Health Spectator

Unfortunately for those of us who appreciate a good steak, there is mounting evidence that red meat consumption may contribute to heart disease and cancer. The American Institute for Cancer Research, in cooperation with the World Cancer Research Fund, of which it is a part, recently released a report, five years in the making, entitled Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective.

The WCRF/AICR report cites evidence that body fat is directly linked to six cancers, including colorectal and post-menopausal breast cancer. (more…)

Could your ever-expanding waistline be more a reflection of the friends you keep than of a personal lack of restraint? Or could whatever maladaptive eating and exercise habits you’ve acquired be a reflection of social acclimation rather than merely foibles you’ve fomented on your own?

Questions such as these arise as one reads through a recent article published in The New England Journal of Medicine by Nicholas A. Christakis and James H. Fowler. What we find most troubling about the findings presented by these researchers is their plausibility.

No reasonable theory we have previously heard regarding obesity has, to our recollection, treated it as a social disease. (Excuse our re-casting the term, but we believe it is even more applicable here than in its normal usage.) We have always been attracted to the view that obesity is simply a perversion of the natural tendency to gain weight in preparation for winter, when food in nature is scarce. In our modern world—in which winter tends to be more an annoyance than a period of near-starvation for most of us—this fattening process never stops. When winter never arrives and we never starve, some of us just grow fatter indefinitely.

One interesting theory to explain this weight gain run amok holds that after considering our modern diet, which in no way resembles the food available to our ancestors when our genetic structure was being determined, the modern conveniences of lighting, heating, air conditioning and protective shelter cause most of us to become desynchronized from the natural circadian rhythms that orchestrate our daily hormone cycles and influence many bodily functions, including metabolism. This desynchronization interferes as well with natural sleep, the daily period during which the immune system works overtime while the body repairs itself. In nature, as the periods of darkness wax and wane with the seasons, so too do our bodies (and their sleep cycles) change in a natural rhythm. From this point of view, obesity is just one symptom of a modern, alienated physical state: dis-ease. Depending on the individual, this disease might manifest as schizophrenia, diabetes, cancer… or obesity.

We find it interesting to contemplate that this particular theory does not in any way contradict the notion of obesity as a disease that can spread through social networks much as might, say, venereal diseases, though both the nature of the diseases themselves and the type and degree of contact are quite different. Indeed, one of the most intriguing notions in Christakis and Fowler’s findings is that geographic proximity is not even a factor in the spread of obesity; rather, the relationship between individuals—of which the most influential is strong mutual friendship—becomes the predominant factor.

Thus, social proximity substitutes for physical proximity, and with that substitution, the venereal analogy holds.

Still, our initial reaction upon seeing the title of the paper—The Spread of Obesity in a Large Social Network over 32 years—was somewhere between aghast and scandalized. The whole notion of obesity as a disease that spread from individual to individual—especially outside the genetically linked family structure—seemed preposterous. The authors note that obesity in a valued friend may cause one to become accepting of the condition, thus becoming more susceptible to it oneself or to accepting behaviors that cause it.

Aside from that, nothing in this paper really attempts to explain obesity: rather, it describes a topology by which the condition appears to spread. Nothing here hints at physical mechanisms or causes; we merely see relationships among those affected. An unfortunate implication one might draw from the authors’ analysis is that the obese exercise some unconscious control over their condition. We think this is an all-too-common medical prejudice that so far remains unproven.

Yet, if instead of the notion of accepting obesity one substitutes, say, infection—that is, a non-voluntary mechanism for the spread of obesity in which the infectious agent might be a complex of practices that the individual does not consciously associate with their consequences, rather than an external pathogen—the potential usefulness of the study’s findings falls back into place without unwarranted etiological assumptions.

Not only is it interesting that mutual friendships show the highest correlation among obese individuals, but those friendships between members of the same sex show the highest correlation of all. Not even marriage or sibling relationships correlate individuals as highly for obesity.

Not only do Christakis and Fowler provide thought-provoking insights into obesity, they build on previous work by Christakis and others emphasizing the undeniable importance of social networks in our overall approach to disease, particularly from the public health perspective. Whether this particular work points to a whole new dimension in the study of obesity or proves a tantalizing but inevitable dead end remains to be seen.

One wonders: how would the results of the study have differed had it mapped the spread of television or cell phones instead of obesity?

For most people, glimpsing the world of science is the equivalent of peeking behind the Wizard-of-Oz screen or falling down the Alice-in-Wonderland rabbit hole: Science remains shrouded in wonder and mystery, and always removed from everyday life.

My personal introduction to the everyday life of science came as a postgraduate (in my case, a post-undergraduate) lab technician.

That post is as low as you can go in science, barely on speaking terms with real scientists. Indeed, one visiting professor from the Max Planck Institute in Gottingen, Germany literally refused to acknowledge either my presence or my greetings until taken aside by my more politically correct employer, who tactfully explained that in the United States, lab technicians were actually allowed to address their superiors. Call it the price of a democracy.

Although I thought him needlessly arrogant at the time, he did, at least, confer on me a proper appreciation of my standing in the scientific world. And he, no doubt, thought me equally arrogant for summoning the temerity to speak to him.

At the time, I was working toward becoming a doctor and found myself hopelessly lost in the heady realms of hard science, which I knew would never confer recognition on one who had recently decided not to get a Ph.D. Since my goal was to become a psychiatrist, I was having a hard time reconciling my desire to help distressed people with my job, which entailed not only the predictable sous-chef-like duties that befell an underling in a chemistry lab, but also the occasional sacrificing (and, to my mind, torture) of animals, at which I became the reluctant local practitioner by decree.

It literally was my job to cut the tails off electric eels so that electrophysiologists could perform experiments with the cells of their electric organs, then return them to their tanks in an attempt to keep them alive for as many such vivisections as possible. Each day or so I would remove another slice of tail, until the hapless animals either died or had no more electric organ to be experimented upon.

It was within this gruesome context that I learned that science was not the neat, orderly progression of knowledge most of us believe it is. In some ways, everyday science is like some people’s description of the military: endless boring repetition punctuated by periods of intense excitement. What’s more, science is as grimly competitive as the business world and equally dog-eat-dog, while its purpose—to judge by the behavior of some scientists—is primarily self aggrandizement.

So scientists are real people, just like the rest of us.

That’s not to say that people don’t become scientists for all the right reasons. But let’s just say that if you’ve ever been appalled by the behavior of business executives, just imagine the amount of ego involved when one needs a Ph.D. just to get through the door. Science can be like the business world on steroids.

The eye-opener for me in this context was the realization that real-life scientists don’t always tell the complete truth in their published papers.

At the time in question, I was working at the Columbia College of Physicians and Surgeons, otherwise known as Columbia Medical School, and one of our competitors at another research institution had just published the results of a study he had performed. We needed to replicate his procedures as a step in our own research, but could not do so no matter how hard we tried. Eventually, my superiors acknowledged what a less naïve practitioner than myself would have realized from the start: an important step or two had been left out of the published procedure, enabling the other lab to stay one or two discoveries ahead of us.

It happens all the time.

Not long after that, a researcher at a famous cancer institute was pilloried for falsifying the data for some ostensibly significant cancer research. This was a particularly egregious example of research falsification; along with a cluster of similar events, it led to public disillusionment with scientific research for some years to come.

So, scientists caught up in the pressure of competition—whether for the Nobel Prize or simply for teaching tenure—will sometimes mislead, exaggerate or outright falsify results. Those are the deliberate cases. Although I’m dropping the dime on some of these guys, I still believe that most scientists are perfectly honest people whose highest goal is finding the truth through the application of the scientific method.

Still, even the most honest of scientists get caught up in the way science can naturally, well… lie. It is inherent in the nature of the scientific model, which proposes a representation for some aspect of reality, that old models eventually wear out.

Eventually some piece of data comes along that simply does not fit the model that we all know to be correct. Whatever the law or theory, the day may come when new data no longer fits within its predicted framework. Think of Newton’s Law of Gravitation, the DNA genetic model, or the inheritance of male-pattern baldness. Chances are, what you think to be true just isn’t; or, it is at least mildly discordant with reality.

Almost everyone knows, for example, that so-called male pattern baldness is inherited from the mother. Baldness is caused by a gene carried on the Y (female) chromosome that is dominant in men and recessive in women. Thus, a man needs only one such gene to be bald, while a woman requires two–one on each Y chromosome. Women carry the gene without manifesting baldness and can pass it to their offspring; the sons who inherit the gene will be bald and the daughters will simply pass the gene on unless they obtain a second baldness gene from their father, in which case they too will be bald.

Practically everyone knows this description of baldness, and it is wrong. No one really has any reason to perpetuate such a myth; companies that sell baldness cures have no vested interest in convincing people of inaccurate models of baldness inheritance, since they simply sell their products to those who display its symptoms. Yet, the myth persists.

It is tempting to say that this is how bad science works. In reality, it is the way science works. First, someone proposes a theory to explain a phenomenon; in this case, the inheritance of baldness. They then test the theory by examining evidence to support or refute that theory. When Dorothy Osborn performed her baldness study in 1916, her findings supported her expectations. She published her findings, and they became common knowledge, since baldness was a subject of interest to many.

Her results were so logical that no one felt compelled to challenge them. Yet, by the 1980s, scientists knew that Osborn’s conclusions were not entirely sound. Today, no one really understands the inheritance of baldness in precise detail, because at this writing, we can’t account for the genes that cause it; it has been established, however, that the simple model described by Osborn is not adequate to describe all the data. It appears that several genes interact in concert to produce baldness, perhaps influenced by triggering factors we do not yet fully understand.

In any case, the original theory—-so appealing precisely because of its simplicity—-turns out not to contain the real scoop on genetic baldness, though it served as a close enough approximation for many years.

The same, of course, is true of Newton’s Law of Universal Gravitation. It works well enough for everyday phenomena, but calculations of planetary orbits (specifically, precession of the perihelion) using Newton’s equations show substantial error over time. Einstein’s general theory of relativity adequately accounts for currently available data, but it won’t astound most physicists if someday someone finds data that requires a revision to that theory, too.

This is simply the nature of science. As a consequence, what any of us believes to be true based on scientific study at any given point in time will likely be proven false or inadequate at some later point in time.

The latest casualty on the list of generally held Great Truths earned Crick and Watson the Nobel Prize in 1962.

There was tremendous beauty in the model Crick constructed to describe our genetic encoding in the DNA double helix with a one-to-one correspondence between the nucleic acid chains of our genes and the resulting proteins that form our living bodies. However, even while I was still involved in research, parts of the thread had begun to unravel as scientists came to realize that genetic transcription was prone to errors or dislocations, much like, say, translating novels between English and Japanese: What you got in the end was roughly equivalent, but might differ markedly at various points.

Specifically, gene splicing could occur in nature, with the order of genes scrambled slightly or simply inverted between two adjacent genes. Not a huge thing on the surface, maybe, but a slight disruption of the presumed order, in any case. And the simple one-to-one correspondence between DNA nucleotides and the proteins whose blueprints they contain has had to be thrown out completely. We now know that a given DNA sequence may control the generation of many proteins. The transcription from code to living being is far more complex than we once thought.

This is not to say that the works of Mendel, Crick and Watson have been completely thrown out the window. Their findings account for the vast majority of the data, but the simple elegance that gave their breathtaking models such beauty has given way to increasing layers of complexity.

As beautiful and as useful as these models may be, they are vastly simplified descriptions of the real world.

Nowhere do these general shortfalls of scientific knowledge prove more problematic than when we approach the long dreamed-of task of creating or designing life. Science has finally reached the point at which the technology exists to sculpt completely or refine slightly the properties of living beings. Many forms of life have already been genetically engineered, including mice, bacteria, corn, alfalfa, soybeans, tomatoes, potatoes, plums, papaya, and more.

The forefront of science generally, and of animal husbandry and agriculture in particular, has become the design of animals and crops based on genetic manipulation.

Some object on religious grounds that this is meddling with God’s design. Others—perhaps more accustomed to seeing the visible incursions of science into daily life rather than the visible incursions of God—see all this as a step in the right direction, or at least as a predictable outcome: the culmination, if you will, of scientific endeavor, as presaged by Mary Shelley’s Victor Frankenstein and his monster.

Still others fear the outcome of this seemingly inevitable series of experiments, just as Frankenstein feared the actions of his monster and rued its creation.

It would be foolish to assert—as the major corporations that genetically modify food so often do—that genetically engineered (GE) crops are no different from conventional crops; if they were identical, there would be no reason to produce them in the first place. As potential improvements upon the naturally occurring varieties at hand, they hold alluring promise. There is an obvious draw in being able to shape or even control the properties of life.

But there is great irony here. Companies use genetic engineering not only as a means of modifying crops—which, except for transgenic strains containing genes from other organisms, might often be accomplished by conventional breeding—but as a means of establishing ownership through the questionable legal loophole that allows patenting organisms. This too has been presaged in works of fiction (think of the strange inventor of live toys in the movie Blade Runner) but has undesirable consequences that favor genetic manipulation on behalf of large companies purely for profit.

Wherever there is a large profit to be made, forces conspire to make that profitable outcome a reality.

Given the degree to which we dimly understand the mechanisms of gene expression and our even lesser ability to predict possible outcomes of genetic manipulation within the larger environmental context, there is indeed much to fear when such a powerful tool is turned over to those whose motivations are as transparent as their marketing literature.

Back in my lab tech days at Columbia Medical School, Dr. David Nachmansohn, the discoverer of the acetylcholine/acetylcholinesterase cycle and the first to isolate these compounds from the tissues of electric fishes, was fond of quoting Einstein.

“God does not play dice with the universe!” he would bellow with a conviction that always amazed and delighted me.

Can we say the same about the modern-day gods who are busy designing the living beings of our future?

I think not.

The headline of a recent news post from Reuters reads, Flouride in tap water may help older teeth too. To the casual reader, this headline seems to indicate that protecting the teeth of old people is just one of the many benefits of fluoridated tap water. But according to a growing array of scientists and health activists, nothing could be further from the truth. (more…)

If you’re prone to colds, infections, asthma, allergies or brittle bones, you might want to check your serum vitamin D levels. Although most doctors don’t call for tests of vitamin D levels when ordering routine lab tests, some experts believe that over 75% of the U.S. population may be deficient.

A study published in the March 23 issue of the Archives of Internal Medicine found that vitamin D levels in Americans have steadily declined over the past two decades. Dr. Adit Ginde of the University of Colorado at Denver School of Medicine stated recently that “over three out of four Americans now have vitamin D levels below what we believe is necessary for optimal health.”

And Hispanics and African Americans are even worse off, he says: “Nearly all have suboptimal levels.”

Why you need vitamin D

Many people are aware that without adequate vitamin D levels, their teeth and bones would suffer due to malabsorption of dietary calcium and failed regulation of the ratio of calcium and phosphorus in the body. But even most doctors practicing today are unaware of the vitamin’s role in promoting overall well being.

Vitamin D modulates blood pressure by suppressing the production of renin in the kidneys and brakes uncontrolled cell proliferation that leads to cancer. Its actions affect insulin secretion by the pancreas and may increase insulin sensitivity, thereby combating obesity. Without adequate vitamin D, you become vulnerable—perhaps even prone—to various cancers; to autoimmune afflictions such as rheumatoid arthritis, fibromyalgia and psoriasis; to bone diseases such as osteopenia (bone loss), osteoporosis and osteomalacia, a condition in which the bones actually ache; to any conditions resulting from poor calcium metabolism; and to heart disease and nervous disorders.

Among those cancers specifically linked to vitamin D deficiencies are breast cancer, prostate cancer, colon cancer and ovarian cancer.³

Dr. Michael Holick, generally considered the world’s foremost authority on vitamin D, thinks that infants born with vitamin D deficiencies who do not receive adequate supplementation during the first few months of life are likely to develop chronic diseases in adulthood, including type 1 diabetes, rheumatoid arthritis and multiple sclerosis.

Holick cites a study performed in Finland that gave infants 2,000 units of vitamin D daily for their first several years. The study then tracked the children into adulthood. The results showed they had an 80% reduced risk of contracting type 1 diabetes as young adults compared to children who did not receive vitamin D supplements.

By comparison, a group of children that suffered from rickets at age one showed a fourfold increased likelihood of developing type 1 diabetes by adulthood. Holick points to other studies done in the United States and Europe showing vitamin D can decrease the risk of contracting colon cancer by 50%, of prostate cancer by 50%, and of ovarian and breast cancers by almost the same amount. Yet, in a study where his team measured the serum vitamin D levels of 49 mothers and their newborn infants, he found that 76% of the mothers giving birth were severely vitamin D deficient, as were 81% of their newborns.

Neurosurgeon Russell Blaylock emphasizes that all brain cells have vitamin D3 receptors, both on the cell membrane and in the nucleus. He thinks vitamin D deficiency may be an underlying factor in autism.⁴ He further notes that the vitamin regulates calcium in all cells—including brain cells—and protects the immune system with antioxidant and antiviral benefits while it regulates cell growth and cell death. Vitamin D-3 plays a major role in a number of mechanisms that protect the brain, such as increasing neuronal levels of glutathione, an important antioxidant that protects against free radicals. Blaylock believes Alzheimer’s and Parkinson’s diseases may arise as a result of brain inflammation caused by vitamin D deficiency—cases where this protection against free radicals has failed.

Studies have linked vitamin D insufficiency to hypertension, atherosclerosis, congestive heart failure and heart attacks.⁵ Crohn’s Disease, ulcerative colitis, seasonal affective disorder (SAD), some depressions and other mood disorders yield to vitamin D supplementation. Even sickle cell anemia has been suggested as a possible consequence of vitamin D deficiency.

One study showed that postmenopausal women who increased their daily vitamin D intake by 1,100 IU reduced their relative risk of cancer by 60 to 77%.⁶

Clearly, maintaining an adequate level of this vitamin is worth the effort.

Optimal levels

Since sunlight is the most common source of vitamin D for most people, it is best to test your vitamin D levels in the spring. That’s the time of year when you are most likely to be deficient after months of sunlight inadequate for vitamin D production. In fact, David Brownstein, MD recommends having your doctor check vitamin D levels at least once a year using a simple blood test that checks serum levels of 25-Hydroxycholecalciferol (a circulating form of vitamin D). Brownstein says optimal vitamin D levels range from 75 to 125 nanomoles per liter (nmol/l).⁷

Currently recommended levels of vitamin D supplements are 200 International Units (IU) per day from birth to age 50, 400 IU per day from age 51 to 70, and 600 international units per day for adults aged 71 and older. Unfortunately, these recommendations were set to ensure against rickets rather than to guarantee strong general health. Most authorities now recommend 1,000 to 2,000 IU of the vitamin daily. Holick and other experts recommend obtaining about 4,000 to 5,000 IU per day for maximum health. Lactating women should receive 4,000 IU per day to assure transfering enough of the vitamin to their milk to satisfy their infant’s needs.⁸

It is safe to consume 4,000 to 10,000 IU of the vitamin daily for extended periods. Indeed, our ancestors may have been awash in vitamin D from hunting, fishing, or farming outdoors.

How to get it

If you spend several hours a week working or resting in the sun, your body may produce adequate vitamin D in summer. In that case, you might only need to supplement from other sources during the remaining seasons. However, research suggests erring on the side of supplementation if—like many Americans—you shower or bathe on a daily basis.

That’s because the production of vitamin D in sunlight results from the interaction of UVB rays with oils on the surface of the skin. These oils readily wash away during bathing. If they wash away before vitamin D is formed or after vitamin D is formed but before it has been absorbed back into the skin, the net result is little or no vitamin D from sunlight. So in our cleanliness-obsessed society, the average American is apt to require other sources of vitamin D besides sunlight.⁹

Moreover, should you suffer from liver, thyroid or kidney disorders, your body may not produce adequate amounts of the vitamin even when exposed to sun. Forty years ago, Adelle Davis observed that a high incidence of rickets was reported in such sunny locales as Greece and Israel, presumably because dietary factors nullified the effects of sunlight, though sun-protective clothing may be a factor.¹³

Rickets, of course, is the classic condition associated with vitamin D deficiency and reflects inadequate calcium absorption due to lack of the vitamin. Until recently, scientists thought that stimulating calcium absorption and utilization was vitamin D’s only role in the body. Now we know that it also regulates gene expression controlling immune and renal functions. These in turn can have profound effects on insulin production, serum calcium levels, diabetes, obesity, cancer immunity and countless immune disorders. Other possible effects from the vitamin are constantly under research.

When conversion of precursors by sunlight goes successfully, the sun is the vitamin D source par excellence. Dosages of vitamin D as high as 50,000 IU have been reported from as little as 30 minutes exposure to strong sunlight, though most authorities place the likely range between 10,000 and 15,000 IU within the continental United States. Latitude, altitude, atmospheric conditions, time of day, the amount of exposed skin and skin pigmentation will influence the quantities of vitamin D produced.

As a general guide, if you live north of Atlanta you will require longer exposure to the sun and will be able to generate vitamin D only during the summer months. Using sunscreens shuts down vitamin D output. A sunscreen with an SPF of 8 reduces your vitamin D production by more than 95%. For African Americans with relatively dark pigmentation, skin pigments alone provide protection from the sun that is equivalent to an SPF 15 to 30 sunscreen, requiring up to 30 times as much exposure as a Caucasian to generate adequate supplies of the vitamin.

Natural sources of vitamin D

Aside from exposure to sunlight, the only reliable natural sources of the vitamin are foods of animal origin. The best of these is cod liver oil, if you can find a brand that does not remove the natural vitamin D. (See sidebar.) Oily fish, such as salmon, mackerel, sardines and herring; oysters and shrimp; liver of all kinds, butter, lard and egg yolks are also good sources, though none compares to the more concentrated vitamins in cod liver oil.

Another reason to consume cod liver oil as a source of vitamin D is that vitamins A and D are synergistic, and high-vitamin cod liver oil is an excellent source of both. Additionally, the presence of vitamin D allows the body to handle much higher quantities of the antioxidant vitamin A safely.¹⁴ But perhaps more important, recent evidence suggests that vitamin D cannot adequately perform some of its essential gene-expression functions without the presence of vitamin A. In the absence of vitamin A, molecules called “corepressors” bind to vitamin D receptors and prevent vitamin D from functioning.¹⁵

Although milk is normally supplemented with vitamin D, the amount tends to be well below the levels that are now known to be adequate for optimal health.

For vegans and others who cannot obtain an adequate supply of the vitamin from their diets, vitamin D supplements are essential. Tablets containing 1,000 IU and even 5,000 IU are now readily available without prescription, so there is no reason for anyone to suffer from inadequate reserves. If you know that you are deficient because your blood has been tested, supplementing with around 4,000 to 5,000 IU per day is a good idea until blood tests show you have reached an optimal level. If you are overweight, it may take longer to achieve normalcy because vitamin D is readily absorbed into body fat for storage. Some sources advocate doubling D supplementation for the overweight.

Vitamin D and Autoimmune diseases

The list of known autoimmune diseases is long and growing. One source states that there are over 80, and that women are the most affected by them.¹⁶

As an example, Type 1 (insulin-dependent) diabetes, classified as a simple hereditary dysfunction a generation or so ago, has more recently become considered an autoimmune disease according to most experts. Along with multiple sclerosis (MS), rheumatoid arthritis, osteoarthritis, irritable bowel syndrome (IBD) and other autoimmune disorders, Type 1 diabetes may arise primarily as a result of vitamin D deficiency and apparently yields, at least in some cases, to treatment with natural vitamin D.

One of the clues that these disorders are linked to vitamin D deficiency springs from an examination of their prevalence at different lattitudes. It turns out that these diseases are all more common at higher lattitudes, which includes Canada, the northern United States and northern Europe. Their symptoms also tend to worsen during winter and spring.

Such diseases continue to worsen in spring because, despite the availability of strong enough sun during the spring months for Caucasian skin to produce vitamin D from exposure near midday, there is a two-month lag involved in overcoming vitamin D deficiency. That lag prevents these diseases from improving immediately upon exposure to the sun, especially for those who are overweight. Indeed, the lag time itself may have served to confound investigators in the past.

Another clue that vitamin D is involved in these autoimmune diseases is that people with inherited deficiencies in their vitamin D3 receptors are known to have a higher incidence of autoimmune diseases of all types.

But now, armed with new insights and new information about the roles vitamin D plays at the cellular level, scientists are beginning to unravel the mysteries. Heart disease, hypertension, schizophrenia and blood levels of inflammatory factors such as C-reactive protein and interleukin-10 all have in common a link to this vitamin that has turned out not to be a vitamin (it can be manufactured by the body in the presence of sunlight) but is nevertheless a substance that controls either directly or indirectly over 200 genes and plays a role in immune system modulation, cell proliferation and differentiation, even cell death.

And all you need to do to minimize your risk of all those diseases is to maintain healthy levels of vitamin D, the sunshine vitamin.

Tuesday, June 23 will be a deadline of sorts for those who would like to be heard raising their voices to oppose carbon pollution. (A form is available at the end of this posting for those who wish to respond or comment.)

On April 2, 2007, the U.S. Supreme Court ruled that six gases—carbon dioxide, methane, nitrous oxide, hydrofluorocarbons, perfluorocarbons and sulfur hexafluoride—were pollutants and that the Environmental Protection Agency (EPA) should regulate them if it found they harmed public health and welfare. The EPA, in turn, released a finding this April that greenhouse gases and other forms of carbon pollution are a danger to America’s health and welfare.

The EPA cannot act upon this finding until it receives comments from the public, and the deadline for providing those comments is June 23—this Tuesday. You can be certain that those individuals and industries who feel that controlling carbon emissions is NOT a national priority have made their opinions known. Therefore, it is important for those who feel it WOULD be helpful for the EPA to regulate such pollution to make their feelings known.

The 2007 Supreme Court ruling came as a result of a suit brought by Massachusetts and other states and environmental groups against the EPA in an attempt to force the agency to use the Clean Air Act to regulate greenhouse gases and other forms of air pollution.

As a result of that ruling and based on its own studies, the agency declared that concentrations of the gases were at unprecedented levels as a result of human activity and that it was highly likely that those elevated levels were responsible for an increase in average temperatures and other climate changes.

Among the ill effects of rising atmospheric concentrations of the gases, the agency found, were increased drought, more heavy downpours and flooding, more frequent and intense heat waves and wildfires, a steeper rise in sea levels and harm to water resources, agriculture, wildlife and ecosystems.

The EPA postings regarding these decisions and their results can be found here.

If you would like to add your name to the list of those responding favorably to the EPA’s decision or comment on what you think should be its future actions, you can respond here:

If you’ve made it this far, chances are better you won’t be getting the swine flu. The fall wave has peaked, experts seem to agree, and while there will surely be more cases to come, they are on the wane. The Centers for Disease Control and Prevention (CDC) is warning that another (winter) wave may occur in January, possibly prompted by students returning home from college during the Christmas holidays, but thus far, the flu pandemic has been a relative non-event as flu pandemics go.

So far, pandemic H1N1 is still crowding out other influenzas, such as seasonal H1N1 and H3N2. Since September, the CDC has tested 420 patient samples that were positive for influenza, and of those, only eight were not pandemic H1N1. Indeed, only one was seasonal H1N1.

The dominance of pandemic flu has not been good for the youngest age groups, however. During week 46 of 2009 (the last for which CDC figures have been reported) 35 influenza-related pediatric deaths were reported. Twenty-seven of these deaths were associated with pandemic H1N1 infections, seven were due to an undetermined influenza A virus subtype, and one was associated with a seasonal H1N1 infection that occurred in March.

Clearly pandemic H1N1 has been harder on children and teenagers than on older people. The H3N2 virus, on the other hand, tends to kill the elderly. But only three cases of H3N2 were reported out of the 420 patient samples previously mentioned, meaning that the pandemic flu’s tendency to crowd out other strains has spared the older age groups, relatively speaking.

Since April, the H1N1 outbreak has killed about 4,000 Americans, according to CDC estimates, of which at least 230 were children under the age of 18.

• WHO says swine flu pandemic might infect 2 billion
• WHO declares swine flu pandemic
• Swine flu virulence still at issue
• Swine flu update
• CDC swine flu statistics

• Weekend Reads: The Dreaded Swine Flu Edition
• Golf Tournament Recap: US Tour Championship
• World battles swine flu as death toll rises
• Fat People Cause Swine Flu or How to Avoid Swine Flu
• Mitch Biggs Claims MonaVie Prevents Swine Flu

Even the Centers for Disease Control and Prevention (CDC) admits it: H1N1 swine flu is a mild disease for most people, but for those whom it hits hard, it is often fatal.

Approximately a third of those who die from the disease do so because of other complications—generally pneumonia or MRSA (methicillin-resistant Staphylococcus aureus) so that the two primary killers once H1N1 gets involved are S. aureus and S. pneumoniae.¹ In part, this reflects the fact—reported here earlier²—that pandemic H1N1 tends to go deeper into the lungs than seasonal flu. According to Dr. Sherif Zaki, a pathologist at the CDC quoted in the November issue of Nature,³ this particular property of the virus is similar to H5N1 avian flu, a far more virulent form of flu that scientists have feared for years might take on a highly contagious human form.

The good news is that this particular scenario has been slow to develop in nature, and may prove difficult to replicate even in the lab. Researcher Bruno Lina at the Jean Merieux/INSERM biosecurity facility in Lyon, France proposes to try to force recombination of H1N1 and H5N1 in the lab and test the survivability and virulence of any resulting products. Based on some of his previous attempts to reassort H5N1 with seasonal H1N1 and H3N2 and the fact that the two viruses in question are different subtypes, he doesn’t expect to find reassortments that are survivable.

Referring to his previous experiments with reassorting H5N1, Lina told Nature, “After a year we only had three reassortments, and none was fit. They just don’t reassort well.”⁴

• More deaths from "new flu"
• Factory farming is key to swine flu epidemic
• U.S. swine flu tally nears 10,000
• New flu strikes lungs: WHO
• Nurse dies of swine flu

• Target Provides Prevention and Treatment Headquarters For Flu Season (NYSE: TGT)
• Game Preview: Kentucky Wildcats vs Gators
• H1N1 Vaccine: Are Elderly Being Rationed?
• Flu Season is Now Open
• Mexican Swine Flu Pandemic? Protecting Yourself In The Event of An Emergency

President Obama today declared the swine flu epidemic in this country a national emergency. Forty-six of the 50 states now have widespread flu contagion.

“It’s important to note that this is a proactive measure — not a response to a new development,” an administration official said.

“H1N1 is moving rapidly, as expected. By the time regions or healthcare systems recognize they are becoming overburdened, they need to implement disaster plans quickly,” he said.

The Centers for Disease Control and Prevention (CDC) says that the extent of swine flu contagion in the U.S. is currently on a par with the peak of the seasonal flu season, which normally doesn’t occur until at least late November and sometimes not until early March.

By declaring the national emergency, the administration enables Medicare, Medicaid and other federal health insurance agencies to waive certain requirements. This will smooth the way for doctors, hospitals and clinics to treat patients. As the flu season peaks, health-care providers such as hospitals are expected to be overwhelmed with patients.

The table below shows figures from the CDC giving the breakdown of lab-analyzed specimens for last week. Note that out of nearly 5,000 positive specimens, over 99% were Type A and approximately 70% were swine flu. This latter figure is slightly misleading, however, because almost 30% of the samples determined to be Type A were not subtyped. This means that virtually all positive respiratory specimens that were analyzed last week have turned out to be swine flu if there subtype was checked.

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The things they try to slip past you. We were catching up on our reading in the general press, in particular reading a piece in the New York Times about New York state requiring its health care workers to get both seasonal and swine flu vaccines, which has the unions of the health workers up in arms. And there it was, in the Times:

Immunologists generally agree that real protection against any disease requires vaccination rates over 90 percent. But because rumors always circulate and many people fear needles, voluntary acceptance never gets that high.

Nice try, NYT. “Real protection against any disease requires vaccination rates over 90 percent”? (Italics mine.) Does that mean real protection as opposed to the illusory protection we get from vaccines otherwise?

Obviously our NYT reporters are confusing issues here. They refer, we think, to so-called “herd immunity,” which, the story goes, requires over 90 percent vaccination rates to protect the remaining 10 per cent or fewer who are unvaccinated from being exposed to the disease. In other words, if you don’t get vaccinated and over 90 percent of the total population does, your chance of getting the disease drops to a rate comparable to that for people who did get vaccinated. That’s assuming, of course, that the vaccine really works and people really do derive immunity from it, both increasingly dubious assumptions these days.

That, apparently, is what the New York Times considers “real protection.” But, as the main thrust of the Times story clearly demonstrates, 58% of health care workers across the country disagree with that analysis and choose not to get vaccinated against the flu—H1N1 or otherwise.

Editor’s note: Today through Sunday (October 2-4) is the 4th International Public Conference on Vaccination, held at the Hyatt Regency hotel in Reston, Virginia. For more information, consult the National Vaccine Information Center Website.

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