Health for life

A diet high in omega-3 polyunsaturated fat lowers levels of problem enzyme

Columbia University Medical Center (CUMC) researchers have found that a diet high in saturated fat raises levels of endothelial lipase (EL), an enzyme associated with the development of atherosclerosis, and, conversely, that a diet high in omega-3 polyunsaturated fat lowers levels of this enzyme. The findings establish a "new" link between diet and atherosclerosis and suggest a novel way to prevent cardiovascular heart disease. In addition, the research may help to explain why the type 2 diabetes drug rosiglitazone (Avandia) has been linked to heart problems.

The study, conducted in mice, was published in the October 4 online edition of Atherosclerosis, Thrombosis, and Vascular Biology.

Like other lipases, EL plays a role in the metabolism of blood lipoproteins, which are complexes of lipids (fats) and proteins. EL, which is secreted by macrophages (a type of white blood cell) and other cells in arteries, was discovered in 1999. Studies have shown that elevated EL is associated with atherosclerosis and inflammation. Until now, however, little was known about how dietary fats might affect this enzyme, said study leader Richard Deckelbaum, MD, the Robert R. Williams Professor of Nutrition professor of pediatrics and of epidemiology and director of the Institute of Human Nutrition at CUMC.

In the current study, a strain of mice susceptible to atherosclerosis was fed a normal diet enriched with either palmitic acid (a common saturated fat) or eicosapentaenoic acid (an omega-3 fatty acid, or polyunsaturated fat, found in fish oil, among other foods). After 12 weeks, the mices aortas were examined for changes in the expression of EL and inflammatory factors. Aortas of mice fed the saturated fat diet showed a significant increase in EL and detrimental changes in inflammatory factors, while those of mice fed the polyunsaturated fat diet showed a significant decrease in EL and beneficial changes in inflammatory factors. Studies in cultured macrophages showed similar results.

"Our study identifies a new way in which the high-saturated-fat Western diet could lead to the development of atherosclerosis, though, of course, these results need to be confirmed in human studies," said Dr. Deckelbaum. "The findings might also explain some of the cardiovascular benefits that have been attributed to omega-3 fatty acids."

The researchers also found, in cell culture studies, that macrophages fed saturated fat showed increased expression of PPAR-gamma, a cell signaling molecule that plays a role in regulating lipid metabolism and inflammatory responses. This increase was blocked when the cells were fed an omega-3 fatty acid.

"These findings are intriguing, because we know that the diabetes drug rosiglitazone (sold under the brand name Avandia) is a strong PPAR-gamma activator and that it has been associated with an increased risk of heart disease," said Dr. Deckelbaum. "So we hypothesized that if rosiglitazone activates ppar-gamma, it might also activate EL, which would explain its effects on the heart."

In fact, when the macrophages were given rosiglitazone, the expression of EL increased markedly. The addition of omega-3 fatty acids to the cells blocked this increase. "This would suggest that besides raising LDL cholesterol levels, rosiglitazone can raise the risk of cardiovascular disease by increasing EL," said Dr. Deckelbaum. "In addition to its potential role in increasing arterial inflammatory responses, EL increases the anchoring of LDL to cell surfaces, which could be associated with increased LDL accumulation in coronary arteries."

Use of Avandia was severely restricted in 2010, when the drug was linked to the development of heart disease.

New research that looked at whether two commonly prescribed statin medicines, used to lower low-density lipoprotein (LDL) or bad cholesterol levels in the blood, can adversely affect cognitive function has found that one of the drugs tested caused memory impairment in rats.

Between six and seven million people in the UK1 take statins daily and the findings follow anecdotal evidence of people reporting that they feel that their newly prescribed statin is affecting their memory. Last year, the US Food and Drug Administration (FDA) insisted that all manufacturers list in their side effects that statins might affect cognitive function.

The study, led by scientists at the University of Bristol and published in the journal PLOS ONE, tested pravastatin and atorvostatin (two commonly prescribed statins) in rat learning and memory models. The findings show that while no adverse cognitive effects were observed in rat performance for simple learning and memory tasks for atorvostatin, pravastatin impaired their performance.

Rats were treated daily with pravastatin (brand name - pravachol) or atorvostatin (brand name - Lipitor) for 18 days. The rodents were tested in a simple learning task before, during and after treatment, where they had to learn where to find a food reward. On the last day of treatment and following one week withdrawal, the rats were also tested in a task which measures their ability to recognise a previously encountered object (recognition memory).

The studys findings showed that pravastatin tended to impair learning over the last few days of treatment although this effect was fully reversed once treatment ceased. However, in the novel object discrimination task, pravastatin impaired object recognition memory. While no effects were observed for atorvostatin in either task.

The results suggest that chronic treatment with pravastatin impairs working and recognition memory in rodents. The reversibility of the effects on stopping treatment is similar to what has been observed in patients, but the lack of effect of atorvostatin suggests that some types of statin may be more likely to cause cognitive impairment than others.

Neil Marrion, Professor of Neuroscience at Bristols School of Physiology and Pharmacology and the studys lead author, said: "This finding is novel and likely lects both the anecdotal reports and FDA advice. What is most interesting is that it is not a feature of all statins. However, in order to better understand the relationship between statin treatment and cognitive function, further studies are needed."

Its recognized that people who are obese have a higher risk for developing type 2 diabetes. Now, researchers reporting in the July 21 issue of Nature have found a link between the two, in the form of a protein - specifically, retinol binding protein 4 (RBP4) - thats secreted by fat cells.

RBP4 has a known function as a transporter of Vitamin A in the body. These investigators found that high levels of the protein can also cause cells to be more resistant to insulin - a condition that precedes diabetes.

This knowledge may lead to the development of drugs that can lower levels of this protein, adding to the arsenal of diabetes therapies.

________
For a summary of the study:
Study identifies fat-secreted protein linked to insulin resistance

For the study itself:
Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes

Migraine headaches are a major cause of ill health and a reduced quality of life. Some individuals suffer from a frequent and severe migraine problem which means that they require regular medication to try and prevent them. A new review_ of the medications, which may help to prevent episodic migraines, appears in the Journal of General Internal Medicine_, published by Springer. The authors, Tatyana Shamliyan from the University of Minnesota School of Public Health, and her colleagues, compare published research on the drugs available to find those which offer the best migraine prevention coupled with the fewest adverse side-effects.


Preventive treatments for migraines aim to reduce the number of migraines suffered by fifty percent. There are a number of different drugs commonly used, all of which may cause some side effects. The researchers carried out a review of studies which tested how well the different types of drugs worked and also their acceptability in terms of adverse effects suffered. The studies used enrolled mostly middle aged women with episodic migraine who suffered an average of five monthly migraine attacks.


The authors found that all approved drugs used in the reviewed trials worked better than placebo in reducing monthly migraine attacks. They all demonstrated similar effects in that they prevented half or more migraines in 200 to 400 patients per 1000 treated. Off-label anti-epilpetics and anti-depressants appeared to cause the most bothersome side effects which usually resulted in the medication being stopped. Off-label beta-blockers and angiotensin-inhibiting drugs caused the fewest side-effects. (Off-label drugs are drugs which have not been approved by the Food and Drug Administration for a specific condition).


The American Academy of Neurology and the American Headache Society currently recommend two types of anti-epileptic drug and two beta-blockers for adult migraine prevention. These guidelines do not consider the balance between the effectiveness and harms of the drugs they recommend. As well as the increased occasion of immediate side effects with anti-epileptics, there is also evidence from other studies that with long-term use they can cause sexual problems such as impotence which would also deter long-term adherence.


Shamliyan and her colleagues suggest that future studies should examine the effects of the approved as well as the off-label drugs, taking into consideration patient demographics, family history of migraine, other illnesses and response to prior treatments. They also suggest that vigilance should be increased to monitor any adverse effects of current migraine-preventing drugs. Only once the necessary evidence is available, will migraine sufferers be given the best possible hope of a better quality of life with a preventive treatment that is more pro than con.

Check out Troeltschs perspicacious response to the Disease Management Care Blog assertion in yesterdays posting that a New York City ban on the sale of 16 oz. calorie dense beverages would "work":

What evidence do you have for the comment "it works?" particularly in light of the fact that soda is simply banned in restaurants, and not any where else in the city?

Troeltsch has both right. 

The proposal, as it now stands, would limit the ban to restaurants, street vendors and concession stands and spares grocery stores. So while New Yorkers couldnt buy that "Big Gulp" to-go, theyd still be able to buy that liter of fructose corn syrup-loaded soda and continue their gluttonous ways in the privacy of their own homes.

And whats more, the DMCB did a literature search and can find no published evidence that a calorie-dense beverage ban reduces the prevalence of obesity. Yesterdays claim that "it works" was simply overzealous. DMCB readers can not only spot non-scientific puffery at meetings, in news reports and in marketing materials, but also in the DMCBs weaker-moment writings.

Well done.

That being said, the DMCB still gives the Big Apple some credit. If you go to the original proposal, youll see that the ban is only one of 26 initiatives that seek to improve nutrition and increase exercise in the citys public schools, alter sidewalk and building codes to promote physical activity, require hospitals to offer healthy menus, increase the availability and appeal of tap water and promote wellness, especially among public employees. This is commercial population health management writ large.

And the DMCB still stands by its original assertions. Mayor Bloombergs attack on obesity in the name of public health should remind health care providers that a similar fate awaits their costly ways if shared savings, accountability, bundling, electronic records, the demos and ACOs fail to bend the curve. Instead of trimming excess calories, our politicians will trim excess costs by proclamation.

The DMCB offers three additional observations:

1) Peter Orzag, one of Mr. Obamas health orm architects, famously asserted that the Affordable Care Acts health mandate provision would increase a collective expectation that we should all buy health insurance, much like seat belt laws prompted most of us to buckle up. There may be something to that in the anti-obesity fight, says the DMCB, and Mayor Bloombergs very public attack on sugary drinks may prompt his city to shift to a new cultural norm

2) The DMCB hopes NYCs Department of Health and Mental Hygiene devotes the resources it takes to adequately measure the impact of the ban. The rest of the country needs to know if this works.

3) Last but not least, if nothing comes of this, this is one more warning to a largely uncooperative and unrepentant food industry.

A small study conducted by researchers at Arizona State University found that low blood levels of vitamin C were associated with decreased fat oxidation - the burning of fat for fuel.

"Free-living individuals with marginal vitamin C status oxidized 25% less fat per kg body weight during a 60-minute treadmill walk as compared to individuals with adequate vitamin C status."

They site a possible mechanism: Vitamin C is used by the body to make carnitine, and carnitine is necessary for fat oxidation.

They also found that the less fat participants oxidized, the greater their fatigue, leading them to speculate that:

"Vitamin C depletion may result in weight gain by two mechanisms: indirectly by fatigability and exercise intolerance and directly by lipid accumulation."

When researchers supplemented the depleted subjects with 500 mg/day of vitamin C, they increased their amount of fat used for energy by a factor of 4.

________
For the study, published in Nutrition and Metabolism:
Marginal vitamin C status is associated with reduced fat oxidation during submaximal exercise in young adults

A large study of nearly half a million older adults followed for about 12 years revealed a clear trend: as coffee drinking increased, the risk of death decreased. Study author Neal Freedman, PhD, MPH, National Cancer Institute, discusses the significance of these findings and the potential links between coffee drinking, caffeine consumption, and various specific causes of disease in an interview in Journal of Caffeine Research, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Journal of Caffeine Research website.

"Epidemiology of Caffeine Consumption and Association of Coffee Drinking with Total and Cause-specific Mortality" presents an in-depth interview exploring the many factors that could contribute to the association between coffee, disease, and mortality.

Dr. Freedman examines the relationship between coffee drinking and behaviors such as smoking and alcohol abuse, the physiological effects of caffeine on blood pressure and cardiac function, and the importance of differentiating between the effects of coffee and caffeine.

Consumption of fatty fish and fish-oil supplements linked to 71 percent higher risk

A second large, prospective study by scientists at Fred Hutchinson Cancer Research Center has confirmed the link between high blood concentrations of omega-3 fatty acids and an increased risk of prostate cancer.

Published July 11 in the online edition of the Journal of the National Cancer Institute, the latest findings indicate that high concentrations of EPA, DPA and DHA – the three anti-inflammatory and metabolically related fatty acids derived from fatty fish and fish-oil supplements – are associated with a 71 percent increased risk of high-grade prostate cancer. The study also found a 44 percent increase in the risk of low-grade prostate cancer and an overall 43 percent increase in risk for all prostate cancers.

The increase in risk for high-grade prostate cancer is important because those tumors are more likely to be fatal.

The findings confirm a 2011 study published by the same Fred Hutch scientific team that reported a similar link between high blood concentrations of DHA and a more than doubling of the risk for developing high-grade prostate cancer. The latest study also confirms results from a large European study.

"The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis and recommendations to increase long-chain omega-3 fatty acid intake, in particular through supplementation, should consider its potential risks," the authors wrote.

"Weve shown once again that use of nutritional supplements may be harmful," said Alan Kristal, Dr.P.H., the papers senior author and member of the Fred Hutch Public Health Sciences Division. Kristal also noted a recent analysis published in the Journal of the American Medical Association that questioned the benefit of omega-3 supplementation for cardiovascular diseases. The analysis, which combined the data from 20 studies, found no reduction in all-cause mortality, heart attacks or strokes.

"Whats important is that we have been able to replicate our findings from 2011 and we have confirmed that marine omega-3 fatty acids play a role in prostate cancer occurrence," said corresponding author Theodore Brasky, Ph.D., a research assistant professor at The Ohio State University Comprehensive Cancer Center who was a postdoctoral trainee at Fred Hutch when the research was conducted. "Its important to note, however, that these results do not address the question of whether omega-3s play a detrimental role in prostate cancer prognosis," he said.

Kristal said the findings in both Fred Hutch studies were surprising because omega-3 fatty acids are believed to have a host of positive health effects based on their anti-inflammatory properties. Inflammation plays a role in the development and growth of many cancers.


It is unclear from this study why high levels of omega-3 fatty acids would increase prostate cancer risk, according to the authors, however the replication of this finding in two large studies indicates the need for further research into possible mechanisms. One potentially harmful effect of omega-3 fatty acids is their conversion into compounds that can cause damage to cells and DNA, and their role in immunosuppression. Whether these effects impact cancer risk is not known.

The difference in blood concentrations of omega-3 fatty acids between the lowest and highest risk groups was about 2.5 percentage points (3.2 percent vs. 5.7 percent), which is somewhat larger than the effect of eating salmon twice a week, Kristal said.

The current study analyzed data and specimens collected from men who participated in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), a large randomized, placebo-controlled trial to test whether selenium and vitamin E, either alone or combined, reduced prostate cancer risk. That study showed no benefit from selenium intake and an increase in prostate cancers in men who took vitamin E.

The group included in the this analysis consisted of 834 men who had been diagnosed with incident, primary prostate cancers (156 were high-grade cancer) along with a comparison group of 1,393 men selected randomly from the 35,500 participants in SELECT.

Hi,

Been staying on the program pretty well. I did have one mishap last Tuesday, but I immediately made the correction and got back on track so the weight loss still seems to be happening. So far this week (on day 6) Ive lost an average of 2.14 pounds. Im happy with that.

Tomorrow is the cheat meal and Im planning on making home made spaghetti. Ive bought all the ingredients and have been reminding myself that they are for Saturday only -- which, oddly enough -- has been working. I think it has only been possible because my meals are healthy and satisfying and, for the most part, Ive not been craving -- just as promised on the program.

This means a lot to me because Ive never been one to be able to clearly distinguish hunger from cravings or even from thirst. Ive discovered that for most of my life I was dehydrated. I did drink water but only an average of one, maybe two, tall glasses of water per day was all I would normally do. I was never a big soda drinker and rarely drank coffee or tea, either. I drank milk pretty often, and occasionally had some orange juice but not often because it would always make my stomach burn. I did not actually realize that I was dehydrated until just a few years ago. Perhaps that is part of the reason I rarely had any "get up and go."

I think that I may have been responding to thirst as if it were hunger. So I would eat when I was thirsty, not being familiar with the distinction. Even now I nearly never think that I am thirsty unless my mouth is actually dry. I can only tell if I am dehydrated by low output of water on the other end. So it is rather important for me, especially, to pay attention to getting 64 ounces of water into me every day. I have three 32-ounce bottles in the fridge with the aim of drinking two of them each day.  The other is for backup or if I need more for some reason.

In the morning, I have some prescriptions and supplements to take. Quite a few supplements, in fact. So I have about three pretty large handfuls of pills to take and it requires an entire 12-oz bottle of water to down them properly. Then I fill the bottle again (from the larger bottles in the fridge so I can passively keep track of my intake.) I may sit my drinking bottle on the counter and swig from it every so often, or I might put it in the fridge to keep the water cold. Somehow, through the day, the water gets downed -- for the most part -- so that works for me.

Since I still dont have an active "thirst detector" I pay attention to the clues my body gives off. Sometimes just seeing the bottle sitting there waiting prompts me to swig a little. Sometimes if I recognize that Ive been sweating I will drink a bottle to replenish. If Ive been doing some house cleaning and my throat feels dry, I drink a little to "whet my whistle."

I try to drink both before and after I swim -- just like my therapist would have me do in her office. Before I go to bed I have one more handful of pills to take so I often drink half a bottle, at least, before bed. I also make sure I have a bottle of water ready in the fridge before I go to bed. Then when I get up in the night and switch sleeping places I grab that bottle of water and have a few sips. I place it on the table beside me and I sip some more during the night sometimes, and I sip a little more when I wake up. Now that Im drinking two or three cups of different kinds of tea during the day that helps keep me from being dehydrated, too. So that is how I deal with "thirst."

Having been eating pretty right for two weeks now, and knowing that eating low carb will eliminate "cravings" I can usually now recognize when I am hungry. I gotta admit that sometimes, especially on the first three days, while I was going through "sugar withdrawals," I got hungry way more often than I thought was right or even possible. What I did was to follow the program advice and simply eat some veggies and a protein when I felt hungry -- whether it made sense to my mind or not. I just said "oh well," and ate. That got me through until things started to normalize.

Now I trust my body when it gives me the sensations that make me realize that I am hungry. I dont worry that it might be "too soon" according to some one elses ideas (and especially not my own!). If I feel hungry I eat. Having the salad ready in the fridge really is helping me to eat right. I fill up my salad bowl and choose a protein. Not always, but sometimes, I eat the salad before the protein is done cooking. That does not bother me either. It does not matter except that I need to eat them together. I figure one right after the other is pretty darn "together." For the most part, I eat them at the same time but do not hesitate to satisfy my hunger whenever it is upon me.

Cravings. Cravings are a whole different animal. Cravings are insistent -- but they always and only insist on something sweet -- or maybe salty. Cravings are pressurized. I remember the first time I recognized the "pressure" right in the middle of a huge craving that I was trying to control with will power. I noticed I was picturing the item of choice at the moment (probably candy or sweets of some kind) but did not want to submit. I suddenly looked inside my body and noticed I was clenching my teeth and my muscles were tight and I might even have been holding my breath. I was shocked that I was under so much pressure! In the past I gave in to the pressure, threw up my hands, and went and got the item in question. When I would eat it the craving would go away and I could breath normally again. I would be comforted by eating the item, but always felt guilty for the bad behavior.

Cravings bring up pictures of "favorite" high carb items in my mind. Rarely do they bring up into inner vision a cucumber, or a salad, or a healthy low carb item. Cravings are indicative of a hormonal imbalance. Cravings come on the heals of previous high carb meals or snacks -- in fact, the more meals you eat with high carb items, the more intense and often come the cravings knocking at your psyche. The more high carb items you eat, the more you want them. At least that is how it is for me, and it seems to be universal from the reading that Ive done. You know what that means? It means you really are experiencing an uncontrollable bodily reaction -- an addiction. Think of a drug addict. They behave exactly the same way -- even going so far as to steal from family and friends to support their habit. Addiction is a powerful negative force inside the body that if left to its own resources will kill you.

That is why it is hard for a carbohydrate addict to tell the difference between hunger and cravings. Cravings take a normal bodily function (hunger) and transform it into a beast within you. If your hunger seems to be in the form of a roaring lion that insists on being fed unhealthy sweets and snacks beyond all reason -- that is probably not normal hunger. But there is a rather simple solution to the problem of taming the lion of carvings.

Im not going to get technical and discuss insulin, blood sugar levels, and ghrelin or even adiponectin -- Im only going to talk about the solution to the cravings. The solution to cravings is a three-day carb fast that allows the "out of balance" to come back into balance. It allows insistent insanity to subside and be replaced with peaceful sanity. The sanity comes when, on those three days, you simply eat raw veggies and protein when you feel the slightest craving. They will come often, but will temporarily subside with veggies and protein.

If you do that for three days (at the most four) you will then begin to experience some peace. You can put that lion to sleep if you keep eating raw veggies and protein for the next week. You will even lower your blood sugar numbers and probably lose some weight, too. If you continue on to week two, you still might stumble a little, but it will be easier to get back on track.

Carbs are not the culprit. Eating carbs too often is the culprit. The body actually needs some carbs to function properly but if you are living on the back of the lion, you are giving your body way too many carbs for it to handle. It is just so odd that if you eat too many carbs, you only want more and more to infinity -- but that is how it is. The only way to reign in the lion is with the three-day carb fast and following the program as outlined on http://blogspot.com/2012/01/normal-0-false-false-false-en-us-x-none.html  There are, of course, other programs that will give you the three-day fast -- but if you are a diabetic or a pre-diabetic ... and if you are a post-menopausal woman (or not).... this one may work for you.

The weekly, hour-long, cheat meal lets you consume your favorite high carb items once a week. You dont have to be completely deprived of your favorite foods. You can keep the lion sleeping while you tip-toe past and eat your favorite things if you follow the guidelines that help you replenish and rev up your metabolism without waking up the lion.

You wont know for sure until you try it. That is what I am doing -- I am trying it out. I am on day six of week two and looking forward to my cheat meal tomorrow but it is not like it was when I was on the back of the lion. The real test will be on weeks three and four and beyond.

I felt quite happy when I spoke to my sister-in-law and she shared that her grandson told her exactly the same thing about the cheat meal that Im trying out. He said he keeps his weight under control with a once a week cheat meal and it was gratifying to hear about his success. It seemed only a coincidence that he is doing what I am starting to do... but Im glad I got confirmation from another trustworthy source.

I hope you are well and have gotten off the lion, too. Comment below and let me know how you are doing. Even if you are not doing well -- sharing about it will help to motivate you. Taking action sometimes comes from simply sharing your testimony about what is happening with you. It gives you a more clear picture. That is what the blogging does for me. Go ahead and take the opportunity to support yourself by commenting below.

Be back soon,

Marcia

The European Association for the Study of Diabetes (EASD)s journal, Diabetologia, has four papers and an Editorial in press, addressing a possible link between insulin glargine (Lantus insulin) and cancer.

You can access their studies and press release here.

From their press release:

"The concerns about a possible link between use of Lantus insulin and increased cancer risk were raised by a German study of around 127,000 insulin-treated patients in an insurance database. The research identified a statistically significant link between patients who had used Lantus insulin and those who had been diagnosed with cancer. Compared with people using similar doses of human insulin, out of every 100 people who used Lantus insulin over an average of about one-and-a-half years, one additional person was diagnosed with cancer. Of particular note in this study was the finding that the increased risk of cancer was dose-dependent. Thus for patients given a dose of 10U, Lantus insulin alone increased the risk of cancer by 9% compared with human insulin; but for a dose of 50U, the increased risk was 31%."

Additional studies were carried in Sweden, Scotland, and the UK:

• The Swedish study found that compared with patients on insulins other than Lantus insulin, patients on lantus insulin alone had double the risk of breast cancer.
  
• The Scottish study found a non-significant increased risk for breast cancer specifically.
  
• The UK study found no link between insulin glargine and cancer.

The studies are observation and not conclusive. More research is needed. The EASD is advising patients not to stop taking Lantus insulin without contacting their healthcare provider. Alternatives may be available.
________

If New York Citys Mayor Michael Bloomberg has his anti-obesity way, the Big Apple will begin banning the restaurant and concession sale of sugary beverages that exceed a volume 16 fluid ounces as early as March of 2013.  The Disease Management Care Blog suspects there is one big reason why Hizonner is deploying brute force in this battle of the bulge, this confrontation of the calories, this attack on adiposity:

It works.

Contrast the approach of simply outlawing obesogenic drinks with kinder and gentler approaches, like those based on education (food labeling and warnings), economic incentives (fat taxes), appeals to self-interest ("youll look and feel better!") or enculturation (starting with food choices in our schools cafeterias).  They all have their role, but lets face it: we dont heed labels, hate taxes, find life-style changes difficult, are suckers for the food industrys marketing and ultimately like the taste rush of corn syrup.  Take a stroll through Manhattan and its pretty obvious we have a problem.

The Big Apple is doing this for our own public health good.

This lesson prompts the Disease Management Care Blog to ponder the largest threat to the success of the "accountability" movement in health care.  By "aligning" economic interests, offering savings-based "gain-sharing," leveraging decision support and enculturating physicians into "systems" of care imbued with best practices championed by physician leadership, we believe our collective taste for high cost testing, technology and pharmaceuticals will fade faster than the flab on The Biggest Loser.

Is that so?  Maybe not, and so the DMCB offers up two observations:

1. Assuming physicians are people and patients have their self-interest at heart, the likelihood that our appetitite for over-testing, the latest tech and brand name drugs will be blunted by electronic health record decision-support warnings, the promise of some savings-based future bonus, appeals at staff meetings to do the right thing or an expectation that physician culture will change is about as realistic as a successful John Edwards White House run in 2016.

2. And assuming that none of that works, the likelihood that future local and national politicians will use the same public health logic and announce a Bloomberg-esque "ban" of some high cost low value tests, technology and drugs is almost certain.

You read it here first.

Image from Wikipedia   

Im baaaaack!

When persons are admitted to a hospital, insurers payment rates are based on the diagnosis, not the number of days in the hospital (known as a "length of stay").  As a result, once the admission is triggered, the hospital has important economic incentive to discharge the patient as quickly as possible.  The Disease Management Care Blogs physician colleagues used to refer to this as "treat, then street."

Unfortunately, discharging patients too soon can result in readmissions.  Thats why the DMCB has agreed with others that diagnosis-based payment systems and a policy of "no pay" for readmissions were working at cross purposes.  Unified bundled payment approaches like this seem to be a good start.

But thats all theoretical.  Whats the science have to say?

Peter Kaboli and colleagues looked at the push-pull relationship between diagnosis-based payment incentives  and the likelihood of readmissions in a scientific paper just published in the Annals of Internal Medicine. 

The authors used the U.S. Veterans Administration (VA) Hospitals "Patient Treatment Files" to examine length of stay versus readmissions in 129 VA hospitals.  The sample consisted of over 4 million admissions and readmissions (defined as within 30 days and not involving another institution) from 1997 to 2010. The mean age started out at 63.8 years and increased to 65.5 years, while the proportion of persons aged 85 years or older increased from 2.5% to 8.8%. Over the years, admissions also grew more complicated with a higher rate of co-morbid conditions, such as diseases of the kidney (from 5% to 16%).

As length of stay went down, readmissions should have gone up, right?

The answer was yes and no.

Yes, if the data were trended over time: Over the 14 year period of observation, the number of days in the hospital (length of stay or LOS) decreased from 6.0 days to 4.3 days.  Yet, as LOS decreased, readmissions also decreased from 16.6% to 15.2%. 

The decreases held up when the LOS was risk-adjusted for hospital and patient characteristics.  There was also no increase in mortality rates

No, if hospitals were compared to each other:  Hospitals with risk-adjusted low lengths of stay had higher readmission rates compared to their average peers.  In that group, each day of saved LOS was associated with a 6% increased rate of 30-day readmissions.

It gets even more complicated.  As the LOS increased beyond the average, each additional day in the hospital was associated with a 3% increased rate of 30-day readmissions.

What should the DMCB learn from these data?  Keeping in mind that the VA is not necessarily generalizable to the typical community medical center,

1. Over 14 years of worth of VA data for 129 hospitals suggest it is possible to have your cake (a lower LOS) and eat it too (lower readmissions).  Thats the good news.

2. While overall performance improved over the years, between hospital comparisons showed there is a "U" shaped relationship between days in the hospital and the likelihood of readmission.  The DMCB agrees with the authors: premature discharge before the patient is ready is associated with an 6% per day readmission rate, while patients who are very sick and have to stay a few extra days in the hospital are also at risk to the tune of 3% per day.  Thats the sobering news.

What are the implications?

Overzealous efforts to discharge patients can backfire with readmissions.  It appears theres an optimum length of stay that minimizes, but will never eliminate, readmissions.

Patients who do go home "too soon" or need extra days in the hospital appear to be at special risk.  Accountable care organizations and population health management service providers should use this information to target patients at special risk of "treat, street and... repeat."

Critics look at employee wellness

Only the Disease Management Care Blog can link population health, a JAMA "Viewpoint" article on personalized medicine and a Wall Street Journal editorial on the alleged futility of worksite wellness.

The DMCB explains.

The JAMA article, written by Drs. Goldberger and Buxton, illuminates the cognitive dissonance over guideline-based vs. personalized medicine. 

The former represents the best care advice for a condition based on a published body of evidence.  Makes sense, but that evidence is typically based on multiple research studies involving populations that are both broad (able to generate statistically significant data) and representative (similar to other patients with the same disease). 

The latter describes tailored medical treatment that is suited to the individual characteristics (and personal preferences) of each patient.  This suggests that within the flow of "populations" that form the basis of a generalized guideline, there are circumstances for some persons that might make a particular treatment of greater or lesser benefit.

While Goldberger and Buxton use a complicated example involving implantable cardioverter defibrillator therapy to illustrate the conundrum, the DMCB has a simpler example.  Current guidelines support yearly mammography in every woman over the age of 50 years. Does that apply for the terminally ill woman in hospice or for a woman who, despite the advice from her physician, decides to forgo the test?

Intellectually reconciling competing policies of guidelines, such as "best practice," "reducing variation," "benchmarks" and "pay-for performance" on one side vs. personalized "informed consent," "patient empowerment" and "clinical judgment" involves subpopulations.  In other words, within any population-based study that shows an intervention is of benefit (mammograms save lives) there are subpopulations where the intervention is of little to no benefit (exceptions to every rule).

Which brings the DMCB to this provocative Wall Street Journal editorial condemning the entire worksite wellness industry. It recycles a number of tiresome criticisms, including outcomes tainted by regression to the mean, over-reliance on process-based outcomes, selection bias, employee discrimination, savings vs. program costs and overdiagnosis.  

Another criticism of the industry is the need for workforce-level (total) savings vs. per-participant savings. Since wellness programs typically focus on subpopulations of employees at greatest risk who are most likely to benefit and willing to participate, the observed savings can be limited to a few patients.  Unless those savings are culled from the large pool of total health insurance claims, they are otherwise invisible and critics will unfairly pounce.

Worksite wellness offers personalized care for limited numbers of patients.  That is its essential value proposition and its curse.  Until we can reconcile the total care via standardized guidelines vs. a more nuanced approach using personal care, it will continue to be criticized.

Study offers new understanding of cardiovascular health benefits of vegan, vegetarian diets

A compound abundant in red meat and added as a supplement to popular energy drinks has been found to promote atherosclerosis – or the hardening or clogging of the arteries – according to Cleveland Clinic research published online this week in the journal Nature Medicine.

The study shows that bacteria living in the human digestive tract metabolize the compound carnitine, turning it into trimethylamine-N-oxide (TMAO), a metabolite the researchers previously linked in a 2011 study to the promotion of atherosclerosis in humans. Further, the research finds that a diet high in carnitine promotes the growth of the bacteria that metabolize carnitine, compounding the problem by producing even more of the artery-clogging TMAO.

The research team was led by Stanley Hazen, M.D., Ph.D., Vice Chair of Translational Research for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic, and Robert Koeth, a medical student at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University.

The study tested the carnitine and TMAO levels of omnivores, vegans and vegetarians, and examined the clinical data of 2,595 patients undergoing elective cardiac evaluations. They also examined the cardiac effects of a carnitine-enhanced diet in normal mice compared to mice with suppressed levels of gut microbes, and discovered that TMAO alters cholesterol metabolism at multiple levels, explaining how it enhances atherosclerosis.

The researchers found that increased carnitine levels in patients predicted increased risks for cardiovascular disease and major cardiac events like heart attack, stroke and death, but only in subjects with concurrently high TMAO levels. Additionally, they found specific gut microbe types in subjects associated with both plasma TMAO levels and dietary patterns, and that baseline TMAO levels were significantly lower among vegans and vegetarians than omnivores. Remarkably, vegans and vegetarians, even after consuming a large amount of carnitine, did not produce significant levels of the microbe product TMAO, whereas omnivores consuming the same amount of carnitine did.

"The bacteria living in our digestive tracts are dictated by our long-term dietary patterns," Hazen said. "A diet high in carnitine actually shifts our gut microbe composition to those that like carnitine, making meat eaters even more susceptible to forming TMAO and its artery-clogging effects. Meanwhile, vegans and vegetarians have a significantly reduced capacity to synthesize TMAO from carnitine, which may explain the cardiovascular health benefits of these diets."

Prior research has shown that a diet with frequent red meat consumption is associated with increased cardiovascular disease risk, but that the cholesterol and saturated fat content in red meat does not appear to be enough to explain the increased cardiovascular risks. This discrepancy has been attributed to genetic differences, a high salt diet that is often associated with red meat consumption, and even possibly the cooking process, among other explanations. But Hazen says this new research suggests a new connection between red meat and cardiovascular disease.

"This process is different in everyone, depending on the gut microbe metabolism of the individual," he says. "Carnitine metabolism suggests a new way to help explain why a diet rich in red meat promotes atherosclerosis."

While carnitine is naturally occurring in red meats, including beef, venison, lamb, mutton, duck, and pork, its also a dietary supplement available in pill form and a common ingredient in energy drinks. With this new research in mind, Hazen cautions that more research needs to be done to examine the safety of chronic carnitine supplementation.

"Carnitine is not an essential nutrient; our body naturally produces all we need," he says. "We need to examine the safety of chronically consuming carnitine supplements as weve shown that, under some conditions, it can foster the growth of bacteria that produce TMAO and potentially clog arteries."

This study is the latest in a line of research by Hazen and his colleagues exploring how gut microbes can contribute to atherosclerosis, uncovering new and unexpected pathways involved in heart disease. In a 2011 Nature study, they first discovered that people are not predisposed to cardiovascular disease solely because of their genetic make-up, but also based on how the micro-organisms in their digestive tracts metabolize lecithin, a compound with a structure similar to carnitine.