Tag Archives: lipids

Health Matters: The Big Test

8 Apr


Also titled “When the odds are not in your favor”
Also titled “That’s a lot of red”

It’s been a while since I talked about my health. In all honesty there wasn’t a ton going on: just a lot of testing. And my schedule running my own magazine, while working full-time and caring for my family leave little time at the end of the day. At any rate, the big test is surely worth making time to write. About a month ago I had blood drawn for this fancy test by Health Diagnostic Laboratory.

The test looks at tons of stuff: lipids, inflammation, genetics, hormones, sterols, insulin resistance, and so on and so forth.

A. lot.

And I knew going into it the answers would not be good. As I said, the genetic odds are not in my favor. So here it goes (sorry this is going to be a long one):

I knew I had high cholesterol. Since starting with my doctor last year we’ve been steadily working toward the real answer behind my cholesterol problems. My total cholesterol is 265. Anything above 240 is high risk. My LDL is 196 (above 130 is high risk). A bright note is that my HDL is 63 (optimal is more than 50), but Doc said she wants it much higher. Here’s a good primer on heart health for more information.

Some notes from the test:
My markedly elevated LDL is suggestive of familial hypercholesterolemia or another related genetic disease, familial defective Apo B100. We’re going to run further tests on this.

Tests like these can even tell you the size of your cholesterol. There’s small/dense stuff and there’s large/bouncy stuff. The large stuff is less harmful. My small dense LDL cholsterol and ApoB are increased, consistent with the presence of small dense LDL particles. Studies have shown that elevated small dense LDL particle concentration is associated with increased risk for coronary heart disease even in the presence of optimal LDL cholesterol values. Small LDL particles may be observed in association with metabolic syndrome and prediabetes (note my insulin resistance below). Statin drugs effectively reduce the number of LDL particles, but do not generally influence the size distribution of the LDL particles. Niacin, omega-3 fatty acids, a low carb diet, fibric acids, and combo therapy (statin + niacin) have been shown to increase LDL particle size.

My LDL particle concentration is also increased, which is a risk for coronary heart disease, even in the presence of optimal LDL cholesterol values. Exercise and weight loss also increase LDL particle size.

My Apo B:Apo A-I ratio was increased. Large case studies have demonstrated that this ratio is superior for predicting risk for myocardial infarction. Decreasing the ratio can be achieved by lowering Apo B and or increasing Apo A-I. Statins reduce Apo B as do fibrates and Niacin. Combo therapy is particularly effective, especially when small dense LDL particles are present. Apo A-I concentration may be increased by exercise or omega-3 fatty acids. Niacin, fibric acids, and combo therapy are also effective.

C-reactive protein and fibrinogen are in the intermediate range. These are acute phase reactants associated with an increased risk for ischemic cardiovascular events. We’ll retest and if they’re still elevated, lifestyle changes will help: including weight reduction, regular exercise, a diet rich in soy protein, viscous fiber, and almonds, can help. Statins, fibrates, niacin, aspirin, and omega-3 fatty acids also help. Fibrinogen levels have been found to be associated with subsequent myocardial infarction and stroke. If your levels are in the upper tertile have a relative risk of future cardiovascular disease 2.3 times higher.

LP-PLA2 was increased, which is an inflammatory risk marker produced by macrophages and is a marker of vascular specific inflammation. Lp-PLA2 circulates in the plasma primarily bound to LDL particles. They are associated with increased risk for cardiovascular disease and events, endothelial dysfunction and peripheral arterial disease. Again, statins, fibric acids, omega-3 fatty acids and niacin help.

My fasting insulin level was elevated, which reflects hyperinsulinemia, an atherosclerosis risk. The combination of my elevated fasting insulin, apolipoprotein B (Apo B), and small LDL size identifies a very high-risk group for the development of ischemic heart disease. I like Doc’s explanation of insulin. Insulin is the key to the door. The door is the cell receptor. If the key is not recognized, the pancreas calls for backup (more keys) and eventually a resistance is built, in which case, among other things, the brain will even start sending out sugar cravings. It’s a wonderful combination (sarcasm) that makes a lot of sense to the way I’ve always felt. I’m taking Metformin to help my doors recognize the keys.

I have an increased free fatty acid concentration, associated with the metabolic syndrome and increased risk for the development of Type 2 diabetes. Basically my body isn’t turning fat into fuel. It’s storing it. With my lifelong struggle to shed fat, this makes a lot of sense.

My ApoE genotype is 3/4. Everyone has ApoE, but it comes in different values: 2/2, 2/3, 2/4, 3/3 (most common), 3/4 and 4/4. It’s our body’s instruction manual. In general, patients with the E4 allele respond less favorably to high-dose statins and may respond better to dietary change or combination drug therapy as a means to lower lipid levels. My 3/4 means my body won’t clear bad cholesterol. Decreasing fat intake as well as supplementing with omega-3 fatty acids are beneficial. This genotype may be th emost in need of supplemental omega-3 fatty acids. Along with an insulin resistance, a low carb or Mediterranean diet may be appropriate. I talk to a dietician in a week. Here’s an interesting article about the possible correlation between ApoE-4 and Alzheimer Disease.

I also have the normal or wild-type genotype for the MTHFR C677T (C/C) polymorphism. I’m also homozygous for the MTHFR A1298C (C/C), which results in significantly reduced activity of MTHFR, potentially leading to diminished production of L-methylfolate, the active form of folate. I guess only 7-12% of people get it. Doc calls these “Mother effers” … which sounds … awesome? Reduced levels of A1298C lead to decreased production of neurotransmitters, reduced conversion of homocysteine to methionine, and reduced s-adenosylmethionine (SAMe) concentrations. CNS neurochemical deficiency, along with buildup of homocysteine and decreased availability of methyl groups from SAMe, may increase risk for cardiovascular disease. It may also predispose me to certain psychiatric disorders and/or memory and attention deficits. I am supplementing with active L-methylfolate in combo with B12.

My total HDL particle concentration is in the intermediate range, an increase for cardiovascular disease. HDL particle concentration can be increased by exercise or omega-3 fatty acids. Statins, ezetimibe, fibric acids, metformin, and combo therapy have increased HDL particle concentration. Niacin increases HDL-P size.

Myeloperoxidase (MPO) is a marker of inflammation and oxidative processes, which may lead to atherosclerotic plaque vulnerability and left ventricular remodeling. In healthy individuals, elevated MP are associated with a 2-fold increased risk for major adverse cardiovascular events. The difference between Lp-PLA2 and MPO is their location relative to the arterial wall and their function. MPO is on the outside of the vessel wall and is a leukocyte derived enzyme that catalyzes the formation of oxidants and results in the formation of oxidized LDL. Lp-PLA2 is produced by macrophages and circulates in association with LDL particles. Inside the vessel wall, Lp-PLA2 on oxidized LDL specifically cleaves oxidized phospholipids to produce bioactive intermediates that upregulate inflammation. Lp-PLA2 is indicative of vulnerable plaque When both MPO and LP-PLA2 are elevated, it creates a situation where oxidized phospholipids are formed, which can subsequently be cleaved to bioactive products, which upregulate and maintain the inflammatory pathway.

In summary, a lot of my problems would normally be treated with statins, but because of my genotype, my body doesn’t really like statins. This fact makes me more thankful than ever to be with Dr. Alexander at New You Health Studio. To say she understands alternative medicine is an understatement. I have total faith in her and I’m so thankful to finally have a doctor who spends time with me, figures me out, and helps me be well.

Here’s a list of the large amount of meds I’m now. Incidentally, I had to get an app to manage when I take everything. Mango Health is a great app!

8 a.m.
Drink Metagenics UltraMeal 360 Plus, which contains the active MTHfolate my body needs because of the “mother effer” gene
Fish Oil
Armour Thyroid


Super B Complex



Niacin ER
Co Q-10
Vitamin E 400 Mixed

I had a bad reaction to the Metformin at first, but I’m seeing this is pretty normal and moving it to bedtime instead of dinner time helped. None of this is cheap. I said I was going to live to a ripe old age but have no money left. Doc laughed at that and denied the idea. The cost of organic foods has been great, but with my diet limitations, we don’t buy as much other stuff. The cost of medical expenses is great, but hopefully it will save me money later in life. The cost of supplements and prescriptions is great, but I am happy knowing exactly what I’m putting in my body.

The good news from the test was that my hormones and thyroid are doing much better. These are the first things we tackled and I’m so happy they’re in check again. My antibodies when I first started, you may remember were in the 800s. They have steadily declined with not eating gluten to 500s, then 300s, now 200s. I broke down and had one of my mom’s homemade cinnamon rolls at Christmas, so that’s probably why it hadn’t dropped farther. My omega-3 levels are also good. 🙂

Anyway, there it is! I know some people were waiting for an update, and I’m sorry it’s a long one. Hopefully this will be the longest. 🙂

Cheers to your health!