The Depression-Heart Link
Majid Ali, M.D.
Evidence for Oxygen Models of Depression and Coronary Heart Disease
My Oxygen Models of Depression and Coronary Heart Disease (CHD) are extensions of my Oxygen Model of Health and Disease. These are unifying models that explains all aspects of depression and CHD—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.
Strong evidence for the oxygen models of depression and CHD was published in Auhgust 2015 in the journal Circulation with the following words: “while deaths from coronary heart disease [CHD], the most common type, have declined dramatically in older Americans over the last few decades, those improvements were not shared equally by people under 55, especially women.” The research “also notes that social and psychological risk factors, such as depression and stress, may play a role in the development of heart disease.”
Below, I reproduce the text of full abstract of the report:
Background—Coronary heart disease (CHD) mortality rates have fallen dramatically over the past four decades in the Western world. However, recent data from the US and elsewhere suggest a plateauing of CHD incidence and mortality among young women. We therefore examined recent trends in CHD mortality rates in the US according to age and sex.
Methods and Results—We analyzed mortality data between 1979 and 2011 for US adults =25 years. We calculated age-specific CHD mortality rates and compared annual percentage changes (EAPC) during three approximate decades of data (1979-1989, 1990-1999, and 2000-2011). We then used Joinpoint regression modeling to assess changes in trends over time, based on inflection points of the mortality rates. Adults aged 65+ years showed consistent mortality declines, which became even steeper after 2000 (women, -5.0% and men, -4.4%). In contrast, young men and women (aged <55 years) initially showed a clear decline in CHD mortality from 1979 until 1989 (EAPC -5.5% in men and -4.6% in women). However, the two subsequent decades saw stagnation with minimal improvement. Notably, young women demonstrated no improvements between 1990 and 1999 (EAPC +0.1%), and only -1% EAPC since 2000. Joinpoint analyses provided consistent results.
Conclusions—The dramatic decline in CHD mortality since 1979 conceals major heterogeneities. CHD death rates in older groups are now falling steeply. However, young adults have experienced frustratingly small decreases in CHD mortality rates since 1990. The drivers of these major differences in CHD mortality trends by age and sex merit urgent study.