Despite the biological and psychosocial changes that may accompany pregnancy and the postpartum period, most women are not diagnosed with PPD. Many mothers are unable to get the rest they need to fully recover from giving birth. Sleep deprivation can lead to physical discomfort and exhaustion, which can contribute to the symptoms of postpartum depression. Risk factors
While the causes of PPD are not understood, a number of factors have been suggested to increase the risk. These risks can be broken down into two categories, biological and psychosocial:

Biological
Administration of labor-inducing medication synthetic oxytocin
Chronic illnesses caused by neuroendocrine irregularities
Genetic history of PPD
Hormone irregularities
Inflammatory illnesses (irritable bowel syndrome, fibromyalgia)
Cigarette smokingThe risk factors for postpartum depression can be broken down into two categories as listed above, biological and psychosocial. Certain biological risk factors include the administration of oxytocin to induce labor. Chronic illnesses such as diabetes, or Addisons disease, as well as issues hypothalamic-pituitary-adrenal dysregulation (which controls hormonal responses), inflammatory processes like asthma or celiac disease, and genetic vulnerabilities such as a family history of depression or PPD. Chronic illnesses caused by neuroendocrine irregularities including irritable bowl syndrome and fibromyalgia typically put individuals at risk for further health complications. However, it has been found that these diseases do not increase risk for postpartum depression, these factors are known to correlate with PPD. This correlation does not mean these factors are causal. Cigarette smoking has been known to have additive effects. Some studies have found a link between PPD and low levels of DHA (an omega-3 fatty acid) in the mother.
Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases. With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the person now experiences a polydipsia and polyuria cycle. Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice. Diagnosis
To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops). Urinalysis demonstrates a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low.A fluid deprivation test is another way of distinguishing DI from other causes of excessive urination. If there is no change in fluid loss, giving desmopressin can determine if DI is caused by:

a defect in ADH production
a defect in the kidneys response to ADHThis test measures the changes in body weight, urine output, and urine composition when fluids are withheld to induce dehydration. The bodys normal response to dehydration is to conserve water by concentrating the urine. Those with DI continue to urinate large amounts of dilute urine in spite of water deprivation. In primary polydipsia, the urine osmolality should increase and stabilize at above 280 mOsm/kg with fluid restriction, while a stabilization at a lower level indicates diabetes insipidus.