Marianne J. Legato – författare

It is a universal fact that men die before women. But the causes of this have long remained unexplored. In this trailblazing book, Dr. Marianne Legato - an expert in gender specific health - examines the reasons behind men's fragility and explains what they need to do to live longer. A bestselling author and Professor of Medicine at Columbia University, Dr. Legato shows how the forces of culture and biology conspire against male mortality. Drawing on the latest research and narrated through the lives of her patients, she delves into problems that both men and women care about - from why the male fetus is at greater risk, to why boys have a hard time adjusting to school, to how elevated levels of the stress hormone cortisol make men more prone to aggression and why they are more likely to die from cardiac arrest or cancer and even depression.Why Men Die First offers specific advice on what men can do to live better, including * how on-one time with young boys reduces anxiety and attention deficit problems * lifestyle changes that can prevent cardiovascular disease and osteoporosis * why young men take on high risk endeavors and how to decrease the stress * how to cope with mid life depression and feelings of emasculation and uselessness * how testosterone shots can mitigate the unpleasant symptoms of aging Dr. Legato brings the possibility of both mental and physical wellbeing to men in this compelling and inspiring book. A superstar physician, celebrated annually in New York Magazine's Best Doctors Issue, Dr. Legato is well poised to take on this urgent topic with her unimpeachable authority and natural warmth.

Heart disease, despite recent improvements, continues to be the single most im­ portant cause of death and disability in the United States. It is estimated that the direct cost of medical care for cardiovascular disease is $6 billion dollars per year. Data compiled by the National Center for Health Statistics reveal a dramatic de­ cline in deaths from cardiovascular disease in the United States (greater than 20% since 1968). This phenomenon has been the subject of in-depth study. It is clear that the decline is real and not a statistical artifact. The decrease in mortality has been noted in all sections of the country, though the onset and rate of decline varies in different regions of the country. Both primary prevention, through changes in risk factors, and basic and applied research leading to earlier recognition and im­ proved treatment have contributed to the decline. They do not fully explain the decline. Further research is needed to clarify this issue. Clinical cardiologists have been exposed to a veritable explosion of new knowl­ edge of mechanisms of cardiovascular disease, development of new improved non-invasive diagnostic techniques, and the pharmacodynamics of agents affect­ ing the cardiovascular system. This new knowledge results from contributions made by individuals from diverse disciplines including cellular and molecular bi­ ologists, geneticists, hematologists, cardiologists, and cardiovascular surgeons.

The Stressed Heart is truly unique in concept and will provide an eXCItmg adventure to the reader no matter what his or her field of expertise and interest. The title, although quite appropriate, does not adequately indicate the range of topics considered or the rational interrelationships among them. Indeed, perhaps the most important point to be learned from the book is that a serious consideration of the response of the heart to mechanical overload, ischemia, or excessive humoral stimuli must include evaluation of each of the topics in the table of contents. The heart responds to stress through alterations in both structure and function. How these changes are brought about is the subject of the initial chapters. These consider first the normal regulation of gene expression in the heart, the rapid response to mechanical overload that leads to both quantitative and qualitative changes in the contractile proteins, and our current understand­ ing of the signals that might be elicited by stress and alter gene expression. One chapter emphasizes the fact that, regardless of the nature of the stress, the common denominator is a discrepancy between energy requirements and expenditure. The central role of cellular acidosis in initiating the sequence of responses to stress and the possible roles of peptide regulators of transcription and protein regulators of translation are considered in detail.

The Stressed Heart is truly unique in concept and will provide an eXCItmg adventure to the reader no matter what his or her field of expertise and interest. The title, although quite appropriate, does not adequately indicate the range of topics considered or the rational interrelationships among them. Indeed, perhaps the most important point to be learned from the book is that a serious consideration of the response of the heart to mechanical overload, ischemia, or excessive humoral stimuli must include evaluation of each of the topics in the table of contents. The heart responds to stress through alterations in both structure and function. How these changes are brought about is the subject of the initial chapters. These consider first the normal regulation of gene expression in the heart, the rapid response to mechanical overload that leads to both quantitative and qualitative changes in the contractile proteins, and our current understand­ ing of the signals that might be elicited by stress and alter gene expression. One chapter emphasizes the fact that, regardless of the nature of the stress, the common denominator is a discrepancy between energy requirements and expenditure. The central role of cellular acidosis in initiating the sequence of responses to stress and the possible roles of peptide regulators of transcription and protein regulators of translation are considered in detail.

Heart disease, despite recent improvements, continues to be the single most im­ portant cause of death and disability in the United States. It is estimated that the direct cost of medical care for cardiovascular disease is $6 billion dollars per year. Data compiled by the National Center for Health Statistics reveal a dramatic de­ cline in deaths from cardiovascular disease in the United States (greater than 20% since 1968). This phenomenon has been the subject of in-depth study. It is clear that the decline is real and not a statistical artifact. The decrease in mortality has been noted in all sections of the country, though the onset and rate of decline varies in different regions of the country. Both primary prevention, through changes in risk factors, and basic and applied research leading to earlier recognition and im­ proved treatment have contributed to the decline. They do not fully explain the decline. Further research is needed to clarify this issue. Clinical cardiologists have been exposed to a veritable explosion of new knowl­ edge of mechanisms of cardiovascular disease, development of new improved non-invasive diagnostic techniques, and the pharmacodynamics of agents affect­ ing the cardiovascular system. This new knowledge results from contributions made by individuals from diverse disciplines including cellular and molecular bi­ ologists, geneticists, hematologists, cardiologists, and cardiovascular surgeons.