I keep thinking that I’m missing something here. Some magical number that makes these drugs to lower cholesterol worth the hype.
I’ve read all the studies and I’ve seen the numbers, but I don’t read ALL of the medical literature that gets published on statins. So maybe I missed the one that showed that statins are worth all the hype and the new recommendations.
There has been much pushback on the newly released 2013 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on reducing atherosclerotic cardiovascular disease risk. The arguments include conflict of interest (8/15 panelists had financial ties) and overzealous interpretation of the data. Here are the scenarios when moderate to high dose statins should be used:
- Anyone with low-density lipoprotein (LDL) cholesterol levels >190 mg/dL.
- Anyone from 40 to 75 years or age with type 1 or 2 diabetes.
- Anyone aged 40 to 75 years with LDL cholesterol levels between 70 and 189 mg/dL and 7.5% or higher estimated 10-year risk of atherosclerotic cardiovascular disease.
- Moderate-dose statin treatment in anyone with an estimated 10-year risk between 5% and 7.5%.
This pretty much covers everyone.
But this aren’t the problem. Or rather, the problems.
First, the queen of all twisting of the data has to do with cholesterol. If you remember how this all started years ago, it was all about total cholesterol. Everyone needed their total cholesterol checked so that we could see whether or not they needed drugs. The entire, laser-like focus on preventing heart disease kept total cholesterol in the crosshairs. We did this, spending mass amounts of money on “educating” doctors and patients that total cholesterol = heart disease = statins.
It got embedded deep. Really deep.
It was not until 10 years later that anyone asked whether lower total cholesterol with drugs was preventing heart attacks and deaths. Turns out they didn’t work really well. Actually, they sucked. So much that these new guidelines do not even take total cholesterol into account. Basically, the suggestions were that we don’t need to look at markers anymore, but we just treat for the sake of treating because the research shows that these drugs help to reduce deaths.
Which brings us to the second problem. They suck at preventing death.
And they did not hide this in the recommendations, as you can see in this review article on the subject. The numbers are given as “NNT,” or number needed to treat over 5 years to see a benefit. This number helps us to understand how many patients need to be treated to benefit a single patient. As an example, using steroids in an acute asthma attack will save 1 person from going to the hospital for every 8 treated, so a NNT of 8. This is considered pretty darn good. Acid blocking drugs in a bleeding stomach ulcer to prevent another episode of bleeding? 15. Probiotics for preventing C. diff infections? 25.
You get the idea.
So what about the use of statins? Here’s the numbers:
- Dying from all causes NNT 138
- Having a cardiac event NNT 49
- Dying from cardiac causes NNT 88
- Having a stroke NNT 155
- Developing diabetes NNT 98
The saddest part about all of this is that society and medicine has degenerated to the point where we are willing to accept a treatment that is so poor that we have to treat 88 people for 5 years to prevent a single death. And the costs to prevent that single heart attack are staggering (think about the costs of 5,280 months of statin drugs).
With these recommendations, we have given up on the hope that the American public can and will make the necessary lifestyle changes to protect their hearts and have instead leaned more heavily on the use of drugs for “prevention” of heart disease.
That is the saddest part of all of these recommendations.
Every since our office discovered the laser lipo unit, it seems like the research supporting this approach to curb inflammation has been everywhere.
Or maybe, just like the new car you just bought you thought no one else had that you now see everywhere, I’m just looking for research along this avenue more.
Either way, it’s interesting, to say the least. It is becoming more and more clear that inflammation coming from that extra fat we you are carrying around your middle is setting your body and health on fire. And not in a good way. This inflammation is driven by hormones released by the fat cells when they become angry from the wrong lifestyle choices.
This particular study requires a wee bit of background. First, there are a few major depots of fat in the human body. Visceral fat is the fat around your organs, sometimes referred to as omental fat (the omentum is the fascial tissue acting like a web connecting all of your internal organs, loaded with fat and blood vessels). There is no doubt that visceral adipose tissue is not a good thing.
Subcutaneous fat is the fat found just under your skin that serves to keep you warm and cushion you when you fall back onto your buttocks. In general, this type of fat has been thought to be less related to chronic diseases like heart disease and diabetes as visceral fat.
Or, at least, that’s what I thought before I delved into some basic background research for this post. About 3 hours later (who needs sleep??) I’ve come to the conclusion that we still have no idea whatsoever about the human body. Why?
Because there is a growing body of research that suggests that our subcutaneous fat may actually help us keep our visceral fat in check. In particular, subcutaneous fat produces more of a compound called caveolin-1 (CAV-1). CAV-1 has been shown to protect against diabetes.
As I read through this, a blog article I did several years ago made much more sense. In the article, I reviewed the findings that, after liposuction that removed subcutaneous fat, there was a bounce-back 10% increase in visceral adipose tissue.
With this in mind, I need to get back to the article. In it, researchers looked at fat removed during surgery from 44 women (average age 47 years old). They were looking at two characteristics of the fat from both the omental (visceral) and subcutaneous fat:
- Larger fat cells than expected (termed adipocyte hypertrophy).
- Smaller fat cells, but more of them (termed adipocyte hyperplasia).
Here’s what they found. When compared to smaller fat cells (hyperplasia):
- Women with larger omental fat cells had a worse ability to manage blood sugar (as measured by GLUT4 mRNA expression) as well as more inflammation (as measured by CEBPB mRNA, OM PLIN, CD68, CD14, CD31 and vWF) and were more likely to release fats into the bloodstream (a process called lipolysis).
- Women with larger subcutaneous fat cells also had a worse ability to manage blood sugar, higher inflammation, lower adiponectin levels (not good–leads to diabetes) and more lipolysis.
While this sounds complicated, the bottom line is that larger fat cells, regardless of location in the body, was far more dangerous than having more, but smaller, fat cells.
This is consistent with what we know about fat cells being the storage for extra calories. Too many calories, super-sized fat cells and not enough blood flow to support the cells and you get a revolt and uprising.
Cold laser has been known for years to fight this situation by increasing blood flow and decreasing inflammation. It fits in very well with our experiences with laser lipo for patients who have abdominal fat that has reached this state of inflammation.
I have certainly written about the powerful effects of lifestyle choices on the risk of breast cancer, but rarely do studies look at the type of breast cancer.
First, a primer on the types of breast cancer as it relates to receptor type. Cellular receptors sit on either the outside of the cell membrane or on the actual DNA of a cell. When a trigger (like a hormone), lands on one of these receptors, they cause changes in the way a cell behaves. Many of these receptors are set up to receive the messages from hormones like estrogen and progesterone.
When estrogen lands on its receptor, one of the effects is to fire a signal down into the nucleus of the cell causing it to divide over and over again. If this is a tumor cell, that’s going to be a very bad thing. In a estrogen receptor positive breast cancer (ER-positive), that cancer cell produces a lot more estrogen receptors on its surface, leading to a perfect scenario for the progression of the cancer. Treatment of breast cancers that are ER-positive involves the use of drugs like Tomoxifen to block this receptor site.
The role of progresterone receptors (PR) in breast cancer is not as clear and it may have more to do with how the PR intacts and affects the ER. There are no direct treatments for PR+ breast cancer; instead, they fall under the same treatments as ER+ breast cancers noted above.
HER2 is another receptor that is found in higher number in about 20-30% of breast cancer tumors. This receptor also stimulates rapid cell division which would also promote tumor growth. Herceptin is the blockbuster drug that was designed to treat HER2+ breast cancers.
When you hear that a tumor is ER+/PR+, HER2+, triple positive or triple negative, these are the hormones that are referred to. In general, the hormone receptor negative and triple negative breast cancers are harder to treat. Because of this, prevention of these types of cancers is even more important.
Which brings us to this particular article. In it, researchers identified 5 main diet patterns:
- Plant-based diet, high in fruit and vegetables
- High-protein, high-fat diet, high in meats, eggs, fried foods, and high-fat condiments
- High-carbohydrate diet, high in convenience foods, pasta, and bread products
- An ethnic diet, high in legumes, soy-based foods, rice, and dark-green leafy vegetables
- A salad and wine diet, high in lettuce, fish, wine, low-fat salad dressing, and coffee and tea
They used these patterns to evaluate the risk between the risk of breast cancer and these diet patterns. Here’s what they found:
- The plant-based pattern led to a 15% lower risk of breast cancer risk.
- However, for hormone receptor negative tumors, the protection was much greater at 34% lower risk.
- The salad and wine pattern, however, led to a 29% higher risk of ER+/PR+ tumors.
Your first reaction may be to question how a good diet, like salad and wine, could increase the risk of breast cancer. But let’s look at what many consider a “salad.” Iceberg lettuce, maybe a tomato and low fat dressing. What did they replace the fat with in these “healthy” dressings? High fructose corn syrup.
You basically have a diet with some good stuff, but the salads are low-value loaded with high fructose corn syrup. Not really part of a healthy diet when you break it down like that.
Either way, it is clear that the plant based diet pattern made a strong impact on one of the more difficult breast cancers to treat.
Biotin and Allergies.
Biotin is one of those nutrients that nutrition textbooks say there is no known deficiency, and yet it is popping up in numerous places with positive effects on health. Here we see that high dose biotin is able to favourably modify gene expression as it relates to allergies.
nutrition.org — Abstracts: Wiedmann et al. 133 (3): 716
Four monthly oral vitamin D3 (cholecalciferol) supplementation on fractures and mortality.
This is an interesting concept–giving a weekly dosage of Vitamin D (a fat soluble vitamin that gets stored rather than washed out like water soluble vitamins).
bmj.com Abstracts: Trivedi et al. 326 (7387): 469
’5-a-day’ fruit and veggies or folic acid-fortified foods on plasma folate and homocysteine.
This study is an important idea for the clinicians who have said that multivitamins were unnecessary because we get all the vitamins we need from our diets. First of all, these clinicians need to ask their patients if they are getting the minimum 8-10 servings of fruits and veggies. I highly doubt it. And, these study does highlight the fact that certain genetic polymorphism will require higher dosages of nutrients than a normal diet can provide.
Monounsaturated Fatty Acids Prevent the Deleterious Effects of Palmitate and High Glucose on Human Pancreatic Beta-Cell Turnover and Function.
This article finds that monounsaturated fatty acids (i.e. olive oil, nuts, avacodos…) not only protected the beta cells of the pancreas (the cells that produce insulin) from damage, but also increased their proliferation. This would make monounsaturated fatty acids absolutely essential for treatment of both diabetes and Syndrome X.
Diabetes — Abstracts: Maedler et al. 52 (3): 726
Short-Term Fasting and Refeeding on Transcriptional Regulation of Metabolic Genes in Skeletal Muscle.
I know this title is a bit too long, but let me see if I can distill the results down. Basically, after a 20 hour fast, participants in this study were fed either a high carb or a high fat meal. The fast caused several genes involved in breakdown of fat for energy to upregulate. Breaking the fast with carbs sent those levels back down to normal and breaking the fast with fat maintained the upregulation. My personal interpretation? Breaking a fast, from a weight loss perspective (this would include breakfast meals) should NOT be done with a high carb meal. I know one of my favorite breakfasts is natural peanut butter on whole grain toast.
Diabetes — Abstracts: Pilegaard et al. 52 (3): 657
Aldehydes, Glutathione in Exhalation of Kids with Asthma Exacerbation.
I can follow along with the idea that oxidative stress and lowered glutathione levels are noted in children with asthma flare ups. However, the authors noted that a 5-day course of oral prednisone lowers the levels in exhaled breath. Huh? We have an appearent defect–lowered gluatathione and oxidative stress–and we fix it with steroids?? Excuse me for stating the obvious, but how about nebulized gluatathione inhaler and antioxidant therapy to address this? If your gas gauge reads low on gas, do you just tow around the car and call it fixed?
AJRCCM — Abstracts: Corradi et al. 167 (3): 395
L-5-methyltetrahydrofolate vs folic acid on plasma homocysteine.
Oral folic acid needs to be converted by the enzyme MHTFR to 5-MTHF before it can be used by the body in the methylation pathways. As has been previously discussed in Updates, the enzyme MHTFR is a common site of genetic differences, with certain genotypes producing a very sluggish enzyme that does not readily activate the oral folic acid. The idea has been that, by giving 5-MHTF directly, you can bypass genetic defects. This study does not support this theory, but it was also done on normal patients without consideration of their genetic makeup.
AJCN — Abstracts: Venn et al. 77 (3): 658