Overweight (Obesity): Secondary Diseases

The following are the most important diseases or complications that may be contributed to by overweight or obesity:

Congenital malformations, deformities, and chromosomal abnormalities (Q00-Q99).

  • Increased risk of congenital malformations such as neural tube defect, hydrocephalus (hydrocephalus), cleft lip and palate, cardiovascular anomalies (e.g., cardiac septal defects), anorectal atresia

Respiratory System (J00-J99)

  • Bronchial asthma
  • Chronic rhinosinusitis (CRS, simultaneous inflammation of the nasal mucosa (“rhinitis”) and the mucosa of the paranasal sinuses).
  • Decreased total lung capacity, increased work of breathing, especially at night!!!

Eyes and eye appendages (H00-H59).

Certain conditions originating in the perinatal period (P00-P96).

  • Fetopathies (damage to the fetus/unborn) of all types – one to two times increased risk in obesity.

Blood, blood-forming organs – immune system (D50-D90).

Endocrine, nutritional and metabolic diseases (E00-E90).

  • Andropause (male menopause)
  • Type 1 diabetes mellitus – childhood obesity: Mendelian randomization analysis: obesity alleles are much more common in individuals with type 1 diabetes in childhood than in the control group (risk of type 1 diabetes increased by 2.7-fold and by about one-third per BMI standard deviation from normal weight)
  • Diabetes mellitus type 2 (insulin resistance) – threefold increased risk in obesity; In about 80% of cases, diabetes mellitus type 2 disease is based on obesity.
  • Hormonal disorders
    • Decreased testosterone serum level (hypoandrogenemia) in men.
    • Increased levels of androgens (male hormones) in pubertal girls – increased hyperandrogenemic and hyperinsulinemic; it is likely that hyperinsulinemia in obese girls contributes to the development of hyperandrogenemia before and in early puberty; in females – hyperandrogenemia, polycystic ovary syndrome (PCO syndrome) – one to two times increased risk in obesity).
  • Hyperinsulinemia – presence of elevated insulin levels in the blood (fasting insulin > 17 mU/l).
  • Hyperleptinemia – presence of elevated leptin in the blood; is involved in the control of hunger and satiety.
  • Hyperlipidemia/dyslipidemia (dyslipidemia) – two to three times increased risk in obesity.
    • HDL cholesterol lowering
    • Hypertriglyceridemia (excessive triglyceride levels in the blood).
    • Notice: More than 50,000 patients in 30 countries were studied as part of DYSIS (Dyslipidemia International Study). The authors could not find a relationship between body mass index (BMI) and LDL cholesterol.
  • Hyperuricemia (elevation of uric acid levels in the blood).
  • Metabolic syndrome – clinical name for the symptom combination obesity (overweight), hypertension (high blood pressure), elevated fasting glucose (fasting blood sugar) and fasting insulin serum levels (insulin resistance) and dyslipidemia (elevated VLDL triglycerides, lowered HDL cholesterol). Furthermore, a coagulation disorder (increased tendency to clotting), with an increased risk of thromboembolism is also often detectable

Factors affecting health status and leading to health care utilization (Z00-Z99).

  • Stress – with higher body weight, the body reacts more strongly to stress.

Skin and subcutaneous tissue (L00-L99)

  • Acanthosis nigricans, which is characterized by darkening and rind formation of the skin folds at the armpits, flexures of the joints, neck and genital area, is associated with an increased risk of mycoses (fungal and yeast infections)
  • Psoriasis (psoriasis)
  • Striae (thighs, arms and abdomen) (40% of obese children).

Cardiovascular system (I00-I99).

  • Apoplexy (stroke) – from a BMI (body mass index) > 30 – increase by 40%.
  • Atherosclerosis (arteriosclerosis, hardening of the arteries).
  • Heart failure (cardiac insufficiency) – from a BMI (body mass index; body mass index) > 30 – increase by 100%; obesity is independent risk factor for diastolic heart failure; systolic heart failure as a direct consequence of obesity, however, is rare.
  • Hypertensive encephalopathy – hypertensive emergency characterized by an increase in intracranial (within the skull) pressure with consequent intracranial pressure signs.
  • Hypertension (high blood pressure) – two to three times increased risk in obesity; especially increased visceral fat mass correlates closely with hypertension.
  • Coronary artery disease (CAD) – diseases of the coronary arteries.
    • BMI of 25 to 29.9 – increases CHD risk by 32% (still 17% when adjusted for risks from hypertension and hyperlipidemia)
    • BMI over 30 – increases CHD risk by 81 percent (adjusted for the risks due to hypertension and hyperlipidemia still by 49%).
  • Left ventricular hypertrophy (LVH) – enlargement of the left heart due to extra work.
  • Myocardial infarction (heart attack)
  • Blood clotting disorders, such as venous thrombosis – from a BMI (body mass index) > 30 – increase of 230% due to an increase in clotting and inhibition of fibrinolysis (inhibition of the dissolution of blood clots).
  • Thromboembolism – increased risk in women with BMI > 24.9 taking oral contraceptives (birth control pills).
  • Atrial fibrillation – from a BMI (body mass index) > 30 – increase by 75%.

Liver, gallbladder and bile ducts – pancreas (pancreas) (K70-K77; K80-K87).

  • Acute and chronic cholecystitis (gallbladder inflammation).
  • Cholelithiasis (gallstones) – over 70% of all gallstones are due to elevated cholesterol and blood fat levels (triglycerides) – threefold increased risk in obesity.
  • Fatty liver hepatitis
  • Pancreatitis (inflammation of the pancreas)
  • Steatosis hepatis (fatty liver) (3-fold increased risk in obesity; >50% of overweight or obese adolescents; 80% in metabolic syndrome).

Mouth, esophagus (food pipe), stomach, and intestines (K00-K67; K90-K93).

  • Gastroesophageal reflux disease (synonyms: GERD, gastroesophageal reflux disease; gastroesophageal reflux disease (GERD); gastroesophageal reflux disease (reflux disease); gastroesophageal reflux; reflux esophagitis; reflux disease; reflux esophagitis; peptic esophagitis) – inflammatory disease of the esophagus (esophagitis) caused by the pathological reflux (reflux) of acidic gastric juice and other gastric contents; two to three times increased risk in obesity.
  • Constipation (intestinal blockage)

Musculoskeletal system and connective tissue (M00-M99)

  • Genu valgum (x-leg position; 55% of obese children).
  • Gout (arthritis urica/uric acid-related joint inflammation or tophic gout).
  • Rheumatoid arthritis
  • Back pain – one to two times increased risk in obesity.
  • Degenerative diseases of the spine and joints – osteoarthritis such as coxarthrosis (osteoarthritis of the hip joint – one to two times increased risk with obesity), gonarthrosis (osteoarthritis of the knee joint – two to three times increased risk with obesity)

Neoplasms – tumor diseases (C00-D48).

Ears – mastoid process (H60-H95).

  • Tinnitus (ringing in the ears)

Psyche – nervous system (F00-F99; G00-G99)

  • Anxiety disorders
  • Chronic migraine – as BMI increases, attacks become more severe and frequent. Among normal-weight individuals (BMI 18.5 to 24.9), four percent reported 10 to 15 headache days per month; among obese individuals (BMI 30 to 35), the rate was 14 percent; among severely obese individuals (BMI over 35), the rate was 20 percent.
  • Dementia
  • Depression
  • Erectile dysfunction (ED; erectile dysfunction).
  • Insomnia (sleep disorders)
  • Libido disorders
  • Alzheimer’s disease
  • Polyneuropathy (disease of the nerves of the peripheral nervous system; depending on the cause, motor, sensory or autonomic nerves may be affected; sensitivity disorders) (BMI ≥ 40); prevalence: 11.1%; in the obese participants with prediabetes (pathological glucose load test): 29% and in type 2 diabetics: 34.6%.
  • Problems in the partnership, for example, due to self-esteem reduction.
  • Sleep apnea syndrome (sleep-related breathing disorders) – threefold increased risk in obesity.

Pregnancy, childbirth and puerperium (O00-O99).

  • Atony – weakness of contraction (atony) of the uterus after the birth of the child and the incompletely or completely born placenta, resulting in severe to life-threatening hemorrhage.
  • Increased risk of miscarriage/preterm birth and stillbirth.
  • Fetal macrosomia (>4 kg at birth).
  • Increased risk of complications during pregnancy for fetomaternal complications (mother and child) – e.g., preeclampsia, eclampsia, gestational diabetes, premature placental abruption, more frequent induction of labor, increased sectio rate (cesarean section rate), and increased risk of postpartum hemorrhage
  • Increased risk of asphyxia (condition with circulatory weakness and respiratory depression to arrest associated with hypoxia (lack of oxygen supply to tissues) and hypercapnia (increased blood carbon dioxide content)).
  • Perineal tear grade III/IV
  • Shoulder dystocia (after delivery of the head, the baby’s shoulder gets stuck in the mother’s pelvis, causing birth arrest) – risk increases with increasing BMI (body mass index; body mass index)

Symptoms and abnormal clinical and laboratory findings not classified elsewhere (R00-R99).

  • Chronic inflammation (inflammation) – to be detected, for example, by elevated high-sensitivity C-reactive protein (hs-CRP)Inflammation (inflammation) triggered by metabolism (metabolism) is also called metaflammation.
  • High fasting glucose was associated with an increased risk of carcinoma according to the results of a large prospective cohort study in Korea – men had a 27% increased risk of dying from carcinoma and women had a 31% increased risk of dying from carcinoma.Among these, the main associated tumor types were pancreatic carcinoma, hepatocellular carcinoma, esophageal carcinoma, colon carcinoma, and also cervical carcinoma
  • Fractures (bone fractures)
  • Heartburn

Genitourinary system (kidneys, urinary tract – sex organs) (N00-N99)

  • Nephrolithiasis (kidney stones).
  • Renal insufficiency (kidney weakness)
  • Reproductive disorders – male and female – one to two times increased risk in obesity.
  • Gynecomastia – enlargement of the male mammary gland (40% of male adolescents).
  • Urinary incontinence (bladder weakness); also stress incontinence – occurs twice as often in obese women as in women of normal weight.
  • Overactive bladder (OAB)
  • Cycle disorders

Injuries, poisonings, and certain other sequelae of external causes (S00-T98).

  • Fractures (broken bones)

Further

  • Meta-analysis confirms that body weight has a significant impact on premature mortality risk (risk of death); excluded from the study were individuals who had ever smoked, deaths in the first five years after weight was recorded, and patients with chronic diseases. The following is the mortality risk as a function of body mass index (BMI):
    • BMI from 25 to less than 27.5: 7% increased mortality risk.
    • BMI from 27.5 to below 30 (obesity grade I): 20%.
    • BMI from 30 to under 35 (obesity grade I): 45 %.
    • BMI from 35 to under 40 (obesity grade II): 94 %.
    • Adults with BMI of 40 or higher (obesity grade III): 3-fold increased risk of premature death.
  • Increased mortality (death rate) or fewer healthy life years:
    • Men (age 20-40 years)
      • BMI > 35: die 8.4 years earlier than normal-weight peers due to retained obesity or have 18.8 fewer healthy life years (here: without type 2 diabetes mellitus or cardiovascular disease)
      • BMI 30 – < 35: -5.9 years of life or have 11.8 healthy life years less
      • BMI 25 – < 30: -2.7 years of life or have 6 healthy years of life less.
    • Women (age 20-40 years)
      • BMI > 35: die 6.1 years earlier or have 19.1 fewer healthy life years due to retained obesity
      • BMI 30 – < 35: -5.6 years of life or 14.6 healthy life years less.
      • BMI 25 – < 30: -2.6 years of life or 6.3 healthy life years less
  • Increased risk of surgery and anesthesia (especially in patients with a BMI > 39.9)
  • Increased risk of accidents (falls, injuries).
  • Gray hair (obesity is the most weighty risk factor after familial disposition).
  • Premature decline in brain white matter from age 40: by age 50, this had already shrunk to a level not reached until age 60 in lean participants.
  • Loss of function of NK cells (natural killer cells): NK cells store excess fatty acids, which contributes to the paralysis of the metabolism of the cells. As a result, NK cells can still recognize tumor cells, but are no longer able to destroy them because the too cytotoxic mechanisms are blocked.
  • Increased formation of the receptor PD-1 (“programmed death-ligand 1”) on the T cells as a result of accelerated immune senescence.

Notice.

  • Obese women who are metabolically healthy (happy obese; synonym: benign obesity) also then have an increased risk of cardiovascular disease (hazard ratio 2.61 (2.36-2.89); metabolically unhealthy women with obesity: hazard ratio of 3.15, which was statistically significant with a 95% confidence interval 2.83 to 3.50).
  • The Tübingen Family Study and the TUebingen Lifestyle Intervention Program (TULIP) come to the interesting conclusion that about 30% of obese people can be described as happy obese (synonym: benign obesity). Despite obesity, these “happy obese” have a similarly good insulin sensitivity as normal weight people. Furthermore, cardiovascular risks (based on intima measurement) and inflammatory mediators do not appear to be elevated either. These patients respond well to lifestyle interventions such as dietary changes and exercise. “Life-style nonresponders” (synonym: unhappy obese), on the other hand, do not respond to the above interventions. Their insulin sensitivity barely reaches 50% of normal, even with regular exercise. As a result, these obese patients are affected by numerous metabolic disorders. These patients accumulate a lot of ectopic fat in liver and muscles and their inflammatory mediators are increased. The above differences appear to be due in part to differential insulin resistance in the brain. Normally, the rise in insulin in the brain after eating results in a reduced desire for further eating. If insulin resistance in the brain is impaired, this feedback loop is disrupted and lifestyle interventions can only have a reduced effect.Epigenetic factors probably have a major influence on insulin sensitivity.