, the emerging cases are usually more strongly genetically determined – if one of the identical twins became ill before the age of 6, the second case fell in 60% of cases. When the disease appeared after the age of 25, the siblings fell ill only in 5% of cases. A small proportion of people with type 1 diabetes have a mutated gene that causes MODA diabetes.

Type 2 has a stronger link to inheritance. The first-degree relatives of a person with type 2 diabetes have a much higher risk of developing diabetes of this type. The more sick relatives you have, the greater the risk. In the case of an illness in one of the identical twins, the risk of occurrence in the other is close to 100%. One of the genes important for the development of type 2 diabetes is KCNJ11, which encodes the ATP-sensitive isotope potassium channel, Kir6.2 and TCF7L2, which regulates the proglucagon gene expression and thus the production of the glucagon-1-like peptide. In addition, inheritance is very important for obesity itself (which is a separate risk factor for type 2 diabetes). As in type 1, many genes are thought to be responsible for susceptibility.

Different genetic syndromes can also take place with diabetes, such as myotonic dystrophy and Friedreich’s disease. Wolfram’s syndrome is an autosomal recessive neurodegenerative disorder whose first symptoms appear in childhood. These include: diabetes insipidus, type 1 diabetes, optic nerve atrophy and deafness.


Blood glucose

The main symptom of diabetes is an increase in blood glucose. Depending on the severity of the disease, it may occur only after or without carbohydrate intake. The content of sugar in the blood (blood glucose) is given in milligrams per 100 ml of blood (mg / dl) or in millimoles per liter (mmol / l); the relationship between them is given by the formula [mmol / l] x 18 = mg / dl. The normal fasting blood glucose level is 70-99 mg / dl (3.9-5.5 mmol / l), in the second hour of the glucose challenge oral glucose test below 140 mg / dl (7.8 mmol / l). For normoglycemia, i.e. the level of sugar in a blood in a healthy human being, the range is 60-99 mg / dl. Lower blood glucose means hypoglycaemia, and higher means:

pre-diabetic status, that is:
impaired Fasting Glucose (IFG): fasting 100-125 mg / dl (5.6-6.9 mmol / l) or
impaired Glucose Tolerance (IGT): in the second hour of the oral glucose challenge glucose test 140-199 mg / dl (7.8-11 mmol / l).

diabetes when:
the glucose concentration measured at any time of the day exceeds 200 mg / dl and symptoms of hyperglycaemia occur (polydipsia, polyuria),
twice the fasting glucose level exceeds 126 mg / dl (7.0 mmol / l),
in the 2nd hour of the oral glucose load test, the glucose level exceeds 200 mg / dl (11.1 mmol / l).

The standards are given according to WHO guidelines.

Glycated hemoglobin

One of the indicators of glucose concentration is the fraction of hemoglobin that has been glycated (by glucose in the blood), glycated hemoglobin (HbA1c). The study reflects the average glucose concentration in the last 2-3 months (more precisely, from the life-span of erythrocytes), of which the last 30 days have the greatest influence (about 50% of the influence on the parameter height). The threshold value depends on the method used by the laboratory, usually HbA1c greater than 6% is considered abnormal (this standard is considered based on the DCCT test). The value of HbA1c in the diagnosis is only of auxiliary significance, in patients it is used as an indicator of the effectiveness of therapy (with the proviso that it reflects the average glycemia), usually taking as a sign of good glycemia control HbA1c ≤7% (General criteria PTD), ≤6.5 % (PTD detailed criteria) and even ≤6.1% (in pregnant women, PGDM and GDM). It should be noted that the recommended levels of HbA1c are different in different countries – in Denmark, the acceptable level of glycated hemoglobin is 5.9%). Patients with low HbA1c have less complications of diabetes – according to research. Too low HbA1c suggests frequent hypoglycaemia. The index is unreliable for variants of hemoglobin – in this case it is recommended to measure glycated plasma proteins (fructosamine).

Other symptoms

The most characteristic symptoms of diabetes include:

polyuria (polyuria) – when the plasma glucose concentration (because it is filtered) exceeds the renal threshold (usually about 160-180 mg%), due to exceeding the maximum transport for glucose, renal tubular epithelial cells are unable to resorb glucose from filtrate (primary urine). Because it is not resorbed in further sections of the nephron, it enters the final urine. Glucosuria (glycosuria) appears, i.e. glucose excretion in the urine, and polyuria – more than 3 l per day (glucose is an osmotically active substance, thus retaining water and entraining it with it).
polydipsia (increased thirst) – increased loss of water in the urine causes enormous thirst and drying of mucous membranes and skin.
polyphagia (bulimia, wolf hunger) – due to the lack of insulin glucose found in the blood can not get into the tissues in which it could be used. Therefore, despite the normal or often increased supply of food, the body is starving (so-called “hunger in abundance”, as sometimes even significant hyperglycemia sometimes co-occurs). The patient is sleepy and tired, feels strong hunger and loses weight when he tries to satisfy him.

An organism that can not use sugar as a nutrient begins to consume large amounts of fat for nutrition. As a result of their disintegration, ketone bodies arise which appear first in the blood (ketonemia) and later in the urine (ketonuria); the breath may pick up acetone (due to the decarboxylation of acetoacetate to acetone due to the oxygen contained in the air). Nausea may occur.

Often, patients lose visual acuity.

The above symptoms are typical of type 1 diabetes, and in type 2 diabetes, hyperglycemia is usually not severe enough to cause a full set of them. However, diabetic complications can develop in patients.

Clinical tests of people suspected of having diabetes

Determination of blood glucose levels after fasting and after meals
A test for detecting the presence of glucose in the urine
Determination of glycated hemoglobin (HbA1c)
Urine and plasma testing for the presence of ketone bodies
Pathophysiological blood test to detect the possible presence of antinuclear antibodies
Glycemic curve (OGTT – oral glucose load test)
The patient’s reaction to insulin administration


The risk of type 1 diabetes depends on genetic predisposition based on HLA types (especially DR3 and DR4) and unknown environmental factors (presumably infections in most cases), as well as an uncontrolled autoimmune response that attacks insulin produced by beta cells. Studies conducted since the 1980s suggest that breast-feeding may reduce the risk of insulin-dependent diabetes mellitus. Various other nutrient risk factors have been studied, but no reliable evidence has been found.

The risk of type 2 diabetes can be reduced in many cases by making changes in diet and increasing physical activity. The American Diabetes Association (ADA) recommends maintaining normal body weight, taking at least 2.5 hours of physical exercise per week (a quick, uninterrupted walk seems to be enough), consuming moderate amounts of fat, absorbing enough fiber and whole grains in food. ADA does not recommend alcohol as a prevention measure, but moderate alcohol consumption may reduce the risk (although higher intake is associated with significant negative effects on the body). There is insufficient evidence of clinical benefit from eating foods with a low glycemic index.

Some studies have shown a delay in the onset of diabetes in patients at increased risk for prophylactic metformin, rosiglitazone or valsartan. Patients taking hydroxychloroquine for rheumatoid arthritis had a reduced risk of diabetes by 77%. Breastfeeding may also be important in the prevention of type 2 diabetes in mothers.

Complications of diabetes

Acute complications

Ketoacidosis (DKA – Diabetic Ketoacidosis) is a dangerous complication and a life-threatening condition. Lack of insulin causes the breakdown of fats and the associated formation of ketone bodies that pass into the patient’s blood and urine. Symptoms include dehydration, deep and quick breathing (Kussmar’s breath, often with the smell of acetone), often abdominal pain, drowsiness. Ketoacidosis can lead to shock and coma. Quick treatment usually provides a full cure. It usually happens to people with type 1 diabetes, due to a complete lack of insulin.

Non-keto hyperosmolar state or hyperosmotic acidosis is relatively rare, usually affecting older people with type 2 diabetes. High blood glucose results in osmotic water loss from cells and further loss of water excreted with glucose in the urine. If fluid deficiencies are not replenished, this leads to extreme dehydration and electrolyte imbalance. The treatment of disturbances of consciousness can lead to coma. In the blood of patients very high levels of glucose are found without the development of ketoacidosis. Prognosis is very seriously unfavorable, mortality is about 40%.

Hypoglycaemia threatens sick patients who are treated with insulin or oral insulin secretagogues. It usually occurs after taking the wrong dose, not eating or stinging the meal with which the medicine was taken, and after physical exercise, which was not compensated by the appropriate dose of glucose in the food or reducing the dose of the drug. Too low glucose in the blood may be manifested in the patient’s sweat, anxiety, agitation, chills and hunger. In extreme cases, you may lose consciousness, coma or convulsions – then hospitalization is necessary. People with diabetes usually recognize the symptoms of hypoglycaemia early and can effectively prevent it by eating or drinking the equivalent of at least 10-20 g of glucose (sweets, sugar, sweet drink). If the patient is unable to take glucose by mouth, glucagon can be given to him intramuscularly (people with the disease usually have a handy glucagon kit) that releases glucose from the glycogen stores in the liver. This method is not effective when glycogen has already been consumed (e.g., prior use of glucagon).


Many years of diabetes lead to many serious complications that affect many organs. The risk of occurrence and progression of chronic complications depends mainly on the metabolic control of diabetes. People with well-balanced diabetes are much less at risk of chronic complications. The cause of complications is damage to blood vessels: microangiopathy, small vessels and capillaries, and macroangiopathy leading to atherosclerotic lesions of medium and large diameter vessels.

Microangiopathy causes damage:

sight organ – retinal vascular changes, or diabetic retinopathy, cataracts, choroidal lesions. Eye blindness is the most serious result of eye damage;

kidney – diabetic kidney disease, i.e. damage to kidney function leading to their failure (the need for treatment with dialysis or kidney transplant);

nerve fibers – neuropathies: diabetic polyneuropathy with characteristic “glove” and “sock” symptoms (sensory disturbances, numbness, pain or burning of hands and feet) and diabetic neuropathy of the autonomic nervous system – symptoms depend on the location of changes and may include, for example: cardiac work, blood pressure abnormalities, gastrointestinal tract disorders (mainly persistent diarrhea), impaired urination, impotence.

Macroangiopathy leads to an increased incidence of cardiovascular diseases, which account for about 80% of the cause of death in this group of patients. The most important vascular complications occurring in diabetics are:

ischemic heart disease and myocardial infarction;

diabetic foot syndrome – impaired blood supply and innervation of the foot, which can lead to ulceration and deformation of the foot, infection and, consequently, necrosis and the need for smaller or larger amputations;

stroke – leading to various degrees of brain damage.

Diabetics may also include:

metabolic changes such as acquired hyperlipidemia,

drop in immunity.

worse wound healing

Dermatological changes are also common in diabetic patients. It happens that it is thanks to their presence that diagnostics begins, as a result of which the underlying disease is diagnosed. The most common skin changes associated with diabetes mellitus include skin infections, ulcerations, so-called thick skin, dark keratosis, sown yellow tufts and diabetic blush. There are less frequent: pruritus, fat loss, ring granuloma, diabetic dermatitis and bullosis diabeticorum. There are also skin reactions associated with the use of antidiabetic drugs


Blood glucose levels change very rapidly. Therefore, in all types of diabetes, the best results of treatment are achieved with active participation of the patient in treatment. The educated patient, leading a proper lifestyle and adjusting the therapy for demand by himself has a high chance of avoiding complications.

Stevia leaves have been used in South America in traditional Indian medicine for the treatment of diabetes for centuries. There are studies on the compound contained in them, rebaudioside A. The hypoglycemic mechanism of stevia is unclear and occurs only at elevated serum glucose.

insulin therapy

Insulin therapy is the basic treatment for type 1 diabetics. It is also applicable to patients with type 2 diabetes, in whom insufficient diet, lifestyle and oral diabetes medications and in women with gestational diabetes are insufficient.

Insulin preparations

For many years, preparations of insulin of animal origin were used, isolated from bovine and porcine pancreas. These insulins differ from the human protein by three and one amino acid, respectively. Since the 1980s, most of the available insulin preparations are of biotechnological origin – insulin produces genetically modified Escherichia coli bacteria or Saccharomyces cerevisiae yeasts. In this way, human insulin and insulin analogs are made, with several amino acid substitutions that give insulin the desired properties.

The insulin lispro analogs (e.g., Humalog) and aspart (e.g., NovoRapid) administered subcutaneously work faster than human insulin with a more pronounced peak effect. There are also long-acting analogues, such as glargine (eg Lantus) and detemir (eg Levemir), slowly releasing. Previously, a similar effect was obtained by making suspensions with the addition of protamine (the so-called NPH insulin – Neutral Protamine Hagedorn, ie, for example: Gensulin N, Humulin N, Insulatard) or zinc. Different insulin preparations start to work for 15 minutes. up to 6 hours after the injection, they work for 3 to 24 hours, the peak activity is from 1 hour. up to 14 hours after administration or without a clear action summit.

Administration of insulin preparations

Insulin preparations in normal treatment are administered subcutaneously, using a pen, for example a pen (insulin pen) or less and less a syringe. There are also needle-free injectors, and at the beginning of 2006 inhalation insulin was introduced to the medical treatment (in a spray eg Exubera from Pfizer).

The administered insulin is supposed to mimic the natural rhythm of insulin secretion by the pancreas – and therefore a certain basic demand (covered with long-acting insulin) and the insulin needed to balance the meals (human insulin or fast-acting insulin analogs). The so-called. Intensive insulin therapy means adjusting the insulin amount to the meals, exercise and other factors that are currently being used by the patient – in contrast to traditional therapy, in which the meals and lifestyle are adapted to the injected insulin.

The special treatment regimen is insulin administration using an insulin pump. An insulin pump ensures constant subcutaneous insulin delivery (usually a fast-acting analog or human insulin) and allows the best glycemic control among the solutions available on the market, especially with varying daily basic insulin demand, but requires a high level of self-therapy, and badly used risk of acidosis ketone.

Oral antidiabetic medications

Oral antidiabetic drugs are used in type 2 diabetes. The main mechanisms of action of particular groups of drugs:

increase insulin secretion (sulfonylurea derivatives and meglitinides, e.g. repaglinide),
they inhibit the release of glucose from the liver (metformin),
inhibit the release of glucose from intestinal carbohydrates (alpha-glucosidase inhibitors),
reduce tissue insulin resistance (thiazolidinedione and related PPAR-γ receptor agonists).
incretin drugs (dipeptidyl peptidase 4 inhibitors)

Physical effort, diet and lifestyle

In the majority of cases, type 2 diabetes can be controlled initially with the right diet and exercise. Because this type of diabetes is usually associated with overweight, weight loss increases insulin sensitivity. Physical effort works similarly, and it helps to prevent complications of diabetes. Appropriate diet (products with low glycemic index, complex carbohydrates, reduced amount of saturated fat, more soluble fiber) reduces postprandial hyperglycemia and allows to prevent complications.

In type 1 diabetes, dietary restrictions are not so important. In addition to the need to adjust the insulin dose to food (or vice versa) it is recommended to avoid products with a very high glycemic index and products that may accelerate the development of complications (such as atherosclerosis). Physical effort helps prevent complications.

In all types of diabetes, it is very important to avoid smoking and drinking alcohol – these drugs increase the likelihood of complications of diabetes.

Diabetes and alcohol

Because some of the symptoms of hypoglycaemia (hand tremors, problems with maintaining the balance, in some patients aggressiveness), are similar to the symptoms of alcohol intoxication, there are cases of failure to provide first aid to people who are in a state of profound hypoglycaemia. Therefore, it is important that people in the patient’s environment know the symptoms of hypoglycaemia and the course of this complication so that they are able to react in the right way. For this reason, in addition to glucagon, people with illnesses often carry various types of diabetes (diabetes cards, dog tags, handbands) informing about the disease and how to deal with the loss of consciousness.

In insulin-dependent diabetes, alcohol consumption increases the effect of insulin, which can lead to acute hypoglycaemia. It is then particularly dangerous, because the liver is less sensitive to glucagon when it is neutralized with alcohol. In this case, the help consists in intravenous glucose administration, which requires immediate hospitalization or emergency call. Alcohol absorbs insulin, blocking its action, but unlike it, it is broken down. The insulin released in large quantities may cause severe hypoglycaemia.

Therefore, it is recommended that the patient should stop or significantly reduce alcohol consumption, so that he can count on professional help in the event of hypoglycaemia and facilitate the interpretation of its symptoms in the environment. In addition, there is an absolute rule that diabetics should not consume alcohol in any form on an empty stomach.

It is recommended that before the planned consumption of alcohol, eat a meal containing long-decaying carbohydrates in order to protect against hypoglycemia which is particularly dangerous in such circumstances. Hypoglycaemia occurs most often 2 to even 5-6 hours after drinking alcohol on an empty stomach.

Oral diabetic drugs interact with alcohol, which can lead to unpredictable escalation of the drug’s effects, or complications in the form of lactic acidosis (in combination with Metformin).

Diabetes can cause problems for people who drive a car. Breathal breathing apparatus, in addition to alcohol in the exhaled air, also react to ketone bodies. The breathalyzer may show 0.3 to 0.5 per mille of alcohol in a diabetic, even though he did not drink alcohol.


Self-control of metabolic control of diabetes is carried out by patients on their own, measuring blood glucose in urine, checking the presence of ketone bodies in the urine. Self-control allows appropriately educated patients to adjust the therapy to current needs, prevent complications of diabetes – acute and chronic, lead a specific lifestyle. The glucose concentration in the blood is tested using a glucometer, the presence of glucose or ketones in the urine – using color-responsive diagnostic strips.

In the light of the study conducted in 2008, diabetes self-control does not improve the control of diabetes in people with newly-diagnosed type 2 diabetes, but is associated with the severity of depression in these patients.

Determination of other indicators to monitor the course of diabetes

In order to follow the development of the disease and treat the emerging complications of the disease as early as possible, it is recommended for patients – apart from constant glycemic control – additional diagnostic tests:

ketone bodies in the urine,
glycated hemoglobin (2 to 4 times a year),
total cholesterol, HDL and LDL cholesterol and triglycerides (once a year),
creatinine (once a year),
albuminuria (once a year),
fundus examination (once a year),
ECG tests (once a year),
stress ECG examinations (once every 2 years),
lower limb arteries using the Doppler method (once every 2 years),
neurological examination (at least once a year).

Future therapies

For type 1 diabetes: pancreatic islet grafts, use of stem cells for the formation of insulin-producing cells, a pump with a feedback mechanism, adjusting the amount of insulin administered to glycemia.

Linoleic acid and diabetes

Due to elevated levels of linoleic acid and a deficiency of gamma-linolenic acid, it is believed that diabetics are deficient in the key enzyme of fat metabolism – stearoyl-CoA desaturase. Studies have shown that increased consumption of gamma-linolenic acid (eg in evening primrose oil) alleviates complications of diabetes.


About 5% of the population has diabetes. In 95% of cases this is type 2. Probably at least half of people with type 2 diabetes are not diagnosed. In recent years, the number of cases has been dramatically increasing, especially in developing countries, and this type of diabetes in children is more and more often detected. Some populations, such as Pima Indians, are extremely susceptible to this disease (50% of patients). The diet rich in fats and carbohydrates is lethal for them because their ancestors have been exposed to hunger for centuries and their genes allow for extremely cost-effective use of food.

Type 1 diabetes is most common in North America – one in four and in Europe – one in five. A completely unique country is Finland, where the prevalence of diabetes is the highest – 3/1000 and is the most new cases. This is probably due to the fact that most Finns come from a relatively small group of settlers. In Poland, according to various estimates, there are between one hundred and two hundred thousand people with type 1 diabetes and about 300,000 people are treated with insulin.

For the prevention and regeneration of the pancreas, it is worth taking a dietary supplement Biofiton Healthy Pancreas.

Phytotablets Biofiton Healthy Pancreas contain plant raw materials whose actions are focused on:

STANDARDIZATION OF SUGAR LEVEL. Biologically active substances contained in bean pods, burdock roots normalize the level of sugar in the blood.
STANDARDIZATION OF CHOLESTEROL LEVEL IN BLOOD. Biologically active substances contained in bean pods, dandelion and burdock roots normalize the level of cholesterol in the blood, thus promoting healthy body mass.
GOOD DRAIN. Leaves of Nettle and Blueberry, Wild Rose Fruit, Marshmallow, Dandelion, Oman and Burdock Root stimulate the pancreas, promoting better digestion.
REDUCING DISCOMFORT. The combined effects of substances derived from Marshmallow, Oman and the Roots of the Nuns and Leaf of Nettle support the reduction of discomfort and improve the work of the pancreas.