Autoimmunity in endocarditis: Only epiphenomenon or the underlying cause?

Abstract

Humans require a balanced diet to survive, which has been established by science. However, science has never considered one crucial question: ancient human beings had very little understanding of science, yet they managed their food sources to achieve a balanced diet in different environments; what made this possible? We would like to propose a theory which addresses this question: The Attention deficit hyperactivity disorder and Obsessive–compulsive personality disorder theory of human behavior (ADHD–OCPD theory). The theory proposes that natural selection favored behaviors that allowed humans to gain access to a balanced diet. The theory argues for Darwinian adaptive radiation in human behavior to achieve a balanced diet in different niches over time and space. The theory goes against the current view that some human populations are primitive while others are more evolved. It is a greatly revised and extended version of the Hunter–Farmer theory [1] proposed by Thom Hartmann. The profiles of some unmedicated ADHD patients [2,3] parallel the stereotypical profiles of some ethnic groups [4,5]. Over thirty years ago, Thom Hartmann proposed the Hunter– Farmer theory [1]. In our view, the characteristics Hartmann ascribes to the hunter fall within the spectrum of a personality disorder defined in the DSM-IV as the Attention Deficit Hyperactivity Disorder (ADHD), whereas the farmer’s traits fall within the spectrum of the personality disorder known as Obsessive Compulsive Personality Disorder (OCPD). We propose that a more precise way of defining Hartmann’s theory is to refer to it as the ADHD– OCPD theory. We propose that the environment played a significant role in shaping the behavior of people of all ethnicities to allow attainment of a balanced diet in native environments. We posit that natural selection may have favored ADHD to varying degrees in environments where no farming and small-scale farming were feasible such as areas traditionally occupied by Pima Indians, African San, Central African Pygmies, the Inuit, some Asian groups and many black African groups. OCPD is postulated to have been selected for in areas where large-scale farming was feasible, which are the areas where civilizations sprouted among the ancestors To the Editor, In clinical practice, it is common to find incomplete criteria for definitive infective endocarditis (IE) but the presence of endocarditis in echocardiogram is often followed by antibiotics which are even maintained in spite of negative blood cultures. Those patients usually lack of typical features of IE, such as fever, cardiac murmur, leukocytosis or elevated C reactive protein. Coincidentally, they are not usually present in nonbacterial thrombotic endocarditis (NTBE) [1]. It is currently known that NTBE is the prior suitable site for colonization and formation of IE. Surgical series have shown that NBTE is more frequent in patients with connective tissue and autoimmune diseases. In the Mayo Clinic series [2], an underlying immune-mediated disorder was identified in 60%, including primary antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). Another study involving 759 patients reported 290 non-infective cases, of which 129 showed autoantibodies [3]. Moreover, nine patients met classification criteria for SLE and two for RA. On other hand, recent evidences suggest that patients with rheumatic heart disease (RHD) may actually have autoimmune diseases with similar valve involvement [4]. Hashimoto’s thyroiditis has been found linked to RHD. When autoimmune disease has been investigated in patients with recurrent diastolic heart failure, 40% of cases showed RHD, fulfilled criteria for SLE, there were not criteria for a diagnosis of past rheumatic fever, and the association to autoimmune thyroid disease was confirmed [5]. Of note, follow-up of patients with positive autoantibodies has not been extensively described. Likewise, studies on long-term outcome rarely focus on the sequence of non-cardiac complications or newly-diagnosed autoimmune conditions after the acute episode. Therefore, it is possible that autoimmune conditions may be implicated in the pathogenesis of NBTE, IE and RHD, so it would be possible to find autoantibodies at anytime and as well as findings of non-cardiac manifestations of autoimmune disease. Perhaps, we should change our hitherto clinical practice and consider three new objectives in a patient with IE: (a) to demonstrate clinical and immunological features of systemic autoimmune connective tissue disease, before and after the acute episode; (b) to demonstrate if non-definitive cases of IE are actually NTBE; and (c) to asses long-term outcomes of NTBE and IE. Those observations may change the paradigm of IE management, and relate and prevent non-cardiac events in the outcome of the patients.