DIABETES AND POST-TRAUMATIC STRESS DISORDER AMONG THE ELDERLY

DIABETES AND POST-TRAUMATIC STRESS DISORDER AMONG THE ELDERLY 

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Pathophysiology of Diabetes among the elderly 

Elderly people tend to experience medical problems most often as a result of weakening immune systems as they age. Diabetes is among the most common medical complications that the elderly face in the U.K and all over the world. Diabetes mellitus commonly known as diabetes is a medical condition used to describe diseases that affect blood sugar levels in the human body. Glucose plays a crucial in a human’s body since it provides energy to the body. Diabetes among the aging population appears unique as compared to other populations. In the elderly, the pathophysiology of this disorder differs, so the therapy approach should be different too (Meneilly, n.d). Diabetes incidence and prevalence increase with age for a number of reasons. It is evident that genetic influences play a role in this disease (Kahn, 1994, Pg. 1066-1085). Therefore, in families with a history of diabetes, the risk of developing the disease increases with age, though no gene responsible has been identified. Additionally, certain ethnicities are more likely to suffer from type 2 diabetes than others, indicating a genetic predisposition (Lipton et al., 1993, Pg. 826-839). 

In addition, some people with diabetes develop a genetic predisposition due to age-related changes in carbohydrate metabolism. The condition may be the result of declining beta-cell responses to incretin hormones GIP and GLP-1 and insulin-mediated glucose disposition (Ferrannini et al., 1996, Pg. 947-953). A genetically susceptible individual is also more likely to develop diabetes in old age if they engage in many environmental and lifestyle factors (Meneilly & Tessier, 2001). Taking multiple medications that could negatively impact glucose metabolism is common among older people with co-existing illnesses. 

Similarly, a reduction in physical activity and an increase in obesity-associated with aging, particularly central obesity, are two factors that can contribute to abnormal glucose metabolism. People who consume more saturated fats and simple sugars in their diet are more likely to develop diabetes than those whose diet contains complex carbohydrates. Women who drink moderate amounts of alcohol seem to be protected against diabetes, whereas elderly adults who consume high amounts of dietary iron may be at greater risk of diabetes. The development of diabetes in the elderly is thought to be linked to trace elements such as zinc and chromium, as well as vitamins such as vitamin C and E. However, specific evidence has not yet been provided. Accordingly, lifestyle modification could help prevent diabetes among older adults considering the above information. As a matter of fact, adapting to diet and activity to prevent diabetes in older people was more effective than in younger people (Anon, 2002, Pg. 393–403). 

When diabetes occurs in the elderly, inflammatory cytokines, such as tumor necrosis factor-alpha and C-reactive protein are associated with an increased risk of the disease (Del Prato, 2009, Pg. 1066–1085). Conversely, elevated levels of adiponectin (an adipocytokine that stimulates insulin production) have been linked with a lower risk of diabetes.  Similarly, the incidence of diabetes appears to be more prevalent in men with a low testosterone level and higher testosterone levels in women.

 Metabolic Alterations 

Numerous studies have been performed on metabolic abnormalities in middle-aged type 2 diabetes patients (DeFronzo, 2009, Pg. 773–795).  A significant insulin-mediated glucose disposal deficit is observed in both lean and obese subjects. Increased fasting concentrations of blood glucose, lower insulin release, and impaired glucose clearance all contribute to impaired glucose disposal. There is no increase in fasting hepatic glucose production in the elderly. Similar to obese younger subjects, obese older subjects have impaired insulin-mediated glucose disposal, but glucose-induced insulin secretion is preserved relative to older subjects. Insulin secretion is markedly impaired in lean elderly subjects, but insulin sensitivity is relatively preserved. Ultimately, obesity is primarily responsible for metabolic defects in older people with diabetes, whereas leanness is responsible for metabolic defects caused by reduced glucose-induced insulin release. As such, administering insulin or giving insulin secretagogues should be the main approach to lean older subjects. Therefore, metformin is commonly prescribed for obese patients as the first step in improving insulin sensitivity. Diabetes patients with obesity and insulin resistance have also shown impaired insulin-mediated vasodilation, which accounts for more than 30% of normal glucose disposal (Meneilly & Tessier, 2001). The above observations illustrate the possibility of drugs that enrich muscle blood flow being beneficial. Indeed, patients with these conditions have shown improved insulin sensitivity when taking angiotensin-converting enzyme inhibitors (Meneilly, n.d.).

 For a long period of time, patients with type 1 diabetes who develop beta-cell failure are thought to be affected by autoimmune phenomena (Naik et al., 2009, Pg. 4635–4644). In addition, it is increasingly recognized that there is a subgroup of patients with type 2 diabetes who have antibodies against their islet cells, and these are referred to as adults with autoimmune diabetes. latent epidemic (LADA). Current data are unclear regarding the prevalence of LADA among insulin-dependent older people with diabetes. Patients with this disease tend to be lean individuals who cannot tolerate oral medications and need insulin therapy early in their illness. There is some evidence that early insulin therapy and antigen-specific immunomodulation may delay insulin therapy in type 2 diabetes patients. Future studies may recommend measuring autoimmune parameters at diagnosis in elderly patients with type 2 diabetes. This hypothesis will, however, need more research to be proven. 

The fact that glucose can stimulate its own uptake without insulin has been recognized for years. The process is known as non-insulin-mediated glucose uptake (NIMGU). In normal individuals, 70% of their glucose is absorbed through NIMGU, and about 50% is consumed through mechanisms other than insulin. Since NIMGU is associated with insulin resistance, it has greater relevance for better glucose metabolism in patients with type 2 diabetes who are older and obese. Regrettably, NIMGU is impaired in diabetic older adults, further impairing their blood glucose control (Forbes et al., 1998, Pg. 1915–1919). However, future therapeutic developments may include the treatment of metabolic abnormalities associated with aging.  It may be those future treatments targeting NIMGU, along with diet changes and GLP administration, will also decrease insulin resistance and increase insulin secretion in older individuals with type 2 diabetes (Meneilly et al., 2001, pp. 1951–1956).   

Molecular Biology 

In elderly diabetics, there is relatively little research on molecular biologic abnormalities. Even today, mutations in the glucokinase gene have not been found to be related to these patients' disease (McCarthy et al., 1994, Pg. 198–204). Insulin activates insulin receptor tyrosine kinases in skeletal muscle after binding to its receptor. Some research suggests that insulin receptor number and affinity are normal in elderly patients, however, insulin receptor tyrosine kinase activity may be defective, making this type of insulin resistance more likely (Obermaier-Kusser et al., 198, Pg. 9497–9504). The aging process is characterized by progressive mitochondrial dysfunction, and decreased insulin release and sensitivity are possible side effects of mitochondrial dysfunction (Hawley & Lessard, 2007, Pg. 699-702). As such, it is clear that more studies are needed to determine the subcellular defects that impede glucose metabolism in elderly diabetic patients.  

Glucose Counter-Regulation 

Several studies have shown that hypoglycemia symptoms with insulin or oral agents increase exponentially with age (Stcepka et al., 1993, pages 115-121). Multiple factors contribute to this phenomenon. Hypoglycemia is controlled primarily by glucagon in normal subjects; glucagon responses are reduced in old subjects, and to an even greater extent, in patients with diabetes (Meneilly et al., 1994, Pg. 403-410). Elderly patients typically are not educated about hypoglycemia warning signs, and therefore are unaware of what they should do when the signs manifest (Kahn, 1994, Pg. 1066-1085). Patients with low blood sugar may also be less aware of autonomic warning signs of hypoglycemia, even after they have been educated about them. Lastly, older patients are less able to take appropriate steps to return to normal blood sugar levels when their blood sugar levels are low. As a result of these abnormalities, hypoglycemia is observed at higher rates in the elderly, including decreased secretion of hormones that oppose blood sugar regulation, reduced recognition and awareness of warning signs, and altered psychomotor functions. 

Two important interventions could potentially prevent hypoglycemia in older people following the above information. In the first place, elderly patients should be taught frequently and carefully what hypoglycemia symptoms mean. Moreover, alternative treatment options, such as oral agents or insulin, such as glipizide or insulin glargine, are also worth considering as they have been shown to reduce the frequency of hypoglycemia in elderly patients. 

Conclusively, age-related changes in carbohydrate metabolism coupled with environmental and genetic factors result in diabetes in the elderly. Those with diabetes who are older experience metabolic changes that differ from those with diabetes who are younger. Older patients should therefore receive different therapeutic approaches because of their distinct metabolic abnormalities. In the coming decades, an improved understanding of the pathophysiology of diabetes in the elderly will assist us in better coping with the epidemic of this disease among the elderly. 

 Pathophysiology of Post-traumatic stress disorder (PTSD) 

Trauma Among the Elderly Post-Traumatic Stress Disorder (PTSD) is a psychological condition that affects many people who have been exposed to traumatic events. A traumatic event can lead to the development of PTSD, which is characterized by intense fear, helplessness, and horror. There are three main clinical manifestations of PTSD: reexperiencing, avoidance behavior and numbing of emotions, and physiological hyperarousal (Weintraub and Ruskin, 199, Pg. 144-152). In elderly persons, post-traumatic stress disorder (PTSD) makes it more difficult for them to manage subsequent life stress and to deal successfully with the phases of aging. Trauma can trigger it at any time during a person's lifetime. Chronic or intermittent symptoms can accompany the disorder, which may be temporary or chronic. The severity of trauma and premorbid psychiatric illnesses increases the possibility of developing PTSD, while certain personality traits and psychosocial support can counteract the adverse effects of the disorder. The prevalence of PTSD among elderly people does not appear to be higher than in young people, and the symptoms of it are similar across ages: reliving traumatic events, avoiding them, and feeling hyper-aroused (Yao et al., 2003, Pg. 232-238). Neurobiology has implicated dysfunction of the adrenergic system and the hypothalamic-pituitary-adrenal axis in PTSD, but no evidence is available to support that aging affects these systems and their function in this condition. In the treatment of PTSD in this age group, antidepressants, cognitive-behavioral therapy, and group therapy are among the most common treatments today. However, there has been no systematic research conducted. 

PTSD in older people can be divided into two categories. The first category involves war survivors such as those who survived Vietnam, Korea, and WWII, Holocaust survivors, and former refugee children are some of those who have been traumatized years or decades ago. PTSD may develop into chronic symptoms in older adults who suffered trauma earlier in life, or it may be exacerbated as the body ages. For instance, a medical condition or decreased physical ability may mean that an individual cannot cope with his or her PTSD symptoms with the coping strategy that was previously used. 

Those who have experienced trauma within the last decade, as older adults, constitute the second group of people with PTSD. Older adults may be more vulnerable to trauma exposure due to a number of reasons. For instance, those with diminished reaction times may have difficulty escaping dangerous situations and avoiding motor vehicle or other accidents. Besides, the likelihood of older people receiving early warnings via automated text messages during a natural disaster may be lower. In addition, this group may also be more likely to suffer serious medical complications in an accident or disaster. 

To fully understand the phenomenon of traumatic memories in this population, it is crucial to consider the effects of aging on cognitive functioning. People tend not to develop cognitive deficits (such as cognitive flexibility, concept formation, goal setting, planning, and organizing) until they are at least eighty (Anderson, 2010, Pg. 37-56). The most common cause of dementia, usually associated with older people, is Alzheimer's disease. In Australia, approximately 9 percent of over-65s and 30 percent of over-85s suffer from dementia (Australian Institute of Health, 2012). From samples of veterans, there is some evidence that dementia is more common in people with PTSD, although the nature of this link is unclear; the presence of PTSD can increase the risk of dementia, or a common risk factor can cause both diseases. Researchers have found that the degree of dementia among trauma-exposed groups, such as Holocaust survivors, is comparable to that in non-trauma-exposed groups (Ravona-Springer et al., 2011, Pg. 709-716).  

Although the elderly population is less likely to develop serious psychological problems after trauma, natural disasters can be particularly taxing on their physical and mental health (Jia et al., 2010, Pg. 1-11). Older natural disaster survivors are more likely to feel grief and guilt than younger survivors, especially when younger relatives have died in the disaster. Studies show that older people may not move as a result of a disaster, preferring to stay in their own city, and there is some evidence that those who do move are at greater risk of developing post-traumatic stress disorder (Viswanath et al., 2012, Pg. 402-407). Several other factors can influence the severity of symptoms, including female gender, disaster exposure levels, and behavior-based or avoidant coping methods (Weinstein & Ryan, 2011, Pg. 4-17). Although they experience a lot of suffering after a disaster, older people are less likely to seek health or general help than younger survivors. 

PTSD often results in changes in the anatomy and physiology of the brain in addition to its psychological effects. Trauma contributes to the reduction in hippocampal size and predisposes to its loss. In patients with PTSD, the amygdala, which processes emotions and modulates fear responses, becomes overly reactive. With PTSD, the medial prefrontal cortex (mPFC), which controls the stress response and amygdala's emotion, is smaller and less active. 

Although PTSD patients tend to suffer from ongoing stress and high levels of the Corticotropin-Releasing Factor (CRF), they sometimes have normal to low cortisol levels in their bloodstreams. In response to cortisol, CRF is decreased. A low cortisol level stimulates high CRF, which in turn stimulates the release of norepinephrine from the anterior cinculate cortex. Psychophysiological measurements such as heart rate, blood pressure, and skin conductance level can indicate hyperactivity of the sympathetic branch of the autonomic nervous system in people with PTSD. Several other neurotransmitter systems, including the serotonin, GABA, glutamate, neuropeptide Y, and endogenous opioid systems, show altered functioning in elderly people with PTSD (Bowirrat et al., 2010, Pg. 335-358). 

As argued by the Dual Representational Theory, further insight into the pathogenesis of PTSD may be found (Brewin, 2001, Pg. 373-393). The presence of two memory systems is highlighted by this understanding. By reflecting on verbally accessible memories (first recorded in the hippocampus than in the general brain memory storage), they can be modified. These kinds of memories are most common in people who have not suffered trauma. Conversely, situationally accessible memory functions primarily through non-verbal processes that are associated with high emotions and the amygdala. Generally, traumatizing memories are stored as situationally accessible memories, which are hard to process, easily triggered by associations, and more likely to trigger emotional distress when triggered. Thus, the elderly who struggle with integrating these painful memories into their broader narrative may have a significant impact on how they view the world and themselves in the future. 

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