Diabetic neuropathies comprise a group of heterogeneous disorders caused by poorly managed or untreated Type 2 Diabetes. Prolonged hyperglycemia (high blood sugar levels) induces increased production of free radicals, which can damage nerve fibres and cause nerve cell death. As such, patients with diabetic neuropathy often experience pain, numbness, hypersensitivity, and reduced function in the legs and arms. There is no known cure for this painful disease. Doctors generally suggest lifestyle changes, such as smoking cessation, weight loss, and blood pressure management. However, lifestyle changes may not always be enough to alleviate symptoms. Unfortunately, it is very difficult to treat
If you’ve ever found yourself in a state of panic or anxiety and tried slowing your breathing, controlling and lengthening the exhales, you know that it’s possible to use that breath to slow a quickened heart rate and calm the nervous system. Our brain controls the cardiovascular (CV) system, but how we react when we feel stress can also instruct the heart and blood vessels on how to respond. Long-term when we don’t cope well, when chronic stress or anxiety cause the sympathetic nervous system (“fight or flight”) to stay turned on all the time it changes how the CV system functions. Insomnia, depression and/or having history of trauma have also been shown to increase the incidence of a cardiac event, regardless of other risk factors for cardiovascular disease (CVD) such as smoking and obesity.
Stress and Cardiovascular Disease (CVD) Risk
The “fight or flight” response we have to acute stress is an adaptive response that’s part of our normal, healthy nervous system. It increases our heart rate and blood pressure, dilates our pupils, all to help us to address and respond to a stressor in that moment. However, chronic stress and anxiety prolongs this effect and over time can cause changes in our blood vessel function and in the heart. It can change cardiac output and redirect blood flow to different tissues.1 Priming the nervous system to be prepared for stress at all times can overwhelm the system and our adrenal glands leading to poorly regulated blood pressure, heart rate and cortisol secretion while increasing the amount of inflammatory molecules in our circulation.
When the body is always anticipating needing a stress response, it can exaggerate the physiological reaction to stress, exceeding metabolic limits. This means it can cause a higher heart rate when not appropriate, using up energy and putting stress on our heart and blood vessels unnecessarily. Combined this not only changes our CV function, but it affects our body’s ability to regulate blood sugar balance and lipids (cholesterol) as well.2
All together this can accelerate the development of atherosclerosis, when the blood vessels develop plaques, promote hypertension (high blood pressure), increase the mass of the heart’s ventricles,2 overall increase the risk of a heart attack and a CV-related death.1
Poor Sleep and CVD Risk
Both insomnia and low sleep hours have been shown to negatively affect the CV system. Insomnia, difficulty falling asleep, maintaining sleep or having poor quality sleep, is associated with increased sympathetic nervous system (SNS) activity as well as adrenal gland activity where cortisol is released. During deep restorative sleep, the nervous system activates the parasympathetic nervous system which prompts “rest and digest” and puts “fight or flight” activities to rest. This causes our heart rate and blood pressure to decrease during sleep. However, for those with broken or disrupted sleep, this changes that process.
Cortisol, a stress hormone, and melatonin, our sleep hormone, have opposite 24-hour curves where cortisol is highest in the morning, and melatonin highest in the night. Cortisol actually blunts melatonin, so if you’re overly stressed or anxious and pumping out a bunch of cortisol at night, you’re likely not going to be able to fall asleep, or you may notice poor sleep quality. Patients with insomnia tend to have higher levels of cortisol and adrenaline (epinephrine) as well as an increased heart rate, and decreased heart rate variability.3
Short-term this might not have a huge impact on overall CVD risk, but long term it can have multiple negative consequences. Insomnia has been associated with increased inflammation and getting less than five to six hours of sleep per night has been shown to increase the risk of hypertension by two-fold.4 It’s also associated with coronary artery hardening, independent of obesity and cholesterol levels.3
In a large review of the research composed of 122,500 patients with insomnia but without CVD at baseline, there was a 45% increased risk of developing CVD or dying from a CVD event within 3-20 years.5
Depression and CVD Risk
The effects of stress and anxiety on our nervous system and CV system is understandable, but depression and depressive disorders have been strongly linked to CVD as well. Studies have found that those with depression are at a greater risk of developing a heart attack, heart failure and stroke, and patients with CVD may suffer more from depression than the general population.6 The prevalence of CVD is three times greater among those with major depressive disorder compared to those without mood disorders.6 Depression has also been linked to earlier development of CVD by about 7.5 years compared to cases without a history of depression.
Part of this is explained by lifestyle habits that those with depression may fall into that can increase CVD risk including physical inactivity, smoking, substance abuse, poorer hygiene and diet, and a reduced adherence to medication and supplement intake. But of course, this isn’t every case of depression.
As we know with stress and anxiety, psychological factors can affect changes in our hormonal and nervous systems. Depression is linked to increased inflammatory reactions, and may affect the function of our platelet cells (involved in blood clotting).6
Observational studies have noticed that social isolation and loneliness can increase the risk of a CVD event by 50%.7 Post-traumatic stress disorder (PTSD) can also increase CV risks. A recent study of active US military service members found that combat deployment was associated with a significantly increased risk of new onset coronary heart disease (CHD).8 In another study, over an average 13 year follow up period, Vietnam veterans with PTSD had over twice the risk of CHD, independent of other CVD risk factors, substance abuse and depression.7 These individuals tended to have lower myocardial blood flow on cardiac scans and increased calcifications of coronary arteries – a marker of atherosclerosis. 7
Interestingly, a new population with increased CVD risk may be the “internet troll”. Recent preliminary research is linking the use of negative social media posts, including angry and hostile posts, with cardiovascular deaths.2 In a study of language used on Twitter, negative emotions including anger and disengagement seemed to be its own risk factor for atherosclerotic heart disease.9 Negative language used on Twitter predicted CVD-associated death better than a comparative model that used health risk factors such as smoking, diabetes, obesity and hypertension.
Treating CV and Mental Health Conditions
How do we address these psychogenic factors that are strongly linked to CVD and CV-related deaths? It forces us to approach our heart health on multiple levels including addressing mental health. In addition to modifying lifestyle factors such as smoking, alcohol use, diet and body weight, we need to consider mental and emotional support. In a randomized trial of individuals with a diagnosed CHD event in the year previous to the start of the study, adding 20 two-hour sessions of cognitive behavioural therapy (CBT) focused on stress management, in addition to conventional treatment, led to 41% fewer recurrent CVD events over a period of about eight years.10 This was compared to those who were given conventional treatment only.
All efforts, including cognitive and behavioural, that can help manage our reactions to stress could potentially lead to better cardiovascular outcomes. This also illustrates the importance of not discounting vague symptoms such as fatigue and chest discomfort in those with depression, PTSD, chronic stress and/or anxiety, especially in women who seem to have less prominent cardiovascular symptoms compared to men.
- Ginty AT, Kraynak TE, Fisher JP, Gianaros PJ. (2017). Cardiovascular and autonomic reactivity to psychological stress: Neurophysiological substrates and links to cardiovascular disease. Auton Neursci. 207: 2-9
- Chauvet-Gelinier J-C, and Bonin B. (2017). Stress, anxiety and depression in heart disease patients: A major challenge for cardiac rehabilitation. Ann Phys Rehabil Med. 60(1): 6-12
- Javaheri S, Redline S. (2017). Insomnia and risk of cardiovascular disease. Chest. 152(2): 435-44
- Fernandez-Mendoza J, Vgontzas AN, Liao D. (2012). Insomnia with objective short sleep duration and incident hypertension: the Penn State cohort. Hypertension. 60(4):929–935
- Sofi F, Cesari F, Casini A, et al. (2014). Insomnia and risk of cardiovascular disease: a meta-analysis. Eur J Prev Cardiol. 21(1): 57-64
- Bucciarelli V, Caterino AL, Bianco F, et al. (2020). Depression and cardiovascular disease: The deep blue sea of women’s heart. Trends Cardiovasc Med. 30(3): 170-6
- Cohen BE, Edmondson D, Kronish IM. (2015). State of the art review: Depression, stress, anxiety, and cardiovascular disease. Am J Hypertens. 28(11): 1295-302
- Crum-Cianflone NF, Bagnell ME, Schaller E, Boyko EJ, Smith B, Maynard C, Ulmer CS, Vernalis M, Smith TC. (2014). Impact of combat deployment and posttraumatic stress disorder on newly reported coronary heart disease among US active duty and reserve forces. Circulation.129:1813–1820
- Eichstaedt JC, Schwartz HA, Kern ML, et al. (2015). Psychological language on Twitter predicts country-level heart disease mortality. Psychol Sci 26: 159-69
- Gulliksson M, Borell G, Vessby B, et al. (2011). Randomized controlled trial of cognitive behavioural therapy vs standard treatment to prevent recurrent cardiovascular events in patients with coronary heart disease: Secondary prevention in Uppsala Primary Health Care project (SUPRIM). Arch Intern Med. 171(2): 134-40