Saturday, 19 December 2009

Thursday, 5 November 2009

Interview with Dr Uffe Ravnskov MD PhD

Is High Cholesterol The Cause of Heart Disease? An Interview with Uffe Ravnskov M.D. PhD.

(not with me, the interviewer does not wish to be associated!)

When did you begin to suspect that the cholesterol theory of atherosclerosis might be wrong? What led you to this conclusion? Before then, had you believed in the cholesterol theory? Was this part of your training?

I have never thought that it was true. I heard about it for the first time in 1962 shortly after having got my MD. My biochemical knowledge was still intact at that time and I knew that cholesterol was one of the most important molecules in our body, indispensable for the building of our cells and for producing stress and sex hormones as well as vitamin D. The idea that cholesterol in the blood should kill us if its concentration is a little higher than normal, as they wrote in the Framingham paper, seemed to me just as silly as to claim that yellow fingers cause lung cancer.

Would you tell my readers about your training, publications, university appointments, other professional activities?

The first seven years as a doctor I worked on different medical departments in Denmark and Sweden. In 1968 I started my academic career at the Department of Nephrology, University Hospital in Lund where I got my PhD. After a few years I organized a research team investigating the association between hydrocarbon exposure and glomerulonephritis. Unfortunately I caught one of my coworkers in producing a fraudulent paper. It was unfortunate, because it is risky to be a whistleblower in the academic world. Instead of excluding the fraudulent researcher it was my research that was questioned. The resistance against my research from my superiors became intolerable and I therefore decided to go into private practice. Nevertheless I succeeded in publishing the main part of my research in major medical journals after having left the department. I have summarized my findings and conclusions on the web as well.

In the late eighties the cholesterol campaign was started in Sweden. I was much surprised because I couldn’t recall anything in the scientific literature in support. I started reading it systematically and I soon realized that I was right. Since then I have published about eighty papers and letter and also books, translated into five languages, where I have presenting my arguments and criticism.

How has your work believe received by your colleagues? By healthcare professionals and consumers around the world?

In the beginning nobody took notice. To ignore criticism is the most effective way to maintain a false idea. My first book was published in Sweden in 1991 and a Finnish edition shortly afterwards. The Swedish one made no impact whatsoever and the Finnish one was put on fire in a television show. Ridicule and slander have been used as well as a means to muffle me. After I had aired my warnings against statin treatment in Dutch television for instance, Dutch researchers described me in a following show as a crackpot who had been kicked from the universities of Copenhagen and Lund. The directors of the show offered my critics a possibility to discuss the issue with me on television, but all of them declined. On his blog Michael Eades has described how one of them later on belittled me in a scientific paper.

But I have also realized that I am not alone. Seven years ago I started THINCS, The International Network of Cholesterol Skeptics (, which by now includes about eighty doctors, professors and other researchers from all over the world, who share my scepticism, and I have received two international awards for my contributions. Also encouraging is the hundreds of emails that I receive every year from patients, who have regained their health after having stopped their cholesterol-lowering treatment...

Your work seems to validate what many integrative health care professionals have been saying for decades. How does the alternative community respond to you?

There is a much more open attitude from these people.

If the cholesterol hypothesis is in error, does this mean that all of its therapies – low cholesterol diet, cholesterol lowering natural therapies and medications -- are wrong?

Absolutely. This kind of treatment is meaningless, costly and has transformed millions of healthy people into patients.

Specifically, what are your views on statins?

Their benefit is trivial and has been seen only in male patients who already have heart disease. Worse is that their many adverse effects are ignored or cleverly belittled by the trial directors. Independent researchers have found many more and in much higher numbers. If they are true it means that today millions of previously healthy people probably consider their weak and painful muscles, their bad memory, their sexual failure and their cancer to be a consequence of increasing age and so do their doctors. The risk of cancer is most alarming. Both animal experiments, epidemiological studies and several of the statin trials have shown that low cholesterol predisposes to cancer. The widespread use of statin treatment probably explains why the decrease of the smoking habit that has been going on in many countries hasn’t been followed by a decrease of cancer mortality. We should have seen a decrease because smoking predispose not only to bronchial cancer, but to all kinds of cancer.

Drug companies market vigorously the highest, strongest doses of statins. Lipitor is pushed at the highest dosage, 80 mg. This dosage is the most powerful for lowering cholesterol and LDL, but it also causes more adverse effects and costs more than lower doses. What are your thoughts about this?

The outcome from these trials is a further demonstration that the small benefit from statin treatment has nothing to do with cholesterol. For instance, although cholesterol plummeted and remained at about fifty percent below the initial value during the whole SEAS trial, it did not change mortality, but it increased the number of cancer with statistical significance. Even worse was the result of the ENHANCE trial, where atherosclerosis in patients with familial hypercholesterolemia progressed the most among those whose cholesterol was lowered the most.

If statins can be helpful in reducing the incidence of heart attacks, who should take them?

In my view nobody. When I was practicing I used to describe the benefit in this way: Considering your age and your previous heart attack your chance to be alive in five years is about 90%. You can increase that chance to 92% if you take a statin pill every day, but then you may also expose yourself to its many adverse effects.

From the data I have seen, statins have not produced a reduction in overall cardiac deaths. Do you have any idea of why this is?

You are right. Heart mortality in Sweden is going downwards, but the reduction started already in the sixties. The cause is most probably that treatment of acute myocardial infarction has improved because the mortality curve has not changed after the introduction of the statins. The reason may be that their small benefit is counteracted by an increasing frequency of heart failure. As you know the statins block not only the synthesis of cholesterol, but also of other vital molecules, for instance coenzyme Q10, and muscle cells, including those of the heart, can’t function properly without Q10.

Do you think mainstream medicine will ever relinquish its view that elevated cholesterol causes heart disease and that statins are the magic bullet?

I hope so. The failures of the most recent statin trials has been commented by several journalists in the major US newspapers. In Sweden a revolution is going on. Here, a general practitioner treated her own obesity successfully by eating a low-carbohydrate diet with a high content of animal fat. When she advised her obese and diabetic patients to do the same, she was reported to the National Board of Health and Welfare for malpractice. After a two-year-long investigation she was acquitted, as her treatment was considered to be in accord with scientific evidence. At the same time, the Board dismissed two experts, who had been appointed for updating the dietary recommendations for diabetics, because it came up that they were sponsored by the food industry. Instead the Board has asked independent researchers to review the scientific literature.

The subject has gained general attention due to a number of radio and television shows, where critical experts including myself have discussed the issue with representatives of the official view. Most important, thousands of patients have experienced themselves that by doing the opposite as recommended by the current guidelines they have regained their health. The effect has been that the sales of butter, cream and fat milk are increasing in Sweden after many years of decline, and a recent poll showed that a majority of Swedish people today think that the best way of losing weight is by a low-carbohydrate, fat-rich diet.

Further progress was achieved this spring. Several times colleagues of mine and also myself have asked the Swedish Food Administration for the scientific basis of their warnings against saturated fat. We have been met with the argument that there are thousands of such studies, or by referrals to the WHO guidelines or the Nordic Nutrition Recommendations. As the main argument in the latter two is that saturated fat raises cholesterol we were not satisfied with their answer and finally the Food Administration published a list with 72 studies that they claimed were in support of their view on saturated fat and twelve that were not.

We scrutinized the lists and found that only two of the 72 studies supported their standpoint; eleven studies did not concern saturated fat at all, and the unsupportive list was incomplete, to put it mildly. We published a short report with our comments to these lists in the Swedish medical journal Dagens Medicin. A response from the Food Administration appeared seven weeks later in which they pointed out that their recommendations were directed to healthy people, not to patients. They maintained that they were based on solid scientific evidence without mentioning anything about saturated fat and without answering our critical comments.

But this is not all. Earlier this year Sachdeva et al reported that the mean cholesterol in 137,000 patients with acute myocardial infarction was lower than normal. As usual, the authors didn’t understand their own findings, but concluded that cholesterol should be lowered even more. A few months later Al-Mallah et al. came up with the same result and conclusion, although they also reported that three years later, mortality was twice as high among those who had been admitted with the lowest cholesterol.

These results created a fierce debate in one of the major Swedish newspapers. It was opened by ninety-one-year old Lars Werk√∂, the ‘Grand Old Man’ in Swedish medical science, retired professor in internal medicine and former head of The Swedish Council on Technology Assessment in Health Care, together with Tore Scherst√©n, retired professor in surgery and former secretary of the Swedish Medical Research Council. “Now it is time to sack the cholesterol hypothesis and to investigate the reason of this scientific breakdown” they wrote. They also criticized American researchers in AHA and NHLBI and their followers for sloppy and fraudulent science.

They were of course attacked by two professors and representatives of the current view, but none of them came up with any substantial evidence, only by personalities.

Are there other risk factors that should be followed? Such as: C-reactive protein, fibrinogen, homocysteine, lipoprotein A. Any other factors?

Such analyses may be helpful for doctors to put the right diagnosis in patients with a disease of unknown origin. But to check healthy people’s blood to find deviations from normal is the freeway to unnecessary medication.

Are there other alternative therapies besides statins that people might consider?

There is no reason for healthy people to take drugs or anything else to prevent heart disease as long as we do not know the very cause. Don’t forget that people who die from a myocardial infarction have on average lived just s long as other people. On my talks I use to ask people, who put the same question to me, if they know a better way of dying.

What diet do you recommend people follow?

I do not give medical advice to people I haven’t seen and examined myself and as I am retired it means that I give no advice at all except to my family and nearest friends. I inform people by writing and lecturing. Then they have to decide themselves what to do.

In 20 years, do you expect changes in how we view heart disease, its causes and treatments?

I am confident that we will see a change in the next few years. There is a growing skepticism among medical scientists. What is happening in Sweden these days may hopefully inspire researchers in other countries to air their skepticism openly. Recently experts selected by WHO and FAO published a new report. Here the authors concluded that there was no satisfactory or reliable evidence to support the idea that saturated fat causes heart disease, or diabetes or obesity. A revolutionary change of direction, you may say. However, they did not change their recommendations.

Together with Kilmer McCully, the discoverer of the association between homocysteine and atherosclerosis, I have presented another hypothesis. We think it is much more likely because we are able to explain the many observations that do not fit with the present one. If anyone wants to read the full paper I shall send it on request.

EDIT Ted has a link to the full pdf in the comments section of the original post.

Finally, I assume that much of what I have mentioned here may seem incredible, but all the facts including references to the scientific literature are available in my new book Fat And Cholesterol Are GOOD For You!

Saturday, 31 October 2009

Drug Decriminalization in Portugal

With apologies to Salon for stealing their text. I'll take it down if anyone objects, but the original article does seem to have disappeared already. Here it is.

Glenn Greenwald is a civil rights attorney, a blogger for Salon, and the author of a new Cato Institute policy study called “Drug Decriminalization in Portugal: Lessons for Creating Fair and Successful Policies.” The paper examines Portugal’s experiment with decriminalizing possession of drugs for personal use, which began in 2001. Nick Gillespie, editor of and, sat down with Greenwald in April.

Q: What is the difference between decriminalization and legalization?

A: In a decriminalized framework, the law continues to prohibit drug usage, but it’s completely removed from the criminal sphere, so that if you violate that prohibition or do the activity that the law says you cannot do you’re no longer committing a crime. You cannot be turned into a criminal by the state. Instead, it’s deemed to be an administrative offense only, and you’re put into an administrative proceeding rather than a criminal proceeding.

Q: What happened in Portugal?

A: The impetus behind decriminalization was not that there was some drive to have a libertarian ideology based on the idea that adults should be able to use whatever substances they want. Nor was it because there’s some idyllic upper-middle-class setting. Portugal is a very poor country. It’s not Luxembourg or Monaco or something like that.

In the 1990s they had a spiraling, out-of-control drug problem. Addiction was skyrocketing. Drug-related pathologies were increasing rapidly. They were taking this step out of desperation. They convened a council of apolitical policy experts and gave them the mandate to determine which optimal policy approach would enable them to best deal with these drug problems. The council convened and studied all the various options. Decriminalization was the answer to the question, “How can we best limit drug usage and drug addiction?” It was a policy designed to do that.

Q: One of the things you found is that decriminalization actually correlates with less drug use. A basic theory would say that if you lower the cost of doing drugs by making it less criminally offensive, you would have more of it.

A: The concern that policy makers had, the frustration in the 1990s when they were criminalizing, is the more they criminalized, the more the usage rates went up. One of the reasons was because when you tell the population that you will imprison them or treat them as criminals if they identify themselves as drug users or you learn that they’re using drugs, what you do is you create a barrier between the government and the citizenry, such that the citizenry fears the government. Which means that government officials can’t offer treatment programs. They can’t communicate with the population effectively. They can’t offer them services.

Once Portugal decriminalized, a huge amount of money that had gone into putting its citizens in cages was freed up. It enabled the government to provide meaningful treatment to people who wanted it, and so addicts were able to turn into non–drug users and usage rates went down.

Q: What’s the relevance for the United States?

A: We have debates all the time now about things like drug policy reform and decriminalization, and it’s based purely in speculation and fear mongering of all the horrible things that are supposedly going to happen if we loosen our drug laws. We can remove ourselves from the realm of the speculative by looking at Portugal, which actually decriminalized seven years ago, in full, [use and possession of] every drug. And see that none of that parade of horribles that’s constantly warned of by decriminalization opponents actually came to fruition. Lisbon didn’t turn into a drug haven for drug tourists. The explosion in drug usage rates that was predicted never materialized. In fact, the opposite happened.

Friday, 30 October 2009

Jebb vs Nutt

Drugs tsar 'sacked over comments'

Friday, October 30 07:10 pm
The Government's chief drugs adviser has been forced to resign in the wake of the row over the dangers of class A drugs. Skip related content
Related content

Home Secretary Alan Johnson asked Professor David Nutt to resign as chairman of the Advisory Council on the Misuse of Drugs (ACMD), saying he had "lost confidence" in his ability to give impartial advice.

He accused Prof Nutt of going beyond his remit as an evidence-based scientist and accused him of "lobbying for a change in government policy".

But Prof Nutt hit back, accusing the Government of "misleading" the public in their messages about drugs and of "Luddite" tendencies. He linked his sacking to "political" considerations, citing the forthcoming election.

Professor Nutt sparked controversy this week when he said ecstasy and LSD were less harmful than alcohol and cigarettes, and criticised the decision to upgrade cannabis to class B.

Speaking after he agreed to step down he said: "It's unusual political times, I suppose, elections and all that. It's disappointing. But politics is politics and science is science and there's a bit of a tension between them sometimes."

He attacked Prime Minister Gordon Brown for making what he said were "completely irrational" statements about cannabis.

Confessing himself "extremely surprised" by the decision he said: "The danger is they (politicians) are misleading us. The scientific evidence is there, it's in all the reports we published."

In his letter demanding Prof Nutt's resignation, Mr Johnson wrote: "It is important that the Government's messages on drugs are clear and as an adviser you do nothing to undermine the public understanding of them. As my lead adviser on drugs harms I am afraid the manner in which you have acted runs contrary to your responsibilities.

"I cannot have public confusion between scientific advice and policy and have therefore lost confidence in your ability to advise me as chair of the ACMD. I would therefore ask you to step down from the council with immediate effect."

Sunday, 27 September 2009

Jebb on Atkins

Atkins Diet 'Dangerous'

August 13, 2003
Daily Mail (London)
by Jenny Hope

THE hugely-popular Atkins Diet is medically unsound and a major health risk, nutrition experts warned yesterday.

They said the high-protein high-fat diet, followed by stars such as Catherine Zeta-Jones and Geri Halliwell, was a giant experiment which could have disastrous effects for millions.

Dr Susan Jebb of the Government-funded Medical Research Council said it would be 'negligent' to recommend it for long-term use and called for research into its safety.

She dismissed the theory behind the diet, that it changes the body's chemistry to burn off fat, as 'pseudo-science'. Adverse effects could include kidney damage and bone loss.

The alert comes from one of the country's leading experts on obesity. Dr Jebb is head of nutrition and health research at the MRC's Human Nutrition Research Centre in Cambridge.

She was speaking at a special summit held in London to warn of the dangers that crash dieting poses to the nation's health.

Dr Jebb said the Atkins Diet was the least healthy of a number of trendy 'faddy diets' followed by people desperate to lose pounds in a hurry. She said: 'Fad diets prey on the overweight, offering quick fixes and psychological tricks. I see no medical benefit at all in them, and in particular the Atkins Diet.

'It is nutritionally incomplete. It works in the short term but so does any diet that reduces the amount of calories eaten.

'The diet is a massive health risk, it's medically unsound. We have no idea what will happen in the long term because no one is evaluating the results of the experiment.

'Obesity is a massive problem in the UK but this is not the way to solve it.' The warning is the latest in a series from health professionals over 'gimmicky' diet regimes, endorsed by celebrities.

A multimillion-pound book industry has grown on the back of claims that extreme eating patterns work.

The Atkins Diet is even challenging Harry Potter for world sales figures books about it are currently in first and third place on the British Hot 100 of online retailer Amazon.

Invented 30 years ago by American Dr Robert Atkins, who died earlier this year, it tells followers to eat vast amounts of meat but severely restrict carbohydrates such as bread, pasta, rice and starchy vegetables.

The theory is that carbohydrates increase the body's production of the hormone insulin, which encourages cells to store fat. This leads to both hunger and weight gain.

Cutting carbohydrates right down, Dr Atkins asserted, turns the body from a carbohydrate-burning machine to one that burns fat.

But Dr Jebb dismissed the claim as 'pseudo-science'.

She said following the diet long-term would mean a dramatic change in eating habits for most people, protein accounts for only around 15 per cent of total calorie intake.

Dr Jebb said: 'It's a profound change and we simply do not know the long-term health implications.

'I certainly think we should be adopting a precautionary principle in terms of public health.' The diet is known to put extra stress on the kidneys, which can lead to kidney stones and more serious damage particularly for those with pre-existing problems they might be unaware of.

There is also a fear of bone problems because the diet encourages the excretion of calcium which would otherwise go to build them.

Although two U.S. studies found the Atkins Diet was safe and effective, Dr Jebb said the dieters involved had been on it for only six months and a year.

She also pointed out that, longer-term, it had proved to be no better at permanent weight loss than a conventional low-fat diet.

Dr Jebb said people had to lose weight sensibly and slowly because 'there is no way to lose a stone in a few weeks without putting your health at risk'.

Among other experts warning about the Atkins Diet is Amanda Wynne of the British Dietetic Association. She says the process of ketosis it triggers where the body burns up stored fat can result in nausea and tiredness, while drastic reduction in carbohydrates can lead to constipation and digestive problems.

Dr Jebb's colleague Toni Steer says: 'If you don't eat fruit and veg, you are excluding a lot of essential minerals and vitamins.

'And we know that consuming these foods reduces your risk of cancer and cardiovascular disease.' Professor David Barker, a specialist in foetal health at Southampton University, has warned that mothers-to-be who follow such diet regimes are putting their baby's health at risk.

The diet would deprive an unborn child of essential nutrients and raise the risk of heart disease, diabetes and strokes in adulthood.

Dr Jane Ogden, a reader in health psychology at King ' s College, London, told yesterday's meeting the Atkins Diet was popular because weight watchers could follow the instructions to the letter.

She said: 'What fad diets do is tell people in black and white what they can and can't do, and they identify with that.'

Friday, 18 September 2009

Kebab text (news report link is down)

Post-Pub Kebabs Add 1000 Calories

4:33pm UK, Tuesday January 27, 2009

Doner kebabs in the UK have been found to contain the equivalent fat to drinking more than one and a half wine glasses of cooking oil.

A nationwide sample of the nutritional content of the takeaway meal found the average doner also contained close to an adult's entire daily recommended intake of salt.
Before adding salad and sauce the average kebab contained 1,000 calories but researchers found some with 1,990.

Last year food scientists tested a doner kebab containing 140g of fat - twice the amount a woman should eat in a day.

This was said to be the calorific equivalent to drinking a wine glass full of cooking oil.

The most gut busting kebabs in this latest study provide 346% of a woman's saturated fat intake, close to drinking two wine glasses of cooking oil.Given that 60% of kebabs have been found to contain cholesterol raising trans fats, fans of the takeaway could be risking their health.

Another big finding was that 35% of the meat sent to kebab shops listed a different meat species than was actually contained.

Six kebabs were found to include pork when it was not listed as an ingredient, two of which were described as Halal - which Muslims are permitted to eat.

Christopher Baylis told Sky News that Lacors want to make sure everyone is given the right information.

We had never assumed that kebabs were a health food option - but it was certainly surprising.

Christopher Baylis, Lacors spokesperson

"The labelling is on the kebabs when they come from the manufacturers. It is bad not to convey exactly what is in the kebab," he said.

The minute weight difference between a small and large kebab is also a problem, said chairman of Lacors, councillor Geoffrey Theobald.

"With obesity rates rising so rapidly in the UK, portion size is as important as what is being consumed," he said.

"Reducing portion size is an easy and cost-effective way for small businesses to help people eat sensibly."

The study sampled 494 kebabs from 76 councils and found that the calorie count varied up and down the country.

The average kebab in the North West of England contained 1,101 calories while in Scotland it was 1,084, in Wales 1,055 and 1,066 in south-west England.

The lowest calorie kebabs can be found in Northern Ireland where the snack weighed in at an average of 843.

Tuesday, 25 August 2009

High fat apoE-/-

Even as low-carbohydrate/high-protein diets have proven successful at helping individuals rapidly lose weight, little is known about the diets' long-term effects on vascular health.
Now, a study led by a scientific team at Beth Israel Deaconess Medical Center (BIDMC) provides some of the first data on this subject, demonstrating that mice placed on a 12-week low carbohydrate/high-protein diet showed a significant increase in atherosclerosis, a buildup of plaque in the heart's arteries and a leading cause of heart attack and stroke. The findings also showed that the diet led to an impaired ability to form new blood vessels in tissues deprived of blood flow, as might occur during a heart attack.
Described in today's Online Version of the Proceedings of the National Academy of Sciences (PNAS), the study also found that standard markers of cardiovascular risk, including cholesterol, were not changed in the animals fed the low-carb diet, despite the clear evidence of increased vascular disease.
"It's very difficult to know in clinical studies how diets affect vascular health," says senior author Anthony Rosenzweig, MD, Director of Cardiovascular Research in BIDMC's CardioVascular Institute and Professor of Medicine at Harvard Medical School. "We, therefore, tend to rely on easily measured serum markers [such as cholesterol], which have been surprisingly reassuring in individuals on low-carbohydrate/high-protein diets, who do typically lose weight. But our research suggests that, at least in animals, these diets could be having adverse cardiovascular effects that are not reflected in simple serum markers."
Rosenzweig and his coauthors found that the increase in plaque build-up in the blood vessels and the impaired ability to form new vessels were associated with a reduction in vascular progenitor cells, which some hypothesize could play a protective role in maintaining vascular health.
"A causal role for these cells has not yet been proven, but this new data is consistent with the idea that injurious stimuli may be counterbalanced by the body's restorative capacity," he explains. "This may be the mechanism behind the adverse vascular effects we found in mice that were fed the low-carb diets."
The study's first author Shi Yin Foo, MD, PhD, a clinical cardiologist in the Rosenzweig laboratory at BIDMC, first embarked on this investigation after seeing heart-attack patients who were on these diets - and after observing Rosenzweig himself following a low-carbohydrate regimen.
"Over lunch, I'd ask Tony how he could eat that food and would tell him about the last low-carb patient I'd admitted to the hospital," says Foo. "Tony would counter by noting that there were no controls for my observations."
"Finally," adds Rosenzweig, "I asked Shi Yin to do the mouse experiment - so that we could know what happens in the blood vessels and so that I could eat in peace."
The investigators proceeded to study a mouse model of atherosclerosis. These "ApoE" mice were fed one of three diets: a standard diet of mouse "chow" (65 percent carbohydrate; 15 percent fat; 20 percent protein); a "Western diet" in keeping with the average human diet (43 percent carbohydrate; 42 percent fat; 15 percent protein; and 0.15 percent cholesterol); or a low-carb/high-protein diet (12 percent carbohydrate; 43 percent fat; 45 percent protein; and 0.15 percent cholesterol).
"We had a diet specially made that would mimic a typical low-carb diet," explains Foo. "In order to keep the calorie count the same in all three diets, we had to substitute a nutrient to replace the carbohydrates. We decided to substitute protein because that is what people typically do when they are on these diets."
The scientists then observed the mice after six weeks, and again at 12 weeks. Consistent with experience in humans, the mice fed the low-carb diet gained 28 percent less weight than the mice fed the Western diet. However, further probing revealed that the animals' blood vessels exhibited a significantly greater degree of atherosclerosis, as measured by plaque accumulation: 15.3 percent compared with 8.8 percent among the Western diet group. (As expected, the mice on the chow diet showed minimal evidence of atherosclerosis compared with either of the other two groups.)
"Our next question was, 'Why do the low-carb mice have such an increase in atherosclerosis?'" says Foo. Searching for an explanation, she and her coauthors proceeded to measure the usual markers thought to contribute to vascular disease, including the animals' cholesterol and triglyceride levels, oxidative stress, insulin and glucose, as well as levels of some inflammatory cytokines.
"In each case, there was either no difference in measurements compared with the mice on the Western Diet [which contains the same amount of fat and cholesterol] or the numbers slightly favored the low-carb cohort," she adds. "None of these results explained why the animals' blood had more atherosclerotic blockages and looked so bad."
Since there was no difference in the noxious or inflammatory stimuli that the animals' blood vessels were exposed to, Foo wondered whether the restorative capacity of the animals might be contributing to the difference. The investigators, therefore, looked at the animals' endothelial or vascular progenitor cell (EPC) counts. Derived from bone marrow, the EPC cells may play a role in vessel regrowth and repair following injury.
"Examinations of the animals' bone marrow and peripheral blood showed that the measures of EPC cells dropped fully 40 percent among the mice on the low-carb diet - after only two weeks," says Rosenzweig. "Although the precise nature and role of these cells is still being worked out - and caution is always warranted in extrapolating from effects in mice to a clinical situation - these results succeeded in getting me off the low-carb diet."
Even more important, he notes, the findings point out that there can be a disconnect between weight loss or serum markers and vascular health, and that vascular health can be affected by macronutrients other than fat and cholesterol - in this case, protein and carbohydrates.
"Understanding the mechanisms responsible for these effects, as well as the potential restorative capacity that may counteract vascular disease, could ultimately help guide doctors in advising their patients," adds Rosenzweig. "This issue is particularly important given the growing epidemic of obesity and its adverse consequences. For now, it appears that a moderate and balanced diet, coupled with regular exercise, is probably best for most people."
Source: Beth Israel Deaconess Medical Center

Monday, 27 April 2009