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April 27, 2006
Second-hand obesity
In the National Briefing section of today's New York Times I found the following blurb:
COAST GUARD RECOMMENDS RISE IN WEIGHT ESTIMATES The Coast Guard recommended that operators of small boats raise weight estimates for passengers to reflect that Americans have grown fatter since the first standards in 1942. The recommendation arises from an investigation of an accident in which an overloaded water taxi capsized in Baltimore in 2004, killing five people. The operator assumed that the average passenger weighed 140 pounds, based on Coast Guard standards. Last October, a tour boat on Lake George, N.Y., the Ethan Allen, capsized, killing 20 of the 48 people aboard. The Coast Guard settled on a voluntary standard of 185 pounds until new rules are established. (AP)
I hope that the FFA has been more diligent in increasing the average passenger weight for airlines making weight calculations. I've flown a lot recently and I can tell you that the average passenger weighs much more than 140 pounds.
The excess avoirdupois that many of us are carrying is much more than just a cosmetic problem and, as this piece points out, it's even more than a health problem only to the overweight individual. Since it is a health problem for a given obese person that can affect those nearby perhaps we should call it second-hand obesity.
Posted by mreades at 2:31 PM | Comments (3)
Justice 1760 style
I read an editorial in the New York Times yesterday and an article today about the recent issue of the supposed cruelty of lethal injection as a means of carrying out the death sentence. If you haven't been keeping up, what's at issue is whether or not lethal injection, which was developed as a more humane way of executing people than hanging, electrocution, gassing, shooting, etc., is a 'cruel' form of punishment itself. The idea that lethal injection, at least as administered in the US, is far from the painless drifting off to sleep that most imagine stems from an article last year in The Lancet, a British medical journal.
The authors contend that although the usual mixture used to execute--a combination of an anesthetic, an agent that paralyzes the muscles, and an agent that stops the heart--includes a drug that puts the condemned person to sleep before the other drugs do their job, that, due to lack of training on the part of the people administering the injection, the anesthetic is often given incorrectly or in too low a dose to render the executee unconscious. If this is true the person receiving such an injection would be fully or partially conscious while being paralyzed, unable to breath or even blink his (or her) eyes and would basically smother to death without any observable evidence of doing so. To an observer it would appear that the condemned was resting comfortably or even snoozing while in reality he (or she) was in agony. If these claims are true, it would mean that the lethal injection method of execution would be comparable in terms of discomfort to the old way of executing supposed witches in this country, which was to tie them down and stack stones on them until they couldn't breathe. It would be a real tragedy if, in an effort to be more humane, we took a step back to much less enlightened times.
The Supreme Court has taken up the issue while In California an execution has been delayed by the courts until the state can obtain the services of a physician to properly administer the deadly injection. So far, no physicians have stepped forward to offer their services.
And don't count on me to volunteer; I wouldn't do it for any amount of money. My own thoughts are jumbled and murky on the death penalty issue, but one thing I'm adamant about is that I would never be the one personally responsible for carrying it out.
Things evolve with time. It wasn't so long ago that capital and corporal punishment were much different than they are today.
A few months ago I posted on an article on the latest diet from a 1760 news monthly The London Magazine. I seemed to remember when I read the thing that there was something in it about an execution. I went back an looked, and sure enough, there was an entire article about the execution by hanging of a true 'gentleman' versus your standard issue common criminal. The article described his demeanor, what he wore (he was dressed to the nines), what he said after mounting the scaffold, and how well he died. I would reprint the entire article here because it is quite interesting, but I about went blind typing the last one on diet, and the execution one is even longer.
In this same magazine there is a section called The Monthly Chronologer that is a day-by-day journal of events since the last issue giving blurbs of the news that the editors thought would be of interest. The entry from Friday, May 23, 1760 is:
Ended the sessions at the Old-Baily [London's famous criminal court]; at which sessions Ann Hullock, for the murder of her bastard child, received sentence of death, and was accordingly executed on the 24th. Seventeen were sentenced to transportation for seven years, one for 14 years, two to be whipped, and one to be branded.
When I look up transportation in my copy of Samuel Johnson's Dictionary (which was compiled in 1755) it gives as one definition:
Banishment for felony
We've evolved from an era called The Enlightenment when criminals were hanged, whipped, branded, and exiled without a second thought to an era where we worry about whether the condemned feel any discomfort. I would say we've made progress.
Posted by mreades at 11:07 AM | Comments (5)
April 24, 2006
Mercury amalgam whitewash
You no doubt read in all the newspapers reports last week about the two articles in JAMA (click here for full text of one and here for the abstract of the other) showing that there was no need to worry about letting the dentist fill your kids' teeth (or your own) with mercury amalgams because, well, because two large studies showed no negative effects in multiple parameters between kids who had mercury fillings and kids who had resin fillings.
It seems kind of strange to me given that mercury is an extremely toxic substance that putting large amounts of it into the body (especially the body of a child) wouldn't cause some kinds of problems somewhere along the line. What do these papers tell us?
The first one evaluated groups of children in the New England area who had fillings done with either mercury amalgams or with a resin material containing no mercury. Researchers evaluated these two groups of children for any changes in intelligence as measured by standardized intelligence tests over a period of five years. As might be expected, the children with the mercury amalgams had greater levels of mercury in their tissues as measured by hair and urine samples.
Children assigned to the amalgam group had a significantly higher mean (SD) urinary mercury level 5 years after baseline than did children assigned to the composite group (0.9 [0.8]; range, 0.1-5.7 µg/g of creatinine vs 0.6 [0.5]; range, 0.1-2.9 µg/g of creatinine, P<.001; Figure 2), although the overlap in the distributions was considerable. Urinary mercury was detected in 63% of the amalgam group and in 45% of the composite group. Hair mercury was similar in the treatment groups (amalgam group, 0.4 [0.4]; range, 0.1-2.3 µg/g vs composite group, 0.5 [0.7]; range, 0.04-6.5 µg/g).
The interesting question is how did the non-amalgam treated group end up with so much mercury? Probably from vaccinations. At the time this study was done all children were getting a panoply of vaccinations all of which contained thimerosol, a mercury-containing preservative. These findings beg the question as to whether or not the study outcomes were truly valid since both groups had fairly significant levels of mercury.
The researchers looked at the changes in intelligence over five years in these children and found that, if anything, the group who had the amalgam fillings increased their intelligence more (my italics) than did those who didn't get the mercury fillings.
Full-scale IQ, general memory index, and visuomotor composite scores increased between the baseline and 5-year assessments in both treatment groups. None of the differences between the change scores in the 2 treatment groups, adjusting for baseline score and randomization stratum, were statistically significant, although for all 3 tests, the differences favored the amalgam group (Table 3). Adjusting for additional covariates did not change the results appreciably.
There was no statistical difference in the intelligence changes between the two groups, but if the actual statistical analysis is examined an interesting thing pops out: the confidence intervals are huge. A large confidence interval means that the data was all over the place. Even though the differences overall were not statistically significant, based on the large confidence interval, many children were at the extremes. What this tells us is just what we would expect. Most kids aren't affected by the amounts of mercury found in the amalgams, but some are. It's these kids who are, who are much like the canaries in the mine shafts, whom we worry about. It's like a pack of wolves or other predators circling a herd of elk; the young, old and sick (i.e., the most vulnerable) are the ones that get nailed. The strong, healthy elk aren't bothered. It's the same with a toxic insult such as mercury--it's the vulnerable kids that are affected. Despite the fact that the averages don't change, some kids can be adversely affected and not have it show up in a study such as this one.
The other study published in the same JAMA issue took place in Portugal where the researchers followed and compared two groups of children--one with mercury amalgams and one without--for seven years looking at memory, ability to focus, visuomotor functions and nerve conduction velocities. As in the first study the children with the amalgams had significantly higher levels of mercury in their tissues, but no statistically significant differences in the parameters of neurological function measured. And like the first study the confidence intervals were wide, indicating a wide distribution of findings. Once again, I'm sure some of the most vulnerable children had problems. It would have been nice to have seen all the data instead of just the tabulation.
In the most recent issue of The American Journal of Forensic Medicine and Pathology there appeared a paper throwing more light on this subject. As the researchers reported:
It rarely occurs that issues such as mercury, dental amalgam, or possible amalgam neurotoxicity may indeed reach the forensic scenario. However, scientific data have given us reason to at least consider the fact that dental amalgam may be a poison, in the strictest medicolegal sense, and that therefore its mode of distribution and accumulation within the body and consequential toxic effects could indeed have relevance from medicolegal perspective. However, much of the possible cause-effect concatenation still has to be proven, and the authors would like to briefly illustrate the results of the present pilot study to stimulate consideration of this issue, in other words as mere "food for thought."
The authors of the study went on to describe the wealth of literature showing the correlation between mercury amalgams and tissue mercury levels. After summarizing the literature, they had this to say:
In essence, amalgam fillings have been shown to contribute to approximately two-thirds of the human body burden of mercury.
These researchers then analyzed the tissue mercury content of cadavers at autopsy and compared it to the number of mercury amalgam fillings. The reason this study is so important is that it is difficult to determine the amount of mercury in the tissues of living people because blood levels aren't a particularly accurate way to measure it. Neither are urine and hair. Most of the mercury stays locked in the tissues, especially brain tissue, making it problematic to measure since most people aren't eager to queue up for a brain biopsy, the only real way to find out.
Since corpses don't much mind a brain biopsy the data these researchers uncovered is, in my opinion, invaluable. They found that there was a direct correlation between the number of fillings and the amount of mercury in the bodies. And they found that most of the mercury was in the brain with lesser amounts in the thyroid gland and kidneys.
As they put it:
Mercury levels increased with the number of dental amalgams for all the anatomic sites. The interaction term between each anatomic site and the number of occlusal amalgam surfaces was statistically significant (P = 0.03), suggesting that the association between mercury levels and the number of occlusal amalgams was dependent on the anatomic site. Mercury levels in the pituitary gland and the cerebral cortex in subjects with more than 12 occlusal amalgam surfaces were more than 10 times higher than levels in subjects with 3 or less occlusal amalgams (both P = 0.0007). Levels in the thyroid and in the renal cortex were respectively about 5 and 4 times higher in subjects with 12 occlusal amalgams or more compared with subjects with 3 occlusal amalgams or less (P = 0.01 and P = 0.04, respectively).And their conclusions after a long discussion of the neurotoxic effects of mercury:
In summary, our research shows, for the first time, that frontal lobe cortex has the highest content levels of mercury associated with occlusal amalgam surfaces and total mercury levels approaching or exceeding 300 ppb (ng/g), wet weight, in some cases. This, in turn, strongly points to the hypothesis--which, in the future, should be looked into in larger and ad hoc studies--that mercury vapor, known to be a neurotoxicant, may indeed lead to some types of neurobehavioral disorders.
Now, I don't know about you, but I'm not all that keen to have mercury amalgams. I may be one of those who can withstand the mercury; in fact, I probably am because I had mercury amalgams as a kid, but had them removed and replaced years ago. When I had them in place, they didn't seem to do me any harm, but who knows, without them I might have become a rocket scientist.
I certainly wouldn't expose any of my children or grandchildren to mercury amalgams just because JAMA came out with a couple of articles claiming that they were harmless. Mercury is toxic, of that there is no question. The amalgams produce mercury vapor, of that there is no question. People with mercury amalgams have higher levels of tissue mercury, of that there is no question. So why inflict children (or yourself) with a poison that is for sure going to go to their brains? Even though it might not harm them.
An even better method is to keep your children away from sugar and refined carbohydrates, make them practice good dental hygiene, and prevent cavities in the first place, then you won't have that decision to make.
Posted by mreades at 8:16 AM | Comments (8)
April 20, 2006
Dr. Lynn Allan Smaha R.I.P.
Today's New York Times carried the obituary of Dr. Lynn Smaha, former president of the American Heart Association, who died suddenly of a heart attack at age 63. I'm not in any way using this post to make light of Dr. Smaha's death and I wish his family my heartfelt sympathies and deepest condolences. I can only imagine what a blow it must be to suddenly lose a spouse and father totally unexpectedly. (Click here for another obituary.)
My point in mentioning Dr. Smaha's passing is to mention that he was a disciple of the lipid hypothesis of heart disease, a staunch advocate of the low-fat diet (although he started to modify his views and at least consider a Mediterranean type diet after the data came in from the Lyon Diet Heart Study) and an even stronger proponent of aerobic exercise. He was also a strong believer in physician's practicing what they preach.
Excerpts from Heart doctors flunk own advice
By Maggie Fox, Reuters [11/07/99]
The advice is clear -- do not smoke, eat plenty of fruits and vegetables, and keep fat intake low to avoid heart disease.
But even heart specialists who are supposed to preach this advice to every patient, every day, are failing to take their own medicine, Dr. Lynn Smaha, president of the American Heart Association, says.
He took his fellow heart specialists to task on Sunday for their bad habits and for their failure to stress to patients that heart disease, in many instances, is self-inflicted.
"There are those among us who do not follow proper diets, who do not engage in physical activity," he told the opening session of the group's annual meeting. "And if we do not do it ourselves, how then can we translate effective techniques to our patients?"
Another statement by Dr. Smaha:
"Cardiovascular disease accounts for more than 40% of U.S. deaths and affects both men and women," says Lynn Smaha, MD, PhD, president of the American Heart Association. "Heart disease strikes men earlier, but the risk for women rises at menopause and continues to increase. Additionally, women are more likely to die from heart attacks." Smaha says women often underestimate their risk of stroke as well.
"Many women don't realize that stroke is just as serious for them as it is for men," says Smaha. "Stroke claims the lives of over 90,000 women a year. In comparison, approximately 40,000 die of breast cancer." Smaha says many of these deaths can be prevented.
"Strokes and heart attacks are often preventable, but American adults have a long way to go in changing their behavior," says Smaha. "On average, 60% of us don't get enough exercise, 55% are overweight, 45% have [LDL] cholesterol levels over 130, and 25% have high blood pressure."
Dr. Smaha, I'm sure, followed his own advice, kept his weight down, ate a low-fat diet, did aerobic exercise, and made sure his cholesterol remained in check--in short he did everything he recommended to others to avoid heart disease, yet he succumbed to a heart attack. If cholesterol were the cause of heart disease, if a low-fat diet was truly 'heart healthy,' if aerobic exercise kept coronary arteries supple and plaque-free, then Dr. Smaha would surely still be with us today.
But he isn't. And I don't think that all the beliefs he had on the proper prevention of heart disease were valid. I do believe, though, that we should all reflect on this tragically early death and ask ourselves if we're doing everything we can do for our own hearts. Although cancer is the disease we all seem to dread, statistically we're much more likely to die of heart disease. And in one third of the cases of heart disease, the first symptom is sudden death, which, I suspect is what happened to Dr. Smaha.
I can tell you that of the many thousands of patients MD and I have taken care of first hand with low-carbohydrate diets not a single one has had a heart problem while under our care. We have treated, say, 10-15,000 patients over the years, most of whom were under our care for an average of two months. Multiplying two months times 10,000 patients gives 20,000 patient-months, which, statistically should have produced a number of heart attacks, especially considering that virtually all of these patients were middle aged and overweight and most had high blood pressure, elevated cholesterol, blood sugar problems, and all the rest of the disorders making up the Metabolic Syndrome. I'm not saying that the low-carb diet we treated these patients with kept them from having heart attacks, I'm simply remarking on the statistics.
I wonder if Dr. Smaha's outcome would have been different had he followed a low-carb diet?
Posted by mreades at 9:02 PM | Comments (7)
April 19, 2006
Low-carb caveat
There was a little girl,
Who had a little curl,
Right in the middle of her forehead
When she was good
She was very good indeed
But when she was bad she was horrid.
So goes the familiar poem by Henry Wadsworth Longfellow, and so goes most of our low-carb diets I suspect. When we are in diet mode and are deeply committed, we are very good indeed, but when we break and hit the carbs (and this includes yours truly) we are horrid. A paper in this week's JAMA presents data confirming what I've long suspected: carb bingeing now and then could actually cause worse free radical damage than regularly eating more carbs on an ongoing basis.
The paper entitled Activation of Oxidative Stress by Acute Glucose Fluctuations Compared with Sustained Chronic Hyperglycemia in Patients With Type II Diabetes shows that patients with diabetes who have fluctuations in their blood sugars incur more free radical damage than those with high but not fluctuating blood sugar levels. Before we get into the nitty gritty of the paper, I will step back a little and go over some of the biochemistry involved so that the data will be more understandable to those who might not have a technical background.
First, let's look at how blood sugar is measured. The standard way is to draw blood (usually after the patient has fasted for 12-14 hours) and test it for a blood sugar level. Although this is the way that diabetics were monitored for years, it's not a particularly accurate means of managing patients with diabetes. The fasting blood sugar test itself is reliable, but it only tells what the blood sugar is at the precise moment the blood was drawn--not what it was the week before or the day before or even the hour before. The typical drill was that diabetic patients would come to the office, have their blood sugar levles checked, and based on the results, leave with their medications or insulin adjusted as necessary. Many diabetic patients who didn't like getting lectured by their doctors on following the proper diet, exercising, etc., learned that if they were very good indeed for the few days before their office visit, their blood sugar levels would be close to normal. They would leave with the congratulations of their doctors ringing in their ears and head back to the trough until a few days before their next visit.
A while back a clever person figured a way to detect blood sugar levels not just at the precise moment the blood was drawn but in a way that measures the average blood sugar level for the previous month or two. The test, called a hemoglobin A1C (pronounced, logically enough, hemoglobin A one see), tells the doctor what the patient's average blood sugars have been over the past couple of months. No more can patients be very good indeed for a day or two before their blood draw because a day or two of lower sugar levels won't change the test values. As you might imagine, the advent of the Hgb A1C test allowed doctors to manage their diabetic patients much better.
Just for grins I'll explain how the test works. If you're not interested, skip on down to the next paragraph. If you take a glass of water and stir some protein into it along with some sugar, over time the sugar will react with the protein in an irreversible way. The sugar will actually attach itself to some to some of the protein chains. The process takes a fair amount of time, but the longer you leave the sugar in the water with the protein, the more of it will attach. If you measure the amount of the protein-sugar complex that forms, you will have a rough measure of how long the sugar and the protein were together. If you don't find much of the protein-sugar compound, then you can figure that the two haven't been together for long; or if you find a lot, then you know they've been mixing it up for a while. The same goes for the amount. If you stir the protein into the water and add a tiny bit of sugar, after a time you will find a small amount of the protein-sugar compound; if you add a lot of sugar, then after the same amount of time you will find more of the protein-sugar compound. By taking multiple samples over time and tabulating the results you will be able to come up with a scale that says if you find this much of the protein-sugar compound after a certain number of days, then you can determine how much sugar was added. This is precisely the way that the Hgb A1C measurement works. Sugar in the blood attaches to protein in the blood. By measuring one of those proteins-sugar compounds (Hgb A1C) you can tell what the average amount of sugar in the blood has been over the past couple of months.
The second test I want to discuss that is critical to an understanding of this paper is the urinary measurement of 8-iso prostaglandin F2 alpha (8-iso PGF). When free radicals attack fatty acids that are a part of the cell membrane the damaged products produced are called isoprostanes. Isoprostanes in general are indicators of free radical damage and oxidative stress. Researchers can perform various experimental procedures and measure the release of isoprostanes in the urine and determine how much oxidative stress and free radical damage their procedure caused. 8-iso PGF is simply a specific isoprostane commonly used experimentally to determine the degree of oxidative stress/free radical damage.
Now that you know what all the tests are and what they mean, the paper is a pretty straightforward affair. It is well known that elevated blood sugar levels cause oxidative stress and free radical damage, which is probably the primary reason diabetic patients have increased risk for atherosclerosis and accelerated aging. The authors of this paper wanted to see if a steadily elevated blood sugar caused the production of more 8-iso PGF, i.e., more free radical damage, than wildly erratic blood sugars that averaged out to about the same as the steady state ones. In other words would a blood sugar level that stayed at around 180 (definitely diabetic) most of the time cause the same, more, or less free radical damage than a blood sugar that fluctuated between 100 (upper end of normal) and 250 (pretty high), but averaged by Hgb AiC measurement at about 180?
The researchers recruited 21 subjects with diabetes and 21 age and sex matched non-diabetic controls. They monitored the diabetic patients on a round the clock basis to determine not just their average sugar levels but their fluctuations as well.
The data showed that the diabetic subjects had much higher urinary levels of 8-iso PGF than did the non-diabetic patients, which would be expected. But the data also showed that diabetic subjects who had large fluctuations in blood sugar levels had even greater 8-iso PGF formation than diabetic subjects with more stable, yet still high, blood sugar levels.
These data were in diabetic patients but I suspect the situation holds true in non-diabetic patients as well. And, unfortunately, especially in followers of the low-carb diet. Why so?
Following a low-carb diet makes one a little glucose intolerant, which is the reason that the instructions for a glucose tolerance test always include the admonition to eat plenty of carbs in the week before the test. Why? Because all the macronutrients--glucose, fat and protein--are broken down by enzymes during the metabolic process. And all the enzymes necessary for the metabolism of the various macronutrients are made on demand but not immediately. If you are on a high carbohydrate diet, then you will have plenty of enzymes on hand to deal with the carbohydrates you consume. If you switch to a low-carbohydrate diet, it takes a while to manufacture the enzymes in the quantities needed to deal with the extra fat and protein that your metabolic system hadn't been exposed to. This deficiency of protein/fat metabolizing enzymes is the reason people starting a low-carb diet become so easily fatigued--they've got plenty of enzymes on hand to break down carbs, they just don't have the carbs to metabolize. Once they produce the enzymes necessary to deal with the load of protein and fat, which takes a few days, they become low-carb adapted and no longer feel fatigued.
Once people become low-carb adapted--as I hope we all are--then the same thing happens if they go face down in the donuts. They don't have the enzymes on board to deal with the sudden influx of glucose, and, as a consequence, their blood sugar spikes higher than it would on a person eating the same amount of carbohydrate who is already carb adapted.
This paper shows that these carb spikes are not benign. As the paper points out
Risk factors of atherosclerosis such as hypertension, regular smoking, hyperlipidemia, and obesity have been described as being associated with elevated urinary excretion rates of isoprostanes.
Since the best thing we can do for ourselves is limit free radical damage as much as possible, the obvious way to do so is to maintain a constant low level of blood sugar, for which the low-card diet is just the ticket. In view of these recent findings when we're good, we should be very good indeed, but when we're bad maybe we shouldn't be quite so horrid.
Posted by mreades at 4:34 PM | Comments (12)
April 18, 2006
Tough meat for vegetarians to swallow
Based on my considerable reading of the medical literature it seems as if everyone bends over backwards to put a healthy face on vegetarianism. A recent issue of Atherosclerosis, however, contains an article that goes against the herd.
Researchers in China recruited 57 healthy post-menopausal women who had been vegetarians for an average of a little over 10 years and age matched them with 61 healthy omnivores to study cardiovascular risk and carotid artery atherosclerotic disease.
To fulfill the criteria of apparently healthy subjects, women with any of the following conditions were excluded: a history of diabetes mellitus or fasting blood glucose over 126 mg/dL; hyperlipidemia (cholesterol level ≥240 mg/dL or triglyceride level ≥200 mg/dL); regular alcohol drinking or smoking; any treatment that might affect lipid metabolism; history of CVD, hypertension (systolic blood pressure (SBP) ≥160 mmHg or diastolic blood pressure ≥95 mmHg), or use of anti-hypertensive medication; or serum creatinine level ≥125 μmol/L; thyroid disease; and malignancy of any kind. Vegetarians were defined as exclusive consumption of a vegetarian diet void of meat, fish, and poultry for at least 5 years.
After an overnight fast the subjects provided blood samples that were evaluated for lipids, homocysteine, vitamin B12, and a host of other parameters. The researchers evaluated the presence and degree of any carotid artery disease present in the subjects using ultrasonography.
After the results were tabulated it turns out that vegetarians have significantly increased levels of homocysteine along with decreased levels of vitamin B12. The low levels of vitamin B12 would be expected because vitamin B12 is found only in foods of animal origin, which is one of the primary indicators that humans have evolved eating meat. Homocysteine, a substance thought to be toxic to the arteries, is involved in the metabolism of methionine and is reduced with folic acid, vitamin B12 and vitamin B6. The interesting thing about the findings in this study is that when patients have elevated homosysteine levels they are usually advised to eat more fruits and vegetables to increase their intake of folic acid and to reduce their intake of meat, which provides large amounts of methionine, the precursor of homocysteine. In the case of the subjects in this study, they were already eating large amounts of fruits and vegetables while avoiding meat altogether, yet ended up with more homocysteine than those subjects consuming meat. (These findings are not unusual; most studies on vegetarians find this same phenomenon.) What this proves--at least to my satisfaction--is that vitamin B12 is more potent at reducing homocysteine that the combination of folic acid and vitamin B6. Another surprising finding was that the folic acid levels were the same in both groups.
Another finding in this study was that the vegetarians had elevated levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), an inflammatory substance implicated in the development of atherosclerosis. After some statistical legerdemain, however, the researchers discounted these findings.
This study demonstrates a significant association between levels of Hcy [homocystene] and sVCAM-1, and between vegetarians and sVCAM-1; however, these relationships were attenuated after adjustment for associated covariates.
As you would expect, the vegetarians had both lower LDL and lower HDL levels than the omnivores, which goes to show that if you want your HDL to go up, you've got to eat meat (or at least fat).
Ultrasonography showed no difference in carotid artery thickness between vegetarians and omnivores, which the authors of the study reported as showing no difference in degree of arterial disease. Surprisingly, one of the factors that was different between the two groups the researchers didn't mention at all: pulse pressure.
The data clearly shows a difference in pulse pressure between the two groups that appears to be statistically significant (I say appears because all the data to make such a determination wasn't provided--only the 'p' factor). An increased pulse pressure indicates that arteries are less compliant, which is an indicator of increased rigidity and, consequently, more disease. And the vegetarians had a pulse pressure of 56.6 compared to 52.6 in the omnivores. I would love to have seen this disparity at least mentioned, if not discussed, in the paper.
What did the researchers think of their findings?
In the present study we showed that CA [carotid atherosclerosis] was not significantly different between vegetarians and omnivores in apparently healthy postmenopausal Chinese women. However, we found that plasma Hcy and sVCAM-1 were elevated and plasma Vitamin B12 was lower in vegetarians as compared with omnivores, which seemed to be contradictory to the common belief that a vegetarian diet is beneficial to CVD.
We could not demonstrate any significant beneficial effects of vegetarian diets on CA in this study.
The authors add this caveat:
Thus, all the evidence and inference should be under careful scrutiny.
Which, of course, means, hey, we know our data goes against what we all know to be true, i.e., that fruits and vegetables are good for us and meat is bad. And even though are data shows differently, these data need to be looked at with a jaundiced eye.
I wouldn't be surprised if the 'peers' who reviewed the article made the authors tack that line on as a condition of having the paper published.
Pass this post along to anyone you know who is a vegetarian for health reasons because it ain't all that healthy. And for those misguided souls who persist in believing that vegetarianism is our natural state on this planet, just enunciate the words VITAMIN-BEE-TWELVE to them clearly. It's like sticking a cross in a vampire's face.
Posted by mreades at 3:20 PM | Comments (4)
April 17, 2006
Slow Burn Fitness for boomers
I read a timely article in the New York Times yesterday about how baby boomers are showing up in emergency rooms in record numbers for fractures, dislocations, sprains, strains, and all kinds of other trauma thanks to their efforts to get in shape and delay the aging process. Orthopedic surgeons are doing a land office business replacing knees, hips, and a host of other parts on amateur jocks who are getting up in years.
"Boomers are the first generation that grew up exercising, and the first that expects, indeed demands, that they be able to exercise into their 70's," said Dr. Nicholas A. DiNubile, a Philadelphia-area orthopedic surgeon, who coined and trademarked the term boomeritis.
"But evolution doesn't work that quick. Physically, you can't necessarily do at 50 what you did at 25. We've worn out the warranty on some body parts. That's why so many boomers are breaking down. It ought to be called Generation Ouch."
Led by baby boomers, loosely defined as the 78 million Americans born from 1946 to 1964, sports injuries have become the No. 2 reason for visits to a doctor's office nationwide, behind the common cold, according to a 2003 survey by National Ambulatory Medical Care.
A Bureau of Labor Statistics study said infirmities associated with the athletic activities of middle-aged adults were the source of 488 million days of restricted work in 2002. When the Consumer Product Safety Commission examined emergency-room visits in 1998, it discovered that sports-related injuries to baby boomers had risen by 33 percent since 1991 and amounted to $18.7 billion in medical costs.
It appears from these statistics that you can't have it all. You can't stay in shape and keep your body from wearing out after you've put a few years on it, or so it seems. If you try to take it easy to spare your joints, you end up with a spare tire around your middle. What a choice to have to make.
But we really don't have to make that choice. We can both stay slim and fit and protect our joints, tendons and ligaments. How? By pursuing a type of exercise MD and I wrote about in the book Slow Burn.
Let me tell you how we came to write Slow Burn
Several years back an article appeared in Newsweek that our agent, Channa Taub, saw about a type of exercise that paid huge benefits but only required a few minutes per week. Channa, being totally exercise averse, figured that even she could endure 15-20 minutes per week, so she went to see visit the trainer who was the subject of the Newsweek piece and whose facility was in Manhattan. When she got there, she listened to the pitch from the trainer then asked if there was anyone closer to her home who did the same program. She was directed to a trainer named Fred Hahn, who had actually trained the trainers in the Newsweek article and who had a facility on the upper West side, much closer to where Channa lived.
Channa went to Fred's place on 78th Street, did a workout, and somewhere along the process she mentioned that she was a literary agent. Fred told Channa that he had been wanting to write a book about his methods. Channa told Fred that she represented a number of authors who wrote on health topics and mentioned MD and me. Fred was excited because he had been using our book Protein Power as the nutritional primer for all his clients and had been trying to arrange for us to come to New York and do a talk on low-carb dieting. Synchronicity again.
Channa called and told me about Fred and his methods and sent me a copy of the Newsweek article. She said that Fred was open to the idea of a collaboration with MD and me on a book about the subject. I read the Newsweek piece and thought it was okay, but nothing earth shattering. I told Channa that on our next trip to New York we would go with her to meet Fred and talk about his program.
Let me digress here to tell you that in both Protein Power
In due course we went to New York and found ourselves in Fred's facility. We all went to lunch and we spent the afternoon talking about Fred's program. Frankly, I took it all with more than a grain of salt.
Fred claimed that 15-20 minutes or so spent doing his program would increase muscle mass at anywhere from 100 to 150 percent faster than traditional strength training, that it would improve cardiovascular fitness (or what people think of as cardiovascular fitness) more than aerobic exercise, enhance flexibility, and increase bone density--all without risk to the joints, tendons, and ligaments. In other words, so Fred said, people could get more strength benefit from his method of training than they could from the three-times-per-week-in-the-gym pumping-iron workouts they were used to, more cardiovascular benefit than jogging or bouncing around in an aerobics class, more healthful joint flexibility than they could obtain from practicing yoga or Pilates, and strengthen their bones, all in 15-20 minutes per week. You can see why I was sceptical.
We told Fred we would think about the book project and left with a number of medical references he gave us. I was eager to get into the literature and see if there was anything to all the information he had given us.
I spent about two weeks poring over all the medical papers I could find, and it turned out that Fred was right. His method of slow training, which replaces quantity of exercise with quality, does tremendously reduce the risk for injury, increases strength and muscle mass faster than traditional weight training, improves flexibility and lives up to all the rest of his claims. I found it to be much like the low-carbohydrate diet--those who have done it swear by it; those who haven't poo poo it. And like the low-carbohydrate diet, there is a wealth of medical literature that supports all the claims.
I called Channa and told her to tell Fred we would co-author the book with him.
This post probably sounds like a Blogfomercial for Slow Burn, but it really isn't. I only wrote it because I read the piece in the New York Times and realized how many people were getting injured unnecessarily simply by following doctors' orders to exercise more. If you're one of those people, you can benefit from Slow Burn style training.
Here's what I learned in a nutshell in my medical research on Slow Burn:
The single best way to increase strength and muscle mass is to strength train.
The best way to strength train is to do resistance exercise, i.e., weight lifting.
The optimal way to lift weight--that which gives you the best result per time spent--is Slow Burn.
When I give talks on this subject almost everyone asks how Slow Burn training can increase cardio-pulmonary (heart and lung) fitness. That's the one idea that people have the most difficulty grasping. Let me tell you how it works.
When you run a few hundred yards (assuming you're out of shape) you end up puffing and panting and with your heart pounding. You assume that your heart and lungs aren't in good working order, and you assume that if you start a regimen of regular jogging or other aerobic exercise that in due course your heart and lungs will get in better shape. If you do pursue such a course, you will find that indeed you do breathe less hard and your heart doesn't pound, so you assume that both your heart and lungs are in better condition. The truth of the matter is that your heart and lungs are about the same as they were when you started--what has improved is your muscular fitness. Let me explain.
In the conditioning process the place where the rubber meets the road so to speak is at the level of oxygen entry into the muscle cells. As muscle cells work, they need oxygen. In an unconditioned muscle oxygen doesn't get into the cell particularly efficiently. Consequently, your body, in an effort to get more oxygen to the working muscle cells, pumps more blood (your heart pounds) that contains more oxygen (thanks to your huffing and puffing). As your muscles become more conditioned, what happens is that the body's ability to get oxygen into the muscle cells becomes much more efficient. After your muscles are conditioned and you run a few hundred yards, your heart doesn't pound and you don't pant because your muscles are getting plenty of oxygen because of the conditioning effect in the muscles themselves. It has nothing to do with your heart or lungs.
Much is made of the great bicyclist Lance Armstrongs cardio-pulmonary fitness, but let me ask you this: if I could transplant Lance Armstrong's heart and lungs into you, do you think you could win the Tour de France? It is doubtful. Lance Armstrong was born with an enormous heart and lung capacity that he uses to full advantage because of the conditioning of his muscles. If he let his muscles decondition, he would puff and pant after a short run just like we would.
If you enjoy exercise and are willing to pay the price for your enjoyment in the potential for bunged up hips, knees, and ankles, then by all means do it. If you are exercising because you want to stay fit and you do it grudgingly just because you think you ought to and figure that soreness and injury are part of the price you have to pay to stay fit as you age, then pick up a copy of Slow Burn
Posted by mreades at 2:21 PM | Comments (19)
April 15, 2006
Even monkeys aren't the same
I've posted often about my reluctance to accept as gospel data derived from studies on animals. Animals aren't just furry little humans--they are different genetically than we are and, despite the fact that animals have cholesterol, insulin, blood sugar, and all the rest, their systems behave differently. Even studies using monkeys or other primates, which are certainly closer to humans genetically than rats, don't always provide data that is applicable to humans. A few humans learned this the hard way in a recent study done in the UK that went horribly awry.
I was reading through some back issues of the New York Times when I came upon an article entitled British Rethinking Test Rules After Drug Trial Nearly Kills 6 about a trial study done testing a new immune stimulant drug. The six healthy men recruited for the study who took the drug almost paid for it with their lives. I'll excerpt the basics of what happened.
In February, when Rob O. saw the text message from Parexel International pop up on his cellphone in London -- ''healthy males needed for a drug trial'' for £2,000, about $3,500 -- it seemed like a harmless opportunity to make some much-needed cash. Parexel, based in Waltham, Mass., contracts with drug makers to test new medicines.
Just weeks later, the previously healthy 31-year-old was in intensive care at London's Northwick Park Hospital -- wires running directly into his heart and arteries, on dialysis, his immune system, liver, kidneys and lungs all failing -- the victim of a drug trial gone disastrously bad.
One of six healthy young men to receive TGN1412, a novel type of immune stimulant that had never before been tried in humans, Rob O. took part in a study that is sending shock waves through the research world and causing regulators to rethink procedures for testing certain powerful new drugs.
Within an hour of receiving the milky white drug in a Parexel research ward in the hospital on March 13, the volunteers were racked with chills, pain and nausea, said Rob O., who asked that his last name not be used, for fear that he might be hurt professionally. A doctor informed him he was ''seriously ill.''
''But no one's going to die?'' Rob O. recalled saying, believing he was participating in a fairly standard trial of a painkiller for arthritis.
The chilling response: ''Two of you might. Who's your next of kin?''
The trial began Monday, March 13, at 8 a.m., when the men began receiving TGN1412, each 10 minutes after the last. Within half an hour, the first patient had a headache and chills, said Ann Alexander, a London lawyer who is representing him. Nevertheless, doctors continued injecting new patients. About the time Rob O.'s infusion started, at 9:10 a.m., the first patient had passed out in an adjacent room, according to Ms. Alexander.
Before long, Rob O. said, he began to ache and shiver, feeling as if he had been ''submerged in arctic ice.'' For the rest of the day, six previously healthy men moaned in uncontrollable pain, vomited and struggled for breath, Rob O. and other participants said. Though a dose of steroids temporarily blunted the symptoms, their vital signs steadily deteriorated, and they were transferred to the intensive care unit.
Two of them were placed on ventilators. Uniformed men wheeled in blood filtering machines, Rob O. recalled, to cleanse the blood of acid. Doctors told him that his immune cells were attacking his organs.
The patients' families were summoned to the hospital at 3 a.m.
As it turned out all six survived, but not without some emotional and physical baggage. Their immune systems are still abnormal and the experience has left them with a sense of dread about future health problems.
With his immune system now essentially disabled, Rob O. says he cannot work, or even take the subway, for fear of infection. His liver and kidney tests are still abnormal. Britain's National Health Service covers his doctor's bills, but he has to pay the $87 cab fare.
''I can't believe that nobody will pay and nobody will be punished,'' Rob O. said. ''If I've lost 20 years of life because my liver packs in at 60 rather than 80, who will cover that?''
Why were these poor people subjected to this torture? Why were they given this drug that ended up almost killing all of them?
The British Medicine and Healthcare Products Regulatory Agency, which approved the trial at Northwick Park, announced Wednesday that ''the way the trial was run'' had not contributed to patient injuries, according to its preliminary investigation. The men experienced cytokine release syndrome, which involves an outpouring of toxic molecules when the immune system's T cells are activated, the report said; it could not have been predicted from previous animal studies using the drug[my italics], the association, TeGenero and Parexel agree.
Tests of TGN1412 in monkeys showed no significant trouble...
So, this drug was thoroughly tested in monkeys, close kin to us, and found not to cause problems. But when injected in humans it comes within an inch of killing them almost immediately. Humans and humans are the same; monkeys and humans are different.
Remember this cautionary tale the next time you hear or read about the results of a study using rats as subjects. Ask yourself if the data really apply to you.
Posted by mreades at 9:03 AM | Comments (5)
April 14, 2006
Trans fats and geography
A letter appeared in today's New England Journal of Medicine from a group of Danish researchers who had traveled throughout the world and sampled McDonald's French fries and KFC chicken for trans fats.
We determined the content of industrially produced trans fatty acids in 43 servings of fast foods bought in 20 countries between November 2004 and September 2005. We and our colleagues decided which cities to include in the study on the basis of planned visits for other purposes. The foods (chicken nuggets and french fries) were purchased from McDonald's and KFC outlets.
They discovered great geographical disparity in the trans fat content of these same food purchased in different countries.
The content of trans fatty acids varied from less than 1 g in Denmark and Germany to 10 g in New York (McDonald's) and 24 g in Hungary (KFC). Fifty percent of the 43 servings contained more than 5 g per serving.
Why the big difference in trans fat content from country to country? It's all in the cooking oil.
The cooking oil used for french fries in McDonald's outlets in the United States and Peru contained 23 percent and 24 percent trans fatty acids, respectively, whereas the oils used for french fries in many European countries contained only about 10 percent trans fatty acids, with some countries as low as 5 percent (Spain) and 1 percent (Denmark). At KFC, some values for trans fatty acid content were above 30 percent. Within the same chain in the same country, large variations in these values were observed -- for instance, between KFC outlets in Hamburg and Wiesbaden in Germany and between Aberdeen and London in the United Kingdom.
The take home message from all this is that it is not only the carbohydrate content of French fries and breaded fried chicken, it is the trans fat content too. Especially in foods made outside the home. It's easy to wolf down a chicken sandwich and an order of fries and come away with the effects of 20-30 grams of trans fats swirling in your blood. Data from the Zutphen Elderly Study published a few years back in Lancet showed that consuming 5 grams of trans fats per day increased the risk of developing cardiovascular disease by 25 percent. Now I'm not sure I buy those figures as being exact, but I do believe there is little doubt that trans fats cause problems and are best avoided. And 25-30 grams per day is a whopping large dose, but it is a dose being consumed by us and our children every single day that we and they eat at fast food franchise outlets.
My advice is to avoid McDonald's French fries and KFC breaded chicken like death. But if you've just got to have some, well, make sure you get it in Denmark.
Posted by mreades at 12:13 AM | Comments (3)
April 13, 2006
My morning horoscope and HDL
As a part of her early morning paper-reading ritual my wife always sees fit to alert me to my horoscope, which, today, in our local paper was:
A closed mouth gathers no foot. Big ambitions may be bandied about, but when push comes to shove it's the guy who does the actual work that gets the glory.
Typically I about half listen to her read these things because I'm usually busy pouring over my own newspapers, but today it got my attention. I had finished all my newspaper reading and was reviewing a recent medical paper from the American Heart Journal entitled The independent correlation between high-density lipoprotein cholesterol and subsequent major adverse coronary events, and what caught my ear in the horoscope reading was the line "a closed mouth gathers no foot." In view of this medical article it made me think of Dean Ornish and his idiotic analogy of HDL-cholesterol as a garbage truck that I wrote about a few days ago. It made me wonder if Dr. Ornish had read this same paper I was reading, and if so, did he feel like he had put his foot in his mouth?
The paper is not particularly brilliant but it contains much valuable information. Researchers from Indiana University School of Medicine identified a group of about 7000 patients who had been seen in a huge outpatient care facility and who had had two lipid measurements (lipids are blood fats including cholesterol. Today a typical lipid profile lab test contains the following blood levels: total cholesterol, LDL-cholesterol, HDL-cholesterol, and triglycerides) taken between the years 1985 and 1997. The researchers compared the starting lipid values to the lipid values years later on these subjects and correlated them with any heart disease that might have developed.
Subjects having a lower HDL-cholesterol level at the first or second test were more prone to develop heart disease. Subjects whose HDL-cholesterol levels fell between the first and second tests were even more prone to develop heart disease. And those subjects whose HDL-cholesterol levels went up between the first and second test seemed to incur some protection against developing heart disease. As the authors of the study report:
The level of risk reduction was nontrivial: every 1 mg/dl higher baseline HDL-C was associated with about 1% lower in cardiac risk. Comparably, for every 1 mg/dl increase in HDL-C change over the average 2.6 year measurement interval, cardiac risk was 0.7% lower.
None of the other lipid parameters showed a significant correlation with the development of heart disease.
We were surprised that, contrary to prior research, LDL-C and its change were not associated with subsequent cardiovascular risk.
I would be surprised if they weren't surprised. Researchers are always surprised when LDL-cholesterol isn't shown to be bad in some way.
This study, along with a lot of others, does seem to show, despite any Dean Ornish HDL-cholesterol-is-a-garbage-truck gibberish to the contrary, that HDL-cholesterol may be protective against heart disease. But if HDL-cholesterol is ever conclusively shown to be a protective factor against heart disease, I would be willing to bet that it will be due to its anti-inflammatory properties, not its cholesterol transport properties.
In either case, if you want to get your HDL-cholesterol levels up, you have to eat fat. Fat intake drives HDL-cholesterol levels up; decreasing fat in the diet--as Dean Ornish has discovered to his chagrin--drops HDL-cholesterol levels.
So, if you want to raise your HDL-cholesterol level by putting something other than your foot in your mouth, try a cheeseburger, hold the bun, hold the fries. It's a lot tastier.
I wonder if Dean Ornish is a Gemini?
Posted by mreades at 1:34 PM | Comments (3)
April 12, 2006
Palm oil fights back
Not long ago I posted on the spurious attack job that Michael Jacobson and the Center for Science in the Public Interest (CSPI) mounted against palm oil. Apparently the palm oil industry isn't taking it lying down. A couple of days ago the Malaysian Palm Oil Promotion Council placed a large ad in the New York Times refuting the claims the CSPI ad made about the saturated fat in palm oil and the industry's being responsible for the decimation of orangutans.
Today's New York Times has a lengthy article about the fracas entitled Fat Fight Becomes a Rumble in the Jungle that focuses primarily on actor Paul Newman's anger over the CSPI's fingering him and his cookies (made with palm oil) as orangutan killers and heart disease promoters. As you might imagine, Mr Newman, who is as liberal as they come, is outraged the he, The Paul Newman, could possibly be accused of being both an anti-environmentalist and a health menace to kiddies (the main consumers of his cookies). And to be so accused by another such bastion of liberalism as the CSPI must have seemed beyond the pale. Although I too have a problem with Mr. Newman's cookies (and it ain't the palm oil that's in them) I can see his point. The CPSI's attacks were, by its leader's own admission, inaccurate and were pure demagoguery in its worst form.
Mr. Newman's daughter, an uber-environmentalist herself, encouraged dad in the early 1990's to start a branch within his food company Newman's' Own using only organic products. Since then Newman's Own Organics has produced a line of foods containing organic ingredients and distributed throughout the country. Mr. Newman donates all the profits from the enterprise to charity.
When Mr. Newman decided to add crackers and cookies to his line, he discovered what all cooks and food manufacturers know: it takes shortening. Problem is shortening is a fat. Fats combine with the flour and surround the flour particles and break or 'shorten' (thus the name, shortening) the long gluten strands into shorter sections so the resulting products are flaky like a croissant or non-chewy like the two outside layers of an Oreo cookie or a cracker. The kind of fat that works the best as shortening for crisper products is saturated fat, which is why butter and lard have been used for ages. In an effort to get away from saturated fats, food manufacturers moved to partially hydrogenated fats, trans fats, which have the same shortening characteristics of saturated fats but up until Jan 1 of this year could be included on the label as polyunsaturated fats. But as we all now know, trans fats are bad actors. So Mr. Newman was on the horns of a dilemma. He wanted an Oreo-like cookie that smacked of good health, but needed shortening to make it. In today's anti-saturated fat world butter and lard were out, so he opted for palm oil, a source of saturated fat, but one that most people wouldn't recognize as such.
But he didn't fool the eagly, saturated-fat-seeking eyes of the folks at CSPI, who went on the attack. What the CSPI found so egregious in Mr. Newman's products compared to, say, a regular Oreo cookie, is that Mr. Newman had the temerity to actually advertise his cookies as a healthy alternative when they contained, horror of horrors, saturated fat. In fact, the CSPI and
Mr. Jacobson and the report's other authors accuse Mr. Newman of "bragging" on his labels for cookies and microwave popcorn that palm oil is free of trans fat and is less saturated than palm kernel oil."These statements are literally true, but mislead people into thinking that palm oil is positively healthy," the report said. "Palm oil is not a health food."
So, who is right and who is wrong in all this finger pointing? Both.
Mr. Newman is correct that palm oil is a more healthful alternative to trans fat, but he's wrong in saying his cookies are healthful; Mr. Jacobson is right that Mr. Newman's cookies aren't particularly healthful, but is off the mark on his criticism of palm oil. Let's look at the facts.
Just because a product is made with all organic ingredients doesn't mean that it's good for us to eat. Pure cane sugar is not good for you whether it's organic or not. If I had to eat a cookie I would rather eat one of Mr. Newman's than one filled with trans fat, but health-wise I would be better off avoiding the cookie altogether.
Michael Jacobson and the CSPI are totally off base in their attack on palm oil in particular and in saturated fat in general. Remember, these were the same guys promoting trans fat-laden margarine over butter just a few years back. There is no conclusive evidence that saturated fats, which are perfectly normal fats and have been part of our diets for millennia, are a danger for heart disease or anything else. In fact, carbohydrates, the macronutrient much beloved by Dr, Jacobson and the CPSI, when over consumed are converted by our own bodies to palmitic acid, a saturated fat. Generally, our bodies tend to detoxify ingested toxins by breaking them down and/or converting them to non-toxic substances, which is precisely what happens with carbohydrates. It wouldn't make sense from an evolutionary perspective for our metabolic systems to convert a non-toxic substance into a toxic one, which would be the case if the Jacobson/CPSI way of thinking were correct.
What I find particularly loathsome about Michael Jacobson and the CPSI is that they apparently created the orangutan 'crisis,' which they knew to be untrue to bash Mr. Newman and others who use palm oil in their products. According the the New York Times:
Mr. Jacobson denies that he has a personal campaign against the Newmans and concedes that their palm oil isn't killing orangutans (my italics). But he still takes their labeling to task.
How could you believe anything this man says? But then, he does get some things correct, although not for the right reasons. After conceding that their products maybe aren't responsible for the destruction of the orangutans, he says of the Newmans:
"They may be environmentally sound, but don't eat these cookies if you really care about your heart."
I agree. Don't eat these cookies (or any others) if you really care about your heart.
Posted by mreades at 11:32 AM | Comments (2)
April 11, 2006
High-fructose corn syrup follies
As anyone who has ever Googled it knows, there is information all over the net on high-fructose corn syrup (HFCS). The information ranges from that put out by groups believing that HFCS is at Satan's right hand to that put out by the Corn Refiners Association, which, as you might expect, says, Hey, HFCS is just sugar in a different form, no better or worse than plain old table sugar. Even the New York Times is entering the fray. In today's issue Nicholas Kristof writes an opinion piece blaming HFSC for the obesity epidemic and wanting to tax it.
The HFCS promoters aren't taking all this abuse lying down. Last week at the Experimental Biology meeting in San Francisco researchers underwritten by the HFCS industry made a presentation showing that HFCS was harmless. These findings were, of course, trumpeted to all the media by the HFCS people, and the media fell into step and reported the findings.
Before we get into what the findings were, let's look at what we do know for sure about HFCS and fructose. First, there is no question that the consumption of fructose has increased dramatically since the development and entry of HFCS into the food supply in about 1970. Depending upon whom you want to rely, the figures as to the actual increase vary, but there is no doubt that the amount of fructose has significantly increased over the past few decades. And there is no doubt that the overall consumption of caloric sweeteners (another term for sugars) has increased over the same period. In fact, sugars of one form or another account for an unbelievable 20-25 percent of calories consumed by the average American. Think about that for a minute. Almost a quarter of our diet is composed of empty calories from a substance that we as humans were never exposed to during the 2.7 million years of our existence as humanoid creatures on this planet as we were being molded by the forces of natural selection to be the creatures we are today. (One of my favorite quotes on this comes from Blake F. Donaldson, M.D. who long ago wrote a book called Strong Medicine. Says Dr. Donaldson: "During the millions of years that our ancestors lived by hunting, every weakling who could not maintain perfect health on fresh meat and water was bred out.")
So fact one, we know were eating more sugar in general and more fructose in particular. We also know that fructose is metabolized differently than other sugars. Glucose, for example, can be used as is by virtually every cell in the body; fructose can only be metabolized in the liver (and in sperm cells). If we eat too much glucose, the metabolic process stores it away as glycogen--if we eat too much fructose, our livers convert it to fat and, typically, store it in the liver. Why? Because glucose metabolism is tightly controlled and fructose, in simple terms, jumps the main control point in the sugar metabolism pathway. Click here to read a fairly accurate and comprehensible essay on this process. Click here for full text of a paper about fructose metabolism. (I don't totally agree with the conclusions in this paper, but the description of the control point in fructose metabolism is accurate.)
If we forget about arguing over exactly how much the increase in fructose consumption has been over the past 30 years and focus only on what we know for sure, we can state the following with pretty much certainty: We're eating more fructose than ever, it's converted to fat in the liver, and fatty liver disease is on the rise. To see a previous post on non-alcoholic fatty liver disease, click here. So, the only conclusion that we can draw from these facts is that a lot of fructose is bad for us.
I'm sure the folks involved in the HFCS industry realize this and decided that they had to take some kind of steps to counter the mass of accumulating evidence indicating that fructose is not just an innocent bystander in the diabetes and obesity epidemics. What better way to do it than to underwrite a study showing that fructose is harmless, then release that fact to the press and count on them to disseminate the info under the imprimaturs of the various media outlets. That would be a way to do it.
But how could you underwrite a study and be sure of the results? Well, if you're in the HFCS biz, you're kind of in a no-lose situation. If you construct the study in such a way the fructose almost can't come out looking bad, but it does despite your best efforts, then you simply don't release the results to the press. If the results get picked up online, who cares? It's just one more negative posting among the thousands of others out there. But if the results are positive or if they're just not negative, then you're armed for the attack using the media.
If I wanted to construct a study that would give non-negative results I would use young, healthy, thin subjects and I would design the study so that these subjects consumed small amounts of fructose over a short period of time because the negative effects of fructose take a while to become manifest.
Lo and behold, that's exactly what they did. (Click here to see the study abstract.) The study subjects were 30 lean women who were randomized into two groups. Both groups ate the same number of calories for one day; one group drank soft drinks sweetened with HFCS while the other group drank their soft drinks sweetened with sucrose (table sugar). The researchers checked blood for glucose, insulin, leptin and ghrelin on this first day. The next day these subjects were allowed to eat whatever they wanted, after which blood values were once again evaluated. That was the end of the study. Would you be surprised to learn that this study showed absolutely no difference between the two groups in terms of any of these blood parameters? Nor would I.
In the first place, we don't know how many soft drinks the subjects consumed. Since sucrose is 50 percent glucose and 50 percent fructose, one half of the sugar in the soft drinks sweetened with sucrose was actually glucose. HFCS is 55 percent fructose, so the difference in fructose between a six pack of soft drinks sweetened with HFCS and the same six pack sweetened with HFCS is about 10-14 grams. Not enough to make a difference in only one day in a lean, healthy person. So, when you get right down to it, the study didn't show squat, but it did give the HFCS people something to issue a press release about and to talk up on their website. Notice in this report from Yahoo Health how the writer pretty much picked up the press release verbatim. That's what the HFCS folks are counting on.
Will Rogers once said, "The only thing I know is what I read in the newspaper."
In these days, if that's all you know, you're in trouble.
Posted by mreades at 11:38 AM | Comments (3)
April 2, 2006
The Dean Ornish HDL-ain't-nothin-but-a-garbage-truck rag
I feel about Dean Ornish the same way as one of my favorite philosophers, David Stove (1927-1994), must have felt about his own philosophy department at the University of Sydney when he wrote about it thusly:
[It] is a disaster area, and not one of the merely passive kind, like a bombed building, or an area that has been flooded. It is the active kind, like a badly leaking nuclear reactor, or an outbreak of foot-and-mouth disease in cattle.
And like some kind of a toxic spill, Dr. Dean Ornish is there emitting effusions of imbecilities into the airwaves year after year, polluting the minds of those gullible enough to listen.
His latest screed is a 'fact' sheet written in response to a presentation that was made November 9, 2003 at one of the scientific sessions of the meeting of the American Heart Association. The presentation was ultimately written up as a paper and published in JAMA in January 2005. Why Ornish is just now getting around to attacking this paper I haven't a clue.
Let's first go through this study; then we'll take a look at what has got Ornish's panties in a wad. Finally, we'll deal with his 'fact' sheet.
The paper entitled Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for Weight Loss and Heart Disease Risk Reduction is another one of those studies not really worth the paper they're written on because of fatal flaws in both the data collection and the study design.
The researchers recruited 160 people from newspaper ads and local TV news blurbs. These subjects were randomly assigned to one of the four following programs: the Atkins diet, the Ornish diet, the Zone diet, or Weight Watchers. Each group of 40 subjects underwent what the researchers referred to as "maximum effort," which amounted to the following intervention:
A single team composed of a dietitian and physician administered diet-specific advice to each group, meeting for 1 hour on 4 occasions during the first 2 months of the study. At the first meeting, the team revealed the diet assignment and provided the corresponding rationale, written materials, and official diet cookbook. Subsequent meetings aimed to maximize adherence by reinforcing positive dietary changes and addressing barriers to adherence.
The Atkins diet group aimed for less than 20 g of carbohydrate daily, with a gradual increase toward 50 g daily. The Zone group aimed for a 40-30-30 balance of percentage calories from carbohydrate, fat, and protein, respectively. The Weight Watchers group aimed to keep total daily "points" in a range determined by current weight. Each "point" was roughly 50 calories, and most participants aimed for 24 to 32 points daily. Lists provided by the Weight Watchers Corporation determined point values of common foods. The Ornish group aimed for a vegetarian diet containing 10% of calories from fat.
In an effort to isolate the effects of the dietary component of each plan, we standardized recommendations pertaining to supplements, exercise, and external support. We encouraged all participants to take a nonprescription multivitamin daily, obtain at least 60 minutes of exercise weekly, and avoid commercial support services. To approximate the realistic long-term sustainability of each diet, we asked participants to follow their dietary assignment to the best of their ability until their 2-month assessment, after which time we encouraged them to follow their assigned diet according to their own self-determined interest level.
Basically here is what happened. The researchers recruited people from the greater Boston area who were overweight and wanted to participate in a weight-loss study. Each person was put in with a group of 39 other people and on the first day were informed which diet they were to go on. The subjects attended three more meetings of about an hour each over the next two months, and were then told to go an do their best and to come back in ten months.
What were the results? Pretty much what you would expect with this level of effort and attention. About half of the subjects dropped out, and the ones who stayed in were lax, to say the least, in following their specific program. After the two months of "maximum effort" the subjects in the Atkins group were eating fewer carbs, the ones in the Ornish group were eating less fat, and the ones in the other two groups were in between. At the end of the year, the groups were pretty much indistinguishable in terms of their diet. For example, subjects in the Atkins group were eating an average of 190 grams of carbohydrate and about 80 grams of fat while those in the Ornish group were eating 218 grams of carbohydrates and 64 grams of fat (21 grams of which were saturated fat, an absolute no no on the Ornish program). So the low-carbers weren't low-carbing and the low-fatters weren't low-fatting.
Those subjects who remained in the study were evaluated at the end of the first two months, at six months and at the end of the year. Researchers evaluated a number of lab values at these milestones looking for differences between the groups. What they found was that there was very little difference, which isn't surprising since most of the subjects went off their assigned diet and kind of tended back toward what they were eating at the beginning of the study. There were some slight differences, however, and it was one of these differences that stuck in Ornish's craw.
Turns out that the dieters in the Ornish group dropped their levels of HDL-cholesterol, the so-called 'good' cholesterol, whereas it went up or stayed the same in the other groups. We'll consider the HDL issue shortly, but first let's look at the fatal flaw in this study.
All the subjects who were recruited were obese. They had BMIs of 35 and weight about 220 pounds on average. To determine their baseline diets the subjects were asked to complete 3-day food records at the start of the study. As reported by these subjects, their intake at the start of the study when they weren't actively dieting was around 1950 calories. I can tell you from long experience that people weighing 220 pounds and who aren't dieting consume one hell of a lot more than 1950 calories a day. If you run 220 pounds through one of the equations commonly used to calculate energy expenditure you will discover that these subjects require somewhere in the range of 2900 calories per day just to maintain their body weight. At the caloric intake they reported at the start of the program, they would be in an almost 1000 calorie per day deficit. What does it all mean? It means that the recording of the diets of these subjects was totally unreliable. And if it was this unreliable at the start, who can say whether or not it remained unreliable throughout. If the macronutrients were analyzed based on the reporting of these subjects, then those figures were totally unreliable as well.
As you might expect, all the lab parameters were pretty much the same between all the groups. There were no statistical differences between total/HDL cholesterol, insulin, and C-reactive protein and no significant effects on blood pressure or glucose. What can be pretty much concluded from this sorry study is that if people don't follow any kind of a diet, nothing much changes. Despite the fact that the study was a major bust in terms of data, there was one difference between the groups: the subjects on the Ornish diet dropped their HDL levels significanlty, which brings us to his 'fact' sheet.
The 'fact' sheet, which can be read in it's entirety by clicking here may contain a few facts, but any hard facts it does contain are soon dissolved in a strong solution of total nonsense. The fact that WebMD chose to publish this nonsense should tell you all you need to know about that outfit.
He starts by showing all the positive findings of the study in regards to his program. Unfortunately, most of these statements are not backed up by the study. He then gets to the real problem with this study as he sees it:
The authors reported that "all but the Ornish diet resulted in significant reductions in the Framingham risk score." However, this finding is very misleading.
The Framingham risk score is a system developed by the people in charge of the long-running Framingham study and is calculated to a great extent by total cholesterol and HDL-cholesterol levels. In this scoring system anything that lowers HDL levels increases the risk for heart disease. Total cholesterol levels fell in all the groups in the above study and HDL levels increased in all the groups except for the Ornish group in which HDL levels dropped. As a consequence, according to the Framingham score, the subjects on the Ornish diet increased their risk for heart disease, which does not set well with Dr. Ornish who has built his reputation on the fact that his program protects against and even reverses heart disease.
Like a politician caught with his hand in the till, Ornish comes up with this convoluted explanation of why all the rules don't apply to him or his program. He has this to say about the HDL levels falling in the group on his diet:
What does this mean? Your body makes HDL to remove excessive fat and cholesterol in your diet, like a garbage truck. Most Americans consume a diet high in saturated fat and cholesterol, so those with higher HDL levels are at lower risk for heart disease since they will be more efficient at metabolizing and removing excessive saturated fat and cholesterol. In other words, those with higher HDL levels have more garbage trucks (HDL) to get rid of the garbage (excessive fat and cholesterol).
However, when someone on a high-fat, high-cholesterol diet changes to a healthy low fat, low-cholesterol diet, their HDL levels may not increase or even decrease because there is less need for it. When you have less garbage, you need fewer garbage trucks to remove it, so a reduction in HDL on a low-fat diet is not harmful.
In contrast, someone who increases the amount of fat and cholesterol in their diet (e.g., an Atkins diet) may increase their HDL because their body is trying to get rid of the extra garbage (fat and cholesterol) by increasing the number of available garbage trucks (HDL). For example, eating a stick of butter will raise HDL in those who are able to do so, but that does not mean that butter is good for your heart.
Interesting, but just like the famous "I did not have sex with that woman, Ms. Lewinsky" speech, it's a bunch of smoke and mirrors. And it doesn't even make sense, but that is never a problem for Dr. Ornish.
HDL does indeed scavenge cholesterol from the tissues and transport it to the liver where it is then repackaged and sent back out to the tissues or is discharged into the GI tract through the bile. The cholesterol in the bile is then reabsorbed into the liver, repackaged and sent back out to the tissues. Here is where the Ornish analogy to the garbage truck breaks down. His terminology implies that the cholesterol is taken to the 'dump' where it is deposited never to be seen again. In actuality, using his terms, what happens is that the garbage trucks take the garbage (cholesterol) to the dump and other trucks pick it up and bring it back. So, if you've got fewer garbage trucks hauling it to the dump, you need fewer to bring it back.
Because it doesn't really make sense that years of natural selection would have designed a system to act this way--taking it away and bringing it back to no useful purpose--researchers have suspected that there is much more to HDL than simply the cholesterol-scavenging aspects. And sure enough, there are.
HDL acts as an anti-inflammatory agent and an antioxidant. It binds harmful substances in the blood, stimulates endothelial cell movement, decreases multiple clotting functions, protects red blood cells, stimulates the synthesis of prostacyclin (an important substance involved in arterial relaxation), and increases the half life in the circulation of this prostacyclin. HDL reduces growth factor synthesis in the vascular smooth muscle cells, stimulates the production of nitric oxide, modulates endothelial function and is antithrombotic. All in all, HDL is something you want more of, Dean Ornish's talk of needing fewer garbage trucks notwithstanding.
As to the idea that lower HDL levels are a function of having less 'garbage' to cart away, recent studies show that people with hyperinsulinemia apparently destroy their own HDL particles at greater rates than those with normal insulin levels, leading to lower blood amounts. Apparently people have lower HDL levels because they have an underlying problem, not because they have less 'garbage' to haul away. And any way you want to cut it, the Ornish diet lowers HDL levels. Not only did the study detailed above show this HDL lowering effect, his own published studies show it as well.
But our Dean doesn't let a little thing like the facts stop him. Not on your life. He ends his 'fact' sheet by explaining the fall in HLD levels seen on his program with the same faulty argument that he has used forever:
At best, HDL is only a risk factor for heart disease. In our studies over the past 25 years, we used actual measures of heart disease to see what happened to patients with severe coronary heart disease who consumed a low-fat, whole foods diet [my italics]. They showed reversal of their heart disease using state-of-the-art measures such as quantitative coronary arteriography, cardiac PET scans, thallium scans, and radionuclide ventriculography in randomized controlled trials published in leading peer-reviewed journals. Also, there were 2.5 times fewer cardiac events in these patients. LDL decreased by 40% on average after one year and HDL decreased by 9%, yet these patients showed clear reversal of their heart disease in every way we could measure.
I posted on this very subject a few days ago. All the published studies he refers to are with subjects who are following his program, which comprises four parts: stress management and meditation, smoking cessation, exercise, and a low-fat, vegetarian diet. As I pointed out in my earlier post meditation and stress reduction reduce the incidence and severity of heart disease all by themselves as does exercise and stopping smoking. Ornish tries to pin whatever success his patients have on his program to the diet, when there are three other components that have been shown to reduce heart disease that he tries to sweep under the rug.
We can turn Australian philosopher Stove's words on Ornish and his idiotic arguments once again:
How did an argument so easily answered ever impose itself upon intelligent people? Easily. It was simply a matter of ensuring...a one-sided diet of examples.
Posted by mreades at 12:56 AM | Comments (6)