User:MAlvis

I am a US engineer, entrepreneur, former USAF instructor pilot in supersonic jet aircraft (1970-1974) and physician, specializing in preventive, non-invasive and invasive cardiology and internal medicine in San Antonio, an FAA senior flight examiner, have answered questions on HealhTap.com in the past and currently on Quora.com (more flexibility for more detailed answers without the disabling biass of many in the medical disease industry). I also have practical mechanical, electronic design, software and system engineering/building experience.

I came across Wikipedia in June of 2004, during a Google search looking for technical information on current commercial digital encoding algorithms for sound.

However, since ~2007, I rarely contribute because of excessive interference from a few who seem to have incorrect ideas/beliefs about medicine and keep deleting my work, justifying this by insisting that I provide academic/research references, most of which are not publicly available on the net. Thus, if you are interested in some of my more current charitable efforts, look me up on Google, Milton Alvis, or on the website HealthTap.com[1].

06/2004: Being favorably impressed with the technical information overview, organization and links about the sound encoding issue provided by others, I decided to look up atherosclerosis[2], commonly incorrectly depicted, a problem for a majority of humans, typically beginning in childhood, perhaps more a problem for people in first world countries with longer life expediencies, and one with which I have technical expertise. I found the Wikipedia definition of atherosclerosis to be rather basic and elected to perform rather extensive editing, so far only with text, to better elucidate the issues. Some images to illustrate some of the issues and a better organizational outline would likely be of considerable help to improved understanding by non-physicians. I have not done these, at least yet.

Since 06/2004, I have started a number of additional Wikipedia definitions and assisted with improving others. I only list those definitions which I personally feel OK about, as of the last time I reviewed them.

A few pages I have initiated since 2004 include: Andreas Gruentzig (the founder of angioplasty), atheroma, cardiac output, cardiolite, cerebral circulation, clinically silent, colesevelam, Drug-eluting stent, Electron Beam Tomography, exenatide, false negative, false positive, fatty streaks, gamma camera, Hounsfield scale (the basis for CAT scan images), IMT, IVUS, Jim Otvos, Lp-LpA2, NCEP, positron electron annihilation reaction (the physical basis of PET scanning), radiocontrast, radiodensity, radiolucent, stroke volume, therapeutic effect, Ultra Low Density Lipoprotein, vein graft disease, vulnerable plaque (the basis for most heart attacks and many strokes ), X-Ray tube and a few other definitions. Additional issues and links, one long known and repeatedly verified, importance of lipoprotein concentrations & particle size, which have had considerable and growing scientific evidence of validity for cardiovascular disease progression over the last few decades are presented in the "2008" addendum below.

Pages I have also worked on include: Acyl-CoA, ACSL1, aspirin, angiogram, angioplasty, ApoA-1 Milano, Apolipoprotein B, arteriole, artery, atherosclerosis, benzonatate, Biomarker discovery, blood pressure, blood vessel, C-reactive protein, capillary, cardiac output, cardiac stress test, cardiology diagnostic tests and procedures, cardiovascular disease, Cholesterol, Chronic CerebroSpinal Venous Insufficiency, coronary catheterization, Crestor, chylomicrons, clarithromycin, coronary artery bypass surgery, carotid Doppler machine, computed axial tomography, coronary heart disease, diabetes mellitus, distilled water, efficacy, emulsion, endothelium, endothelium-derived relaxing factor, eteplirsen, freon, gamma camera, glyceryl trinitrate, glycosylated hemoglobin, heart sounds, high density lipoprotein, hydrochlorothiazide, hypercholesterolemia, impedance plethysmography, intermediate density lipoprotein, ischaemic heart disease, John Lenczowski, Kruppel-like factors, lipoprotein (69.91.2.137), low density lipoprotein, Multiple Sclerosis, myocardial infarction, Natural law, necrosis, paresthesia, PCSK9, phytosterol, pioglitazone, pramlintide, platelets, rosuvastatin, side-effect, Asterisk (PBX), Surface-enhanced Raman spectroscopy, SPECT, stents, statins, sulfonylurea, Theaflavin-3-gallate, Tim Russert, tire, thiazolidinedione, thin client, tomogram, vascular smooth muscle, very low density lipoprotein and W. Edwards Deming.

2008: The most effective strategies for reducing atherosclerotic progression and cardiovascular event rates have been altering known, though not 100% fully understood, internal physiologic behaviors which drive the disease, i.e. accumulation of macrophage white blood cells into the inner walls of arteries with some of the cells dying, more macrophages entering and a host of subsequent processes, some of which, e.g. artery enlargement, compensate for and mask presence of the disease, up to a point. The two most consistently powerful factors, in both clincial trials and my own clinical experience, for slowing disease progression have been changing (a) fractionated lipoprotein patterns (including quantified particle concentrations and sizes), not cholesterol or cholesterol fractions per-se (The cholesterol carried by all the lipoproteins is identical, the difference is the protein not the cholesterol.) and (b) blood glucose levels, HbA1c, to abnormally healthy values, i.e. levels more typical of childhood (under age 5) before the atherosclerotic process typically begins.

Additional factors, usually helpful, are reducing systolic blood pressure (at least below 120 mmHg), low level but chronic white blood cell activation (commonly termed inflammatory processes and reflected by C-reactive protein at very low levels, i.e. the hs-CRP test, and many other clinical markers), visceral fat, stopping smoking, staying physically active, reducing lipoprotein little a, maintaining or increasing muscle mass, possibly reducing homocysteine etc.

At the same time, many other strategies, long promoted, such as taking extra doses of vitamins E and/or C, beta-carotene, etc. (antioxidants with the goal of reducing free radical induced cellular damage), in double-blinded prospective randomized human trials of these strategies have repeatedly turned out to show no protective effect and, in some trials, outcomes have been slightly worse than placebo. While the antioxidant issue is clearly relevant, the few seemingly simpler approaches tried to date, vitamins E and C high dose supplementation, have not worked out.

This is a link to a video [[3]], examining autopsy specimens from a 58 year old sudden death heart attack victim, illustrates to issues and that pre-event, high grade lumen narrowing (the rational for "stress" testing) is neither a typical or reliable indicator for future heart attacks. These animations, [[4]] and [[5]], though a bit dramatized, illustrate the sequence of events.

Unfortunately, judging from my experience working with patients for years, most of the public has long been partially mislead by:

• a belief that atherosclerosis starts in 40-year-olds (i.e. when symptoms become more common), rather than the reality, known for over 5 decades from autopsy observations, that it typically beings in childhood, before age ten, yet typically remains asymptomatic, untreated and ignored for decades

• the long focus on lumen narrowing/blockage, technically termed stenosis, commonly termed the "plumbing view" on which bypass surgery and angioplasty are based and long promoted by most in the medical profession (based on angiograms and misunderstandings) rather than the reality that the problem is within the wall of arteries and largely undetected by angiography, much less stress tests, see atheroma & cardiac stress test,

• the long focus on cholesterol as opposed to the correct issues of (a) lipoprotein particle structure, size and plasma concentration driving the progression vs. lack of progression of atherosclerosis combined with several others behaviors, such as (b) blood pressure (repeated wall stretching with each heart beat) (c) blood glucose regulation, etc, and

• the oversimplified (and misleading, in my view) diet exercise cholesterol admonitions of the NIH and its NCEP subcommittee, given the chosen bias of the committee to focus on what are believed to be the least expensive, as opposed to the most effective, strategies (which are debated due to expense & differing interpretations of evidence) to reduce progressive disease burden for the masses, despite the typical ineffective implementation of these admonishments. (Careful review of the long reports of the committee does reveal discussion of the bigger picture.) Additionally, for over two decades the promoted dietary focus was low fat intake as opposed to the more relevant low internal body visceral fat stores and the role of carbohydrate intake and internal body cell-to- cell and inter-tissue signaling and management in driving arterial disease.

As of the year 2000, the NCEP committee's goals were reducing heart attack death rates of those with expected mortality rates greater than 3%/year, 30%/decade based on limited phenotypic characteristics which were presumed fairly easy for most physicians to assess and recognize. As of ~2002, the committee revised its goals to rates greater than 2%/year, 20%/decade, an improvement. However, scientific evidence has repeated demonstrated that the methodologies promoted do not work as well as hoped. Additionally, multiple surveys have demonstrated that most physicians, including most cardiologists, are not effective in helping people reach the NCEP promoted guidelines. Additionally, how many people, (including the famous and respected ABC newsman specializing in politics who died "unexpectedly" June 2008) would deliberately choose the NCEP odds as good enough, if they knew what they were choosing? The AHA published in 2003, that for ~65% of men and ~47% of women, heart attack was the first symptom of cardiovascular disease; what a devastating first symptom; stroke is even worse. In my experience, most people find being aware of the most effective strategies (currently known) and verifying the effectiveness of these strategies for their own health and benefit (e.g. tracking carotid IMT changes, promoting excellence of heart function (not just normality), assessable by unusually carefully performed and read high quality echocardiogram, etc., preferably before onset of symptoms, to be a better approach.

As of 2007, there are still only two laboratories in the world, Berkeley HeartLab (http://www.bhlinc.com) and Liposcience (http://www.liposcience.com), which actually perform lipoprotein analysis for clinicians and patients. In 2006, the Mayo Clinic recruited Liposcience to establish a substation facility at their facility. While I have no financial or management role in either lab company, I believe that the better of the two is Liposcience. Liposcience is an basic science academic research spin-off company founded by and as a result of the research work of Jim Otvos on a better way to measure the many different lipoproteins at lower cost and with better accuracy. Liposcience uses computer automated nuclear magnetic resonance spectroscopy (with both gradient gel electrophoresis and shadowing electron microscopy as references) and report all data referenced to blood samples from Framingham Heart Study first generation children, the blood samples having been both saved and provided by the CDC. Liposcience only performs arterial disease and disease treatment related lab work. However, many labs, in addition to Liposcience, offer HbA1c to track glucose level, important well below levels currently considered Diabetes Mellitus, see Metabolic Syndrome.

An additional good web resource, with more accurate (yet still simplified) graphical illustrations than most presentations, for better understanding of how the atherosclerotic disease process creates a wide spectrum of evolving scenarios ranging from asymptomatic (though creating CHF over years) all the way to sudden-death heart blood supply problems is http://www.shapesociety.org. The graphics at this site also help visually explain why stress testing does not recognize/diagnose arterial disease and why heart artery bypass surgery and angioplasty/stent treatment approaches only partially treat some symptoms of arterial disease in the heart, and other, arterial systems of the body. Be aware that http://www.shapesociety.org promotes both CAT scans and carotid ultrasound for screening. Personally and professionally, I believe there are many well justified concerns and reservations about CAT scan radiation exposure and I rarely recommend them for screening in favor of better and safer ways to approach arterial disease self-protection. However both coronary and carotid ultrasound (they also promote carotid ultrasound) can be very useful, if carefully done and read with the patient seeing and understanding the images as part of a more sophisticated patient education and treatment strategy to avoid becoming symptomatic with advanced cardiovascular atherosclerotic disease consequences; see the pages on atheroma and vulnerable plaque.