....... Continuing from my previous blog entry, major credit goes to the Health Sciences Institute, the gastroenterologist Dr Georges Mouton and the sources listed at the end of this entry. As promised I commence the blog entry with discussion about the microorganism concentration in your probiotic dosage.....
4. Strength in numbers: A good, strong probiotic should have at least 1 billion microorganisms per daily dose... anything less would have a limited effect. To put things in perspective, the human body is home to over 100 trillion bacteria. So, even children need billions of good bacteria in supplements to reap their benefits. But there’s no point in taking a probiotic with a high number of 'friendly' bacteria if it is of poor quality.
5. Time of manufacture guarantee: Probiotics are of a delicate nature. Whether they are kept in the fridge or on the shelf probiotics will lose viability. This means that ‘billions count at the time of manufacture’ will decrease with time. Therefore high quality probiotics should be made with plenty more billions than what is stated on the pack. Always opt for a billions count which is viable until the time of expiry.
6. Too much of a good thing: In general, it is good to take a number of different probiotic strains. However, a high quality multi-strain probiotic will contain 5 or 6 different probiotic strains, and not 20. Too many probiotic strains have been shown to ‘cannibalise’ each other within the capsule. Make sure your probiotic supplement has been tested to ensure that the different strains used can survive together in harmony!
On that note, that is the end of today's blog entry. Next time, I will commence with a look at the importance of prebiotics (notice, not probiotics). What exactly are prebiotics? Find out in my next blog entry...
To your abundant excellent health
Dr Ike
Holistic Health Coach and Functional Health Expert.
Sources:
McFarland, L.V. & Bernasconi, P. (1993) ‘Saccharomyces boulardii : A review of an innovative biotherapeutic agent.’ Microbial Ecology in Health and Disease; VOl. 6. Pp. 157 – 171.
Hochter, W. et al (1990) ‘Saccharomyces boulardii in acute adult diarrhoea. Efficacy and tolerance of treatment.’ Munchener Medizinische Wochenschrift; Vol. 132 (12) pp. 188- 192.
Cetina-Sauri, G. & Basto, S. (1994) ‘Therapeutic evaluation of Saccharomyces boulardii in children with acute diarrhea. Annales de Pediatrei; Vol. 41 (6) pp. 397-400.
Dr Benes, Z. et al (2006) ‘Lacidofil (Lactobacillus acidophilus Rosell-52 and Lactobacillus rhamnosus Rosell-11) alleviates symptoms of IBS.’ Nutrafoods, Vol. 5 pp 20 – 27.
Vanderhoof, J.A. et al. (1999) ‘Lactobacillus rhamnosus (GG) in the prevention of antibiotic –associated diarrhea in children with respiratory infections: a randomised study. Pediatrics 1999; 104(5): e64.
EFSA Panel Members, ‘Scientific Opinion on the substatiation of health claims related to non characterised microorganisms pursuant to Article 13(1) of Regulation (EC) NO 1924/2006’ EFSA Journal 2009, (7):1247, pp. 64.
Chapman, C.M.C., et al., (2010) ‘Health Benefits of probiotics : are mixtures more effective than single strains ?’ European Journal of Nutrition; Vol 50 (1) pp.1-17.
Kumar et al. (2005) ‘Beneficial effects of probiotics & prebiotics on human health’ Pharmazie Vol. 60 (3) p. 163-171
Saavedra, J. & Tschernia, A. (2002) ‘Human studies with probiotics and prebiotics: clinical implications.’ British Journal of Nutrition, Volume 87 (6) Supplement s2, pp. 241 – 246.
Health Sciences Institute Publications (2011)
Saturday 25 June 2011
Monday 20 June 2011
How to choose the best probiotic for your needs (1) ...........
This is based on the research and reports of the gastroenterologist Dr Georges Mouton, guiding how we can choose the best probiotic for our individual needs:
1)Different probiotic strains: Probiotics have different genera, species and strains with a diverse range of properties and benefits for the person taking them. The best probiotic supplements acknowledge this and apply specific strains to target specific health conditions. For example, the Saccharomyces boulardii strain will help with diarrhoea and the Lactobacilli strains can help those taking antibiotics. When it comes to probiotics, there is no ‘one-size-fits-all’, because we all have varying needs and a different bacterial make-up in our digestive tracks.
2) It’s all in the research: It’s important that the probiotic you choose lists the individual probiotic ‘strain’ names, because the health benefits of probiotics are species- and strain-specific. For instance:
Lactobacillus = genus
acidophilus = species
NCFM® = strain
When you have the actual probiotic strain name (and not just the genus and species), you should be able to Google it and see a list of clinical trials which have successfully proven the benefits of that specific strain.
3) Quality control: As well as being scientifically tested for specific health conditions, probiotic strains should all pass the following criteria to help guarantee their effectiveness:
* Ability to survive at room temperature (even refrigerated probiotics need to be stable whilst away from the fridge)
* Ability to resist gastric acidity & biliary salts (so that they survive their journey to your gut, where they get to work)
* Ability to stick to the intestinal wall (it is only then that probiotics can multiply in the gut)
* Ability to inhibit pathogens once in the intestines
In-vitro testing (testing for safety in humans) should be carried out on probiotics to make sure they can pass these essential criteria. Again, these tests are carried out on probiotic strains themselves, and not just the genus and species.....
I will continue in my next blog entry, commencing with information on microorganism concentration in your daily probiotic dosage.
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert
Sources:
McFarland, L.V. & Bernasconi, P. (1993) ‘Saccharomyces boulardii : A review of an innovative biotherapeutic agent.’ Microbial Ecology in Health and Disease; VOl. 6. Pp. 157 – 171.
Hochter, W. et al (1990) ‘Saccharomyces boulardii in acute adult diarrhoea. Efficacy and tolerance of treatment.’ Munchener Medizinische Wochenschrift; Vol. 132 (12) pp. 188- 192.
Cetina-Sauri, G. & Basto, S. (1994) ‘Therapeutic evaluation of Saccharomyces boulardii in children with acute diarrhea. Annales de Pediatrei; Vol. 41 (6) pp. 397-400.
Dr Benes, Z. et al (2006) ‘Lacidofil (Lactobacillus acidophilus Rosell-52 and Lactobacillus rhamnosus Rosell-11) alleviates symptoms of IBS.’ Nutrafoods, Vol. 5 pp 20 – 27.
Vanderhoof, J.A. et al. (1999) ‘Lactobacillus rhamnosus (GG) in the prevention of antibiotic –associated diarrhea in children with respiratory infections: a randomised study. Pediatrics 1999; 104(5): e64.
EFSA Panel Members, ‘Scientific Opinion on the substatiation of health claims related to non characterised microorganisms pursuant to Article 13(1) of Regulation (EC) NO 1924/2006’ EFSA Journal 2009, (7):1247, pp. 64.
Chapman, C.M.C., et al., (2010) ‘Health Benefits of probiotics : are mixtures more effective than single strains ?’ European Journal of Nutrition; Vol 50 (1) pp.1-17.
Kumar et al. (2005) ‘Beneficial effects of probiotics & prebiotics on human health’ Pharmazie Vol. 60 (3) p. 163-171
Saavedra, J. & Tschernia, A. (2002) ‘Human studies with probiotics and prebiotics: clinical implications.’ British Journal of Nutrition, Volume 87 (6) Supplement s2, pp. 241 – 246.
1)Different probiotic strains: Probiotics have different genera, species and strains with a diverse range of properties and benefits for the person taking them. The best probiotic supplements acknowledge this and apply specific strains to target specific health conditions. For example, the Saccharomyces boulardii strain will help with diarrhoea and the Lactobacilli strains can help those taking antibiotics. When it comes to probiotics, there is no ‘one-size-fits-all’, because we all have varying needs and a different bacterial make-up in our digestive tracks.
2) It’s all in the research: It’s important that the probiotic you choose lists the individual probiotic ‘strain’ names, because the health benefits of probiotics are species- and strain-specific. For instance:
Lactobacillus = genus
acidophilus = species
NCFM® = strain
When you have the actual probiotic strain name (and not just the genus and species), you should be able to Google it and see a list of clinical trials which have successfully proven the benefits of that specific strain.
3) Quality control: As well as being scientifically tested for specific health conditions, probiotic strains should all pass the following criteria to help guarantee their effectiveness:
* Ability to survive at room temperature (even refrigerated probiotics need to be stable whilst away from the fridge)
* Ability to resist gastric acidity & biliary salts (so that they survive their journey to your gut, where they get to work)
* Ability to stick to the intestinal wall (it is only then that probiotics can multiply in the gut)
* Ability to inhibit pathogens once in the intestines
In-vitro testing (testing for safety in humans) should be carried out on probiotics to make sure they can pass these essential criteria. Again, these tests are carried out on probiotic strains themselves, and not just the genus and species.....
I will continue in my next blog entry, commencing with information on microorganism concentration in your daily probiotic dosage.
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert
Sources:
McFarland, L.V. & Bernasconi, P. (1993) ‘Saccharomyces boulardii : A review of an innovative biotherapeutic agent.’ Microbial Ecology in Health and Disease; VOl. 6. Pp. 157 – 171.
Hochter, W. et al (1990) ‘Saccharomyces boulardii in acute adult diarrhoea. Efficacy and tolerance of treatment.’ Munchener Medizinische Wochenschrift; Vol. 132 (12) pp. 188- 192.
Cetina-Sauri, G. & Basto, S. (1994) ‘Therapeutic evaluation of Saccharomyces boulardii in children with acute diarrhea. Annales de Pediatrei; Vol. 41 (6) pp. 397-400.
Dr Benes, Z. et al (2006) ‘Lacidofil (Lactobacillus acidophilus Rosell-52 and Lactobacillus rhamnosus Rosell-11) alleviates symptoms of IBS.’ Nutrafoods, Vol. 5 pp 20 – 27.
Vanderhoof, J.A. et al. (1999) ‘Lactobacillus rhamnosus (GG) in the prevention of antibiotic –associated diarrhea in children with respiratory infections: a randomised study. Pediatrics 1999; 104(5): e64.
EFSA Panel Members, ‘Scientific Opinion on the substatiation of health claims related to non characterised microorganisms pursuant to Article 13(1) of Regulation (EC) NO 1924/2006’ EFSA Journal 2009, (7):1247, pp. 64.
Chapman, C.M.C., et al., (2010) ‘Health Benefits of probiotics : are mixtures more effective than single strains ?’ European Journal of Nutrition; Vol 50 (1) pp.1-17.
Kumar et al. (2005) ‘Beneficial effects of probiotics & prebiotics on human health’ Pharmazie Vol. 60 (3) p. 163-171
Saavedra, J. & Tschernia, A. (2002) ‘Human studies with probiotics and prebiotics: clinical implications.’ British Journal of Nutrition, Volume 87 (6) Supplement s2, pp. 241 – 246.
Saturday 11 June 2011
Do Statins Cause Diabetes and Heart Disease?
This is a controversial topic, not because the science and evidence is not sound, but because of the vested commercial interest in statins. A good friend of mine called Jim told me how when his cholesterol level was reported as elevated, he was advised to commence taking statins. However, he was so troubled by his research into the side effects of these drugs, he decided to dig deeper. His findings convinced him to take a different route - nutritional, exercise and healthy lifestyle modification. Today, he is much the healthier for it - with lowered cholesterol levels to boot.
So today I am posting an article by Mark Hyman MD, a respected and accomplished practitioner of functional medicine and healthy lifestyle advocate, because this article raises some serious questions that need answers. There needs to be a debate, and more information as well as research done, so that what health professionals call proper, rational risk - benefit analysis can be carried out when deciding to place patients on these drugs - or not. His article follows below:
I WAS READING A SCIENTIFIC PAPER in the Journal of the American Medical Association a number of years ago by Dr. David Jenkins from the University of Toronto. He showed that using a combination of soy, fiber, almonds, and plant sterols (cholesterol-lowering fats) could lower cholesterol levels as much as statin medications.(i) Diet can lower cholesterol as much as statins — a surprise to many but common in my practice. Using a comprehensive approach of diet and lifestyle change, I routinely see effects that are more powerful than any medication. That was not why the article struck me. It was a finding buried in the text of the paper.
What I found fascinating was that the patients who lowered their cholesterol with statins had higher levels of insulin, while those who lowered their cholesterol through diet had lower insulin levels. Why is that important? Because elevated insulin levels are the first step on the road to diabetes — they make you gain weight around the middle, cause high blood pressure, increase inflammation, and promote stickiness of the blood. Each of these conditions, in turn, contributes to heart attacks and heart disease.
On reading this, the question that lingered in my mind was: Did statins contribute to the development of pre-diabetes and diabetes which are among the most significant risk factors for heart disease? In other words, did lowering cholesterol with statins — a treatment purported to reduce the risk of heart disease — actually increase the risk of heart disease by some other mechanism?
In treating thousands of patients with pre-diabetes, diabetes, high cholesterol, and heart disease, I have noticed one thing: Lowering insulin through diet and lifestyle corrects almost all of the risk factors for heart disease. It lowers blood pressure, increases good cholesterol (HDL), lowers triglycerides and bad cholesterol (LDL), leads to weight loss, lower levels of inflammation (C-reactive protein), and thins the blood. Lowering insulin even increases the light fluffy harmless cholesterol and lowers the level of small dense harmful cholesterol particles.
Lowering insulin is a good thing. However, statins — the best selling class of drugs on the market — appear not to do this. Do they actually increase the risk for diabetes and thus heart disease by increasing insulin levels?
The Truth about Statins and Insulin
The answer, according to a recent study in the Lancet, is yes statins do increase the risk of diabetes.(ii) The authors completed a meta-analysis of both published and unpublished randomized controlled trials from 1994 to 2009 for a total patient group of 91,140 who were treated with statins or a placebo. In the patients treated with statins there was a 9 percent increase in the risk of diabetes. The authors suggest this is a minimal risk and that current guidelines for cholesterol treatment should not change. I would suggest we think a little more deeply.
The study did not analyze any data for pre-diabetes, which dramatically increases the risk of heart disease well before a formal diagnosis of diabetes can be made. It could be that by taking these medications many people developed pre-diabetes or their pre-diabetic condition worsened. If this is true, the full risk of statins was not appreciated. The researchers also failed to consider a simple question: Why should we use a medication with significant potential risks when other treatments have proven MORE effective for reducing the risk of heart disease?
The treatment I’m talking about is dietary and lifestyle change-popularly referred to as lifestyle medicine. The recent “EPIC” study published in the Archives of Internal Medicine studied 23,000 people’s adherence to 4 simple behaviors-not smoking, exercising 3.5 hours a week, eating a healthy diet (fruits, vegetables, beans, whole grains, nuts, seeds, and low meat consumption), and keeping a healthy weight (BMI less than 30). In those that adhered, 93 percent of diabetes, 81 percent of heart attacks, 50 percent of strokes, and 36 percent of all cancers were prevented. (iii)
The fundamental focus of lifestyle or functional approaches (which includes nutrition, exercise, and stress management) is the restoration of normal function and balance in each individual. When you do this, risk factors and symptoms go away automatically. Conventional interventions, on the other hand, are primarily focus on blocking, interfering with, or excising a biochemical or physical manifestation of disease. This is the reason biology shifts towards normal when using lifestyle medicine, instead of medication, and the only side effects are good ones: weight loss, more energy, better sleep, increased well being, a reduction of most disease, and increased longevity.
While it is still a matter of public debate, there is ample evidence that lifestyle therapies equal or exceed the benefits of conventional therapies such as medication and surgery. Nutrition, exercise, and stress management can no longer be considered alternative medicine. They are essential medicine, and often the most effective and cost-effective therapies to deal with the chronic disease epidemic that afflicts millions of Americans and is now the primary cause of death worldwide.
Addressing the Global Burden of Chronic Disease
Chronic disease has replaced infectious and acute illnesses as the leading cause of death in the world, both in developed and developing countries.(iv) In 2002, the leading chronic diseases, including heart disease (17 million), cancer (7 million), chronic lung diseases (4 million), and diabetes (1 million), caused 29 million deaths worldwide. These ailments are almost entirely attributable to lifestyle risk factors including poor diet, sedentary lifestyle, and tobacco and alcohol use. The misperception that these diseases affect primarily developed and affluent societies has led to a misappropriation of resources, which fails to deal with the exponential growth of chronic lifestyle- and diet-related disease.
By 2030, 50 million will die from preventable chronic diseases compared to less than 20 million from infectious diseases. We need to include chronic disease in our global efforts to improve health. In Haiti, the poorest nation in the Western hemisphere, the major admitting diagnoses to the largest and main public health hospital where I worked after the earthquake in January 2010 was not tuberculosis or AIDS, but heart disease, diabetes, and hypertension related heart failure.
The major global health policy makers and agencies do not allocate appropriate resources to the prevention of chronic lifestyle diseases either because they have yet to recognize the problem or the economic and social benefits of focusing on chronic disease are underestimated. Heads of state, health ministries, the World Health Organization, academic and research institutions, non-governmental organizations, private donors, the World Bank, and the United Nations allocate only a fraction of their resources to chronic disease prevention despite a rich evidence base for the role of lifestyle and diet in the prevention of the major chronic diseases.
When compared to doing nothing, the argument can be made for high cost, technological interventions. When compared to changing our medical care system from one focused on treating end-stage disease, to one whose goal is to prevent disease and promote optimal health through nutrition, lifestyle, stress management, and adjunctive complementary therapies, the conversation shifts dramatically.
Diet, Lifestyle, and Chronic Disease: A Model for Increased Quality of Care and Lower Costs
Let’s briefly look at the science of nutrition and compare it to efforts for preventing or treating chronic disease with medication. This will highlight the powerful, cost-effective, and critical role nutrition plays in the cause, prevention, and treatment of chronic illness.
Science provides a firm foundation for moving nutritional and lifestyle interventions to the center of medical practice and public policy.(v) A single nutrient, food, or lifestyle habit when studied as an isolated intervention, while helpful, may not show significant effect, but when assessed collectively, the power of lifestyle over pharmacological approaches to prevent and treat chronic disease is overwhelming. That is why we have to stop looking at single nutrients or interventions and look at the whole picture. In his recent article in the Journal of the American Medical Association, Dr. David Ludwig of Harvard calls for a shift from a nutrient-based to a whole foods-based approach to our dietary guidelines.(vi) He indicts our current dietary guidelines showing how these recommendations have led to our chronic disease epidemic. Let us eat food, he says — real, whole, fresh, complex, interesting food. It’s the whole picture, not just fats or carbs or this or that nutrient that makes a difference.
For example, healthful lifestyle practices in an elderly population that included eating a whole foods Mediterranean-style diet, exercising moderately, not smoking, and moderate alcohol consumption were associated with nearly a 70 percent reduction in death from all causes.(vii) What’s remarkable is that these people didn’t start this healthy lifestyle until they were 70 years old, yet they still reduced their risk of death by 70 percent compared to a similar group of elderly who didn’t follow a healthy lifestyle.
Other studies(viii), (ix), (x) showed similar results including an 83 percent reduction in heart disease,(xi) 91 percent reduction in diabetes in women,(xii) and a 71 percent reduction in colon cancer in men.(xiii)
The Lyon Diet Heart Study,(xiv) showed a 79 percent reduction in heart disease in patients with established heart disease after a few years of following a Mediterranean diet. In another study of patients with existing heart disease, an integrated lifestyle approach of a plant-based diet, exercise, smoking cessation, and stress reduction found a 50 percent reduction in heart attacks and heart disease related deaths.(xv)
The evidence is simply overwhelming that healthful dietary patterns which include whole grains, legumes, nuts, vegetables, fruits, olive oil, fish, and, perhaps, moderate alcohol intake are associated with a decrease in chronic disease and death from all causes. The harmful effects of trans and certain saturated fats, refined carbohydrates, and other food additives or toxins are well known in the medical literature.
It is time to start putting into practice what we know, and stop the domination of our medical practice by the pharmaceutical industry. The Lancet paper on how statins increase the risk of diabetes should be front-page news. Medications such as statins that cost more, are less effective, and lead to serious side effects including diabetes should not be our first line of treatment for preventing or treating heart disease. The recent proposal that statins be handed out with cheeseburgers and fries at fast food restaurants is dangerous and misses the point.
You can’t eat a horrible diet, avoid exercise and expect to be healthy. A whole foods, plant-based diet, moderate physical activity, not smoking, and creating a supportive social network of friends and family is the best medicine. It works in ways we don’t yet understand and don’t need to-just eat real food, enjoy, and don’t worry. Your body knows what to do from there.......
This excellent and wide ranging article by Dr Hyman should be a wake up call for all those who are faced by the prospect of taking statins - why not dig deeper and work with your doctor or other health professional from a better informed position? After all, it is your life at stake!
Also, the serious questions raised reveal the necessity of further large scale, high quality research. I leave you with this thought provoking quote from Dr Hyman:
Nutrition, exercise, and stress management can no longer be considered alternative medicine. They are essential medicine.
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert.
Sources:
(i) Jenkins D.J., Kendall, C.W., Marchie, A., et. al. 2003. Effects of a dietary portfolio of cholesterol-lowering foods vs Lovastatin on serum lipids and C-reactive protein. JAMA. 290(4): 502-10
(ii) Sattar, N., Preiss, D., Murray, H., et. al. 2010. Statins and risk of incident diabetes: A collaborative meta-analysis of randomised statin trials. Lancet. 375(9716): 735-42.
(iii) Ford E.S., Bergmann M.M., Kroger J., et. al. 2009. Healthy living is the best revenge: findings from the European Prospective Investigation Into Cancer and Nutrition-Potsdam study. Arch Intern Med. 169(15): 1355-62.
(iv) Yach D., Hawkes C., Gould C.L., et. al. 2004. Global burden of chronic diseases: Overcoming impediments to prevention and control. JAMA. 291(21): 26
(v) Rimm E.B., and M.J. Stampfer. 2004. Diet, lifestyle, and longevity-the next steps? JAMA. 292(12): 1490-2. No abstract available.
(vi) Mozaffarian, D. and D.S. Ludwig. 2010. Dietary guidelines in the 21st century-a time for food. JAMA. 304(6): 681-682.
(vii) Knoops K.T., de Groot L.C., Kromhout D., et. al. 2004. Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: The HALE project. JAMA. 292(12): 1433-9.
(viii) Trichopoulou A., Costacou T., Bamia C., et. al. 2003. Adherence to a Mediterranean diet and survival in a Greek population. N Engl J Med. 348(26): 2599-608.
(ix) Salmeron J., Manson J.E., Stampfer M.J., et. al. 1997. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA. 277(6): 472-477.
(x) Liu S., Willett W.C. 2002. Dietary glycemic load and atherothrombotic risk. Curr Atheroscler Rep. 4(6): 454-461.
(xi) Stampfer M.J., Hu F.B., Manson J.E., et. al. 2000. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 343: 16-22.
(xii) Hu F.B., Manson J.E., Stampfer M.J., et al. 2001. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med. 345: 790-797.
(xiii) Platz E.A., Willett W.C., Colditz G.A., et. al. 2000. Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men. Cancer Causes Control. 11(7): 579-588.
(xiv) de Lorgeril M., Renaud S., Mamelle N., et. al. 1994. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet. 343: 1454-1459. [published correction appears in: Lancet. 1995; 345(8951): 738]
(xv) Ornish D., Scherwitz L.W., Billings J.H., et. al. 1998. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 280: 2001-2007.
So today I am posting an article by Mark Hyman MD, a respected and accomplished practitioner of functional medicine and healthy lifestyle advocate, because this article raises some serious questions that need answers. There needs to be a debate, and more information as well as research done, so that what health professionals call proper, rational risk - benefit analysis can be carried out when deciding to place patients on these drugs - or not. His article follows below:
I WAS READING A SCIENTIFIC PAPER in the Journal of the American Medical Association a number of years ago by Dr. David Jenkins from the University of Toronto. He showed that using a combination of soy, fiber, almonds, and plant sterols (cholesterol-lowering fats) could lower cholesterol levels as much as statin medications.(i) Diet can lower cholesterol as much as statins — a surprise to many but common in my practice. Using a comprehensive approach of diet and lifestyle change, I routinely see effects that are more powerful than any medication. That was not why the article struck me. It was a finding buried in the text of the paper.
What I found fascinating was that the patients who lowered their cholesterol with statins had higher levels of insulin, while those who lowered their cholesterol through diet had lower insulin levels. Why is that important? Because elevated insulin levels are the first step on the road to diabetes — they make you gain weight around the middle, cause high blood pressure, increase inflammation, and promote stickiness of the blood. Each of these conditions, in turn, contributes to heart attacks and heart disease.
On reading this, the question that lingered in my mind was: Did statins contribute to the development of pre-diabetes and diabetes which are among the most significant risk factors for heart disease? In other words, did lowering cholesterol with statins — a treatment purported to reduce the risk of heart disease — actually increase the risk of heart disease by some other mechanism?
In treating thousands of patients with pre-diabetes, diabetes, high cholesterol, and heart disease, I have noticed one thing: Lowering insulin through diet and lifestyle corrects almost all of the risk factors for heart disease. It lowers blood pressure, increases good cholesterol (HDL), lowers triglycerides and bad cholesterol (LDL), leads to weight loss, lower levels of inflammation (C-reactive protein), and thins the blood. Lowering insulin even increases the light fluffy harmless cholesterol and lowers the level of small dense harmful cholesterol particles.
Lowering insulin is a good thing. However, statins — the best selling class of drugs on the market — appear not to do this. Do they actually increase the risk for diabetes and thus heart disease by increasing insulin levels?
The Truth about Statins and Insulin
The answer, according to a recent study in the Lancet, is yes statins do increase the risk of diabetes.(ii) The authors completed a meta-analysis of both published and unpublished randomized controlled trials from 1994 to 2009 for a total patient group of 91,140 who were treated with statins or a placebo. In the patients treated with statins there was a 9 percent increase in the risk of diabetes. The authors suggest this is a minimal risk and that current guidelines for cholesterol treatment should not change. I would suggest we think a little more deeply.
The study did not analyze any data for pre-diabetes, which dramatically increases the risk of heart disease well before a formal diagnosis of diabetes can be made. It could be that by taking these medications many people developed pre-diabetes or their pre-diabetic condition worsened. If this is true, the full risk of statins was not appreciated. The researchers also failed to consider a simple question: Why should we use a medication with significant potential risks when other treatments have proven MORE effective for reducing the risk of heart disease?
The treatment I’m talking about is dietary and lifestyle change-popularly referred to as lifestyle medicine. The recent “EPIC” study published in the Archives of Internal Medicine studied 23,000 people’s adherence to 4 simple behaviors-not smoking, exercising 3.5 hours a week, eating a healthy diet (fruits, vegetables, beans, whole grains, nuts, seeds, and low meat consumption), and keeping a healthy weight (BMI less than 30). In those that adhered, 93 percent of diabetes, 81 percent of heart attacks, 50 percent of strokes, and 36 percent of all cancers were prevented. (iii)
The fundamental focus of lifestyle or functional approaches (which includes nutrition, exercise, and stress management) is the restoration of normal function and balance in each individual. When you do this, risk factors and symptoms go away automatically. Conventional interventions, on the other hand, are primarily focus on blocking, interfering with, or excising a biochemical or physical manifestation of disease. This is the reason biology shifts towards normal when using lifestyle medicine, instead of medication, and the only side effects are good ones: weight loss, more energy, better sleep, increased well being, a reduction of most disease, and increased longevity.
While it is still a matter of public debate, there is ample evidence that lifestyle therapies equal or exceed the benefits of conventional therapies such as medication and surgery. Nutrition, exercise, and stress management can no longer be considered alternative medicine. They are essential medicine, and often the most effective and cost-effective therapies to deal with the chronic disease epidemic that afflicts millions of Americans and is now the primary cause of death worldwide.
Addressing the Global Burden of Chronic Disease
Chronic disease has replaced infectious and acute illnesses as the leading cause of death in the world, both in developed and developing countries.(iv) In 2002, the leading chronic diseases, including heart disease (17 million), cancer (7 million), chronic lung diseases (4 million), and diabetes (1 million), caused 29 million deaths worldwide. These ailments are almost entirely attributable to lifestyle risk factors including poor diet, sedentary lifestyle, and tobacco and alcohol use. The misperception that these diseases affect primarily developed and affluent societies has led to a misappropriation of resources, which fails to deal with the exponential growth of chronic lifestyle- and diet-related disease.
By 2030, 50 million will die from preventable chronic diseases compared to less than 20 million from infectious diseases. We need to include chronic disease in our global efforts to improve health. In Haiti, the poorest nation in the Western hemisphere, the major admitting diagnoses to the largest and main public health hospital where I worked after the earthquake in January 2010 was not tuberculosis or AIDS, but heart disease, diabetes, and hypertension related heart failure.
The major global health policy makers and agencies do not allocate appropriate resources to the prevention of chronic lifestyle diseases either because they have yet to recognize the problem or the economic and social benefits of focusing on chronic disease are underestimated. Heads of state, health ministries, the World Health Organization, academic and research institutions, non-governmental organizations, private donors, the World Bank, and the United Nations allocate only a fraction of their resources to chronic disease prevention despite a rich evidence base for the role of lifestyle and diet in the prevention of the major chronic diseases.
When compared to doing nothing, the argument can be made for high cost, technological interventions. When compared to changing our medical care system from one focused on treating end-stage disease, to one whose goal is to prevent disease and promote optimal health through nutrition, lifestyle, stress management, and adjunctive complementary therapies, the conversation shifts dramatically.
Diet, Lifestyle, and Chronic Disease: A Model for Increased Quality of Care and Lower Costs
Let’s briefly look at the science of nutrition and compare it to efforts for preventing or treating chronic disease with medication. This will highlight the powerful, cost-effective, and critical role nutrition plays in the cause, prevention, and treatment of chronic illness.
Science provides a firm foundation for moving nutritional and lifestyle interventions to the center of medical practice and public policy.(v) A single nutrient, food, or lifestyle habit when studied as an isolated intervention, while helpful, may not show significant effect, but when assessed collectively, the power of lifestyle over pharmacological approaches to prevent and treat chronic disease is overwhelming. That is why we have to stop looking at single nutrients or interventions and look at the whole picture. In his recent article in the Journal of the American Medical Association, Dr. David Ludwig of Harvard calls for a shift from a nutrient-based to a whole foods-based approach to our dietary guidelines.(vi) He indicts our current dietary guidelines showing how these recommendations have led to our chronic disease epidemic. Let us eat food, he says — real, whole, fresh, complex, interesting food. It’s the whole picture, not just fats or carbs or this or that nutrient that makes a difference.
For example, healthful lifestyle practices in an elderly population that included eating a whole foods Mediterranean-style diet, exercising moderately, not smoking, and moderate alcohol consumption were associated with nearly a 70 percent reduction in death from all causes.(vii) What’s remarkable is that these people didn’t start this healthy lifestyle until they were 70 years old, yet they still reduced their risk of death by 70 percent compared to a similar group of elderly who didn’t follow a healthy lifestyle.
Other studies(viii), (ix), (x) showed similar results including an 83 percent reduction in heart disease,(xi) 91 percent reduction in diabetes in women,(xii) and a 71 percent reduction in colon cancer in men.(xiii)
The Lyon Diet Heart Study,(xiv) showed a 79 percent reduction in heart disease in patients with established heart disease after a few years of following a Mediterranean diet. In another study of patients with existing heart disease, an integrated lifestyle approach of a plant-based diet, exercise, smoking cessation, and stress reduction found a 50 percent reduction in heart attacks and heart disease related deaths.(xv)
The evidence is simply overwhelming that healthful dietary patterns which include whole grains, legumes, nuts, vegetables, fruits, olive oil, fish, and, perhaps, moderate alcohol intake are associated with a decrease in chronic disease and death from all causes. The harmful effects of trans and certain saturated fats, refined carbohydrates, and other food additives or toxins are well known in the medical literature.
It is time to start putting into practice what we know, and stop the domination of our medical practice by the pharmaceutical industry. The Lancet paper on how statins increase the risk of diabetes should be front-page news. Medications such as statins that cost more, are less effective, and lead to serious side effects including diabetes should not be our first line of treatment for preventing or treating heart disease. The recent proposal that statins be handed out with cheeseburgers and fries at fast food restaurants is dangerous and misses the point.
You can’t eat a horrible diet, avoid exercise and expect to be healthy. A whole foods, plant-based diet, moderate physical activity, not smoking, and creating a supportive social network of friends and family is the best medicine. It works in ways we don’t yet understand and don’t need to-just eat real food, enjoy, and don’t worry. Your body knows what to do from there.......
This excellent and wide ranging article by Dr Hyman should be a wake up call for all those who are faced by the prospect of taking statins - why not dig deeper and work with your doctor or other health professional from a better informed position? After all, it is your life at stake!
Also, the serious questions raised reveal the necessity of further large scale, high quality research. I leave you with this thought provoking quote from Dr Hyman:
Nutrition, exercise, and stress management can no longer be considered alternative medicine. They are essential medicine.
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert.
Sources:
(i) Jenkins D.J., Kendall, C.W., Marchie, A., et. al. 2003. Effects of a dietary portfolio of cholesterol-lowering foods vs Lovastatin on serum lipids and C-reactive protein. JAMA. 290(4): 502-10
(ii) Sattar, N., Preiss, D., Murray, H., et. al. 2010. Statins and risk of incident diabetes: A collaborative meta-analysis of randomised statin trials. Lancet. 375(9716): 735-42.
(iii) Ford E.S., Bergmann M.M., Kroger J., et. al. 2009. Healthy living is the best revenge: findings from the European Prospective Investigation Into Cancer and Nutrition-Potsdam study. Arch Intern Med. 169(15): 1355-62.
(iv) Yach D., Hawkes C., Gould C.L., et. al. 2004. Global burden of chronic diseases: Overcoming impediments to prevention and control. JAMA. 291(21): 26
(v) Rimm E.B., and M.J. Stampfer. 2004. Diet, lifestyle, and longevity-the next steps? JAMA. 292(12): 1490-2. No abstract available.
(vi) Mozaffarian, D. and D.S. Ludwig. 2010. Dietary guidelines in the 21st century-a time for food. JAMA. 304(6): 681-682.
(vii) Knoops K.T., de Groot L.C., Kromhout D., et. al. 2004. Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: The HALE project. JAMA. 292(12): 1433-9.
(viii) Trichopoulou A., Costacou T., Bamia C., et. al. 2003. Adherence to a Mediterranean diet and survival in a Greek population. N Engl J Med. 348(26): 2599-608.
(ix) Salmeron J., Manson J.E., Stampfer M.J., et. al. 1997. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA. 277(6): 472-477.
(x) Liu S., Willett W.C. 2002. Dietary glycemic load and atherothrombotic risk. Curr Atheroscler Rep. 4(6): 454-461.
(xi) Stampfer M.J., Hu F.B., Manson J.E., et. al. 2000. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 343: 16-22.
(xii) Hu F.B., Manson J.E., Stampfer M.J., et al. 2001. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med. 345: 790-797.
(xiii) Platz E.A., Willett W.C., Colditz G.A., et. al. 2000. Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men. Cancer Causes Control. 11(7): 579-588.
(xiv) de Lorgeril M., Renaud S., Mamelle N., et. al. 1994. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet. 343: 1454-1459. [published correction appears in: Lancet. 1995; 345(8951): 738]
(xv) Ornish D., Scherwitz L.W., Billings J.H., et. al. 1998. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 280: 2001-2007.
Wednesday 1 June 2011
Are you tired all the time?
If you are, you might find the substance NADH - Nicotinamide Adenine Dinucleotide helpful. Also known as Coenzyme number one, this substance has recently become available as a nutritional additive, and is a key player in cellular metabolism along with ATP, promoting production of greater levels of ATP and hence higher energy levels available for driving cellular processes. NADH is involved in more than a thousand different metabolic processes. No wonder people feel tired all the time if they lack NADH...
Hence a growing body of evidence from researchers and doctors shows the significant effect of NADH on keeping us energetic and healthy. So do some due diligence on this compound for yourself - you never know, this might be the missing energy link you have been searching for....
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert
Sources
^ a b c Pollak, N; Dölle C, Ziegler M (2007). "The power to reduce: pyridine nucleotides—small molecules with a multitude of functions". Biochem. J. 402 (2): 205–18. doi:10.1042/BJ20061638. PMC 1798440. PMID 17295611.
^ a b c d e f g Belenky P; Bogan KL, Brenner C (2007). "NAD+ metabolism in health and disease" (PDF). Trends Biochem. Sci. 32 (1): 12–9. doi:10.1016/j.tibs.2006.11.006. PMID 17161604. Retrieved 2007-12-23.
^ Unden G; Bongaerts J (1997). "Alternative respiratory pathways of Escherichia coli: energetics and transcriptional regulation in response to electron acceptors". Biochim. Biophys. Acta 1320 (3): 217–34. doi:10.1016/S0005-2728(97)00034-0. PMID 9230919.
^ Windholz, Martha (1983). The Merck Index: an encyclopedia of chemicals, drugs, and biologicals (10th ed.). Rahway NJ, US: Merck. p. 909. ISBN 911910271.
^ Biellmann JF, Lapinte C, Haid E, Weimann G (1979). "Structure of lactate dehydrogenase inhibitor generated from coenzyme". Biochemistry 18 (7): 1212–7. doi:10.1021/bi00574a015. PMID 218616.
^ a b Dawson, R. Ben (1985). Data for biochemical research (3rd ed.). Oxford: Clarendon Press. p. 122. ISBN 0-19-855358-7.
^ a b Lakowicz JR, Szmacinski H, Nowaczyk K, Johnson ML (1992). "Fluorescence lifetime imaging of free and protein-bound NADH". Proc. Natl. Acad. Sci. U.S.A. 89 (4): 1271–5. doi:10.1073/pnas.89.4.1271. PMC 48431. PMID 1741380.
^ Jameson DM, Thomas V, Zhou DM (1989). "Time-resolved fluorescence studies on NADH bound to mitochondrial malate dehydrogenase". Biochim. Biophys. Acta 994 (2): 187–90. PMID 2910350.
^ Kasimova MR, Grigiene J, Krab K, et al. (2006). "The free NADH concentration is kept constant in plant mitochondria under different metabolic conditions". Plant Cell 18 (3): 688–98. doi:10.1105/tpc.105.039354. PMC 1383643. PMID 16461578.
^ Reiss PD, Zuurendonk PF, Veech RL (1984). "Measurement of tissue purine, pyrimidine, and other nucleotides by radial compression high-performance liquid chromatography". Anal. Biochem. 140 (1): 162–71. doi:10.1016/0003-2697(84)90148-9. PMID 6486402.
^ Yamada K, Hara N, Shibata T, Osago H, Tsuchiya M (2006). "The simultaneous measurement of nicotinamide adenine dinucleotide and related compounds by liquid chromatography/electrospray ionization tandem mass spectrometry". Anal. Biochem. 352
Hence a growing body of evidence from researchers and doctors shows the significant effect of NADH on keeping us energetic and healthy. So do some due diligence on this compound for yourself - you never know, this might be the missing energy link you have been searching for....
To your abundant excellent health,
Dr Ike
Holistic Health Coach and Functional Health Expert
Sources
^ a b c Pollak, N; Dölle C, Ziegler M (2007). "The power to reduce: pyridine nucleotides—small molecules with a multitude of functions". Biochem. J. 402 (2): 205–18. doi:10.1042/BJ20061638. PMC 1798440. PMID 17295611.
^ a b c d e f g Belenky P; Bogan KL, Brenner C (2007). "NAD+ metabolism in health and disease" (PDF). Trends Biochem. Sci. 32 (1): 12–9. doi:10.1016/j.tibs.2006.11.006. PMID 17161604. Retrieved 2007-12-23.
^ Unden G; Bongaerts J (1997). "Alternative respiratory pathways of Escherichia coli: energetics and transcriptional regulation in response to electron acceptors". Biochim. Biophys. Acta 1320 (3): 217–34. doi:10.1016/S0005-2728(97)00034-0. PMID 9230919.
^ Windholz, Martha (1983). The Merck Index: an encyclopedia of chemicals, drugs, and biologicals (10th ed.). Rahway NJ, US: Merck. p. 909. ISBN 911910271.
^ Biellmann JF, Lapinte C, Haid E, Weimann G (1979). "Structure of lactate dehydrogenase inhibitor generated from coenzyme". Biochemistry 18 (7): 1212–7. doi:10.1021/bi00574a015. PMID 218616.
^ a b Dawson, R. Ben (1985). Data for biochemical research (3rd ed.). Oxford: Clarendon Press. p. 122. ISBN 0-19-855358-7.
^ a b Lakowicz JR, Szmacinski H, Nowaczyk K, Johnson ML (1992). "Fluorescence lifetime imaging of free and protein-bound NADH". Proc. Natl. Acad. Sci. U.S.A. 89 (4): 1271–5. doi:10.1073/pnas.89.4.1271. PMC 48431. PMID 1741380.
^ Jameson DM, Thomas V, Zhou DM (1989). "Time-resolved fluorescence studies on NADH bound to mitochondrial malate dehydrogenase". Biochim. Biophys. Acta 994 (2): 187–90. PMID 2910350.
^ Kasimova MR, Grigiene J, Krab K, et al. (2006). "The free NADH concentration is kept constant in plant mitochondria under different metabolic conditions". Plant Cell 18 (3): 688–98. doi:10.1105/tpc.105.039354. PMC 1383643. PMID 16461578.
^ Reiss PD, Zuurendonk PF, Veech RL (1984). "Measurement of tissue purine, pyrimidine, and other nucleotides by radial compression high-performance liquid chromatography". Anal. Biochem. 140 (1): 162–71. doi:10.1016/0003-2697(84)90148-9. PMID 6486402.
^ Yamada K, Hara N, Shibata T, Osago H, Tsuchiya M (2006). "The simultaneous measurement of nicotinamide adenine dinucleotide and related compounds by liquid chromatography/electrospray ionization tandem mass spectrometry". Anal. Biochem. 352
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