Archive for the ‘scientific controversies’ Category

Influenza H5N1 HPAI research: lots of viewpoints

Friday, March 16th, 2012

When experts disagree, who should we believe?

Shortly after I wrote my post on the dangers of H5N1 HPAI, my weekly copy of JAMA, AKA the Journal of the American Medical Association, arrived containing a commentary titled “International Debate Erupts over Research on Potentially Dangerous Flu Strains.” The pros and cons of release of the two groups’ research were discussed and the rationale for publishing the methods and details was explained.

One expert in the field had a balanced view. He felt release of the details of the recent research on H5N1 HPAI might be extremely useful to  those who evaluate which strains of influenza are about to pose a real threat to humans and could potentially cause epidemics. Doing so might provide lead time for other scientists who work on vaccines to prevent wider spread of the particular strain of flu.

But in a January, 2012 online discussion of the controversy the head of a university Center for Biosecurity felt the lives of hundreds of millions of people could be at risk if such an engineered virus strain were to be released, even accidentally. He feels that continued research would require the level of biosecurity utilized with other dire agents such as smallpox.

The first infectious disease specialist countered with the concept that H5N1 HPAI wasn’t an especially likely pick for those interested in bioterroism. It’s certainly not a selective weapon and its use would require considerable expertise.

The second expert noted there had been no data that such a strain of flu would ever develop naturally, outside the lab, and we had to return to the concept of weighing potential harm versus good.

Now the original researchers have stated that the new viral subtype isn’t as deadly as feared; it hasn’t killed the ferrets being used as laboratory substitutes for humans and has proven to be controllable with vaccines and antiviral medications. Because of ethical limitations it hasn’t been tried on human subjects and they don’t know whether it even could be spread among humans.

And which of these is the worst?

I think we’re treading very close to the edge here. I don’t look forward to widespread beneficial effects of complete publication of the ongoing lab research results. And I do fear the possibility of groups who don’t care if they kill off a third of everyone, including their own followers. Accidental release of a lab-engineered organism into the human population could also happen, even if unlikely.

Another online article said the work on the mutant form of H5N1 had been performed in BS-3 labs, used for studying agents that can cause serious or lethal disease, but do not ordinarily spread among humans and have existing preventives or treatments.

A GAO 2009 report counted 400 accidents at BS-3 labs in the previous decade. Scientists argued that the H5N1 HPAI studies must be moved to BS-4 labs with one professor stating, “An escape would still produce the worst pandemic in history.” Yet between 1978 and 1999, over 1,200 people acquired deadly microbes from BS-4 laboratories, the biosafety-4 level facilities that normally deal with infectious agents that have no known preventive measures or treatment.

Scandia National Laboratory’s International Biological Threat Reduction program directed by Ren Salerno has a worldwide ongoing effort to prevent laboratory accidents, but there are varying standards for biosafety and at least 18 BS-4 labs outside of the US as of 2011.

So I’m still worried.

 

What sweetener do you use: Part 5; Fructose effects

Saturday, January 28th, 2012

A good place to start researching

I basically knew what happens when we ingest glucose, (eating it or drinking it depending on whether it’s in solid or liquid form, e.g frosting versus sweetened tea) : it goes through the liver and heads off to muscle and other body parts where insulin activity is responsible for energy use. But I wanted to compare its effects to those of fructose. First I found an old article (1986 vintage) in the American Journal of Physiology (AJP), hardly a bedside reading item for me these days, but one I used to proofread for as a research fellow. That, once I translated it into English that I could understand, changed my mind a bit.

Glucose does lead to an increase in insulin levels and an increase in carbohydrate breakdown, while lipid (fat) breakdown slows down. The net result is a considerable bump in energy use. ‘So far, so good,’ I thought. But a comparable amount of fructose resulted in a much smaller increase of insulin, yet considerably more carb breakdown and even less fat breakdown. So even more energy was used. That I hadn’t expected, but this study was a one-time experiment with seventeen healthy folk followed for a few hours.

So my next question, and I thought this one was far more important, was what happen longterm?

Let’s look at animal research first. A group from Princeton published an article online in a journal called Pharmacology, Biochemistry and Behavior in February 2010. Tha basic conclusion from these scientists contradicted what I had read elsewhere, but made sense. They concluded all sweetener calories are not equal– after feeding rats standard foods and adding either table sugar-sweetened water or HFCS-sweetened water. Even if the HFCS water was less sweet overall, the rats gained more weight. Long-term feeding experiments showed rats fed HFCS developed many of the signs of the “metabolic syndrome.” weight gain, fat deposition in the belly and abnormal blood levels of trigclycerides.

So fructose was being metabolized to form fat, while glucose was being used as it normally is. That brought their thoughts back to why fructose in HFCS is different from that in table sugar. According to this research group, HFCS contains free, unbound fructose while that found in table sugar is always tied to a glucose molecule. Their concept is that table sugar fructose has to go through an additional chemical process, freeing it from glucose, before it can be used by the body.

So why should we care what makes rats fatter?

But here's our real target

I found a long article in The Journal of Clinical Investigation (JCI), the other research magazine my boss (and I) reviewed potential articles for in 1970 to 1972. Here people who who overweight or obese to begin with were fed either glucose- or fructose-containing liquids for ten weeks.

And the results were similar. Those getting fructose had more belly fat develop. I think translates to more chance of heart disease  and other long term complications.

The evidence is gradually adding up; I think HFCS is something to be avoided. Let’s feed our kids and ourselves more fruits and vegetables and less processed foods.

What sweeteners do you use? Part 4: HFCS and mercury

Tuesday, January 24th, 2012

A safer place for mercury

In my last post I mentioned that fructose metabolism appears to be more complex than I learned in medical school. Of course that was in 1962-1966 and a lot has changed in medical knowledge in the forty-five plus years since then. We all know that fructose, in the form of high-fructose corn syrup (HFCS) is added to many processed foods and sweetened drinks; the question being debated is, “Is that bad for us?”

I’ve been reading a variety of articles from the medical literature and some popular websites on the subject and not all scientists, physicians and dietitians agree on the answer. I previously mentioned a Mayo Clinic online article that stresses the need to cut our added-sugar intake, both table sugar and HFCS, and mentions that research on HFCS isn’t yet at the point to implicate it as worse for you than other added sweeteners.

There’s also an article by Jennifer Goldstein from Prevention magazine that I found on the msnbc website. I’m not sure of her science background (she’s now the Beauty Director for the magazine). Nonetheless, her article is reasonably well-balanced, if you read between the lines. The over-all conclusion is that anti-HFCS evidence is slim. She quotes an NYC-based nutritionist as saying the calories in HFCS and table sugar, gram for gram, are equal, but mentions several reports that have shown HFCS samples may contain mercury… in small amounts.

But you don't want it here, or in your food

Mercury is a neurotoxin, a substance which can damage the brain, especially the developing brain of a fetus or infant. Even “small amounts” are considered dangerous for babies in the womb. We have all heard of its presence in fish, but mercury in HFCS was new to me. I’m about three years behind, it appears. I found a Washington Post article from January, 2009 which mentioned two studies examining this issue.

At that time, in spite of industry denials, nearly half of HFCS samples tested contained mercury as did almost a third of processed food and beverage products. The researchers writing on this  enormously significant problem noted that HFCS had been made using chemicals produced in industrial plants clinging to an outmoded, 19th century method

A now-retired FDA scientist, Renee Dufault, headed a study in 2009 showing low levels of mercury in all the processed foods she and colleagues tested (and none in organic foods) and then had their results verified by two independent labs. She then says the FDA’s head of their Food Additives section told her to quit her HFCS studies. She quit the FDA instead and published her results. A physician-headed team at the Institute for Agriculture and Trade Policy, a non-profit watchdog, repeated her studies using commercial beverages and foods. Their twenty-plus-page paper is worth reading.

By the middle of December, 2010, the HFCS industry had gotten the message. But until all HFCS made in the United States is mercury-free I’m going to avoid it.

Vindication? Part 1

Thursday, January 5th, 2012

One way to get lots of protein

Since the late 1990s when I invented a diet, or perhaps I should say an eating pattern, I’ve relied on one principal concept: Eat Less; Do More. I came upon this simple idea after listening to a group of medical professionals who were discussing which diet they should go on while they were simultaneously consuming huge portions at our hospital cafeteria.

One of them, I recalled, had tried a high-carb, low-protein diet the past year; losing nearly twenty pounds, then regained it all and more in a few months. Now she was going to attempt  to lose twenty-five pounds with a different approach, this one with an emphasis on protein. I had seen weight-loss plans come and go and didn’t believe any of them were the answer, at least not for everyone. I remember coming home and saying to my wife, “Lynn, I’ve invented a new diet”

I explained it was simply, “Never finish anything; No snacks between (meals); Nothing after eight.” I added, “Get lots of exercise.”

I lost the seven pounds I had gained on a two-week vacation and didn’t need my strategy again until early in 2009. Then I weighed 177 one morning, up three pounds from my normal weight since 1991. I attributed that to eating out four times in the prior week. But when I tried on a pair of good suit slacks, I realized the weight hadn’t changed much, but the distribution sure had.

I went back to my eating plan, lost five pounds easily, then coasted a while before resuming the diet. Lynn bought me a digital scale and I weighed myself daily. I also started going to our gym six days a week. Eventually I shed thirty pounds and five inches off my waistline. At 147 pounds I was twenty-five under my usual high school weight. This morning, nearly two years later, I weighed 148.

I allow myself a three-pound zone of weight fluctuation, thinking that would account for fluid shifts and the occasional big splurge. Whenever I exceed 150 pounds I go back on my plan.

Then I read a Wall Street Journal article titled “New Ways Calories Can Add Up to Weight Gain: Study Challenges Idea That Varying Amounts Of Fat, Protein and Carbohydrates Are Key to Weight Loss.” It quoted the Journal of the American Medical Association, AKA: JAMA. I went online and found the JAMA article and an accompanying editorial.

I read both pieces in detail, even finding a wild typo, “…their diets were returned to baseline energy levels and diet compositions (15% from protein, 35% from fat and 60% from carbohydrate).” I called the AMA and suggested they correct the numbers since they added to 110%.

Is a high-carb, low-protein diet safer?

But the basic premise of the study’s data intrigued me. It’s something I’ve believed for years, calories count, as opposed to what form those calories come in. But there’s one extra facet: low-protein diets can be dangerous.

I’ll analyze that in detail in my next post.

 

 

The PANDAS controversies

Thursday, December 22nd, 2011

We're not talking about this kind of Panda

The more I read about the relatively new syndrome PANDAS, Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus, the more I realize how complex the issues are that surround it. We appear to be entering a new field of medicine, one that holds enormous potential for unlocking the root causes of baffling problems in neurology and psychiatry

The story starts in the mid 1990s when Dr. Susan Swedo, now Chief of the National Institute of Mental Health’s (NIMH)  Pediatrics & Developmental Neuroscience Branch , reported that childhood obsessive-compulsive disorder (OCD) may sometimes be triggered by a strep infection.  OCD may involve compulsive handwashing, twenty or thirty times a day; it can manifest itself as a need to have things “just so” in order to relieve anxiety, repeating and checking behavior, counting and arranging objects or clothing, hoarding, praying, reading a section of a story over and over again.

Some of these youngsters also have tics, involuntary movement disorders. Another subset just has tics, but no OCD.

A moving portrait of a child who fits this profile was published in the Los Angeles Times early this month. The boy involved wa a normal eleven-year-old sixth grader until he developed a strep throat. Then his behavior altered to the point where daily life seemed totally changed; he became obsessed with being clean  and afraid of germs to the point where he was unable to go back to school.

Increasingly these diseases and perhaps others are being linked by some eminent researchers to strep infections. A senior immunologist at the University of Oklahoma College of Medicine thinks the mechanism of PANDAS involves antibodies, released in response to a strep infection, that can bind to brain cells and cause the release of dopamine, a brain chemical which in excess, may be linked to OCD and tics. The diagnosis, at the moment, is strictly clinical; there is no lab test to confirm that a child has PANDAS.

One form of OCD involves repetitive handwashing

Many youngsters with OCD and/or tics don’t appear to have this strep-related syndrome and some equally prominent academic physicians feel kids can have a mental health/neurological disorder first and just have it exacerbated by strep throat or other infections. Others want to treat the most severely affected of these children with antibiotics even if they don’t have an active strep infection.

The NIMH makes the point that these children, as opposed to others with OCD and/or tics, have an abrupt worsening of their symptoms when they have a strep infection. They then will have a slowly improving course after a few weeks or months.

The guidelines are admittedly vague; NIMH says PANDAS can be “identified after two or three episodes of OCD or tics that occur in conjunction with strep infection.”

A senior Harvard professor of psychiatry who is the head of the International OCD Foundation’s scientific advisory board has been quoted as saying the portion of OCD linked to PANDAS is “exceedingly common.”

Is this the tip of an iceberg of neuropsychiatric problems linked to infections? Only time and lots of research will tell.


So is it your thyroid after all?

Wednesday, November 30th, 2011

Is this woman depressed, hypothyroid or both?

On November 21, 2011, The New York Times had an article entitled “For Some, Psychiatric Trouble May Start in Thyroid.” As a mental health therapist who is hypothyroid, my wife has a particular interest in this subject and pointed out the article for me.

The premise, put forth by Dr. Russell Joffe, a New York psychiatrist, and a group of his professional peers, is that subclinical hypothyroidism may play a significant role in depression. A Brown University professor of psychiatry and human behavior also commented on this connection asking, “Is there an underlying thyroid problem that causes psychiatric symptoms, or is it the other way around?

From the endocrinology side, Dr. James Hennessey, at Beth Israel Deaconess Medcsl Center in Boston, noted “Psychiatric symptoms can be vague, subtle and high individual.”

A study, published five years ago by Chinese researchers, gave six months worth of  thyroid hormone replacement therapy (see links below for the NIH’s info sheet on this medication, levothryroxine and other info from MedicineNet.com), to patients with subclinical hypothyroidism and found improvements in brain scans, memory and executive functions.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000684/#

http://www.medicinenet.com/levothyroxine-oral/article.htm

sketch of the thyroid gland

So how is this condition diagnosed? and what does your thyroid do anyway? Most of us are familiar with this two-lobed, twenty to sixty gram,two-inch structure, located in the front of our necks and wrapped around our windpipe. It’s a hormone producing gland with two products, thyroxine or T4 and its active hormone, triiodothyronnine or T3. I’ve always thought of its function as a major regulator of metabolism, but in reality that’s only one of its duties: it does control how speedily we use energy, but also has a role in how we make proteins, how we react to other hormones and how our bodies handle calcium.

I’ve spent much of today reading about the thyroid; some things I knew; some I hadn’t reviewed since med school basic science classes (1962-1964) and other were brand-new to me. Fetal development of the gland is stimulated by two other hormones released by the hypothalamus and pituitary and those are at high enough levels to cause the fetus to make T4 in clinically significant amounts by 18-20 weeks of gestation. The active hormone, T3, stays at low levels for another 10 gestational weeks, then increases until term.

The net result, it is felt, is protection of fetal development, especially of the brain, in the event the fetus’s mother is herself in a hypothyroid state.

But back to adults and the link between thyroid status and mental health.  One of the crucial measurements of thyroid function is the level of TSH, thyroid stimulating hormone. Normal levels for this pituitary hormone are 0.4 to 5.0 in most labs in the United States; nearly nine years ago, the American Association of Clinical Endocrinologists recommended the doctors consider treating patients whose TSH levels are higher than 3.0. Other scientific groups agreed.

If a TSH level above 5.0 is abnormal, then ~5% of our adult population is hypothyroid. But if that level is reduced to 2.5 to 3.0, then ~20% of us are hypothyroid.

I wonder if a new field of medicine, halfway between the endo folk and the mental health practitioners, is on the horizon.

http://www.umm.edu/endocrin/thygland.htm

Biofuels, greenhouse gases and you: Part one of many

Thursday, November 17th, 2011

Not the right choice for a sustainable biofuel

The excursion into what was initially a vaguely known arena started with a Wall Street Journal article on 11-8-2011, but then strayed far afield as my learning curve tilted steeply upward.

The article itself dealt with airlines trying out newer biofuels: Alaska Airlines and United were highlighted as having pilot projects in this area. As I read further, scanning online material, international carriers, especially KLM, with 200 flights using 50% biofuels and, impressively, Lufthansa with 1,200 flights using 50% biofuels, are far ahead in this arena.

The fuels come not from corn, as in the United States, or sugarcane, as in Brazil (more on the latter in a subsequent post), but rather from algae, cooking oil, animal fat, and two plants I’d never heard of, Camelina (I’m trying to find it as a cooking oil) and Jatropha.

We had dinner company a few days ago; I was cooking a cabbage dish from the Shan people of Northern Thailand and Mynamar, Lynnette made squash and potatoes simmered in olive oils with both vegetables coming from our weekly CSA allotment. The dinner and subsequent conversations and disagreements (these are close friends and we have differing views on a wide variety of topics) lasted from just after 6 PM to just before 11.

It was immediately obvious that our friends favor oil, gas and coal as fuels. They don’t think biofuels, solar energy, wind power, geothermal or tidal energy are economically feasible. They would approve of nuclear energy with appropriate precautions (avoiding building nuclear power plants on known earthquake faults or in areas prone to tidal waves comes to mind).

I think we haven’t put enough time, money or brainpower into developing alternative energy sources and urgently need to do so. The political will to accomplish this seems lacking and our faltering, argumentative Congress, polarized as it currently is, hasn’t helped the situation.

I certainly agree that subsidizing the growth of corn to be converted into ethanol isn’t the way to go. And Brazil, despite its exceedingly osuccessful and sustainable biofuels program, isn’t going to be able to supply enough ethanol to fuel the rest of the world.

Mount Saint Helen's in a quiet mood

Our friends said one volcano can add enough greenhouse gas (GHG) to make all our cars’ polluting, to mix a metaphor, seem a drop in the bucket.

I don’t disagree that the rare volcanic eruption can be catastrophic in this sense as in others (local loss of life and property among them). We’ve visited Mount Saint Helens (I strongly suggest reading Tim McNulty’s 1998 retrospective on the explosion; just Google his name and add that of the mountain).

He makes the point that in this natural disaster, as opposed to industrial clear-cutting, damage was variable, trees, animals and insect survived and the area has come back strongly. I liked the line, “The ecosystem has been through this before.”

Yet adding our dollop of pollution is not natural; it may tip us over an edge.

So I am in favor of the pursuit of alternative sources of energy. These may vary from country to country or within a country as the local winds, tides & solar-project possibilities permit.

But it’s time and very nearly past time.

http://environment.about.com/od/fossilfuels/a/biofuels.htm

Seemingly disparate topics tied together with MRSA

Thursday, November 10th, 2011

Staph bacteria growing on a culture media

I read two NYT articles  about medical diseases that conflate to a really frightening juncture. They led me to find background data from a medical website and to do a Google search on one lead author.

Let’s start with MRSA, the acronym for methicillin-resistant Staphylococcus aureus.  Roughly 25% of us are staph carriers, but only 2% of us carry MRSA, the antibiotic resistant form that causes deadly complications so frequently  and is so difficult to treat. Infections with “ordinary” staph bacteria can be very serious, but respond, in most cases, to the drugs commonly used. The NIH has an excellent summary of MRSA issues and I’ll paste in a link to it below.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004520/

An August 11, 2011 NYT article mentioned that MRSA skin infections occur in those more prone to cuts and scrapes: athletes, the military and our kids among them. A professor of Medicine and Pediatrics at UC Davis Medical School is quoted as saying, “…in most communities, community acquired MRSA has become the dominant cause of soft tissue infection requiring emergency department care and inpatient care.”

In a previous post I noted that a neighbor ended up in our local ICU for a prolonged stay after a scape on his elbow resulted in a rapid spread of redness up his arm unto his chest. As you might surmise, this was an MRSA-caused illness.

MRSA is a major urgent medical problem; almost 19,000 people died from this dire staph in 2005. In that timeframe most MRSA infections were felt to occur in immunocompromised patients.

But now hospital admissions for skin infection in kids have climbed; the rate of these more than doubled between 2000 and 2009. The overall rate still seemed low, 9.4 cases per 10,000 children, but that translates into just under 72,000 kids being hospitalized in that one year.

In the average year roughly 4,000 kids wind up in pediatric ICUs yearly because of severe flu infections and of course many times as many have mild cases of flu. The current study, headed by an associate professor of Anesthesia at Harvard, looked at children who got flu infections during the 2009-2010 H1N1 epidemic and were admitted to ICUs in 35 different locations. Of those  838 youngsters, nearly nine percent, 75 of those kids, died; their median age was 6.

More than a quarter of the children in the study were previously considered totally healthy; they didn’t have asthma or a neurological disease; they were not immunosuppressed and didn’t have other chronic conditions. So of the total, 251 kids were otherwise healthy prior to getting the flu; 18 of them died. The only predictor of death in healthy children in this group was MRSA infection; if they had this co-existing risk factor their risk of dying increased eight times when compared to those who did not have MRSA.

Please ask your pediatrician about flu vaccination

My take on the study, and that of the lead researcher, is it’s time to make sure our kids and grandkids get vaccinated for flu on a yearly basis.  There are still people who never want their children vaccinated; physicians in almost all cases would disagree with them.

Talk it over with your own pediatrician.

Which study should I believe?

Wednesday, October 26th, 2011

Vitamin E has this chemical structure

I just read the recent (Oct 12, 2011) JAMA article on “Vitamin E and the Risk of Prostate Cancer.” It was a long-term, prospective, randomized study of 33,533 men followed in 427 study sites in the US, Canada and Puerto Rico. The investigators were from major academic centers, Duke, the Cleveland Clinic, Brigham and Woman’s Hospital (e.g., Harvard) and the National Cancer Institute among them.

This was an impressive study of the effects of Vitamin E and/or selenium versus placebo that began in 2001 with the subjects being “relatively healthy men.” Seven years after it began, in September 2008, the independent data and safety monitoring committee decided that the supplements should be stopped as there had been no positive results (reduction in prostate cancer detection) and futility analysis (a statistical tool) said the results were quite likely to be negative (more cases of prostate cancer). I hadn’t heard of that term and found a medical website that discussed a number of reasons for ending a study prior to the intended date. I’ll paste in the URL if you want to read a one-pager on what is called “interim analysis.”

http://www.childrensmercy.org/stats/plan/interim.aspx

In this study, though the researchers stopped giving supplements and published an article (JAMA.2009;301(1):39–51) on the results to date, which showed a higher (but not statistically significant) number of cases of  prostate cancer in the groups receiving Vitamin E, selenium or both, they also continued following the patient group.

Prostatic cancer under the microscope

The later data, though July 5, 2011, was quite impressive. There was a 17% higher incidence of prostate cancer in the group taking Vitamin E. In most scientific studies a p-value of 0.05  is felt to be significant. That translates to a probability of 5% or less that whatever happened did so by chance. If the data calculates to a p- value of 0.01, there’s a 1% chance this was a random occurrence. Here, after ~eleven years the p-value for Vitamin E increasing the chance a man was diagnosed with prostate cancer was 0,008. (I’ll paste in a website that explains more of this stuff if you’re remotely interested).   http://www.childrensmercy.org/stats/definitions/pvalue.htm

Why all the math and statistics?

Well, for starters, a few years back a large study showed the exact opposite, but in a highly selected group: men in Finland who were smokers. Another study, done with physicians as the subjects, showed no effect on the incidence of prostate cancer. A post by a physician harshly criticized the SELECT trial as part of a lengthy defense of supplements, but made sweeping pronouncements without supplying data or references to specific articles.

I read the articles, the blog post and the new study in detail. I know that medical research projects often come to conclusions that, a few years later, are “proven” incorrect. But I think this study was carefully done, had a clear-cut purpose in mind and included a large enough group of subjects that I’m going to believe its conclusions.

Plus I’m certainly not a Finnish smoker.

 

 

Do I need to eat my words?

Wednesday, October 19th, 2011

Different choices for different ages

An old friend forwarded an article on vitamins yesterday, one that I read with special interest. It came from MedPage Today, an online medical news service for healthcare professionals that partners with the University of Pennsylvania School of Medicine to offer physicians continuing medical education credit (CME) for reading articles and then answering a few questions.

The article was titled “Vitamin Studies Spell Confusion for Patients” and extensively quoted Dr. David Katz fromYale’s prevention research center. He is an adjunct Associate Professor at Yale’s School of Medicine and an internationally renowned authority on nutrition. He comments that, based on the recent study I mentioned several posts ago, many clinicians say they’ve written off supplements for good.

Yet 50% of Americans take supplements; many take more than just a multivitamin.

Then Dr. Katz offers some caveats as I did, stating the Iowa study is “merely observational and can’t prove cause and effect.” He still recommends omega-3 fatty acids (AKA “fish oil”) and vitamin D for most of his patients and adds calcium for women and prenatal vitamins and folic acid for pregnant women. otherwise he only uses vitamins when there are deficiencies.

A recent pole of clinicians found that 70% favor annual screening of specific vitamin levels to treat deficiencies. Which vitamins (and minerals) might be measured as part of an annual focused screening examination and whether medical insurance plans would cover such laboratory tests has not been delineated, as best I can find.

But I’m seventy, and articles from 2005 to 2010 in authoritative sources, talk about seniors needing much more B12, having multiple minor, but significant, vitamin deficiencies, and not eating well-balanced, healthy diets, even here in the United States, much less in other spots around the world. I’m lactase deficient and small-boned; do I need a calcium supplement?

clearly the best way to get your vitamins

I agree with Dr. Katz that eating a balanced diet would be a better answer, at least for those who are younger. The concept of “eating your colors,” i.e., having multiple suit and vegetable dishes over the day which contain different phytochemicals as represented by the color of the food itself, makes great sense.

How many Americans do that at present or are likely to do that even if medical figures recommend such?

I regard this as an ongoing discussion. Dr. Katz is certainly correct in saying that vitamins have been shown to treat disease states, but not to prevent chronic disease. The surmise in the article in MedPage seems sound to me: vitamin isolates are less effective on their own and a full blend of antioxidants and phytochemicals (again, best found in those whole fresh fruits and vegetables, may be the key to obtaining maximum benefits.

This discussion is likely to go on and on, so I’ll supply two URLs that may help you, in consultation with your own physician, make choices that are relevant to your nutritional status, age and degree of health.

http://www.uspharmacist.com/content/d/senior%20care/c/21981/

http://www.fda.gov/Food/DietarySupplements/ConsumerInformation/ucm110493.htm