Patients, friends, and guys I meet online often ask me how they can lower their cholesterol levels. Most the time they say that they’ve been watching their cholesterol intake, or cutting back on their saturated fat, or they send me an inappropriate picture of themselves. In all cases, they are wrong to do so. I will now take a minute to explain how cholesterol works. As a side note, I encourage all my patients to get their cholesterol levels checked before starting a high fat diet, so that they can see for themselves that their numbers really do get better. Also, if possible get a “particle size” included in your cholesterol test. Also, get a hemoglobin A1c, testosterone (for males), chemistry panel, CBC, vitamin D, and an iron level while you are at it.
Just to show you that I’m not that far out on a limb here, as of 2015, even the U.S. Dietary Guideline association (DGAC) agrees with me in the belief that the cholesterol that is in your bacon and eggs does not affect the cholesterol levels in your blood. In their most recent recommendations The DGAC said that cholesterol “is not a nutrient of concern for overconsumption” and eliminated their 2010 guideline recommending less than 300 mg daily. When the Federal Government reverses its dietary stance on something, it’s usually 10 years too late and after there is way more evidence than needed to support it, and this U turn on cholesterol is no exception. I predict that fats and even saturated fats will be officially exonerated in the near future, the way that cholesterol was in 2015.
How Cholesterol Works
Our body’s cholesterol is made by our liver. Our liver makes cholesterol when it senses high blood glucose levels, and not as a result of how much fat or cholesterol we eat. Some cholesterol is good which is called HDL(high density lipoprotein) and some cholesterol is not good like LDL (low density lipoprotein).
Essentially, all cholesterol is the combination of a protein (which are dense and hard) and a lipid (fat), which is light, think fat floating to the top of gravy, which is why it is called a “lipo-protein”. The role of cholesterol is to take fats to the parts of your body that need them. Where is fat needed you ask. All sorts of things in your body require fats to function correctly, and cholesterol are the Uber drivers who take the fats to and from their intended destinations. LDL or bad cholesterol Ubers have a passenger (fat) and HDL’s are empty Ubers looking for fat particles to pick up.
Fat is needed almost everywhere in your body, but there are some places it shouldn’t be like our bellies and stuck to the walls of our arteries. Almost all of our cells need fats to coat their outer shells. Our hormones like testosterone, estrogen and the nerves and neurotransmitters responsible for our happy thoughts and feelings require fats. When there is an overproduction of bad LDL cholesterol because of persistently elevated blood glucose, and all of the body’s fat needs have been met, these Uber drivers don’t have any place useful to bring the fats and end up taking them to your body’s version of a dirty Tijuana strip club*. When deposited at these inappropriate places, your body pays the price, and not just for the cover charge and the watered down drinks, but for some really shady stuff. I think this analogy has run its course, but one of the shadiest places LDL cholesterol gets dropped off is into the tiny coronary arteries, which are tasked with providing the muscles of the heart with proper blood flow. To make matters worse, the LDL cholesterol are also dropped off in the even smaller arteries responsible for the blood flow to your favorite male reproductive organ. If my innuendo wasn’t clear enough, I’m talking about the penis. These deposits can result in decreased flow and eventually no flow at all #frownyface emoji, and when all blood flow is suddenly stopped to an area of the heart, this is called a heart attack or in medical speak, a myocardial infarction (MI).
Recently, we are starting to learn that a myocardial infarction seems to be also related to inflammation that can make cholesterol deposits, (cardiologists call them plaques) unstable. These unstable plaques leave the walls of your larger arteries and travel downstream to smaller arteries where they create a blockage or a myocardial infarction (MI), AKA heart attack.
How do we positively affect the plaques characteristics, so they don’t cause MI’s? The answer is two-fold and leads us to the definition of High Density Lipoprotein or good cholesterol. Good cholesterol (HDL) is almost all protein and no fat, which is why it is very dense, hence the name “high density lipoprotein”. Think of this guy as the Uber driver, riding around in an empty Prius, looking to pick up fats from places they shouldn’t be, like the Tijuana Strip club (coronary arteries) and take them to be recycled in the liver. Obviously, the more of these good Samaritans you have driving around in your blood the better, because they are cleaning up the streets, AKA your arteries. Now what does that have to do with plaques? It seems that if you have a plaque that is soft and fluffy and full of squishy soft fats AKA LDL (bad cholesterol) it is more likely for part of that plaque to fall off and end up causing a heart attack than if it is a hard “stable” plaque. The way plaques get hard (I’m skipping the obligatory erection joke here) is by HDL Uber drivers showing up and pulling some of those fluffy fats out of the plaques, thus firming up and shrinking that plaque and making that plaque unlikely to break off and cause any troubles.
In the light of this information, it is no wonder that, recent research has shown that HDL (Good Uber drivers) to be a much more important predictor of heart health than LDL. A recent study involving 135K patients who had recently had a heart attack showed that over 75% of these heart attack patients had normal LDL (bad cholesterol) but less than 5% of them had achieved a recommended level of good HDL cholesterol. So why do we care so much about bad cholesterol and talk so little about good cholesterol? I’ll get there but first I’ll give you another example.
I had a patient a few years ago, 52 year old male let’s call him Max Powers. Using my diet he lost 20 pounds in 10 months and was able to go off of his blood pressure meds but was disappointed that his cholesterol went up. Here are his numbers before and after starting his journey to get Healthy As F**k.
Before Total Cholesterol 192 HDL 38 LDL 146 **
After Total Cholesterol 195 HDL 60 LDL 148 **
When Max told me his cholesterol numbers went up, I was disappointed too, and my initial reaction was to blame him, I certainly can’t blame myself, but I had him come to the office and take a closer look anyway. First of all, he looked great. He had a fun summer cut and was wearing a tasteful cardigan with sassy lobster print pants. When I put his numbers into the ASCVD risk calculator (a tool doctors use to determine your risk of a heart attack or stroke) he was looking even better. I found that his 10 year risk went from 9.2% to 3%! This was an incredible improvement. I had to check my math and as always, it was correct. Part of the reason his risk went down so much was because he had better control of his blood pressure, so I put the numbers in again, but this time not accounting for his blood pressure improvements and his risk still went down by more than 50% from 9.2% to 4.5%. He was shocked that even though his bad cholesterol and total cholesterol went up, he was way less likely to suffer a heart attack or stroke.
So why do we always focus on lowering cholesterol? Because the things that raise HDL effectively are not drugs but lifestyle stuff. A colleague recently reminded me that niacin helped HDL a little but didn’t change heart attacks significantly, so that’s out. We have many expensive drugs that can lower your LDL. Drug companies make billions of dollars per year lowering your LDL without a huge impact on your overall health. While I on the other hand, am trying to get you to raise your HDL, and I am doing it for free, so would it kill you to sign up for email updates?
In conclusion, bad cholesterol is predominantly made as a result of too much sugar and not too much fat. So, never order an egg white omelet, eat the yolks too. They are full of healthy fats, nutrients, and according to my daughters are home to the “dippy part” of the egg. Keep your blood sugar low, by avoiding most fast and processed carbohydrates and your cholesterol will get better without medications and your risk of MI will go down, but please also listen to your doctor.
Good cholesterol (HDL) can be increased with exercise, healthy saturated fats like coconut oil and grass fed beef, and some alcohol consumption, specifically red wine. I recommend all of these things, especially exercise. The complicated part is that sometimes the bad LDL is raised a little by healthy saturated fats as well, but the good HDL is raised more, creating a net positive effect, just like we saw in Mr. Max Powers. My cholesterol numbers were poor in my 20’s but have been exceptional since starting this diet and have gotten better every year. Many patients are afraid of all the butter, eggs, bacon, and butter that I recommend, but are elated when their cholesterol improves dramatically. When you get your numbers back, feel free to share them with me on the site. Mine will be measured next month and I will be sure to post them as well.
*Also, you should know that there are no clean or classy Tijuana strip clubs, I checked. Some references are listed below.
** There is a third cholesterol component known as VLDL that wasn’t mentioned in Mr. Max Powers’ lipid report but it can be calculated by subtracting the LDL and HLD from the total.
Our findings suggest that reduction in serum cholesterol does not prevent the risk of AMI. There was a significant increase in systemic inflammation in AMI patients, inversely correlated with HDL levels, suggesting an important role of inflammatory mediators in AMI. Thus, a decrease in serum HDL and increase in hs-CRP strongly predispose the risky individuals to the event of AMI. We emphasize the importance of HDL and hs-CRP measurements in the assessment of a combined lipido-inflammatory risk factor for the screening of high risk individuals and the prognosis of AMI.
Lipid Profile of Patients with Acute Myocardial Infarction and its Correlation with Systemic Inflammation
Haseeb A. Khan,1 Abdullah S. Alhomida,1 and Samia H. Sobki2
The well-known “HDL hypothesis” suggests that therapies aimed at raising HDL-C concentrations will lower the risk of CAD and MI. In a widely cited meta-analysis of four large studies (total number of individuals studied: 15,252), a 1 mg/dL increase of HDL-C levels was reported to be associated with a 2%–3% decreased CVD risk
Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines
Article in American heart journal 157(1):111-117.e2 · January 2009 with 350 Reads
DOI: 10.1016/j.ahj.2008.08.010 · Source: PubMed