I’ve been meaning to make this video for a long time, and finally got all the pieces together. I’m obviously not a video editor, but I’m learning. Feel free to share this with any family or friends who you know who are having, or have had a breast biopsy. This video would be good preparation for their appointment in regard to asking pertinent questions and more efficiently addressing their concerns.
If there are any other medical topics you think might be worth a similar treatment, let me know; and maybe I’ll get around to it :^l
This is my October contribution to the NWTC Newsletter, What’s Cooking. Since it is October, I saw no harm in a little morbidity.
We’re all gonna die! Someday. That’s an obvious given, a constant, the elemental fact of life with which we will be confronted. One day. That momentous day, in which the age-old question that has plagued mankind subsequent to the onset of sentience is answered—is there a God; is there a spiritual realm in which I will have an awareness of; will I find St. Augustine’s Eternity? The problem is; you won’t be able to tell anyone else the answer. No, that glorious answer belongs to you alone, and all the antecedent arrivals to the hereafter.
The Mayan “Long Count” calendar wraps up a 5,126 year era on 21 December, this year, in a few months, and is supposed by some to mark the end of the world as we know it. How the end comes is anyone’s guess; perhaps it’s a collision with a planet called Nibiru en route from the star V838 Monoceros;
Monocerotis, from where Nibiru is coming (courtesy of NASA)
or, perhaps it’s a collision with one of a thousand (that we know of) Near Earth Objects (NEO) that are already in the neighborhood. Well, 5000 years doesn’t seem all that significant against the backdrop of a 4.5 billion year-old earth, and the chance of a planetary collision is less likely than me winning the Powerball, and what do a bunch of extinct old Mayan’s know anyway. Therefore, before sinking into the Paranoia of these end-of-the-world scenarios, perhaps we should focus on the more common causes of our material end.
I knew a neurosurgeon where I trained who never drank out of an aluminum can because he thought he’d get Alzheimer’s despite the lack of medical evidence for a causal relationship—but, he is a neurosurgeon, which makes one go…hmmm. After all, Alzheimer’s is the eighth most common cause of death in the U.S., which makes that frosty can of MGD on a blistering summer day behind a fishing pole on a stone beach radiating shimmering waves of heat look less appealing…okay, not really—but then, I’m not a neurosurgeon either. Alright, let’s consider causes of death one, two and three; heart disease, cancer, and cerebrovascular disease (stroke), which accounted for 60% of all deaths in 2000. Let’s further consider some of the most common causes of cancer; breast, colorectal, endometrial, kidney, ovary, lymphoma, and pancreatic, the first three for which a link to obesity has been firmly established, and the remainder for which there at least seems to be an association.
The sixth most common cause of death is diabetes mellitus of which type II is also strongly associated with obesity. The fifth most common cause of death are unintentional accidents, an example being like going for an innocent bike ride on a beautiful day and suddenly finding yourself launched head-first into space with the overwhelming thought…is this my day? (Ahem…true story—last Memorial Day)
So, it is clear that there’s plenty to be paranoid about, if not fearful, unless you face the thought of death with the equanimity of a saint, unless you are a saint. Not being a saint, I admit to finding myself a few degrees to either side of fearful, depending on the day, my mood, and whether or not I’ve attended church lately. But, if you want to exert a force towards longevity and delay of that momentous day, it is clear where your efforts should be focused—not on avoiding beverages in aluminum cans, but on defeating obesity, given the well-documented link between it and heart disease, diabetes, cancer and stroke; and by only riding your bike on flat grassy fields.
Now all those things seem rather mundane and common (maybe because they are), and much less dramatic than a planet called Nibiru colliding with the earth; but at least they are things we have some control over. Still…I’ve noticed that my exposure to aluminum cans has fallen, and I did notice a particularly bright star in the sky the other night, and I do have a Mossberg 12 gauge leaning in the corner with four shells in the tube, and a pile of nonperishable food in the basement next to my beer-fermenting carboyl for December 21st when the world goes crazy because I’m no saint, and don’t plan on going gentle into that good night.
And you thought I was kidding.
My August contribution to the NWTC newsletter, “What’s Cooking.”
Although brilliant, he was not known as a tidy researcher, and so, when leaving for an August holiday with his family it seemed of no particular significance that he should leave a stack of petri dishes in a dusty corner of his laboratory, an irregular glass pillar of staphylococcus bacterium subject only to the barely perceptible currents of air in a closed room, and neglect. The month of August in London is a warm month; had it been January, perhaps the dust blown through a loose pane would not have been so heavy with fecundity; as it was, the month was August, and the warm particles of dust were heavy with a fecund ripeness of portent as they wafted lazily towards the pile of glass in a forgotten corner.
One month later, he approached the pile of culture plates, much as he would a stack of dirty dishes, with reluctance and a pang of mild regret for having not done them before he left on vacation. As he reached for the plate on the top, most exposed to the air, he noticed three dark purplish spots, scattered amongst the coalescing colonies of staphylococci, around which there was a ring of…nothing. The day was September 3rd, 1928.
Alexander Fleming recognized the antibacterial nature of the purple spots, and published his findings in the British Journal of Experimental Pathology in 1929, where the discovery languished for the next decade, a few sheets of printed paper buried amongst shelves and shelves of those dusty periodicals found only in a smattering of academic institutions of industrialized countries across the world. By 1939, Sir Alexander abandoned his research of the Penicillium mold after failing to find a chemist skilled enough to refine the active agent.
On a Saturday, May 25th of 1940, another researcher, Dr. Howard Florey, a subscriber to the Journal of Experimental Pathology, tested eight mice that were injected with a lethal dose of streptococci bacteria. The four mice that received the penicillin his team had extracted from the Penicillium mold lived. The four controls that didn’t receive penicillin did not. In 1941, the first human received penicillin after suffering an infection from a rose thorn, and in 1943 Dr. Florey traveled to North Africa to test penicillin on wounded soldiers. His results were hailed as a miracle.
The popular antibiotic, Augmentin, was developed by SmithKline Beecham in the seventies, a US patent filed in 1979, a patent granted in 1984, and the drug first sold in the nineties, nearly twenty years later. Although the FDA was created in 1936, it wasn’t until the 1960’s that its role was expanded in the premarket approval process, driven by the thalidomide tragedy in which thousands of European babies were born with deformed limbs after their mothers ingested the drug for the treatment of nausea.
In 1940, Penicillin went from the lab bench to practical use in the battlefields of Northern Africa three years later. In 1977, Augmentin began the FDA premarket approval process to achieve practical use some twenty years later.
It is now 2011, and modern medicine is running out of antibiotics. There are few new drugs in the pipeline, and invisible bacilli and cocci are multiplying and dividing in a most fecund and Darwinian fashion, developing resistance to the antibiotics developed since the first serendipitous sticking of a penicillium mold spore to one of Dr. Fleming’s culture plates while he was away on vacation.
There are strains of the common skin bacterium, Staph aureus, now resistance to Vancomycin, which had been used to treat the S. aureus that was resistant to Methicillin, which had been used to treat the S. aureus that was resistant to Penicillin. One strain of the innocuous gut organism, E. coli, is resistant to at least 14 antibiotics—the same strain that killed dozens of people in Europe this past spring, and caused the hospitalization of hundreds more. Some of these virulent strains of E. coli release a Shiga toxin that causes bloody diarrhea and kidney failure; and the common antibiotic, Cipro, can make it worse because it triggers a massive release of the toxin as the bacteria dies; fortunately, there is another antibiotic that does not cause a release of the toxin, and that the antibiotic is not resistant to…yet.
So, as we swim through the omnipresent microbial soup in our own Darwinian pursuit of longevity and procreativity, it is important that you minimize your risk by practicing good hygiene; washing your hands, doing your dishes in a dishwasher or fresh hot water with detergent, cleansing your produce, and growing your own if so inclined. You can avoid needless exposure to antibiotics, and if you suffer a bad case of bloody diarrhea while on a trip overseas, don’t take the Cipro you’ve brought with for just such an occasion on the outside chance it might trigger the release of a lethal dose of Shiga toxin.
I stumbled across an article in a German medical journal that reviewed strength training in the elderly. Well, over half my patients probably fall in the category of “elderly,” so, I thought I’d summarize it briefly here. I addressed this in my book, and the conclusions reached in the article reaffirm my argument for resistance training as an important component of fitness across all age groups, and gender.
The review covered medical studies over the past five years that collectively totaled thousands of participants.
Without strength training, we begin losing muscle mass from our 30th year to our 50th year in a gradual fashion, but, from 50 years of age and on wards there is an acceleration of lean muscle mass of 15% per decade, which may approach 30% by the 8th decade. Currently, only about 10-15% of the elderly do resistance training, which is unfortunate.
A common misconception is that there are significant side effects to resistance training in the elderly, most commonly that of musculoskeletal injury; however, in the studies reviewed, the adverse effects of exercise didnt’ seem to be commonly reported.
The studies show that resistance training will reverse the age-related loss of muscle tissue, increase bone density, counteracting to some extent osteoporosis, and can even decrease the symptoms of fibromyalgia.
So, then, how much exercise?
Three times a week; 3-4 sets of 10 repetitions per muscle group at an 80% intensity of what you can lift with one repetition.
I would suggest working with a trainer, to get started, at the YMCA, or other local fitness center; especially if you’re a bit short in the weight-lifting experience department. I’ve read other literature that suggests that multiple sets are not necessary if the first set it performed to muscle failure, and that subsequent sets are of diminishing return.
Resistance training does not have to mean free weights, although three are convenient dumbbell stacks in which you can dial a specific weight. Other options would include a set of resistance bands of varying resistances, and of course a circuit weight machine (not free weights).
I think that a lot of elderly folks, especially women, discount the importance of resistance training, as a tool for improving the quality of life of those golden years.
Weight management, aerobic exercise, and strength training are all components of a healthy lifestyle, longevity, and quality-of-life.
The telomere test for approximation of your biological age has been getting some press lately, so I thought I’d research it a bit and make it the topic for June’s NWTC “What’s Cooking” newsletter.
I’ve been interested in telomeres for a few years because of their relationship to aging.
Have you checked your telomeres lately? Do you need to? What the heck are telomeres?
There is a new test that you will soon encounter in the mass market media. The advertisement will read something like, “How much longer will you live,” or maybe, “Find out when you’re supposed to die.” Or, perhaps it will be more positively framed as something like, “Find out your biological age, and how to prolong it.” The test will require a blood sample (possibly saliva) and a payment of about $300, give or take. I’m guessing that the additional information, regarding the prolongation part, will be extra, likely having to do with daily supplements, specialty foods or other allegedly crucial interventions.
The telomere test is a provocative melding of actual science and the various human emotions in orbit around the all-too-real planet of our individual mortality. You have to admit that each of us has, at least to some extent, a morbid curiosity of if not the actual end-of-days, at least our own end-of-day; and, the desire to somehow impact it. This is what some selling the telomere test will promise—a calculation of your biological age, and how to prolong it…by taking vitamins, increasing physical activity, avoiding weight gain or obesity, and correcting insulin resistance (diabetes).
Telomeres are like protective caps on the end of chromosomes, and when the wear out, cells stop dividing and eventually die; so, long telomeres are good and short ones are less good, unless you’re 120 years-old, in which case short ones are expected; or so the argument goes. Of course, it’s not that simple, or predictable for a host of reasons. Let me explain.
You have 23 pairs of chromosomes (46 total) in each cell in your body. Each chromosome is made of your DNA that is specific to you alone in all the universe, unless you’re an identical twin. DeoxyRiboNucleic Acid is kind of like a zipper in that it is made of two matching molecular strands that can unzip and divide into two so that proteins in the cell can assemble new, matching strands so that where there was one, there now are two. This works because each zipper strand has four different kinds of teeth (nucleotide base pairs) call them A, C, G, and T. Each tooth will match up with only one other: G with C, and A with T. And it is the specific sequence of the base pairs that encodes specific genes, like blond hair and blue eyes, or risk of colon and breast cancer. Some genes might have only a few base-pairs, and others, thousands.
23 pairs, 4 different kinds of nucleotides, only two matching pairs—doesn’t sound like big numbers; but, each chromosome can contain up to 10 billion base pairs in a twisted tangled chain. 46 invisible threads in an invisible nucleus in an invisible cell that tell us what we are, if not who. Pretty amazing stuff; and all supposedly arising from a lightning bolt striking a primordial soup long ago; or God—it’s your choice.
The problem with cell division is every time the DNA unzips you lose 30-150 base-pairs off the ends. It’s called “the end replication problem.” Since the telomeres serve as the protective caps, losing a hundred pairs is no big deal—the gene sequences remain safe on the inside as the telomere sacrifices a little bit of itself. The telomeres have about 10,000 base pairs, which comes to 66.6 (10,000/150) cell divisions before they wear out and die.
The age-related diseases; cancer, diabetes, atherosclerosis and heart failure have all been associated with shorter telomere length; as are also obesity and smoking. The question is, do short telomeres cause all this bad stuff; or, does all this bad stuff cause shorter telomeres?
In these studies of associations, and the telomere test itself, it is the White Blood Cell (WBC) whose telomere is being measured. All of our other cells (brain, heart, etc.) have telomeres too, which are widely variable at birth and across population groups; but, they are much harder to sample for obvious reasons, as opposed to a finger stick for a tiny drop of blood. Perhaps the WBC telomeres are more a marker of inflammation, which is the root cause of the metabolic syndrome, diabetes, heart disease, and many types of cancer. Perhaps the telomere test is more a marker of lifestyle choices, the results of which should be no surprise, than it is of longevity.
I don’t think the telomere test is ready for prime time. There are too many variables and too many assumptions; and more importantly, what will it tell you that you don’t already know: that you should stop smoking, lose weight, and control your blood sugars if diabetic? Well, let me say it then. Stop smoking, lose weight, and control your blood sugar. That will be $300 please, and you didn’t even have to give me a blood sample.
Additional Online Only Edition:
The nucleotides in DNA are; Adenine, Cytosine, Guanine, and Thymine; A, C, G, and T; and in humans, the telomere is made of repeating sequences of TTAGGG repeats for a total telomere length of 8-15 kilobase (kb) pairs, or 8-15,000 base pairs. This sequence is shared with mice, rats, and birds; and slime mold has an extra “T” (TTTAGGG). Hmmm…I wonder if there’s slime mold in primordial soup.
The cells in our bodies are called somatic cells; they have differentiated from stem cells into specific cell types; and as such, suffer from mortality, being good for about 50-70 divisions before cell senescence or apoptosis, which basically means cell death or disintegration. In contrast, embryonic stem cells are as immortal as a cell can be in that it has high levels of a protein complex, called telomerase, which can rebuild telomeres; so, in the stem cell, the telomeres don’t wear out. Some cancer cells also have high levels of telomerase, which is a factor in a tumors relentless growth.
Most of the studies drawing age-related associations have been with the telomere length of WBCs, which may be a more accurate measurement of the inflammatory state. The telomere lengths of various organs are widely variable from person to person, and from organ to organ within an individual. Do those individuals with shorter telomeres at birth of the heart cells have a shorter life span than those of an individual with longer ones? Do people that die at a young age from illness have shorter telomeres than age-matched controls?
I think the telomere is a factor in aging, and potentially, eventually, subject to interpretation and intervention for longevity; but at this time the test result is, I think, nothing more than a curious novelty, no more accurate than having your palm read at a carnival.
I’ve posted some sample chapters of The Relativity Diet on the “About the Relativity Diet Page.”
Over the next few days I will be reposting my last three monthly contributions to the NWTC Newsletter, as well as the June contribution; and I think I’ll write about the telomere/knowing when you’re supposed to die issue for July just because it’s something I’ve been interested in over the years–telomeres, which are protective caps on the ends of your chromosomes, and when they wear out, bad things happen; or, maybe not so bad if you believe in God. So, I guess it would be bad for Stephen Hawking who has the view that the brain is really no different than a computer. When it gets old and wears out, it’s just something to be discarded.