Although genetic deficiencies are currently considered rare, variations in these genes may predispose to common obesity. Many candidate genes are highly expressed in the central nervous system.

Several additional loci have been identified. Also, several quantitative trait loci for BMI have been identified.

Confirmed and hypothesized associations include:

Some studies have focused upon inheritance patterns without focusing upon specific genes. One study found that 80% of the offspring of two obese parents were obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.

The thrifty gene hypothesis postulates that due to dietary scarcity during human evolution people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would more likely survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies. This is the presumed reason that Pima Indians, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle.

Numerous studies of laboratory rodents provide strong evidence that genetics plays an important role in obesity.

The risk of obesity is determined by not only specific genotypes but also gene-gene interactions. However, there are still challenges associated with detecting gene-gene interactions for obesity.

Various developmental factors may affect rates of obesity. Breast-feeding for example may protect against obesity in later life with the duration of breast-feeding inversely associated with the risk of being overweight later on. A child's body growth pattern may influence the tendency to gain weight. Researchers measured the standard deviation (SD [weight and length]) scores in a cohort study of 848 babies. They found that infants who had an SD score above 0.67 had catch up growth (they were less likely to be overweight) compared to infants who had less than a 0.67 SD score (they were more likely to gain weight).

A child's weight may be influenced when he/she is only an infant. Researchers also did a cohort study on 19,397 babies, from their birth until age seven and discovered that fat babies at four months were 1.38 times more likely to be overweight at seven years old compared to normal weight babies. Fat babies at the age of one were 1.17 times more likely to be overweight at age seven compared to normal weight babies.

In the recent decades, family practices have significantly changed, and several of these practices greatly contribute to childhood obesity:

- With a decreasing number of mothers who breast-feed, more infants become obese children as they grow up and are reared on infant formula instead.

- Less children go outside and engage in active play as technologies, such as the television and video games, keep children indoors.

- Rather than walking or biking to a bus-stop or directly to school, more school-age children are driven to school by their parents, reducing physical activity.

- As family sizes decrease, the children's pester power, their ability to force adults to do what the want, increases. This ability enables them to have easier access to calorie-packed foods, such as candy and soda drinks.

- the social context around family meal-time plays a role in rates of childhood obesity

Several studies have shown that obese men tend to have a lower sperm count, fewer rapidly mobile sperm and fewer progressively motile sperm compared to normal-weight men.

Obesity in Germany has created a cholesterol problem. High cholesterol is known to cause premature death, angina, heart disease and strokes.

There has been an increase of children with Type 1 diabetes between 1996 and 2011. Diabetics are at higher risk for complications such as heart attack and stroke. In Germany, 600,000 people suffered from diabetes near the end of World War II compared to eight million now.

Obesity can increased risk for secondary diseases such as diabetes, cardiovascular disease, certain cancers and Alzheimer's. Children who get diabetes can expect to lose 10 to 15 years off of their lives. Diabetes also affect the eyes, kidneys and nerves in the legs.

Obesity is a "very strong promoter of cancer." Obesity causes an increased risk for colon cancer and breast cancer.

Sedentary lifestyle increases the likelihood of development of insulin resistance. It has been estimated that each 500 kcal/week increment in physical activity related energy expenditure, reduces the lifetime risk of type 2 diabetes by 9%. A different study found that vigorous exercise at least once a week reduced the risk of type 2 diabetes in women by 33%.

A sedentary lifestyle plays a significant role in obesity. Worldwide there has been a large shift towards less physically demanding work, and currently at least 30% of the world's population gets insufficient exercise. This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home. In children, there appear to be declines in levels of physical activity due to less walking and physical education. World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland found an increase and a study from the United States found leisure-time physical activity has not changed significantly. A 2011 review of physical activity in children found that it may not be a significant contributor.

In both children and adults, there is an association between television viewing time and the risk of obesity. A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.

Several associated risk factors include the following:

- Genetic factors (inherited component):

- Family history of type 2 diabetes

- Insulin receptor mutations (Donohue syndrome)

- LMNA mutations (familial partial lipodystrophy)

- Cultural variables, such as diet varying with race and class; factors related to stress, socio-economic status and history have been shown to activate the stress response, which increases the production of glucose and insulin resistance, as well as inhibiting pancreatic function and thus might be of importance, although it is not fully corroborated by the scientific evidence.

- Particular physiological conditions and environmental factors:

- Age 40–45 years or older

- Obesity

- The tendency to store fat preferentially in the abdomen (also known as "abdominal obesity)", as opposed to storing it in hips and thighs

- Sedentary lifestyle, lack of physical exercise

- Hypertension

- High triglyceride level (hypertriglyceridemia)

- Low level of high-density lipoprotein (also known as HDL cholesterol or "good cholesterol")

- Prediabetes, blood glucose levels have been too high in the past, i.e. the patient's body has previously shown slight problems with its production and usage of insulin ("previous evidence of impaired glucose homeostasis")

- Having developed gestational diabetes during past pregnancies

- Giving birth to a baby weighing more than 9 pounds (a bit over 4 kilograms)

- Pathology:

- Obesity and overweight (BMI > 25)

- Metabolic syndrome (hyperlipidemia + HDL cholesterol level 2.82 mmol/L), hypertension (> 140/90 mmHg), or arteriosclerosis

- Liver pathologies

- Infection (Hepatitis C)

- Hemochromatosis

- Gastroparesis

- Polycystic ovary syndrome (PCOS)

- Hypercortisolism (e.g., Cushing's syndrome, glucocorticoid therapy)

- Medications (e.g., glucosamine, rifampicin, isoniazid, olanzapine, risperidone, progestogens, glucocorticoids, methadone, many antiretrovirals)

Obesity is one of the leading preventable causes of death worldwide. A number of reviews have found that mortality risk is lowest at a BMI of 20–25 kg/m in non-smokers and at 24–27 kg/m in current smokers, with risk increasing along with changes in either direction. This appears to apply in at least four continents. In contrast, a 2013 review found that grade 1 obesity (BMI 30-35) was not associated with higher mortality than normal weight, and that overweight (BMI 25-30) was associated with "lower" mortality than was normal weight (BMI 18.5-25). Other evidence suggests that the association of BMI and waist circumference with mortality is U- or J-shaped, while the association between waist-to-hip ratio and waist-to-height ratio with mortality is more positive. In Asians the risk of negative health effects begins to increase between 22–25 kg/m. A BMI above 32 kg/m has been associated with a doubled mortality rate among women over a 16-year period. In the United States, obesity is estimated to cause 111,909 to 365,000 deaths per year, while 1 million (7.7%) of deaths in Europe are attributed to excess weight. On average, obesity reduces life expectancy by six to seven years, a BMI of 30–35 kg/m reduces life expectancy by two to four years, while severe obesity (BMI > 40 kg/m) reduces life expectancy by ten years.

Developing asthma due to abdominal obesity is also a main concern. As a result of breathing at low lung volume, the muscles are tighter and the airway is narrower. It is commonly seen that people who are obese breathe quickly and often, while inhaling small volumes of air. People with obesity are also more likely to be hospitalized for asthma. A study has stated that 75% of patients treated for asthma in the emergency room were either overweight or obese.

Genes partly play a role in obesity. Scientists at the German Institute of Human Nutrition and the University Hospital of Leipzig stated that identified two genes that promote fat accumulation in the abdominal cavity. The increased activity of the genes also promotes the release of an enzyme that is responsible for the formation of cortisol. A permanent increase in cortisol levels contribute to obesity.

Based on studies, it is evident that obesity has a strong association with vascular and metabolic disease which could potentially be linked to Alzheimer's disease. Recent studies have also shown an association between mid-life obesity and dementia, but the relationship between later life obesity and dementia is less clear. A study by Debette et al. (2010) examining over 700 adults found evidence to suggest higher volumes of visceral fat, regardless of overall weight, were associated with smaller brain volumes and increased risk of dementia. Alzheimer's disease and abdominal obesity has a strong correlation and with metabolic factors added in, the risk of developing Alzheimer's disease was even higher. Based on logistic regression analyses, it was found that obesity was associated with an almost 10-fold increase risk of Alzheimer's disease.

Like many other medical conditions, obesity is the result of an interplay between environmental and genetic factors. Studies have identified variants in several genes that may contribute to weight gain and body fat distribution; although, only in a few cases are genes the primary cause of obesity.

Polymorphisms in various genes controlling appetite and metabolism predispose to obesity under certain dietary conditions. The percentage of obesity that can be attributed to genetics varies widely, depending on the population examined, from 6% to 85%. As of 2006, more than 41 sites on the human genome have been linked to the development of obesity when a favorable environment is present. The involvement of genetic factors in the development of obesity is estimated to be 40–70%. Some of these obesogenic or leptogenic genes may influence obese individuals response to weight loss or weight management.

The incidence of idiopathic GHD in infants is about 1 in every 3800 live births, and rates in older children are rising as more children survive childhood cancers which are treated with radiotherapy, although exact rates are hard to obtain.

The incidence of genuine adult-onset GHD, normally due to pituitary tumours, is estimated at 10 per million.

In the United States, the prevalence of obese or overweight adult dogs is 23–53%, of which about 5% are obese; the incidence in adult cats is 55%, of which about 8% are obese.

In Australia, obesity is the most common nutritional disease of pets; the prevalence of obesity in dogs in Australia is approximately 40%.

Normal weight obesity is the condition of having normal body weight, but with a high body fat percentage, leading to some of the same health risks as obesity.

Compared to non-obese animals, obese dogs and cats have a higher incidence of osteoarthritis (joint disease) and diabetes mellitus, which also occur earlier in the life of the animal. Obese animals are also at increased risk of complications following anesthesia or surgery.

Obese dogs are more likely to develop urinary incontinence, may have difficulty breathing, and overall have a poorer quality of life compared to non-obese dogs, as well as having a lower life expectancy. Obese cats have an increased risk of diseases affecting the mouth and urinary tract. Obese cats which have difficulty grooming themselves are predisposed to dry, flaky skin and feline acne.

The body mass index (BMI) does not capture information about percentage body fat (PBF), which is a better predictor of risk due to obesity.

The term "metabolically obese normal weight" (MONW) refers to people with normal weight and BMI, but who display some metabolic characteristics that may increase the risk of developing metabolic syndrome, in the same way as obesity. MONW subjects have excess visceral fat, and are predisposed to insulin resistance, hypertension and cardiovascular disease. These people show benefits from energy restriction and weight loss, for example a 4- to 12-week period of diet and exercise.

Some studies have suggested that the main factor which explains the metabolic abnormalities in MONW individuals is fat distribution. On the basis of these studies, a scoring method has been proposed to identify MONW individuals, based on the presence of associated diseases or biochemical abnormalities related to insulin resistance.

Growth hormone deficiency in childhood commonly has no identifiable cause (idiopathic), and adult-onset GHD is commonly due to pituitary tumours and their treatment or to cranial irradiation. A more complete list of causes includes:

- mutations of specific genes (e.g., GHRHR, GH1)

- congenital diseases such as Prader-Willi syndrome, Turner syndrome, or short stature homeobox gene (SHOX) deficiency

- congenital malformations involving the pituitary (e.g., septo-optic dysplasia, posterior pituitary ectopia)

- chronic renal insufficiency

- intracranial tumors in or near the sella turcica, especially craniopharyngioma

- damage to the pituitary from radiation therapy to the head (e.g. for leukemia or brain tumors), from surgery, from trauma, or from intracranial disease (e.g. hydrocephalus)

- autoimmune inflammation (hypophysitis)

- ischemic or hemorrhagic infarction from low blood pressure (Sheehan syndrome) or hemorrhage pituitary apoplexy

There are a variety of rare diseases which resemble GH deficiency, including the childhood growth failure, facial appearance, delayed bone age, and low IGF levels. However, GH testing elicits normal or high levels of GH in the blood, demonstrating that the problem is not due to a deficiency of GH but rather to a reduced sensitivity to its action. Insensitivity to GH is traditionally termed Laron dwarfism, but over the last 15 years many different types of GH resistance have been identified, primarily involving mutations of the GH binding protein or receptors.

The disease is caused due to a variety of reasons:

- It can be due to aging, wherein muscles become weak due to a lack of exercise, and the individual gains weight due to the same reason.

- In other cases, the cause is genetic, wherein the individual is born with a reduced ability to grow muscle mass.

Pregnancy also poses as another high risk factor for vitamin D deficiency. The status levels of vitamin D during the last stages of pregnancy directly impact the new borns first initial months of life. Babies who are exclusively breastfed with minimal exposure to sunlight or supplementation can be at greater risk of vitamin D deficiency,as human milk has minimal vitamin D present. Recommendations for infants of the age 0–12 months are set at 5 ug/day, to assist in preventing rickets in young babies. 80% of dark skinned and or veiled women in Melbourne were found to have serum levels lower than 22.5 nmol/L considering them to be within moderate ranges of vitamin D deficiency.

A large percentage of children that suffer from PEM also have other co-morbid conditions. The most common co-morbidities are diarrhea (72.2% of a sample of 66 subjects) and malaria (43.3%). However, a variety of other conditions have been observed with PEM, including sepsis, severe anaemia, bronchopneumonia, HIV, tuberculosis, scabies, chronic suppurative otitis media, rickets, and keratomalacia. These co-morbidities tax already malnourished children and may prolong hospital stays initially for PEM and may increase the likelihood of death.

In light of the increase of vitamin D deficiency throughout Australia the federal government introduced mandatory fortification of vitamins and minerals such as vitamin D in certain foods like edible oil spreads as indicated in the: Australian Standard 2.4.2. It is mandatory for all food manufacturing companies producing table spreads like butter and margarine to have no less than 55 mg/kg of vitamin D, as a response to a growing public health requirements.

In response to recent advances, public policies are being reconsidered to ensure vitamin D is evidently being measured. With the vitamin D deficiency resurfacing the nutrient reference value guidelines were established, in turn creating the dietary vitamin D recommendations.

The dietary vitamin D guidelines are assuming limited exposure to UVB sun light are:

Infants, Children and Adults <50 years: 5 µg/day

Adults >50 - <70 years: 10 µg/day

Adults >70 years: 15 µg/day

Malnutrition and being underweight are more common in the elderly than in adults of other ages. If elderly people are healthy and active, the aging process alone does not usually cause malnutrition. However, changes in body composition, organ functions, adequate energy intake and ability to eat or access food are associated with aging, and may contribute to malnutrition. Sadness or depression can play a role, causing changes in appetite, digestion, energy level, weight, and well-being. A study on the relationship between malnutrition and other conditions in the elderly found that malnutrition in the elderly can result from gastrointestinal and endocrine system disorders, loss of taste and smell, decreased appetite and inadequate dietary intake. Poor dental health, ill-fitting dentures, or chewing and swallowing problems can make eating difficult. As a result of these factors, malnutrition is seen to develop more easily in the elderly.

Rates of malnutrition tend to increase with age with less than 10 percent of the "young" elderly (up to age 75) malnourished, while 30 to 65 percent of the elderly in home care, long-term care facilities, or acute hospitals are malnourished. Many elderly people require assistance in eating, which may contribute to malnutrition. Because of this, one of the main requirements of elderly care is to provide an adequate diet and all essential nutrients.

In Australia malnutrition or risk of malnutrition occurs in 80 percent of elderly people presented to hospitals for admission. Malnutrition and weight loss can contribute to sarcopenia with loss of lean body mass and muscle function. Abdominal obesity or weight loss coupled with sarcopenia lead to immobility, skeletal disorders, insulin resistance, hypertension, atherosclerosis, and metabolic disorders. A paper from the "Journal of the American Dietetic Association" noted that routine nutrition screenings represent one way to detect and therefore decrease the prevalence of malnutrition in the elderly.

The physical implications of obesity in children include sleep apnoea, breathlessness, a reduced tolerance to exercise and orthopaedic and gastrointestinal problems including non-alcoholic fatty liver disease. Children who reciprocate these physical health disadvantages tend to struggle to concentrate more in- school and find it harder to fit in, being marginalised due to the inability to partake in physical exercise. According to the Dieticians Association of Australia 25-50% of overweight or obese children with turn out to be obese as adults. Long-term effects of obesity, therefore, include cardiovascular disease (hypertension and high blood pressure) and particular types of cancers in particular colon, kidney and breast cancer. Non-alcoholic fatty liver disease (NAFLD) is one of the most common risk factors associated with obesity being characterised as a buildup of fat within the liver cells. Musculoskeletal defects such as osteoarthritis are also said to have a strong link with obesity due to excessive amounts of weight being exerted on the joints. Individuals who have a Body Mass Index (BMI) that is equal to or greater than 25 kg/m2 are also said to have an increased chance of premature morality.

The symptoms are basically the same as that of sarcopenia and obesity. The individual may show a BMI that is appropriate and healthy to his or her age but will look fat in appearance.