Archive for category The Medical Tent
It would be great if an acclaimed — and more importantly, extremely widely read — U.S. newspaper could boast “Health” and “Science” sections that boasted consistently impressive articles. This one is getting a lot of attention, and with good reason: something like two-thirds of adult Americans are considered overweight, millions of them are trying to shed pounds, and Gina Kolata’s article in effect conveys the message that they are screwed.
I’m going to assume that anyone reading this has read the article and the study it draws from or at least has tabs open to these, because I am not going to review it in depth.
A couple of very quick, seemingly obvious, and (perhaps deliberately) underemphasized or omitted points:
A guy I hang around with is convinced that milk is about the worst thing a person can ingest, save for red meat, which he sees as a virtual guarantee of colon cancer (there is probably an association, but he takes the issue to an extreme). Of course, this same fellow is a “truther” (thinks the U.S. government was behind the 9/11 terror attacks) and has paranoid tendencies across the board. And when he says milk is bad, he’s not referring to the hormones people are concerned about; he means milk per se, at least cow’s milk and other milk derived from animals. Read the rest of this entry »
So lately I’ve been helping to take care of a dog that has proven to be a remarkable, and damned near heartbreaking, challenge. (Well, considering we all live indoors and have plumbing and electricity and stuff. I don’t want to get too high-flown here. A Jack London story this ain’t.)
Ellie is a 12- or 13-year-old Australian Cattle Dog mix, weighing in at about 60 pounds. (An alternative name for this breed is “Blue heeler.”) I first became acquainted with her toward the end of last year. A friend of mine does a lot of house-sitting and pet-sitting, and I often lurk nearby when she does; Ellie’s family is a frequent client. My initial meetings with Ellie were on the turf of her owner Jil’s parents, who live less than a mile from Jil and her husband and own a similarly aged, better sighted, more arthritic pooch named Mollie. Mollie’s owners are also frequent clients of my friend the sitter. When Jil is out of town, Ellie usually stays at Mollie’s, and when Jil and her parents are both out of town (which happens more often that you might think, not that I’m reading your mind), the dogs and my friend all stay at Mollie’s. Which is a hell of a nice house, since you asked.
With that burst of irrelevant details out of the way, I’ll describe the problem and the (apparent) (re)solution. Read the rest of this entry »
File this one under “No shit, Sherlock”:
A new study of the relationship between alcohol intake and wheel-running in hamsters has found that exercise may provide an effective alternative for reducing alcohol intake in humans.
[S]aid Alan M. Rosenwasser, professor of psychology at the University of Maine, chronic alcohol abuse and circadian disruption become reciprocally destructive and result in negative effects on physical and emotional health.
“Dopamine is the primary chemical released within the brain in response to any type of reward, including exercise, drugs, food, and sex,” [study corresponding author J. David Glass] said. “For humans, exercise may be an effective, beneficial, and naturally rewarding substitute for any type of addiction.”
To be fair, all of this may actually be news to addiction researchers even though drinkers with a running problem themselves have been aware of these things for decades, and the research team did establish a common link–circadian rhythm regulation–offering insight into why, other than the variously triggered dopamine-reward system that was elucidated a long time ago, exercise helps keep people on the wagon. Still, the fact that scientists are just now catching on to the vital role exercise plays in managing chemical dependency underscores a greater clinical reality: All too often, exercise is never mentioned by psychiatrists treating all manner of substance-abuse problems and mood disorders, with the primary and typically sole intervention being a prescription drug with or without the suggestion to attend support groups.
This is not surprising. A Consumer Reports survey of over 1,500 Americans with clinical depression suggests that far more people embrace pills than embrace talk therapy, despite the fact that those who attended at least seven therapy sessions reported as much symptom relief as those who relied on drugs alone. Four in five respondents, in fact, replied that they would rather go the pharmacological route.
This is understandable, given that taking a pill as a lot less work and, in many cases, is a lot cheaper than visiting a therapist. But this doesn’t take into account efficacy, and many people have spent years trying to find an SSRI or other drug that produces the desired effects.
Of course, this is a false dichotomy, since many people on medication are also in therapy. But it’s clear that people are hungering for a magical solution to a complex problem, and it’s unlikely that clinically depressed people will ever fully return to baseline using pharmacotherapy alone.
Of ancillary note: More and more people who seek help for mental-health problems report anxiety as one of their symptoms, and the type of therapist people employ (psychiatrist vs. psychologist vs. social worker, etc.) does not appear to have an effect on the efficacy of therapy.
What I find interesting is how people who share some distinct trait, belief, or status–however rare–seem to gravitate toward one another without any conscious effort whatsoever. If agnostics and people who believe in some amorphous “higher power” are not included, the percentage of atheists in the U.S. apparently ranges from around 5% to around 15%, depending on the parameters of the survey. Yet well over half of the people I associate with are atheists by any measure. Similarly, this Web MD slide show cites the 2% figure I have seen elsewhere with respect to the fraction of the population believed to be afflicted with bipolar disorder; I’d have to say that a far greater fraction of my friends and associates have been diagnosed as bipolar.
Anyway, the slide show is a great overview. The curse of bipolar disorder is that people with it, especially in its less explosive forms, usually find the manic or hypomanic phases not only tolerable but enjoyable, and may often be more productive in some areas of their lives (or at least believe that this is the case). So when the depression hits, they find it easy to believe that their moods are under conscious control and that if they simply fight to reclaim the high of days and weeks past, it can happen. Since this is not how things work, people already experiencing “organic” depression excoriate themselves for their perceived weakness and incompetence, perpetuating a very nasty cycle within a population already apt to have alienated most everyone in their lives and thus operating largely in isolation.
Humans break so damned easily.
Some time ago, some playful rapscallion signed me up to get daily e-mail updates from OneNewsNow.com, a site representing the truly demented and prevaricating arm of U.S. Christianity. I was tempted to cancel “my” subscription, but after reading a few of these updates and visiting the site, morbid fascination and a longstanding personal propensity for finding reasons to become tweaked over the doings of idiotic liars won out over common sense, so I continue receiving messages housing all manner of laughable bullshit about homosexuality, abortion, and everything else that the religious right has uniquely mangled in its antiheroic insistence on infecting mainstream society with its worthless take on social and medical issues.
The latest crapburst is a post about the supposed lack of merits of embryonic stem-cell research, and it’s more of a joke than the usual mindless litanies churned out by this vile band of backward souls. I realize that the reason this site exists is to raise money for the American Family Association by pandering to the lowest common denominator of cross-happy dolts in this country and that its writers are not quite as stupid as they appear, but nevertheless, “articles” like this one are inexcusable and could be drolly dismantled by any eighth-grader with a handle on scientific and general reality.
Anyway, the skinny: Read the rest of this entry »
Most people know that there are various blood “types,” as defined by two major contributors: protein antigens on the surface of erythrocytes (red blood cells, or RBC’s) classified as either “A” or “B”, and a plus or minus designation rooted in the Rh factor (“Rh” derived from the Rhesus monkey). Other immunological factors exist, but do not normally affect compatibility in the realm of blood transfusions.
As a result, there are eight blood types: A, B, AB, and O, each with its own + or – appendix.
Out of the gate, it is important to recognize that people build antibodies against antigens that do not exist within their own systems, and do not mount such defenses against their own antigens (well, they sometimes do, and this is what results in autoimmune diseases, which can be severe or even fatal, as with lupus). The implications of this is that if you have blood type A, you will have anti-B antibodies in your blood and conversely. If you are type O, meaning you have neither A nor B antigens on your RBC’s, you have both anti-A and anti-B antibodies floating around.
Things are the same with the Rh-factor. If you are Rh-negative, your bodies produce anti-Rh antibodies. These can cross the placenta, meaning that if an Rh+ male mates with an Rh- female and the fetus turns out to be Rh-, the fetus–if Rh+, the genetically likely outcome–can be attacked by the potential mother’s circulating anti-Rh antibodies. This is the reason underlying the early-term administration of RhoGAM, which consists of anti-Rh antibodies that work in a seemingly paradoxical fashion: given to Rh- pregnant women, they desensitize the woman’s own response to the presence of an Rh+ fetus and prevent hemolytic disease of the newborn, which would otherwise kill at least 10,000 brand-new babies every year in the U.S. alone.
So, breaking things down, it’s easy to see why certain blood types do not mix. My own very common blood type is O+, which means that I could donate to anyone who is type A, B, or AB (since there is nothing for their anti-A or anti-B antibodies to attack) as long as the recipient is also Rh+. This is why people with blood type O- are called “universal donors.” Similarly, someone who is AB+ makes no antibodies to anything relevant, and is thus a “universal recipient.”
These factors are nicely summed up in this graphic:
You might rightfully wonder why someone with, for example, type-O blood–whose serum contains type-A and type-B antibodies–can be given harmlessly to those with various other blood types, since the donor blood could theoretically antagonize the RBC’s of the recipient. For whatever reason donor antibody-recipient antigent reactions are negligible compared to the parallel reverse situation. More importantly, when people receive blood, it is usually in the form of “packed RBC’s,” meaning that the serum of the donor–and along with it, all antibodies–has been stripped out and that only RBC’s themselves are given. Nevertheless, for other hematological reasons, the possibility of graft-versus-host disease exists and remains an important consideration in the transfusion milieu.
I wrote this post almost entirely off the top of my head, so it may not be entirely trustworthy. If I glitched anything, I trust that someone will correct me. But the bottom line is that your blood type not only needs to be a part of your medical record, but is also something you should know yourself. In my experience, most people have no idea. So don’t get into a car crash or other evil, unpredictable situation if you are among the unknowing.
|I wrote recently about my mother’s Golden Retriever, who turned nine in September, being diagnosed last month with Lyme disease and experiencing the rapid antibiotics-induced improvement typically seen in dogs and people in whom the illness is caught early. Unfortunately, she’s really fallen apart in recent days and is now in a Portsmouth veterinary hospital.
I haven’t seen her since last weekend or so, but evidently she had some lethargy that quickly went from mild to incapacitating, and, alarmingly, had an eye went from normal in appearance one day to 100 percent bloodshot the next.
My mom rushed her to the vet, who drew blood and took X-rays an in turn sent them along to where she now rests. In addition to the ophthalmological issue, she was found to be anemic (very weird since she was recently placed on an all-meat diet), febrile, and dehydrated. She also had abdominal tenderness, and the X-rays revealed some arthritis in her spine (possibly unrelated to everything else, given her age and breed).
From what little knowledge of medicine still lingers in my chemically damaged brain, I would have to think that a multisystemic problem like this is almost as likely to be autoimmune as infectious, but the seemingly rapid onset and the fever still point to something infectious. The fact that the doxycline she’s on obviously hasn’t cleared things up suggests a misidentification of the causative agent, an idea supported by a few things Nubble’s vet mentioned about the blood test that resulted in a diagnosis of Lyme.
Anyway, she’s in good hands know and being seen by various specialists. This poor dog, naturally, is the sweetest animal you could ever meet and never objects to the various tests she is subjected to or behaves in a surly way even when she is clearly under duress. And it’s a shame she can’t vocalize exactly how this has all progressed from a subjective standpoint.
Why can’t things like this, if they have to happen at all, strike animals like Michael Vick instead?
I live less than a half-mile from my parents and their recently-turned-nine Golden retriever, Nubble.
When I first moved back to New Hampshire almost a year ago, I, lacking a dog of my own, immediately appointed myself Nubble’s unofficial recreation director. She had never been a runner, with her daily exercise generally consisting of a walk of close to a mile through Bellamy Park. Within a month or so I was–while recognizing that she was no young Komen–taking her for about four runs a week, covering anywhere from about two miles to as many as five or six. She loved the work, it seemed (working-class breeds are about the only dogs worth having) but I was worried to some degree about her age and overtaxing her.
By mid-summer, I had tabled the idea of running Nubble thanks to the heat and, having scaled back to daily walks, stuck with her and other retrievers’ primary love, swimming. But in August, something started going wrong. One day, out of the blue, as we started out the door, Nubble displayed a limp, clearly favoring her left hindleg. I couldn’t think of anything she’d stepped on or otherwise done to bring this on. In any case, this precipitated a visit to the vet, who, after an X-Ray, believed that Nubble might be suffering from a damaged anterior cruciate knee ligament (actually the cranial cruciate ligament in dogs, but whatever). She was tentatively scheduled for surgery, but then showed a remarkable resurgence over a period of days, calling into question the diagnosis and radiography.
Several weeks later, Nubble experienced a relapse of her symptoms and had a lot of difficulty just getting up from the floor to say hello when friends arrived. It seemed that she might have just been getting older and manifesting the “retriever hips” and rheumatoid arthritis that strike a lot of older, heavier dogs. So, with surgery having been ruled out as an option, Nubble began a completely changed dietary regimen, and started a course of Rimadyl (carprofen, a veterinary NSAID), which essentially functioned as a miracle drug for a few weeks. She also started undergoing biweekly acupuncture and was given a couple of herbal-type medicines.
A couple weeks ago, when I was in Colorado, Nubble decompensated dramatically over the course of a day. She would not even come downstairs for breakfast, which is hardly her style. Both hindlegs had become almost useless. My mom took her to the vet that morning, and the doc noticed that Nubble was extremely feverish ( I would never pick this up in a dog, but then again I’m not exactly a veterinarian).
Every year, as part of her general care, Nubble receives the Lymevax vaccine to prevent against Borreliosis, better known as Lyme disease and involving a vexing range of symptoms, ordinarily starting with arthritis but potentially involving a a host of organ systems. I had believed for some reason that Lyme–transmitted by Ixodes deer ticks and, in humans, sometimes involving a characteristic roundish rash at the site of the tick bite–was not much of a factor in New Hampshire. I was wrong.
Despite Nubble having been vaccinated, it seemed clear to her vet that she was suffering from Lyme disease. The doc gave her doxycylcine, also the treatment of choice in humans, and promised that she would be at least 75% better within a day. She was.
Nubble’s blood test did not suggest that she was infected with the causative agent, a spirochete known as Borrelia burgdorferi. But there are are multiple strains of the bacteria as well as issues with the serology itself. The ELISA screening test is roughly 70% sensitive, meaning that a third of cases might be missed. If someone is flagged as infected (as determined by the presence of antibodies to a particular bug, which is what the ELISA test–also used for HIV and other nasties–is all about), then a Western blot, derived from the polymerase chain reaction, can be used to confirm. But absent an initial positive, all a practitioner has to go on is intuition. Thankfully, Nubble’s vet is uncommonly sharp.
Now, she’s as frisky as I have ever seen her. She’s be on the doxycycline (which I keep wanting to call “dogsy-cycline”) for a while longer, but she has her legs, mobility, and life in general back, and never stopped being the sweetest dog you’ll never meet anyway.
I really don’t have to editorialize any further than I have in the post title. Anyone who doesn’t think that Christopathy doesn’t threaten greater American society need only read this to receive a wake-up call.
The Alliance Defense Fund is seeking permission to intervene in a court decision ordering the Food and Drug Administration to sell the “Plan B” pill to minors.
The Plan B pill, otherwise known as the “morning-after pill,” is a very strong dose the same hormones used in oral contraceptive pills. Some doctors believe it could cause an abortion to an expectant mother. Matt Bowman is an attorney with the Alliance Defense Fund.
“This is a case where pro-abortion activist groups have put their political agenda over the health of minors by attempting to force a court to expose them to a troubling drug,” he contends.
Bowman says there is no research on what potential medical problem the Plan B pill might cause for a minor. He adds that most minors who take the pill do so without parental knowledge.
First. let me say that I understand that groups like this one do not speak for most people who call themselves Christians. Even those who are personally opposed to birth control and drugs like Plan B would not interfere with the rights of others to use them. I’m targeting a particular, and virulent, subset of the flock with these observations.
With that out of the way: The claims made by the Alliance Defense Fund are, as usual, high-octane unadulterated bullshit. First of all, anyone who uses the term “pro-abortion” immediately discredits himself. No one likes abortion. But for a host of well-established reasons, the choice must remain.
As a result of a March court decision, 17-year-olds can buy Plan B over the counter. Girls under 17 can only get a prescription form of the drug, consisting of the synthetic progestin hormone levonorgesterel.
Beyond that, this idea that Plan B “could cause an abortion to an expectant mother” is screamingly incoherent. For one thing, Plan B is not an abortifacient–it prevents implantation from occurring at all. For another, how many expectant mothers–that is, pregnant women who hoped to carry to term–would take this drug? Do men sworn to celibacy seek prescriptions for Viagra?
Then there’s the implicit claim that particular risks to minors are likely to exist. This is asinine. All ovulating females would be expected to react to the same way to this medication. The idea that teenagers would tolerate a dose of Plan B more poorly than older women is nothing but special pleading aimed at achieving he ends of cross-eyed Bible-boppers. Besides, it’s not as though this is a maintenance drug–it’s a one-shot deal, for obvious reasons.
The Alliance Defense Fund is unabashedly interfering in women’s health issues, and doing so with the usual freshets of lies. If its members have an aversion to Plan B, then they can simply not take it, and they can shut the fuck up about what’s supposedly good for everyone else.
Of course, they’ll get nowhere with this from legal standpoint, but it’s the thought–and the intent–that counts. These people are assholes who remind the world of two unyielding truths: Christheads venture into areas where they don’t belong, and Christheads lie with aplomb.
Hey! Do you know what’s REALLY driving up the cost of health care in the USA? Why, according to Douche Limbaugh, it’s people who exercise! Yep. People interested in fitness are responsible for expensive health care. See if you can follow this “logic”
Apparently, Douche can’t tell the difference between the costs of one-time acute injuries such as a sprained ankle and long-term chronic maladies such as heart disease and the complications associated with them. And let’s not even get into the whole quality-of-life thing.
But when you’re a doughy Oxycontin abuser I guess it makes perfect sense. One thing I will say about Douche, he knows his audience. I’m sure there aren’t many “fitness freaks” in that group. And what’s with his not-so-thinly-veiled jealousy that I hear about injuries being a “badge of honor”? I’ve known a great many athletes who have been injured and not a single one of them is in any way proud of their injuries. In fact, injuries do nothing but frustrate the athlete. I’d go so far as to suggest that, at least to many distance runners, “injury” is almost synonymous with “I was stupid”.
That the diagnosis of Crohn’s disease eluded this girl’s doctors for eight years is far more remarkable than her diagnosing herself thanks to histological evidence she uncovered while in Biomedical Problems class (must be nice to have access to such a course as a high-schooler). Still, this is a hell of a story.
For eight years, Jessica Terry suffered from stomach pain so horrible, it brought her to her knees. The pain, along with diarrhea, vomiting and fever, made her so sick, she lost weight and often had to miss school.
Her doctors, no matter how hard they tried, couldn’t figure out the cause of Jessica’s abdominal distress.
Then one day in January, Terry, 18, figured it out on her own.
In her Advanced Placement high school science class, she was looking under the microscope at slides of her own intestinal tissue — slides her pathologist had said were completely normal — and spotted an area of inflamed tissue called a granuloma, a clear indication that she had Crohn’s disease.
You can watch her talk about her experiences in this video.
There are allusions to “bonobo scat spattered walls” here at the Refuge. Time to go one better. I am scheduled for a colonoscopy tomorrow. This will be my second such procedure so I have an idea of what to expect. I haven’t found any problem with the procedure itself, but the prep is tad, shall we say, messy. Here’s what it looks like:
Three days prior, no more fresh fruit or vegetables, and no nuts. This kills me because that’s about one third of my diet. OK, so I can live on canned fruit for a while, but morning cereal without my usual blueberries, strawberries, etc. is depressing. Oh, and no dried fruit stuff either due to skin and/or seeds. There goes more snack food.
So now the “fun” stuff. The day before the procedure (today) it’s a clear liquid only diet. And Jell-O. Joy of joys. At 2 PM I am to take 2 Dulcolax tablets to “get things moving”. At 6 PM, I am instructed to mix an entire 238 gram bottle of Miralax in a 64 ounce bottle of sports drink (I chose lemon-lime) and drink 8 ounces every 10-15 minutes until it’s finished. So that’s nearly two liters of laxative-spiked Gatorade in maybe an hour and a half. Here’s the part I love on the instruction sheet: “Expect everything you drink to pass through the rectum”. That’s an understatement. If past experience is any guide that should read “Expect everything you drink to rocket out of your anus at near hypersonic velocity. You may wish to flush mid-rifle to ensure that the bowl doesn’t overflow.”
And just in case that’s not enough, it’s two more Dulcolax tablets at 8 PM.
I think it would be easier if they just had you sit on a firehose. If there’s anything left in there after this procedure, I’d have to guess that it’s welded in place.
Obviously, there’s nothing to eat or drink after midnight. In fact, that’s one of the first things they ask when you check in: “Have you had anything to eat or drink since midnight?” The instructions are quite explicit, so asked if anyone ever answered “yes” to that query. The nurse said that it sometimes happens, and in fact, one fellow answered “Yes, I had a chili-dog for breakfast this morning.”
Needless to say, his procedure was cancelled for that day.
…the fact that most overweight people regain most or all weight they lose does not imply that it carries no health risks or that weight loss just isn’t possible for some people. If you carry on certain behaviors that promote slimming, than abandon them and return to old ones, of course you’ll get fat again. That’s common sense.
I write this because of a passage in an otherwise excellent posting about quackery and its shoddy label, “evidence-based medicine”:
I am broadly sympathetic to Paul Campos’ claim that medical guidelines on obesity tell you much more about the attitudes towards fat in the upper middle class social stratum that doctors occupy, than about reliable scientific evidence on same.
But policy demands certainty. And so you get obesity guidelines advising everyone to diet and excercise to shed their excess pounds, even though it’s as close to a scientific certainty as anything is that most people simply regain any weight they manage to diet off. And you get absurdly precise economic forecasting, even though in many cases, the better answer would be “who knows?”
Perhaps a lot of doctors and others are biased in favor of alarmism to some extent, and carry around prejudices. However, one can’t just throw out all of the unequivocal evidence that extra weight is a health hazard just because white-coats rub you the wrong way. Paul Campos is a crank and has been for years.
An article published yesterday on Scientific American’s Web site deals with a phenomenon that underscores just how many ways an especially advanced mammalian forebrain can misfire, and and this case the consequences are far more dramatic, and overtly pathological, than the presentation.
In [body integrity and identity disorder] (BIID), or apotemnophilia, individuals say that a limb, or part of it, feels “intrusive” or “over-present.” They usually report that they have had the desire to remove the limb since early childhood, but do not understand why. This desire can be so strong that they sometimes resort to damaging the limb irreparably, thus forcing doctors to amputate it. Almost all BIID sufferers have no other psychological disturbances, and almost always say that they feel much happier when the limb is eventually amputated.
Insanely, this kind of behavior has hitherto been regarded as perhaps faddish or at least self-indulgent:
Voluntary amputation, for example, [has been] regarded as a fetish, perhaps arising because an amputee’s stump resembles a phallus, whereas imaginary extra limbs were likely to be dismissed as the products of delusions or hallucinations.
Things are changing in the neurological community.
Paul McGeoch of The Brain and Perceptual Process Laboratory at the University of California, San Diego, and his colleagues tested the hypothesis that BIID occurs as a result of abnormal activity in the right SPL. They recruited three male BIID sufferers (apotemnophiles) who expressed a desire to have their left leg amputated, and a fourth who wanted both legs removed. The researchers tapped the participants’ feet with a bundle of fiberoptic filaments, while recording the electrical activity of their brains using magnetoencephalography (MEG). Their responses were compared with those of four controls.
In the controls, tapping either foot caused activation of the right SPL. In the three apotemnophiles who wanted one leg amputated, tapping the unaffected foot evoked a response in the right SPL, but tapping the affected one did not. In the fourth apotemnophile, neither foot evoked a response. These findings, which are published in Nature Precedings, confirm the researchers’ hypothesis. They suggest that the brain does not register the limb as a part of the body, and contains no representation of it. As a result, the limb is not incorporated into the body image, so the apotemnophile has no sense of ownership over the limb–he feels that it does not “belong” to him, and so wishes to have it removed.
The Atlantic Monthly published an article about this over eight years ago. The medical findings and the response of scientific minds to them are fascinating in both the more recent piece and the one from a half-decade ago.
Under 200. That’s the usual target for total cholesterol as reported in popular media. But are all 200s the same?
I just received my profile from a recent blood test. Here’s what it said.
Total cholesterol: 204
LDL (bad cholesterol): 131.6
HDL (good cholesterol): 57
The total is computed as LDL+HDL+Tri/5. These are fairly typical numbers for me as compared to the last half dozen years, although my HDL usually is a few points higher and my LDL and tri usually are a few points lower. This 204 would normally place me at borderline high. However, my doctor is not very concerned, and neither am I. Why?
First of all, I have only one risk factor (being a male over age 45). Second, my HDL is on the high side for men my age and this leads to a favorable LDL/HDL ratio of only 2.3. Further, at 5’10” and 142 pounds, my BMI is about 20.5. As an avid runner, my resting pulse is in the low 50s, my blood pressure is typically 110/70 (and sometimes as low as 105/60), and a recent echo cardiogram showed no problems. OK, so what’s the beef? Surely mitigating factors and health status need to be considered instead of a single number, right? Yeah, but there’s more to it than that. It’s an unfortunate but true observation on my part that people tend to focus on the one number and that number can be misleading. I know a lot of people who can recite their total cholesterol value but have no idea of the “numbers inside”. I doubt that they are atypical.
Consider two men with minimal risk factors, Ralph and Larry. For the sake of simplicity, let’s assume both have a triglyceride value of 75. Ralph’s LDL and HDL are 140 and 30 while Larry’s are 125 and 65. Ralph’s total cholesterol is 185 while Larry’s is 205. If we just look at the total, Ralph seems to be in a much better position than Larry, yet Larry’s LDL is considered safe while Ralph’s is borderline high, and similarly, Larry’s HDL is considered protective of heart disease while Ralph’s is definitely too low.
Knowing the tendency of folks to “like it simple”, I wonder why there isn’t a single “cholesterol index” that could combine these considerations. Why do we bundle all forms together when high HDL is considered protective, yet it raises the “scary” total? It seems that a fudge factor could be added for the LDL/HDL ratio (just like there’s one for triglycerides). I think it would be a little easier for people to grab onto, and then their doctor could look at the numbers inside and the patient’s lifestyle, and offer the most promising strategies to combat a too-high index.
Oh, and my doc says I should probably watch my diet a little closer. I tend to agree as I do have a tooth for the cookies.
The treatment could boost cup size while reducing stomach fat. It involves extracting stem cells from spare fat on the stomach or thighs and growing them in a woman’s breasts. An increase of one cup size is likely, with the potential for larger gains as the technique improves.
Professor Kefah Mokbel, a consultant breast surgeon at the London Breast Institute at the Princess Grace hospital, who is in charge of the project, will treat 10 patients from May. He predicts private patients will be able to pay for the procedure within six months at a cost of about £6,500.
Although the stem cell technique will restore volume, it will not provide firmness and uplift.
The cells will be isolated from a woman’s spare fat, once it has been extracted from her thighs or stomach, using equipment owned by GE Healthcare, a technology company. The concentrated stem cells will then be mixed with another batch of fat before being injected into the breast. It takes several months for the breast to achieve the desired size and shape.
Until now, when fat was transplanted to the breast without extra stem cells, surgeons had difficulty maintaining a blood supply to the new tissue. Surgeons believe the double concentration of stem cells under this technique promotes the growth of blood vessels to ensure a sufficient blood supply circulates to the transplanted fat.
Evidently this has been going on in Japan for a half-dozen years.
As reported on Science Daily, researchers in Switzerland have found that the equivalent of two cups of coffee blunts the increase in blood flow to the heart muscle itself that occurs with exercise, and that the effect is increased at conditions simulating high altitude. These findings (free full text) were part of a study published over three years ago in the Journal of the American College of Cardiology. I have no idea why mention of it appeared in one of my news feeds just yesterday, but it’s interesting enough to warrant comment.
The researchers, including lead author Mehdi Namdar, M.D., F.A.C.C., studied 18 young, healthy people who were regular coffee drinkers. The participants did not drink any coffee for 36 hours prior to the study testing. In one part of the study, PET scans that showed blood flow in the hearts of 10 participants were performed before and immediately after they rode a stationary exercise bicycle. In the second part of the study, the same type of myocardial blood-flow measurements were done in 8 participants who were in a chamber simulating the thin air at about 15,000 feet (4,500 meters) altitude. The high-altitude test was designed to mimic the way coronary artery disease deprives the heart muscle of sufficient oxygen. In both groups, the testing procedure was repeated 50 minutes after each participant swallowed a tablet containing 200 milligrams of caffeine, the equivalent of two cups of coffee.
The caffeine dose did not affect blood flow within the heart muscle while the participants were at rest. However, the blood flow measurements taken immediately after exercise were significantly lower after the participants had taken caffeine tablets. The effect was pronounced in the group in the high-altitude chamber.
Blood flow normally increases in response to exercise, and the results indicate that caffeine reduces the body’s ability to boost blood flow to the muscle of the heart on demand. The ratio of exercise blood flow to resting blood flow, called the myocardial flow reserve, was 22 percent lower in the group at normal air pressure after ingesting caffeine and 39 percent lower in the group in the high-altitude chamber. Dr. Kaufmann said that caffeine may block certain receptors in the walls of blood vessels, interfering with the normal process by which adenosine signals blood vessels to dilate in response to the demands of physical activity.
“Although these findings seem not to have a clinical importance in healthy volunteers, they may raise safety questions in patients with reduced coronary flow reserve, as seen in coronary artery disease, particularly before physical exercise and at high-altitude exposure,” the researchers wrote.
On the surface, this comes as a surprise to those of us who routinely load up on coffee before endurance training and competitions. In fact, I can’t name on personal-best time from the mile to the 50K that did not involve some amount of caffeine ingestion beforehand.
I can, however, make a reasonable hypothesis about these results. Coronary arterial blood flow, unless severely compromised by stenosis or spasm, would not be a limiting factor in exercise, especially in untrained persons like the ones in this study. In people free of airway obstruction and anemia, the limiting factor in exercise is likely to be end-organ utilization; that is, people’s muscles are not sufficiently dense in mitochondria to process all of the oxygen delivered to them. Aerobic training increases both mitochondrial density in working muscles and the enzyme activity associated with aerobic metabolism, but either this or oxygen delivery to active tissues generally remain the limiting factor in performance.
Ventilation even at fast (aerobic) running speeds supplies the body with more than the full amount of oxygen it can out to use, at least at sea level; this oxygen very quickly diffuses across the alveolar membranes in the lungs and saturates available red-blood cells. Athletes can remove the limitations imposed at this point in the chain by taking banned “blood boosters” such as erythropoetin (EPO) and its synthetic derivatives; when highly trained people do this, the limiting factor in their exercise output is generally regarded as “substrate failure”–again, a concern within the working muscles themselves.
Throughout all of this, the heart is pumping perhaps up to 10 percent of its own output to itself in order to sustain near-maximal aerobic effort. Simply put, coronary artery blood flow would have to decline significantly in order for this to become limiting, and this is in trained people. Healthy normals like the 18 subjects in the study would never notice the difference.
Anyway, you’ll pry my coffee out of my cold, dead fingers long before you’ll see me give it up for fear of negative cardiac consequences, with or without competitive running in the mix.
The NY Times has an article about a study suggesting people who drink a lot and get red in the face when they do it may have a high risk of esophageal cancer.
Many people get flushed when they drink alcohol because of general dermal vasodilaton, but this article concerns a special class of people who are deficient in the enzyme ALDH2, or aldehyde dehydrogenase. Normally, ethyl alcohol is broken down into carbon dioxide and water in a series of oxidation reactions: ethanol –> acetaldeyde –> acetic acid –> CO2 and H2O. ALDH2 is responsible for the second step in this chain, meaning that people who lack it altogether experience a build-up of acetaldehyde in their bodies, with extremely unpleasant results. In fact, the drug disulfiram (Antabuse), sometimes given as a drinking deterrent, acts by inhibiting ALDH2 activity. (Side note: in the case of methanol poisoning, ALDH2 oxidizes formaldehyde into formic acid, an extremely retinotoxic substance. This is why people who mistakenly drank “wood alcohol” in days of yore would often go blind a couple of days later.)
Many East Asians are affected by this enzyme deficiency. People who are homozygous for it have a lifelong, built-in “Anatbuse reaction” and can never drink. Heterozygotes, on the other hand, can eventually reach levels of chronic consumption rivaling any other imbiber’s, and these are people mentioned in the article as being at risk for esophageal CA.
The malignancy, called squamous cell esophageal cancer, is also caused by smoking and can be treated with surgery, but survival rates are very low. Even moderate drinking increases the risk, but it rises sharply with heavier consumption. An ALDH2-deficient person who has two beers a day has six to 10 times the risk of developing esophageal cancer as a person not deficient in the enzyme.
It’s not clear from the article whether the mechanism for the increased risk among ALDH2 people has been elucidated, but my guess is that it hasn’t.