Monthly Archives: January 2017

The Apo-B/Apo A-1 Ratio Predicts Severity of Heart Disease

The Apo-B/Apo A-1 Ratio Predicts Severity of Coronary Artery Disease

References: Lipid Health Dis, Hunt Study,

I get asked all the time about whether folks should be on a statin, or whether their lipid panel is trouble. They tell me their total cholesterol. Their doctor just told them to be on a statin. What should they do? Now, I say, “Let’s look at your lipids and see if you really are at risk. Turns out, your total cholesterol just isn’t the issue at all.” The HUNT Study from Norway has thrown a significant monkey wrench into the whole affair be discovering that women who have cholesterol above 200 live longer than women below 200. So, why are we treating you to lower your level below 200? What are your real risks?

Along comes the Singulex company and starts with a new test I hadn’t seen before, the Apo – B / Apo A-1 ratio. Sounds like a lot of excessive slicing and dicing. So, I did some reading and here is what I found out.

Apo – B is essentially the docking protein of the LDL particle. Got that? It’s the site of binding the LDL particle to a fat cell. Simple. And just what is the LDL particle doing? It is essentially carrying extra fat you have manufactured in your liver, to your fat cell for storage. You make extra fat when you eat too many carbohydrates. Through most of human history, we had extra, easily available carbohydrates only a couple of times a year: most notable at the end of the harvest season when the fruit trees and the grains were ripening, and we could eat like a pig. At that time, you want your LDLs to go up, delivering fat to your fat cells. Easy as pie. What happens when you stop eating carbs? Not quite as easy, but even better than than pie. Your LDLs start to change size and shape, and your HDL’s start to climb. And your triglycerides fall like a rock.

When you stop eating carbohydrates, your liver doesn’t have to manufacture triglycerides. Net effect is that you make fewer and fewer LDL particles, but they get bigger and bigger and fluffier and fluffier. And harmless. This unpacks the lunacy of measuring total cholesterol and using that as criteria for being on a statin. The analogy I make is “having a pickup truck full of basketballs would be, (What, 50 basketballs?) is much safer than having a 5 gallon bucket full of golf balls, (500 golf balls?) Golf balls are deadly, basketballs are harmless. It is only the small, dense, dangerous, LDLs that cause heart disease.

Back to the Apo – B / Apo A-1 ratio. The Apo A-1 protein is the docking protein on the HDL particle. It sucks lipids out of stuffed white cells in the walls of arteries that are trying to clean up the mess of small dense, LDLs. If those white cells die, they turn into a lipid pool that sets off all sorts of inflammation and becomes the basis for plaque. You want HDLs. They are your friend. You want more Apo A-1 Protein. Get it?

What the the ratio do? Turns out, it is the MOST accurate ratio for predicting risk for heart disease. You want less than 0.6. It means your HDL is climbing higher. That’s the bottom number, the denominator. And your LDL is falling, that’s the top number. And it takes into account the size and fluffiness of both particles. That’s it. It’s what you want to know to keep yourself safe.

How can you change it? Simple as pie. Aka, no pie. No sugar, no carbs. More fat and carbs in the form of “above-ground vegetables”. You now have a marker you can demonstrate is getting better and better with your eating.

WWW.What will work for me. I love having data that gets to the “heart of it”. With data, and knowing how to interpret it, I can drive my own metabolism. There is lots of research now showing it is the best. Upshot for me. Eat less carbs, more eggs and spinach.


Pop Quiz

‪1. Your Apo B protein is what?

The docking protein on your LDL particle. The more LDLs you have, the more Apo B you will have. In other words, as LDLS get smaller and denser and more numerous, your Apo B goes up.

‪2. You Apo A – 1 is what?

The docking protein on your HDL particle. That’s the good one. You want more HDLs.

‪3. How do you raise your HDLs?

Eat few carbs. Repeat, eat fewer carbs. I’ve raised my HDL’s from 28 to 61 in 4 months by eating 5 eggs a day. The best I could get with Niacin was up to 31.

‪4. So, explain in your words what the Apo B / Apo A-1 ratio is?

It is the bad cholesterol particle count divided by the good particle count. When it gets below 0.6, you’re good. Any lowering is on the path to good.

‪5. I need to keep my cholesterol count below 200. T or F

False, false, false. Read the HUNT study. Look at your ratio. Get a cardiac calcium scan. And if you can’t stop eating ice-cream, well, maybe you should be on a statin.

Eat Chilies, Live Longer

Eat Chilies, Live Longer!

Reference: PLOS 1, Medical News Today, BMJ,

Whoo Hoo! I get to eat chilies and hot sauce and live longer to boot. Isn’t that a bit of fun to cheer up your gloomy January morning? Show me the proof.

That’s what this study reveals, released just this week in the on line journal PLOS 1. The authors from the University of Vermont took a sample of elder Americans over age 18 from our national nutrition survey called, NHANES, and followed them for 18 years. 16,179 carefully randomized Americans, followed for 18 plus years end up being 273,877 human years of follow-up with 4,946 deaths. You are getting to large enough numbers for the ability of statistical analysis to be meaningful and true. The risk reduction of death was from 33.6 percent for “non-consumers” to 21.6% for chili-eaters. That’s an absolute risk reduction of 12% or a relative risk reduction of 36% stated as an RR of .64. That’s a lot.

Pretty good? Huh! So, how? A prior study in the British Medical Journal, found the same thing. It was much, much bigger, but in China, not America. The Chinese eat some seriously spicy food. In that study, 199,293 men and 288,082 women were followed for a total of 3,500,004 years. They asked how many days a week spicy food was eaten, and found that adding a day added an increment of reduction, for a relative risk reduction of 14%. Their findings were also statistically significant. Again, they noticed a reduction on cardiovascular mortality.

Again, how? There may be many mechanisms. We know that populations who eat more chilies have less cancer. Capsaicin is known to disrupt the cell cycle and has been advocated as an anti-cancer drug in the form of a product called Capsol T. The ability of capsaicin to reduce lipids has also been documented. The antioxidant effect of capsaicin is well known. It has been found to alter the biome in the gut.

Goodness, gracious. Chilies are good for you. One day a week is good, two is better, seven is best. One of the articles suggested that part of why chilies may be good for you is that you eat less, you are satisfied faster. Hmmm. Perhaps because you are frantically fanning your mouth and pushing your plate away. What ever works!

WWW. What will work for me. I have used Capsol T in my practice. It is a combination of green tea and chilies, and when used every 4 hours arrests the cell cycle in cancer. But I also have chili sauce on my dining room table. For Christmas I was given Ghost Chilies as a condiment and I have been putting one flake on my eggs in the morning. Now, after 4 weeks, I’m up to 4-5 flakes. And I must admit, I love it. It’s a new flavor that is tasty and delightful. It makes my three egg breakfast something I look forward too. Building up slowly might be the way to go.


Pop Quiz

1. Eating chilies daily will lengthen my life. T of F

Possibly. Population studies aren’t quite generalizable, because you may not be one of the ones who benefits, but the population you are in will. 13% less mortality.

2. The benefits of eating chilies come from cardiovascular risk reduction. T or F

Partially true again. We aren’t sure of exactly what the mechanism is. It appears to be multifactorial, meaning we still can’t put a finger on it.


‪3. The hottest chili in the world is the Ghost Chili? T or F


Well, actually false. The Hottest Chili is now the Carolina Reaper, a hybrid of the Ghost Chili from Assam, India and a Habanero bred at the Puckerbutt Pepper Company.


‪4. You should start eating chilies today. T or F


Well, true on general principles but it’s pretty clear it takes a while to get your body used to it. Starting low and going slow is likely the way to go.


‪5. Chilies came to us from the New World in Ecuador, and spread all around the world. T or F


False. Mexico, but close enough. Now, the most chilies in the world are grown in India,

The Case Against Sugar: A Book by Gary Taubes

The Case Against Sugar, By Gary Taubes

Reference: The Case Against Sugar by Gary Taubes

It has been worth the wait. It was my Christmas present, and didn’t come till this last week. What a treasure. Gary Taubes new book has a different tone. He’s mad. We wants to know why sugar fell off the stage of scientific inquiry in the 1960s and 70s with fat becoming the enemy for the next forty years.

That’s what he details in this book. First of all, the curious addictive quality of sugar that we all demonstrate. Of course we act that we. It has served us well as long as we were living in the jungle and sweet only occurred just before the 6 month starvation season. Sugar makes you eat more so you put on weight, store calories and have enough to make it through the next dry patch.

But there is much much more. Did you know, for example, that the American cigaret industry really took off because they started soaking their tobacco leaves in sugar it allowed smokers to inhale much deeper, and get more seriously addicted? That was great for tobacco sales. Not so good for smokers. That’s still how cigarets are being made today.

But the most troubling part that Gary details is the clear historical record of populations being exposed to sugar, and then becoming fat, then obese, then diabetic, then cancerous, then heart attacks and kidney failure. Population after population showed this all around the world.

And our American scientific community blamed it on us. We were lazy and we ate too much. It could all be easily cured by better Puritan values of “eat less and exercise more”. We know that is what our health care system has said to us for years. Where did that come from? That’s the indictment. The sugar industry has funded critical players on the American nutrition scene for decades, never insisting that they tell outright lies, (well, maybe) but more that they focused the spotlight on fat and just ignored sugar, letting it slide out of sight. Because American medicine has not invested in its physicians understanding nutrition, there really hasn’t been the ability of American medicine to really understand adult human nutrition. We just learn by rote, memorize some convenient rules, and tell folks to get out there and eat less and exercise more.

As readers of this column you should know that it is not the calories you eat that make you fat, it is the hormonal effects of those calories that affects the amount that you eat for the next 12-24 hours.. For example, teens at a summer camp given identical calorie content of either high fat or high sugar breakfasts, are proven to eat more, later in the day, when they eat carbs. It is the insulin response to carbs, and sugar, that sets us off down the path of gaining weight and eating more. Insulin is your storage hormone, not your blood sugar controlling hormone.

Gary even has a nice section on the really dangerous chemical called fructose. It is half of table sugar (sucrose is a glucose hooked to a fructose). Fructose immediate damages your liver, forcing you to make small, dense, dangerous LDLs, making fatting liver, raising insulin, and starting the path to hypertension, diabetes, high cholesterol…….. Humans appear to tolerate fructose well enough when it comes in the package of an apple. But in table sugar, and in every form of added sugar (70% of all prepared foods have sugar added to them: bread, pasta sauce, ketchup, peanut butter etc) we get too much, to our peril.

The verdict is in. This is a brilliant book. He’s mad. There’s more in it about cancer, about kidney failure..the prosecutor is talking to the jury, and he’s mad. It’s a good thing some of those wicked food scientists who shaped American nutrition back in the 60s-80s are dead. Because they would have to hang their heads in deep shame. They harmed us so much, for a few pieces of silver.

WWW. What Will Work for Me. I just finished reading the book. It’s actually just as good as his others. The case is made for us cutting it out. Then I read today the study showing that our food stamp program has 10% of it spent on sugared sodas. And the food industry lobbies heavily to not let us restrict that. So our poor folks get sicker. So, let’s punish them and take their health care away now.

Pop Quiz:

‪1. Sugar is a natural food, but not so terrible other than it’s empty calories. T or F

False, false, false. It’s as dangerous as alcohol. Causes as many metabolic damaging effects. And probably just as addictive

‪2. About 20 years after starting to eat sugar, folks starting getting sick. T or F

That’s what hundreds of studies have detailed.

‪3. Cancer rates in societies without sugar are just the same as ours. T or F

False, false, false. Cancer rates rise in proportion to populations eating sugar. Insulin is one of cancers most potent growth factors.

‪4. I’ll be ok if I cut down and only have sugar on weekends. T or F

It may be true. If your fat cells are small enough, the human body has lots of resilience in it. You likely need to cleanse it out of you with good behavior for the next week.

‪5. If I eat a food with sugar secretly inserted in it, what happens next.

A: I eat more.

Prolactin, A Problem for Older Guys

Prolactin, A Problem for Older Guys

References: Jr of Endocrinology, Wikipedia, Nature Reviews,

Ever heard of prolactin? Bet not. From its name, you can surmise that it has something to do with helping lactation: “pro” – lactation. And that’s just what it was discovered to do. It is secreted from the anterior pituitary in response to breast stimulation, and helps milk let down. A mother can successfully breast feed when she has her infant stimulate her nipple. That was figured out in the 1970s. Since then, we have found over 300 other functions that in which it participates.

Prolactin isn’t just made in the pituitary. It’s made in lots of other places in much smaller amounts. It is quite similar in structure to growth hormone, nature being efficient with hormone design and building off one hormone to make more functions. It has 198 amino acids in it, so is a peptide hormone. As we dig deeper into biology, we are finding that the human metabolism is far more complicated than anything we ever imagined. Orgel’s Third Law alludes to that: Nature is more complicated than you imagine, even when you take Orgel’s Third Law into account.

Now, here’s the rub. One of it’s functions is men’s refractory period. The refractory period is the time after an orgasm during which a man is unable to be aroused again, cannot achieve an erection, and would rather read a book. That period is usually short in teen years (5 minutes) but gradually lengthens with age. With the right environment, it might only be a few minutes – hours in the 20-3os. By the age of 50-60, it can be a few days. Prolactin appears to be the mediator of that refractory period. As men age, their prostate gland enlarges, and the prostate also makes prolactin.

That’s where this week’s study comes in. Ten men in Germany, who were otherwise healthy, had their prolactin measured and then shown erotic films and instructed to masturbate. This is hard to turn into a double blind trial, as you can imagine, so it was single blinded and crossed over so that then subjects didn’t know when they were getting a prolactin inhibitory drug called cabergoline. The cabergoline arm of the study was found to have significant reductions in prolactin, and enhanced of all parameters of sexual drive (<0.05), function (<0.01) , and perception of length of the refractory period (< 0.01). The authors suggest that this is a possible route for study as we look into future effects on men’s sexual health.

Prolactin has over 300 actions in the body. It may play a role in brain cells making myelin, it probably mediates women’s infertility while breast feeding, in infants making surfactant in their lung, in immune tolerance of the mother’s immune system to the fetus, the production of new brain cells… Orgel had it right. Nature is complicated, and we are just unpacking the surface. The interplay still to be discovered has a way to go.

WWW. What will work for me. Well, it turns out cabergoline is now a drug on the market used for men’s sexual health called Dostinex. And we are finding the measurement of prolactin starting to seep into standard blood assays. In my practice, my most used blood panel has it as a newly added feature, and I’m finding a lot of men and women have modestly elevated levels. I tell folks that a tiny percentage may have a pituitary tumor, but what to do with slightly elevated levels is still uncertain. There are web sites on how to lower it naturally for both men and women.

Pop Quiz

‪1. Prolactin is a hormone that helps women breast feed their infants. T or F T.

That is what it was discovered to do

‪2. Elevated prolactin plays a roll in some men who have sexual dysfunction. T or F

Again, true.

‪3. Prolactin is secreted at the end of a sexual encounter and accounts for the sense of satisfaction afterwards and the inability to become aroused again. T or F


‪4. It is easy to measure prolactin. T or F

‪It is almost becoming routine, and lots of folks have modestly elevated levels.

‪5. Prolactin causes cancer. T or F

Whoa Nellie. Not so fast. It may be a growth factor for some cells, and cancers tend so shop around and find what growth factors they can use. Prolactin is similar in structure to growth hormone, but it isn’t really a cancer causer.

Hormone Replacement with Estrogen Improves Lung Function

Hormone Replacement with Estrogen Improves Lung Function

References: Pro Natl Acad of Sci, Townsend Letter, Menopause,

Did you ever wonder how women adapt to being pregnant? One of the key adaptations is that they have to breathe for two, and that’s while their abdomen is being pushed up by the pregnancy. Can’t you imagine breathing enough with a basketball under your belt? This question arises when I see a women who has lung disease. Can we help her adapt to the challenges of that lung disease with hormones? And the answer is yes! This is particularly important because nonsmoking women actually have more chronic lung disease (called COPD) than non-smoking men.

The first research came out in 1995 with the Drs Massaro showing that pregnant rats almost double their oxygen uptake ability. They do it in a unique way. They generate more and smaller alveoli than male rats, (the tiny air sacs where air exchange happens) leading to greater surface area for oxygen to diffuse across. The same researchers then took immature rats and showed that their lungs made many more small alveoli when given artificial estrogen, compared to controls. So, it was estrogen that does it!

Testosterone in the same context didn’t do it. And then, mature rats who had their ovaries removed lost lung surface area and increased the size of their alveoli, all leading to less oxygen capacity.

The authors conclusion was that estrogen plays a key role in lung function in female rats, and can result in regeneration of new and improvement in existing alveoli.

This then lays the table for us to think about humans. The authors wrote a review article on estrogen and women with pulmonary dysfunction. Menopause becomes a critical risk period. With the loss of estrogen, alveoli decline and what may have been adequate prior to menopause because inadequate after. Considering how many women have chronic lung disease without even smoking, this becomes a critically important issue for the safe and optimal care of a post menopausal woman, with any lung disease. The same applies for men. They need some estrogen too, and if their testosterone gets too low, their estrogen conversion doesn’t happen enough to support lung function.

WWW. What will work for me. I’ve always considered estrogen replacement to be critical for brain and bone function. Then we added heart disease, and reduced breast cancer risk. Now, it’s clear that lung function is part of the mix. It only makes sense. What is part of your optimal healthy environment is still part of that combination when menopause arrives and estrogen declines. No wonder women with higher estrogen live longer. No wonder the Leisure Study found that women who use hormone replacement for over 15 years live the longest. I’m adding this to may armamentarium of reasons to be on BHRT.

Pop Quiz

‪1. Pregnant rats demonstrate markedly increase oxygen absorbing capacity. T or F


‪2. Must of this increased capacity in pregnancy comes from smaller and more numerous alveoli? T or F

Again, right on the mark

‪3. Rats with ovaries removed recover more and better alveoli when estrogen is replaced. T or F

You are on a roll. Keep it up

‪4. Humans also get better lung function when they are given estrogen after menopause. T or F

Again, true

‪5. Which makes it obvious that the Leisure Study shows that women live longer when they are on hormone replacement. T or F

Perfect. A good start for the new year.