Nonetheless, I need to tell you and all of your readers how much better I feel after reducing carbohydrate intake and eating lots meat and that oh-so-controversial nutrient, FAT! I am not overweight, not have I ever been (47 years old, 123 pounds, a lot of muscle). But I have blood sugar “issues”. In between meals (particularly high carb ones) and at the end of the day (pre-dinner), I have blood sugar “crashes” that make me irritable, anxious, etc…and can even result in binge-eating. I doubt seriously that I would qualify as hypoglycemic medically speaking, but I am sensitive to changes in blood sugar. The absolutely worst is eating cereal for breakfast…I have the shakes within a few hours and am ravenous. But NO MORE! I feel absolutely great–all day long.

I am lucky enough to live in France–the French, with their low incidence of CVD eat a lot of charcuterie (sausages, meats, foie gras, etc…)…Their only sin is eating a lot of baguettes, which as Mary Enig suggests, contributes to a high rate of degenerative diseases. The sad part is that the French have bought into the low-fat mantra generated by the US medical establishment and are now abandoning their healthy ways. Hope that changes soon.

Keep up the good work!

And, sadly but predictably, since the French have abandoned their ways in favor of the US low-fat approach, obesity has been on the rise in France.

Another great post! I can’t thank you enough for all that you do, really! this blog is such a a God send. I read PP 10 years ago. Then PPLP, but it wasn’t until a year and half ago when my fasting blood glucose levels came at 125 that I took action. You see, I aways been a husky kind of guy, lift weights, jog a little, not your typical couch potato. I was really shocked when that FBG test stared at me, I decided to take action. Following the PPLP now my FBG is 102!
I just got my blood test results and they are as follows:

Fasting glucose——103, last time was 110
HbA1c——————Not measured, last time was 5.6
Total Chol————-303, up fom 260
Direct LDL————-209
Calculated LDL ——233
HDL———————-56, up from 47
Triglycerides———70, down from 88

I am not concerned about the Chol. levels, but I am curious as to why my tot. Chol has increased.

Maybe I am one of those individuals with less LDL-C receptors and thus have a higher LDL-C.

It’s difficult to say why you total cholesterol increased. It could even be a lab error. My bet, based on observing the cholesterol levels of thousands of patients on low-carb diets, is that it will drop with time. It’ll probably be back to normal by your next lab test.

“Research suggests that eating a high-protein, low-carbohydrate diet can cramp your testosterone levels. High amounts of dietary protein in your blood can eventually lower the amount of testosterone produced in your testes, says Incledon, who observed this relationship in a Penn State study of 12 healthy, athletic men.”

Whenever you see the words “research suggests” you’d better run. No, low-carb diets don’t “cramp” testosterone levels. In fact, it is just the opposite. The people who wrote this are probably the same kind of people who would finger low-carb diets as being too high in cholesterol. Well, cholesterol is the molecule from which testosterone is made. Cut cholesterol (think very low-fat, vegan diets) and you reduce testosterone. Also, it’s not just the overall amount of testosterone that’s important, it is the amount of free testosterone (that which isn’t bound to a binding protein making it unavailable for use), and it is well established that insulin resistance decreases free testosterone. How. Elevated levels of insulin drive the liver to make more SHBG (sex hormone-binding globulin), which binds more testosterone. More bound means less free. So a diet that reduces insulin levels (the low-carb diet is best at that) also reduces SHBG, which results in more free testosterone.

My mom needs to lose weight and get healthy and I recommend a low carb diet for her all the time. She now found out she has Diverticulosis. What would you say are the optimal foods she should eat with this condition? She’s just not sure what to eat in her condition.

Most docs would recommend a high-fiber diet, but all my patients with diverticulosis have done fine on low-carb diets. Increasing the fat intake usually makes the colon work better anyway.

Why do you have to resort to other tactics to avoid the statin? The studies show that women of any age irrespective of their heart disease status gain no decrease in all-cause mortality by going on statins. So why go on them at all. Especially since you experience negative side effects. Ask your doctor to show you a study that is a double-blind, placebo-controlled study showing you will benefit from statin therapy in terms of a decrease in all-cause mortality. There is no such study.

So, it is the number of vehicles, the type of vehicle and the type of passenger that is critical. Particles don’t just take up room as in a traffic jam–they get into the arterial wall and based upon their characteristics, do damage.

And as far as accuracy of a VAP-derived Apo B, it has been validated as accurate and may even be more accurate than immunoturbidometry for technical reasons. The NMR LDL-P is also a calculation (uses a formula). Finally, both LabCorp and Quest and all other labs report Apo B

The number of vehicles, the type of vehicles and the type of passengers are simply putative risk factors – no one that I know of has shown that any of these are real (as opposed to putative) risk factors, so why spend a lot of time and money making the tests ever more accurate. Why not simply get a calcium score, which is a much more direct measure of plaque and quit fooling with putative risk factors? The literature is full of case reports of people who have low lipid levels and a lot of plaque and people with scary lipid levels with no plaque. So why not just measure the plaque and be done with it. An EBT scan for a calcium score can be had for about $400, which is about the same or even less than all the fancy lipid tests.

Dr Mike – you say that Mg Citrate is a salt; does it absorb better than Mg Oxide? I’ve had good luck with it not causing stomach upset, but may switch if the chelates are substantially better.

Mg Citrate definitely absorbs better than Mg Oxide. The chelates don’t necessarily absorb better than Mg Citrate, they just don’t compete with other elements for absorption.

He is probably in his early 30’s. The medical schools are still turning them out…

I would appreciate any comments.

What can I say? Your doc sounds all too typical. It’s a real shame.

I agree with you that cholesterol is not “the” answer it has been presented to be, and I am not advancing the “cholesterol hypothesis.” As a point of clarification, tests such as apoB and the NMR LipoProfile test are NOT cholesterol tests, and therefore they do not “slice cholesterol more and more thinly.” Rather, these tests are direct lipoprotein assays (not direct measurements of the cholesterol inside the lipoproteins, but a direct measurement of the lipoprotein particle numbers themselves).

I agree with you that cholesterol is not a causal agent in atherosclerosis. There are correlations between cholesterol levels and atherosclerosis, but correlation does not equal causation, and two people with identical cholesterol levels can have VERY different numbers of lipoprotein particles transporting that cholesterol, and VERY different levels of cardiovascular risk.

Furthermore, the correlations between lipids and cardiovascular disease become progressively weaker as lipid levels drop, so using lipid measurements in an attempt to predict and manage cardiovascular risk is especially dicey for people with low levels of LDL-C and non-HDL-C (the two guideline goals of therapy). The inverse is generally true for HDL-C (although HDL is an extremely complex topic).

The fact remains, however, that when we dissect an atherosclerotic plaque, it’s full of cholesterol. The ONLY way for cholesterol to penetrate the endothelial lining of the arterial wall is for a lipoprotein particle to carry it inside, and when the number of lipoproteins (especially LDL particles) is high, the risk of this penetration occuring is higher. A growing number of studies around the world (including some truly enormous ones -i.e. AMORIS followed 175,000 patients for 5 years) have shown that the number of lipoprotein particles is a stronger predictor of cardiovascular endpoints than cholesterol.

So has cholesterol been “the” answer? No. Can we do better with lipoproteins? Yes (which is why guidelines are starting to slowly move towards lipoprotein particle numbers).

Will lipoprotein particle numbers be “the” answer. No. Atherosclerosis is a multi-factorial disease, with a host of contributory factors. But lipoprotein particle numbers DO work better than cholesterol, and I hope we can agree that having tests which allow us to assess and manage cardiovascular risk better than we can with cholesterol tests is a good thing.

Best Regards,

Marc

I didn’t mean to literally slice cholesterol thinner and thinner. I was using ‘cholesterol’ as a metaphor for the lipid hypothesis. As far as I’m concerned, lipoproteins are a component of the overall category of lipids. I know they are proteins, but their job is to transport lipids. Some factor being a putative risk factor because it correlates with disease is not proof of cause. Many people with low levels of LDL and low particle numbers develop coronary artery disease. You tell me how the cholesterol gets there in their lesions.

MRE