Giving high doses of statins to patients with heart disease doesn’t lower the risk of future heart trouble any more than moderate doses of the cholesterol-lowing drugs do, a new study finds.
Having heart disease raises the risk of heart attack and stroke, as blood vessels become clogged and cut the normal flow of blood and oxygen to the heart. These patients are typically prescribed statins on a long-term basis, to lower levels of vessel-clogging LDL (“bad”) cholesterol. But experts remain conflicted about exactly how low LDL cholesterol levels should go.
“Our study demonstrates that physicians treating patients with heart disease and elevated levels of cholesterol with statins have to ensure that patients meet a target of less than 100 mg/dL to prevent further [heart] events,” said study author Dr. Morton Lelbowitz. He is a senior physician with the Clalit Research Institute in Tel Aviv, Israel.
According to the U.S. Food and Drug Administration (FDA), millions of Americans currently take statins, including well-known brands such as Crestor (rosuvastatin), Lipitor (atorvastatin), and Zocor (simvastatin), among others. But the FDA also stresses that the heart benefits of lowering cholesterol levels with statins is “indisputable.” What is in dispute is what the ideal target cholesterol level should be.
For example, while the American Heart Association does not advocate for any specific LDL target level, the European Society of Cardiology recommends that LDL be brought down to a relatively “low” level of 69 mg/dL or less.
To examine the issue, investigators tracked more than 31,600 patients, ranging in age from 30 to 84, all of whom had been diagnosed with heart disease between 2009 and the end of 2013. All had been taking statins for at least one year.
Nearly 30% were found to have “low” LDL levels, meaning a reading of 70mg/dL or less. More than half had a “moderate” LDL level of between 70.1 and 100mg/dL, while nearly 20% had “high” levels exceeding 100 and as high as 130.
Patients were followed for an average of 1.6 years, and during that time more than 9,000 either died or faced a serious cardiac event, including heart attack, stroke, chest pain (angina), heart bypass surgery or surgery to unblock arteries (angioplasty).
Showing posts with label LDL cholesterol. Show all posts
Showing posts with label LDL cholesterol. Show all posts
Friday, July 22, 2016
Wednesday, December 9, 2015
Wisdom Wednesday: Homocysteine
Homocysteine is an amino acid, one of the building blocks for protein. However, homocysteine is not found in the diet. Rather it is manufactured in the body from another amino acid methionine.
Methionine is one of nine essential amino acids that cannot be synthesized in the body and must be in the diet. Methionine is found in most proteins – red meat, turkey, chicken, fish, soy, many cheeses, and yogurt.
When homocysteine is created it is an intermediate metabolite. Vitamin B6 then converts it to cysteine or vitamin B12 and folic acid convert it back to methionine. However, deficiencies of these vitamins or other co-factors can allow homocysteine to accumulate in the blood stream.
In normal metabolism, when damage occurs to an artery wall, a little C-reactive protein (CRP) is created. This stimulates the homocysteine to combine with LDL (low density lipoprotein) and creates a patch over the damaged area of the artery. If, over time, the plaque begins to come loose, the body sends calcium into the plaque to secure it to the artery wall.
In abnormal metabolism (pathology), any of these factors that elevate can allow this repair process to run wild creating atherosclerosis and heart disease. Unfortunately, the first factor discovered in this process was LDL cholesterol. So it was labeled as “bad” and statin drugs were developed to lower the LDL and total cholesterol.
The statin drugs actually do work (a little bit) but they do so because they lower the CRP, not because they lower the LDL cholesterol. In fact, the data never supported the claim that high cholesterol is associated with coronary artery disease. Over half of patients suffering their first heart attack have normal or even low cholesterol.
Wednesday, January 21, 2015
Wisdom Wednesday: Red Yeast Rice
About once a month a patient will tell me their primary care physician recommended red yeast rice because their cholesterol is high. It was bad enough when I just had to counsel patients against the use of this dangerous supplement. Now I have to convince them that their doctor gave them bad advice.
Red yeast rice (RYR) is made from yeast (Monascuspurpureus) grown on rice. It is a dietary staple in some Asian countries. Processed red yeast rice supplements include red yeast rice extract (RYRE), which is any extract of red yeast rice, and Xuezhikang, an alcohol extract of red yeast rice.
RYR contains several compounds known as monacolins, which block the production of cholesterol. One of these, monacolin K, has the same structure as the drugs lovastatin and mevinolin. Studies suggest that RYR use may lead to a 10-33% reduction in low-density lipoprotein (LDL, or “bad”) cholesterol.
While that all sounds good, physicians should not be recommended this supplement, nor should anyone take it.
There are several problems with this supplement:
The first issue is dosage. There is no standardized amount of monacolins or lovastatin in these products. One tablet may contain as much as 20mg of lovastatin (twice the recommended starting dose to lower cholesterol) and the next tablet may contain little or none of the active compounds. If the supplement company standardizes the active compounds, like the manufacturer Pharmanex did with Cholestin, the FDA ruled that should be considered a drug not a dietary supplement. The U.S. District Court followed suit and ruled that Cholestin is an unapproved drug and it was removed from the U.S. market.
The second issue is potential toxicity and death from citrinic acid. Again, the levels of this toxic chemical vary from tablet to tablet and brand to brand.
Monday, December 8, 2014
Most Seniors Could Use Statins under New Guidelines
Guidelines for the treatment of blood cholesterol released late last year by the American College of Cardiology and the American Heart Association target people most likely to benefit from taking statins such as Zocor (simvastatin) and Crestor (rosuvastatin).
The new study of more than 6,000 black and white Americans age 66 to 90 found that 70% were eligible for stain therapy, including 97% of those 66 to 75 years of age and all of the men. The findings appear in a research letter published November 24th in the journal JAMA Internal Medicine.
“The guidelines are a significant change from prior guidelines that relied heavily on levels of bad cholesterol to determine who to treat,” letter author Dr. Michael Miedema, a research cardiologist at the Minneapolis Heart Institute Foundation, said in a foundation news release.
“Instead, the new guidelines recommend focusing statin therapy on the individuals that are at the highest risk for heart attack and stroke, even if their cholesterol levels are within normal limits,” he explained.
The guideline recommend statins for people with heart disease, diabetes or high cholesterol levels, but also recommend the drugs for people who don’t have these conditions but do have a higher than 7.5% risk of heart attack or stroke in the next 10 years based on a risk calculator.
“Older individuals will likely cross the 7.5% threshold based on age alone, even if they have normal cholesterol levels and no other cardiovascular risk factors, and our study confirms this notion,” Miedema said.
Monday, August 4, 2014
Effects of Extended-Release Niacin with Laropiprant in High-Risk Patients
BACKROUND – Patients with evidence of vascular disease are at increased risk for subsequent vascular events despite effective use of statins to lower the low-density lipoprotein (LDL) cholesterol level. Niacin lowers the LDL cholesterol and raises the high-density lipoprotein (HDL) cholesterol level, but its clinical efficacy and safety are uncertain.
METHODS – After a prerandomization run-in phase to standardize the background statin-based LDL cholesterol-lowering therapy and to establish participants’ ability to take extended-release niacin without clinically significant adverse effects, we randomly assigned 25,673 adults with vascular disease to receive 2 g of extended-release niacin and 40 mg of laropiprant or a matching placebo daily. The primary outcome was the first major vascular event (nonfatal myocardial infarction, death from coronary causes, stroke, or arterial revascularization).
RESULTS – During a median follow-up period of 3.9 years, participants who were assigned to extended-release niacin-laropiprant had an LDL cholesterol level that was an average of 10 mg per deciliter lower and an HDL cholesterol level that was an average of 6 mg per deciliter higher than the levels in those assigned to placebo. Assignment to the niacin-laropiprant, as compared with assignment to the placebo, had no significant effect on the incidence of major vascular events. Niacin-laropiprant was associated with an increased incidence of disturbances in diabetes control that were considered to be serious, as well as increases in serious adverse events associated with the gastrointestinal system, skin, and unexpectedly, infection and bleeding.
CONCLUSIONS – Among participants with atherosclerotic vascular disease, the addition of extended-release niacin-laropiprant to statin-based LDL cholesterol-lowering therapy did not significantly reduce the risk of major vascular events but did increase the risk of serious adverse events.
MY TAKE:
Please reread the first sentence – Patients with vascular disease are at increased risk of for subsequent vascular events despite the use of statins. The slight benefit from statins comes from reducing inflammation, not from lowering LDL cholesterol.
What this summary doesn’t disclose is that Merck also added another drug to the niacin-statin combination to prevent flushing. Niacin, even in small doses can cause a flushing of the skin accompanied by itching. In previous studies about 25% of participants discontinued niacin therapy due to these side effects. The researchers admit that they don’t know if the negative side effects were related to the niacin or the third drug.
Clinically, I use the niacin without the statins and it works great. I use a much lower dose, up to 500 mg rather than the 2 g used in the study. Yes, my patients “flush” but I have long believed that the flush is important to the biochemical metabolism of niacin. Recent research indicates that the flush comes from the epithelial cells of the body using cholesterol in the formation of prostaglandin inflammation. This chemical process would lower LDL and raise HDL levels through normal biochemical pathways in the body.
Any nutrient – vitamin, mineral, phytochemical – can act like a drug if the dosage is too high. This is a constant concern in daily practice. Nutrients facilitate biochemistry while drugs mandate. I’ll admit that I occasionally cross that line. When I do, it is for short term therapy and I monitor my patient closely.
Drug-nutrient interactions are common place. I have textbooks and internet web sites dedicated to this subject. I am not surprised at the results of this study. I think the study should have been reversed – test niacin and a placebo against niacin and a statin in a double blind study.
Finally, the premise is all wrong. Manipulating the LDL and HDL levels with drugs, vitamins, or even combinations of drugs and vitamins is not the answer. When a patient has high cholesterol, you need to ask why it is high rather than just force it down. Is it diet and lifestyle? Do they have hypothyroidism? Do they suffer from dysbiosis? Commonly, the answer is more than one of these issues is at fault. Correct the metabolism and the serum lipids will come into balance. High cholesterol is a test result, not a disease.
THE BOTTOM LINE:
If you want to reduce cholesterol levels, lower LDL and raise HDL, niacin can be an excellent tool. Work with a nutritionist who will view your serum lipids as a reflection of the health of the body rather than a disease process.
Source: New England Journal of Medicine -July 17, 2014
METHODS – After a prerandomization run-in phase to standardize the background statin-based LDL cholesterol-lowering therapy and to establish participants’ ability to take extended-release niacin without clinically significant adverse effects, we randomly assigned 25,673 adults with vascular disease to receive 2 g of extended-release niacin and 40 mg of laropiprant or a matching placebo daily. The primary outcome was the first major vascular event (nonfatal myocardial infarction, death from coronary causes, stroke, or arterial revascularization).
RESULTS – During a median follow-up period of 3.9 years, participants who were assigned to extended-release niacin-laropiprant had an LDL cholesterol level that was an average of 10 mg per deciliter lower and an HDL cholesterol level that was an average of 6 mg per deciliter higher than the levels in those assigned to placebo. Assignment to the niacin-laropiprant, as compared with assignment to the placebo, had no significant effect on the incidence of major vascular events. Niacin-laropiprant was associated with an increased incidence of disturbances in diabetes control that were considered to be serious, as well as increases in serious adverse events associated with the gastrointestinal system, skin, and unexpectedly, infection and bleeding.
CONCLUSIONS – Among participants with atherosclerotic vascular disease, the addition of extended-release niacin-laropiprant to statin-based LDL cholesterol-lowering therapy did not significantly reduce the risk of major vascular events but did increase the risk of serious adverse events.
MY TAKE:
Please reread the first sentence – Patients with vascular disease are at increased risk of for subsequent vascular events despite the use of statins. The slight benefit from statins comes from reducing inflammation, not from lowering LDL cholesterol.
What this summary doesn’t disclose is that Merck also added another drug to the niacin-statin combination to prevent flushing. Niacin, even in small doses can cause a flushing of the skin accompanied by itching. In previous studies about 25% of participants discontinued niacin therapy due to these side effects. The researchers admit that they don’t know if the negative side effects were related to the niacin or the third drug.
Clinically, I use the niacin without the statins and it works great. I use a much lower dose, up to 500 mg rather than the 2 g used in the study. Yes, my patients “flush” but I have long believed that the flush is important to the biochemical metabolism of niacin. Recent research indicates that the flush comes from the epithelial cells of the body using cholesterol in the formation of prostaglandin inflammation. This chemical process would lower LDL and raise HDL levels through normal biochemical pathways in the body.
Any nutrient – vitamin, mineral, phytochemical – can act like a drug if the dosage is too high. This is a constant concern in daily practice. Nutrients facilitate biochemistry while drugs mandate. I’ll admit that I occasionally cross that line. When I do, it is for short term therapy and I monitor my patient closely.
Drug-nutrient interactions are common place. I have textbooks and internet web sites dedicated to this subject. I am not surprised at the results of this study. I think the study should have been reversed – test niacin and a placebo against niacin and a statin in a double blind study.
Finally, the premise is all wrong. Manipulating the LDL and HDL levels with drugs, vitamins, or even combinations of drugs and vitamins is not the answer. When a patient has high cholesterol, you need to ask why it is high rather than just force it down. Is it diet and lifestyle? Do they have hypothyroidism? Do they suffer from dysbiosis? Commonly, the answer is more than one of these issues is at fault. Correct the metabolism and the serum lipids will come into balance. High cholesterol is a test result, not a disease.
THE BOTTOM LINE:
If you want to reduce cholesterol levels, lower LDL and raise HDL, niacin can be an excellent tool. Work with a nutritionist who will view your serum lipids as a reflection of the health of the body rather than a disease process.
Source: New England Journal of Medicine -July 17, 2014
Wednesday, December 18, 2013
Idea of Healthy Obesity Is Tested
The idea that there are obese people who are nonetheless healthy may be a myth.
December 13, 2013
Although some overweight or obese people have normal cholesterol, glucose levels and blood pressure – elements of so-called metabolic health – a new study suggests that obesity itself increases the risk for heart disease, stroke, diabetes and death.
Last week the Annals of Internal Medicine published a report that followed more than 61,000 adults, most for at least 10 years. About 9 percent of the subjects were obese and metabolically healthy – that is, they had normal LDL, HDL and total cholesterol, along with healthy blood pressure and blood sugar levels.
Compared with metabolically healthy people of normal weight, the obese group had a 24 percent increase in risk for total and nonfatal cardiovascular events like heart attack and stroke, and death by any cause.
Increased weight, waist circumference, blood pressure, and insulin resistance all rose together. However, increases in triglycerides, glucose, or LDL cholesterol were not associated.
“The message here is pretty clear,” said the lead author, Dr. Caroline K. Kramer, a researcher at the University of Toronto. “The results are very consistent. It’s not O.K. to be obese. There is no such thing as healthy obesity.”
MY TAKE:
The study appears to be pretty obvious – if you are overweight, your health suffers. However, if you look more closely, it says something more profound – They found no correlation between high triglycerides, high glucose, or high LDL cholesterol and increased cardiovascular events. Waist circumference was a better indicator of health risk! Please note they did see a correlation between insulin resistance and cardiovascular events.
More than 50 percent of Americans having their first heart attack have normal or even low cholesterol. We don’t need to put statin drugs in the drinking water; we need to focus on the real risk factors of metabolic syndrome – central obesity (weight around the middle), insulin resistance, and low thyroid function.
What is the difference between insulin resistance and fasting blood glucose? The fasting glucose tells you how well your body controls blood sugar levels without the stress of eating (adding more sugar) for at least 8 hours. That’s like an open book test, setting the bar too low. By the time the fasting glucose is high, insulin resistance is out of control and you are a full blown diabetic.
The glycohemoglobin A1c is a simple test that measures insulin resistance. It actually measures the percentage of red blood cells (RBCs) that are saturated with glucose. Normal is below 5.7 percent. Because RBCs live about 120 days, this test measures your average blood glucose over the course of the past two months.
BOTTOM LINE:
Watch your weight, especially your waist line. Have yearly laboratory tests, but insist on a glycohemoglobin A1c and don’t be too concerned with the serum lipids. If you want to see if your cholesterol is really a risk factor, have an L(p)a run. It is the only lipid test that really correlates with increased risk of cardiovascular events.
December 13, 2013
Although some overweight or obese people have normal cholesterol, glucose levels and blood pressure – elements of so-called metabolic health – a new study suggests that obesity itself increases the risk for heart disease, stroke, diabetes and death.
Last week the Annals of Internal Medicine published a report that followed more than 61,000 adults, most for at least 10 years. About 9 percent of the subjects were obese and metabolically healthy – that is, they had normal LDL, HDL and total cholesterol, along with healthy blood pressure and blood sugar levels.
Compared with metabolically healthy people of normal weight, the obese group had a 24 percent increase in risk for total and nonfatal cardiovascular events like heart attack and stroke, and death by any cause.
Increased weight, waist circumference, blood pressure, and insulin resistance all rose together. However, increases in triglycerides, glucose, or LDL cholesterol were not associated.
“The message here is pretty clear,” said the lead author, Dr. Caroline K. Kramer, a researcher at the University of Toronto. “The results are very consistent. It’s not O.K. to be obese. There is no such thing as healthy obesity.”
MY TAKE:
The study appears to be pretty obvious – if you are overweight, your health suffers. However, if you look more closely, it says something more profound – They found no correlation between high triglycerides, high glucose, or high LDL cholesterol and increased cardiovascular events. Waist circumference was a better indicator of health risk! Please note they did see a correlation between insulin resistance and cardiovascular events.
More than 50 percent of Americans having their first heart attack have normal or even low cholesterol. We don’t need to put statin drugs in the drinking water; we need to focus on the real risk factors of metabolic syndrome – central obesity (weight around the middle), insulin resistance, and low thyroid function.
What is the difference between insulin resistance and fasting blood glucose? The fasting glucose tells you how well your body controls blood sugar levels without the stress of eating (adding more sugar) for at least 8 hours. That’s like an open book test, setting the bar too low. By the time the fasting glucose is high, insulin resistance is out of control and you are a full blown diabetic.
The glycohemoglobin A1c is a simple test that measures insulin resistance. It actually measures the percentage of red blood cells (RBCs) that are saturated with glucose. Normal is below 5.7 percent. Because RBCs live about 120 days, this test measures your average blood glucose over the course of the past two months.
BOTTOM LINE:
Watch your weight, especially your waist line. Have yearly laboratory tests, but insist on a glycohemoglobin A1c and don’t be too concerned with the serum lipids. If you want to see if your cholesterol is really a risk factor, have an L(p)a run. It is the only lipid test that really correlates with increased risk of cardiovascular events.
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