Dr. Ashley Burkman, ND

Heart Attack Patients More Prone to Post-Depression

Heart attack patients are 3 times more likely to develop major depression when compared to general population.¹ After an initial heart attack, depression increases the risk of subsequent heart attacks. Interestingly, individuals with depression are more likely to develop heart disease.¹⁵ The stress of a major life-threatening event like a heart attack can be cause enough for the development of depression, and physicians are more aware of the importance of monitoring for depressive disorders in cardiac patients.

Research Focused on Preservation of a Complex Connection

Recently, research has been focusing on the preservation of a complex connection in the brain, called the limbic system. The limbic system controls emotional health, motivation and memory.³ After a heart attack, the limbic system seems to be a vulnerable place to apoptosis, or cellular death. Rat models have demonstrated benefit in reducing inflammation after a heart attack as a way to reduce degradation of limbic system.²

Cardiac Arrest and Increased Inflammatory Signaling

When cardiac arrest occurs, there is a purposeful increase in inflammatory signaling to help reduce the severity of the heart attack. It is when this signaling is perpetuated long after the cardiovascular event that increases the risk of unnecessary damage to healthy brain structures.⁸

Caspases

Caspases are one of the many enzymes that control apoptosis, purposeful cell death, and when over stimulated can accidentally harm healthy cells and structures.¹⁰ After a heart attack, levels of caspsase enzymes are elevated within minutes and remain elevated until signals of inflammation cease.^8,11 In the limbic system, consistently elevated caspsase enzymes increase the risk of damage its delicate structures, pushing researchers to find a way to reduce this lingering elevation.

Reducing the overstimulation of this inflammation-causing enzyme is a promising method in reducing the risk of depression in heart attack victims.

Gastrointestinal System

In addition to nervous system tissues, like the limbic system, the gastrointestinal system is also subject to deterioration post heart attack. The lining of the digestive tract is the gateway from the outside world to the inside body, including to the nervous system. Rat models have shown promise in supporting the digestive tract lining via probiotic supplementation pre medically induced heart attack in reducing caspsase induced limbic system degradation.⁸ It was found that placebo rats, those that did not receive probiotics prior to induced heart attack, had higher amounts of lipopolysaccharides (LPS) in circulation, molecules that activate inflammatory responses. LPS come from gram-negative bacteria residing in the digestive tract. ¹⁴ Compromise in the intestinal lining leads to greater risk for LPS to enter the circulation, which increases stress responses and perpetuates inflammatory signaling.^13,14

Probiotic Strains and Gastrointestinal Lining Compromise

Probiotic strains have been tested in rat models to assess their ability to reduce gastrointestinal lining compromise.^8,12 Lactobacillus helveticus, Bifidobacterium longum and Lactobacullius farciminis were three of the specific probiotic strains that successfully protected against heart attack induced LPS increase in circulation.^8,12 Rats that did not receive the probiotic mixture prior to heart attack exhibited more depressive behaviors including decreased social and sexual behaviors, reduced sleep quality and memory loss, in addition to having quantifiably more LPS in circulation.^2,8

Probiotics and Immune Modulating Effect

Probiotics have a known immune modulating effect, likely stemming from their ability to crowd out harmful bacteria in the digestive system. This offers protection against the perpetuation of inflammatory LPS induced destruction of healthy tissues in the body after a stressful event, including heart attack. ^7,8,10 Addressing underlying digestive flora imbalances may prove to be a substantial way to reduce the pathogenesis of cardiovascular limbic system degradation.

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Dr. Ashley Burkman received her Doctor of Naturopathic Medicine degree from the National University of Health Sciences in Chicago. She is deeply rooted in classical naturopathic medicine, practicing the belief that the human body has an innate ability to heal itself. She works with patients toward lifestyle adjustments in order to bring about long-term health. Viewing the body as an integrated whole and addressing all aspects of what determines health is the cornerstone of both naturopathic medicine and Dr. Burkman’s practice.

Dr. Ashley Burkman is a licensed naturopathic physician in the state of Connecticut. Commitment to the growth of her profession has lead her to participate in the several campaigns to expand the scope of practice of naturopathic physicians in several states. She is also a member of both the Connecticut Naturopathic Association and American Association of Naturopathic Physicians.

Dr. Burkman, an Iowa native, enjoys perusing local farmers markets, spending time with friends and family, and searching for new hiking trails to conquer. She attends comedy shows and baseball games regularly and has a soft spot for cats.

Dr. Burkman and Dr. Lauren Young practice as fully licensed Naturopathic Physicians at Connecticut Natural Health Specialists, LLC, in Manchester, CT. Most major health insurances accepted. New patients are encouraged to call for an appointment.

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References:

1. Williams, RB. Depression After Heart Attack. Depression After Heart Attack. 2011. Available at: http://circ.ahajournals.org/content/123/25/e639.full. Accessed February 9, 2015.
2. Wann, BP, Bah, TM, Kaloustain, S, et al. Behavioural signs of depression and apoptosis in the limbic system following myocardial infarction: effects of sertraline. ResearchGate. 2009. Available at: http://www.researchgate.net/publication/5293131_behavioural_signs_of_depression_and_apoptosis_in_the_limbic_system_following_myocardial_infarction_effects_of_sertraline. Accessed February 9, 2015.
3. Hesselink, JR. HE TEMPORAL LOBE & LIMBIC SYSTEM. Available at: http://spinwarp.ucsd.edu/neuroweb/text/br-800epi.htm. Accessed February 9, 2015.
4. What causes depression? – Harvard Health. Harvard Health. 2009. Available at: http://www.health.harvard.edu/mind-and-mood/what-causes-depression. Accessed February 9, 2015.
5. Kaloustian, S, Wann, BP, Bah, TM, et al. Apoptosis time course in the limbic system after myocardial infarction in the rat. Apoptosis time course in the limbic system after myocardial infarction in the rat. 2008. Available at: http://www.academia.edu/4799691/apoptosis_time_course_in_the_limbic_system_after_myocardial_infarction_in_the_rat. Accessed February 9, 2015.
6. Wann, BP, Bah, TM, Boucher, M. Result Filters. National Center for Biotechnology Information. 2007. Available at: http://www.ncbi.nlm.nih.gov/pubmed/17245469. Accessed February 9, 2015.
7. Halade, GV, Ma, Y, Ramirez, TA, et al. Reduced BDNF attenuates inflammation and angiogenesis to improve survival and cardiac function following myocardial infarction in mice. Reduced BDNF attenuates inflammation and angiogenesis to improve survival and cardiac function following myocardial infarction in mice. 2013. Available at: http://ajpheart.physiology.org/content/305/12/h1830. Accessed February 9, 2015.
8. Girard, S, Bah, TM, Kaloustian, S, Lada-Moldovan, L, Rondeau, I. Lactobacillus helveticus and Bifidobacterium longum taken in combination reduce the apoptosis propensity in the limbic system after myocardial infarction in a rat model. ProQuest. 2009. Available at: http://search.proquest.com.libproxy.bridgeport.edu/docview/213829206?accountid=26484. Accessed February 14, 2015. Girard, S, Bah, TM, Kaloustian, S, Lada-Moldovan, L, Rondeau, I. Lactobacillus helveticus and Bifidobacterium longum taken in combination reduce the apoptosis propensity in the limbic system after myocardial infarction in a rat model. ProQuest. 2009. Available at: http://search.proquest.com.libproxy.bridgeport.edu/docview/213829206?accountid=26484. Accessed February 14, 2015.
9. Malick, M, Gilbert, K, Barry, M, Godbout , R, Rousseau, G. Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction. National Center for Biotechnology Information. 2014. Available at: http://www.ncbi.nlm.nih.gov/pubmed/25451696. Accessed February 14, 2015.
10. Apoptosis: Caspase Pathways. Apoptosis: Caspase Pathways. 2014. Available at: http://www.rndsystems.com/cb_detail_objectname_fa98_apoptosiscaspasepathways.aspx. Accessed February 13, 2015.
11. McIlwain, DR, Berger, T, Mak, TW. Caspase functions in cell death and disease. National Center for Biotechnology Information. 2013. Available at: http://www.ncbi.nlm.nih.gov/pubmed/23545416. Accessed February 14, 2015.
12. Ait-Belgnaoui , A, Durand, H, Cartier, C, et al. Result FiltersPrevention of gut leakiness by a probiotic treatment leads to attenuated HPA response to an acute psychological stress in rats. National Center for Biotechnology Information. 2012. Available at: http://www.ncbi.nlm.nih.gov/pubmed/22541937. Accessed February 12, 2015.
13. Alexander, C, Rietschel, ET. Bacterial lipopolysaccharides and innate immunity. National Center for Biotechnology Information. 2001. Available at: http://www.ncbi.nlm.nih.gov/pubmed/11581570. Accessed February 14, 2015.
14. Wang, X, Quann, PG. Endotoxins: lipopolysaccharides of gram-negative bacteriaResult Filters. National Center for Biotechnology Information. 2010. Available at: http://www.ncbi.nlm.nih.gov/pubmed/20593260. Accessed February 15, 2015.
15. Depression and Heart Disease. NIMH RSS. Available at: http://www.nimh.nih.gov/health/publications/depression-and-heart-disease/index.shtml. Accessed February 14, 2015.