Category Archives: 1. Know Thyself : Your Data Dashboard

High Cholesterol is Good for You

High Cholesterol is GOOD for Women – the HUNT Study

Published Oct 26th, 2015

Reference: Petursson, Jr Eval Clin Pract. AHA Cholesterol Guidelines

Have you been badgered lately by a health provider who has insisted that you be on a statin? They show you your “numbers” and your cholesterol is high.   You blanche. You’ve seen all the ads on TV for statins. All your friends are on statins. What to do? The last time you tried statins, you had terrible leg pain just walking across the room.

Well, what you do is pull the rug out from the argument and read the article above.   It shows that moderately higher cholesterol is protective. Worse, it shows that mortality is HIGHER if you lower your cholesterol.   What are the details? This is a big research study – following men and women prospectively for 10 years (52,087 Norwegians and a total of 510,297 observation years). It shows a U shaped curve for mortality from cardiovascular disease with the greatest mortality happening in the “mid-range”.

The authors suggest that it’s time to get some nuance into cholesterol guidelines.   The total cholesterol is just not the story line we want to follow.   The authors suggest that perhaps better “numbers” would be to take the Total Cholesterol/HDL ratio and aim to get that below a certain threshold. (Most folks say around 4.5) That would take into account the protective effect of HDLs.   As we talked about in this column, a more recent update on ratios shows that the Trigylceride/HDL ratio is the best predictor of all.   Perfect is when you get to less than one. You have virtually eliminated all risk of vascular disease if you can achieve that ratio.

And you can eliminate it, almost completely with lifestyle change. How?   It’s actually easy. You have to understand the role LDL’s play in your body. If you premise that they represent the fat manufactured in your liver, being transported in the blood to fat cells, where the fat will be stored, you will understand exactly how to change them. The human body was not designed to eat lots of processed carbs. We were designed to eat very coarse, dense carbs, like spinach, broccoli, dandelions, ….whole foods, raw and very low in free carbs.   Our colons’ bacteria digested those “high fiber” foods and released glucose very, very slowly.   When we eat refined bread, our liver is overcome, we cannot process the glucose and we force our blood sugar up, our insulin up, and that turns on the production of fat in our liver. Hence, if you want to get rid of your LDLs try your own experiment.   Stop eating carbs, at least the ones that come in processed foods like bread, cookies, sugar, ice cream, donuts.   Eat meat, animal fat (bacon and butter and eggs) and all the green vegetables you want.   Measure your LDLs before and after two-three weeks. You will be cured in a month of “high” LDLs and your HDLs will climb like a rocket. Even your nervous family doctor will be happy because you wont meet criteria to be treated for your allegedly high cholesterol.

So, just what is the take home of this study? Most women are well served with higher cholesterol, because many, many women naturally have very high HDLs. That is partially genetics, partially estrogen, partially discipline and exercise.

WWW. What will work for me. It’s just so ridiculously obvious and simple.   High LDLs mean you are eating too many processed, free modern carbs. You can prove it to yourself in weeks. I’ve done it so many hundreds of times with my customers, I’m just annoyed that our health care system can’t figure it out for themselves. Just get lab twice, a month apart, and try the experiment for yourself.   Presto.   My problem is that I sin, and when I test myself, my wonderful good results go away pretty fast.   Bummer.   This being consistent is not my strongest suit.


Pop Quiz


  1. High cholesterol is good for women.   T or F

Yup. And if you aren’t sure, get a CT cardiac scan and prove your calcium score to be zero, and then sleep sweetly.

  1. So women with a cholesterol of 250 may not need a statin. T or F

That’s it. Taking them will cause harm. You are safer without them. At least if you are Norwegian – or believe yourself to be close enough.

  1. If your doctor insists on a statin, you can ask for a one month reprieve, go on a low carb diet (<20 grams a day) and get retested, and then avoid the statin. T or F


  1. LDLs represent the consumption of too many carbohydrates, resulting in the manufacture of fat by the liver, being transported to the fat cell. T or F


  1. We humans are better served eating tons and tons of spinach rather than donuts. T or F


Calcium Heart CT Scoring Can Improve your Statin Decision Making

Heart Calcium Scoring and Statin Use

Reference: New York Times, Journal of the American College of Cardiology Oct 2015

The use of statins for reduction of risk in coronary artery disease is controversial, in part because of the appearance of commercial conflict of interest.   It is BIG business in BIG medicine. And lots of folks have pretty horrible side effects.   And you have to treat 1000 people to prevent 7 heart attacks a year, for which you have one death.   Hmmm.   Math seems to be a bit dubious at times.   And your doctor is graded and paid “quality assurance” bonuses based on the percentage of patients in his or her practice that are taking statins when they meet guidelines.   It is all well intentioned, as a method of promoting quality, but it results in a certain intensity of persuasion and coercion when you say you don’t like the side effects.

With all that emotion and coercion, is there a better tool that might refine the ability to make a decision?   What would happen if you could get an additional risk scoring procedure done for $ 99 that showed you didn’t need to be on a statin? Wouldn’t that be handy?

That’s what this study asked.  The MESA study is 6,814 multiethnic folks between 45 and 84 without evidence of coronary artery disease who were whittled down to a pure group of 4,758 folks without confounding items like missing data, or complete lack of lousy LDLs, etc.   They were followed for 10.3 years and observed for the development of coronary artery disease events.   The new cholesterol/statin guidelines were applied to this group, of whom 2,377 qualified to be on them.   The majority of them (77%)qualified because according to the ACC risk calculation tables, they had a greater than 7.5% risk of having a heart attack/event over 10 years.   Was that really their risk?   From that group who were supposedly meant to be on statins, 41% had a calcium score on CT scan of “0”. That was ZERO.   No calcium in their arteries.     They did have heart attacks.   Yes, they did. At a rate of 1.5% per 1,000 years. Pretty small.   More than lightning, or shark attacks.  But not enough to take on the risk of statins.     And not at the 7.5% rate that is the acknowledged rate for being enough risk for taking a statin.

What are the risks of taking statins? Well, Mayo’s opinion is measured and valid. At the other end is Dr. Mercola, who would be less measured, but possibly more honest because he’s not in the system and there by maybe speaks a bit more honestly, albeit off the walls.   Or just read the FDA’s concerns.

What does the CT scan find?   Well, it can add up the calcium in plaque in your arteries and actually find calcium that is in the wall of the arteries rather than just bulging out. It takes years for calcium to build up, so it is old plaque. Recent new, raw dangerous plaque is not seen on calcium scanning. It get missed. And the CT does find all sorts of other tidbits, like lung nodules that you don’t know what to do with. But on balance, it’s information.

WWW. What will work for me. I’m dancing a jig. I’m thrilled. I’ve been doing this for four years and I now have literature support that what I’m doing makes sense. Now, if you have risk, you want to know how to turn it off.   That’s were it gets really interesting.   The fine art of getting rid of LDL’s actually isn’t that hard. I can show you how in about a month. And then there is TNF-α, CRP, sdLDL, HDLs and other blood cytokine and risk factors that can show you how to improve your score and get out of risk, without the statins. If you are interested, start by not eating sugar and white flour, and come let me show you how. I’ve been on vacation for a week here in Italy. The gelato has been wonderful. I’m going to measure my HDLs when I get home. I think I just accumulated a bit of risk. Stay tuned.   I’m back in the saddle.



Pop Quiz

  1. You can measure your risk of heart attack by an inexpensive CT scan of your heart that measures your calcium load? T or F

That’s it.

  1. If your score is zero you have a greater than 10 % risk of having a heart attack in 10 years. T or F

Are you kidding? You didn’t read the column. Go back. Read it again. Score of zero means your have a 1.5% chance in 1,000 years. That’s low.

  1. Current ACC guidelines say it is worthwhile to treat you is your risk is greater than 7.5% chance in 1,000 years.


  1. About 50% of people who currently meet the current guidelines for statins have a calcium score of zero.   T or F

True. (Makes you feel pretty confident in those guidelines, doesn’t it)

  1. You get some radiation from a CT scan of your chest.

Also true. But in the world of risk benefit, I’ll take that risk over taking statins for 1,000 years.




How Low Should You Go?

The Sprint Study: How Low Should Your Blood Pressure Be?

Sept 14, 2015

Reference: New York Times , NIH National Heart and Blood Institute Sept 2015

This is really a big deal.   I’m very relieved to hear at because it was just two years ago that a huge meta-analysis said it was no big deal to treat high blood pressure until it was 160/95.   Now we have exactly the opposite and to a remarkable degree.

This is the Sprint Study. In it, 9,300 adults from about 100 medical centers across America and Puerto Rico with high blood pressure were recruited to two arms. One group was treated to a systolic (the upper number) pressure of 140. The other was pushed down to 120 or lower.   The study was meant to be concluded in 2017 but was released this week because the preliminary findings were so robust that the authors felt it to be unethical to continue and not release their findings.   The extra effort of pushing blood pressure down to 120 or lower resulted in a 30% additional decrease in “bad things” like stroke and heart attack, and death about 25% less.   We have had about a 70% drop in stroke since the 1970s when we started to treat high blood pressure, so this should be in addition to that. This is a pretty simple study with a pretty dramatic finding, and just about every expert in the field agrees with the importance of it, and the need to implement this into clinical practice.

What’s my read on it.   Well, I can’t help but agree with it.   It makes sense. But I have a very different take on it. First of all, basic human physiology. As folks get older in indigenous societies around the world, their blood pressure drops. In America, it’s like a rite of passage that our blood pressure rises and by age 70 some 70% of us have high blood pressure.   That means it’s our environment that is askew here in America. And just what is it in America that is doing it to us? And what is high blood pressure?

Second answer first.   High blood pressure isn’t just your pressure gauge being higher. It is actually better called “Endothelial dysfunction” – which basically means the lining of your blood vessels is out of whack, and can’t relax. That results in high blood pressure. It can’t relax because of a shortage of nitric oxide, brought on by inflammation and toxins. The most notable toxin is sugar and fructose, that pushes you towards making more uric acid. Uric acid soaks of nitric oxide and with that, your blood pressure rises.   American’s eat 10% of their total calories in the form of fructose alone. (Not everyone agrees with this analysis.) Another toxin is lead.  Another is trans fats (though they are fading.).   But the biggest problem may be your waistline. Fat is inflammatory. Fat tissue is not just passive calorie storage, it is the source of potent inflammation. And that goes everywhere in your body, and annoys your blood vessels. And that contributes to high blood pressure.   Finally, carbohydrates are the final “toxin”.   They cause insulin to be secreted. Insulin tells your kidneys to hang on to salt. It’s that simple. You have shown it yourself when you go on a diet for three days and don’t eat any carbs. You lose 8 pounds.   Seven of those pounds were from the salt water you hung on to. High blood pressure is a disease of too much salt water stuffed into too small a space. The pressure has to go up. In the last 2000 years, and last 100 in particular, we have developed more and more foods that are more “glycemic” and hence, more insulin inducing.

WWW. What will work for me. This study is slightly insane. It’s advocating for treating high blood pressure more aggressively.   In the world of treatment, that is correct. But there is a better world. Prevention. And that starts with weight loss.   Prove it for yourself. Lose 10 pounds and watch your blood pressure drop. Lose 20, and watch it plummet.   The choice is ours.   Do we have the will to change our environment, and lose weight, eat less sugar, less carbohydrates, less trans fats, or would we rather take a pill. This is a huge study. It confirms that changing our environment is crucial. And if you can’t, well, then. Here are three pills.


Pop Quiz

  1. If we pay attention to this study, we should take pills until our blood pressure is below 120 instead of below 140.   (One extra pill a day on average) T or F


  1. This study was meant to be concluded in 2017 but was such a remarkable result, the authors felt compelled to release it earlier.   T or F

That’s exactly what happened.   Very significant

  1. Our environment has changed in the last 200 years by the addition of more fruits and vegetables. T or F

Well, actually probably true, because we can get vegetables year around now which we couldn’t before, but what has happened is that we really eating much less vegetables and fruits, and instead are eating a lot more sugar and refined flour products.

  1. We have not gained much weight recently in America.   T or F

Are you kidding, we are getting fatter by about 1 pound per person per year.

  1. Losing weight lowers our insulin, and helps our kidneys stop holding onto salt.   T or F

Bingo, making weight loss more important than an extra pill.

Biohacking Vegetables 101

Biohacking Vegetables101

Reference:   Wikipedia, Biohacking Conference,   PBS,

What is Biohacking?   If I may give the simplest explanation, it’s figuring our how to do what you were designed to do, in the best and most satisfying fashion. Well, when we talk about our own health and life style, it’s all about creating choices with food, sleep, brain health, relationships, activities and exercise that gives us the best chance at being the best we can be.   Some of “biohacking”s proponents are about research on the cheap, outside of the traditional academic world and without the constraints or ethical guidelines developed in those venues.   Research that may harm people should be monitored and restricted.   There is a fine boundary with lifestyle choice and making decisions that could harm people.   For example, is it harmful to tell people to eat more vegetables cut out carbs from their diet? That would be the basis for the Bulletproof Diet.   Considering the massive failure of modern medicine to provide us with smart food guidelines, and the confounding ability of our food and pharmaceutical injury to create dangerous and harmful products, it’s no wonder the biohacking world has developed. My interpretation is that it is “us” figuring out for ourselves, what works best.   This email column is a “biohacking” exploration.

How would we apply biohacking to vegetables?   By way of example, this is how I would consider it.  I would first explore what vegetables do to our bodies. Most green vegetables like spinach, kale, cucumbers, asparagus and broccoli are actually quite high in protein, and relatively low in free sugars.   Broccoli, as one example, has as much protein as steak when it comes to protein content per 100 calories.   Our bodies respond to them without much insulin release because the sugars are released so slowly that we don’t need to release insulin. We metabolize the sugars as fast as they are digested.   That is a nice example of first understanding core biology and physiology. Do the research about how your body functions.

A good biohacker would come to the conclusion that the majority of human food should be from vegetables that are green and have a slow insulin response. Insulin lasts for 6 to 8 hours.   To have the main hormone that controls weight gain, appetite, glucose control be one that last 6-8 hours must mean that for 60 million years, the main diet for humans and their ancestors must have been foods that matched that and provided calories in a fashion that lined up with that endocrine need.   That means green vegetables should be core to our diet.

Then think about root vegetables like potatoes and carrots, or grains like corn, rice and wheat or fruits like apples and pears and you find foods that are filled with many more carbohydrates and mature in September and October. They have a lot of sugar, and less protein. They stimulate insulin. They encourage your body to secrete insulin to store calories for the winter.     A good biohacker would conclude, knowing that about when these foods ripen (fall – or just before winter or just before dry season) that they should be limited to those times of year we seek to gain weight.   You want to gain weight if you are aiming to go into a period of starvation.

The challenge of our time is to figure out how to lose weight, not gain weight. We have been inundated with food filled with high calorie, carbohydrate laden foods. And we have gained weight.    Get the drift?   You can be a biohacker too.

WWWW. What Will Work for Me. (AKA: Biohacking) A good biohacker would conclude that the proper way to lose weight would be to back off completely from all foods that simulate insulin. That comes down to avoiding sugar, grains, root vegetables and too much meat.   What’s left is green vegetables and fat, and a bit of meat.   Want to lose weight? Salads with olive oil, spinach with bacon,……. Read the Book, The Bulletproof Diet by Dave Asprey. He lost 100 pounds. Look up the Bulletproof Diet Cookbook by Chris Kane.


Pop Quiz

  1. Biohacking is the attempt by people in every walk of like to be the best they can be. T or F

That about sums it up.

  1. It’s detractors claim it can be unethical? T or F

Possibly true if you are doing research without informed consent on things that can be dangerous.

  1. Our medical food guidelines represent a massive experiment that has caused immeasurable harm, without informed consent. T or F

True. So what’s the deal? We all got fat, diabetic and high cholesterol on those guidelines.

  1. We can trust that we will soon be following the biohacking crew with food guidelines.   T or F

True.   Institutional medicine will gradually get there.

  1. Want to lose weight, biohack yourself and get off carbs. Watch the weight melt away.

Of course your Do

  1. Want to biohack a bit further and see if avoiding some foods helps you feel better?

Give it a try.   Avoiding some foods is not unethical behavior. Just common sense.


Kidneys, Insulin and Salt Retention

Why You Can Lose/Gain 5 Pounds in One Day – Insulin, Kidneys and Salt

June 29th, 2015

Reference: Horita, Int Jr of Hypertension

Ever stepped on the scales and gained five pounds in a day?   Better yet, ever started a diet and lost 5 pounds the first week? “It’s just water weight, “ you say. And you are correct. But the details are pretty elaborate.

Here are the details, as elaborated by Horita in his review article.   There are likely four or five key reasons why being overweight leads to high blood pressure, but leptin resistance is certainly in the mix.   Leptin is your “stop eating hormone” made by fat cells that goes back to your brain and signals that you have had enough to eat. As we get overweight, we become leptin resistant. Long term elevated leptin leads to increased adrenaline in the blood, raising blood pressure. And as we get heavier, we also become insulin resistant, with gradually rising blood insulin first, then rising glucose later.   In addition to leptin, there are arcane hormones such as tumor necrosis factor (TNF) that causes sodium excretion at high concentrations and retention at low concentrations.   Figure that out?!@   Or angiotensin that saves salt and is closely related to insulin resistance.   Then, there is the WNK family with its five subtypes and you get the picture of increasing complexity. Insulin affects all the WNKs. Whew.

But what is the effect of insulin on the kidney? That is the key to discuss today.   Insulin, the hormone your body makes to store glucose, has another effect entirely on the kidney. It essentially turns on sodium retention in virtually every part of the kidney.   When you save sodium, you save water too.   When you hang onto water, you increase the volume of your vascular tree. (Blood vessels.)   That’s a bit like adding more water to a fixed size water balloon. The pressure has to go up.   Now, interestingly enough, insulin also stimulates the production of nitric oxide, the chemical your body uses to relax your blood vessels, making your total volume of body water go up. So, your balloon gets a bit bigger.   Did you get that? With a bigger balloon, you gain water weight. With insulin, you stuff more water in it.

This becomes a pretty simply formula to gain weight.   A piece of chocolate cake for dessert is just 200 calories and weighs less than 4 ounces. But you add ice cream on the side and you just turned on insulin in a dramatic fashion.   With that you start the whole cascade of saving salt water.   You gain 5 pounds.

And what happens when you diet?   You avoid carbs and sugar for a day or two. You just eat “salad”. Salad is composed of low glycemic spinach and arugula, with tomatoes and cucumbers, topped with olive oil – none of which stimulates insulin. Your insulin level starts to fall.   If you are overweight, your insulin level starts out at 11-20, which is supposedly normal, but enough to stimulate sodium retention.   After a few days of consistently low glycemic food, and fat, your insulin level keeps drifting down and your kidneys get the memo, “No insulin”.   Your retention of sodium slows down dramatically, your volume of distribution, the size of your water balloon, shrinks. Your weight suddenly looks like you just lost 5 pounds.   Voila, you feel so proud.

This is the mechanism of every ad shouting at you, “Lose 15 pounds in the first two weeks”.   You can lose 15 pounds in the first two weeks.   Thirteen and a half of water.   You actually lost one and a half fat pounds! But that’s one and a half you weren’t able to lose before. Just don’t get discouraged when those 13 come back.

WWW.   What will work for me.   If you weigh yourself daily, you see your weight bounce up and down by 3-5 pounds all the time.   When I stay off carbs completely for 4 days in a row, I feel mercilessly dizzy if I don’t eat extra salt.   With that extra salt, usually in the form of Tobasco sauce or “Slap Ya Mama” Cajun spice, I feel just fine.   And my blood pressure is down 15-20 points in just a week. If my blood pressure can do it, so can yours!   What’s the wise person to do? Calculate your basal metabolic rate for your age, height, weight and gender, add your exercise calories, and eat less calories a day than that result.   Make sure they are low glycemic vegetables, fat and modest protein calories.   And watch your blood pressure fall.


Pop Quiz

  1. Insulin, your natural calorie storage hormone also affects how much salt your kidneys hang on to. How?

By stimulating your kidneys to reabsorb most of the salt that passes through

  1. Insulin also increases the size of your body water? T or F

True. It stimulates Nitric Oxide production which increases the “size of the water balloon.”

  1. Insulin resistance is strongly related to high blood pressure. T or F

True. (If you didn’t get this one by now, I would be distressed)

  1. It makes sense to lump high blood pressure together with high blood glucose, cholesterol and high insulin.   T or F

True. That’s why we call the collection of them the metabolic syndrome.

  1. Fat has no effect on insulin. T or F

True.   As long as it’s natural fat, not manufactured, transfat or vegetable oil.

  1. You can lower your blood pressure by getting off sugar, wheat, flour, bread and all root vegetables and grains. T or F

Bingo.   Give it a try.

Know your Basal Metabolic Rate

Do you know your Basal Metabolic Rate?

Reference: Wikipedia,  Physiology Reviews

June 8, 2015

We use about 60% of our calorie needs each day just staying alive.   The fuel needed to keep us warm, to keep our brains functioning, our heart pumping, our hair growing, our gut moving – all of that, is your basal rate.   Measuring it exactly is a bit tricky because one needs to measure the amount of carbon dioxide you exhale, (how much you are burning) when you aren’t digesting food, aren’t alarmed, angry, upset, in an environment of supportive temperature – and each of those elements has proponents and arguments. Finally, fat tissue needs to be extracted. Because women biologically have more fat, their weight is a bit higher so in general, a correction needs to be made for that.   As we age, our muscle mass declines, and our rate of exercise declines.   We need less fuel, or we gain weight.

There are several schools of thought with varying formulas.   I will refer you to each of them with links so you can calculate your own.

It should be noted, however, that in every review, they find as much as 25% inter-subject variability, even in the most controlled environment.   Some of us just need less. (So we get fat, faster. We survive starvation, longer.) And now, the literature on underreporting of calories is starting to ramp up too.

The Mifflin St. Jeor Equation is as follows: (My favorite)

For men: BMR = 10 x weight (kg) + 6.25 x height (cm) – 5 x age (years) + 5

For women: BMR = 10 x weight (kg) + 6.25 x height (cm) – 5 x age (years) – 161

The Katch-McCardle Formula depends on knowing your percent body fat.

BMR (both men and women) = 370 + ( 21.6 x lean body mass in kg )

Harris Benedict Formula simply converts your activity level with a predictive formula.

To determine your total daily calorie needs, multiply your BMR by the appropriate activity factor, as follows:If you are sedentary (little or no exercise) : Calorie-Calculation = BMR x 1.2•   If you are lightly active (light exercise/sports 1-3 days/week) : Calorie-Calculation = BMR x 1.375

•   If you are moderately active (moderate exercise/sports 3-5 days/week) : Calorie-Calculation = BMR x 1.55

•   If you are very active (hard exercise/sports 6-7 days a week) : Calorie-Calculation = BMR x 1.725

•   If you are extra active (very hard exercise/sports & physical job or 2x training) : Calorie-Calculation = BMR x 1.9

Each of these has proponents and detractors. Depending on what you want to do. If you want to lose weight, you need to be eating less than you are burning – and you need to be getting access to your fat energy. The only way to do that is to turn off insulin.   Without insulin, your fat cells open up and share freely. With insulin, your fat cells are shut and you only have 1500 calories of carbs to burn before you are starving hungry, hypoglycemic and ready to eat the furniture.

WWW. What will work for me.   I like the Mifflin St. Jeor Equation the best.   I had a monster exercise day on Saturday, biking 18 miles in the Tour de Marsh in Horicon. That allowed me to have 800 extra calories for the day, without gaining weight.   But the Harris Benedict formula comes close.   It also explains to me why petit women (say, 5’3”, who are overweight (say 165)) gain weight when eating 1600 calories a day, with little to no exercise.   We all aren’t the same, and taking into account our age, body fat and exercise level gives us a reality check. Or maybe, as we get older, our denial of what we are eating increases as patterns deepen. This getting older stuff and needing less calories is a drag!

Pop Quiz:

  1. My basal metabolic rate is the calories I burn doing nothing but staying alive. T or F


  1. As we age, we need fewer calories because our bodies shrink, our muscles shrink, we aren’t as active. T or F

T (See, it’s easy to get an A)

  1. The formulas can vary depending on your body fat percentage and gender. T or F


  1. Activity allows you to consume more calories. T or F

True. Makes it almost worthwhile

  1. Despite all our careful measurement, there remains a 25% error rate in our prediction of what our calorie need is. T or F


  1. This variability may be because we underreport our calories when asked to recall what we ate. T or F


Food and Inflammasomes

Fire, Fire, Cells on Fire: Inflammasomes II

Reference:   Scientific American June 2015, Wen Nature Immunology

June 1, 2015

We learned last week that inflammasomes are activated when “stranger” and “danger” signals are present.   Bacteria and viruses can do it, but so can foreign chemicals like asbestos and amyloid in our brains.   The inflammasome is essentially a little factory that propels the inflammatory process forward and turns on the signaling in the cell and its surroundings that trouble is brewing.   When you have a cut finger and get redness around it, it is because your local macrophages have made inflammasomes inside themselves that are putting out the chemicals that make that factory become assembled, and then produce its inflammatory signaling messages.

But that’s not all. Food can do it. Eating too much food sets off inflammation.   Fatty acids can do it too.   A healthy liver has many immune cells within it, and is the first recipient of calories after a meal. The liver can become inflamed and swollen when it is overwhelmed with too many calories.   We have an epidemic of fatty liver in obese children right now. It appears that fructose plays a central role in that process.

What happens when you eat too much fructose (sugar)?   We know that it essentially exhausts your liver because it forces the liver to use up its ATP, resulting in a burst of uric acid and a burst of triglyceride release – as dramatic as with drinking alcohol.   Your liver gets swollen and doesn’t work very well.   You can see large globules of fat in it.   It can’t make an orderly progression of LDLs to transport the extra calories to your fat cells, where the fat can be stored. Instead, you have a wild, uncontrolled release of free fatty acids into the blood.   We call those triglycerides.

We know that triglycerides reflect a higher risk for heart disease than total cholesterol, particularly in women. And that would make perfect sense because triglycerides reflect the presence of inflammation in the liver, spewing out inflammatory messages to the whole body.

The interesting thing about food is that its inflammatory effect seems to be about 24 hours and then it cools off. Immune cells stop responding to the inflammatory messages after a while. The next door to be opened is just what on earth keeps the inflammatory process going and going.   Adenosine may be that signal. And when you eat fructose and overwhelm your liver, you break down ATP and make adenosine. That points a particular finger at fructose again!

How can we turn all this off? Fasting! Or eating a “ketogenic” diet that makes you put out beta-hydroxybutyrate.   Imagine, turning off inflammation by eating fat.

WWW. What will work for me. I know this is true. Eating fat reduces inflammation. My 70% fat diet for the last 4 months has reduced my CRP from 3.8 to 0.3, in just 4 months.   I’m getting better at saying no to sugar if I can just keep away from brownies and chocolate.   I believe that the alleged triglyceride activation of inflammasomes is actually a misplaced association – the triglycerides reflecting the excessive intake of fructose/sugar we Americans are obsessed with. It’s the sugar.

Pop Quiz

  1. Inflammation can be started by eating too much food? T or F


  1. Sugar seems to be able to turn on inflammation as well? T or F


  1. Fructose, from sugar, makes for fatty liver? T or F


  1. Inflammasomes in the liver are caused by eating too much food and too much sugar. T or F

I’m beating a dead horse here, but I want you to get the point.

  1. You can turn off inflammation by eating a keto-genic diet – aka, high fat? T or F


  1. Beta-hydroxybutyrate is the compound your body puts out when you are burning fat, either from your fat cells or from the food you eat – and it happens only when you eat less than 20 grams of carbs a day. T or F

Pretty close to accurate. Some quibbling on details.

Inflammasomes – a Primer on Inflammation

Inflammasomes: a Primer on Inflammation

Reference:   World Jr Diabetes, Scientific American May 2015,

Diabetes, gout, Alzheimer’s, asbestosis, erectile difficulty, heart attacks all have something in common. They are primarily diseases of inflammation. Yup, inflammation is the problem. (Redness, swelling, pain, warmth) All of these “diseases” share a common pathway. They may affect different organs (fat tissues, liver, joints, brain lung, heart) but they share a common pathway on how the illness comes about.   That changes the way we think about them. Instead of treating the organ, it’s time to start thinking about treating the underlying pathway.   That means we have to understand the underlying pathway. Inflammation.

What is inflammation?   Everyone is familiar with “stranger” inflammation. When a bacteria invades your body because you cut your finger, your innate immune system recognizes that it is a stranger, just like a virus, a parasite or a fungus, and your innate system puts out signals that danger is at hand.   Besides “stranger” initiated inflammation, there is also “danger” initiated inflammation. If you crush a cell with trauma, pieces of DNA, or ATP or fatty acids show up in the space between cells where they aren’t normally present. Your guardian immune cells assume that “strangers” must be around for damage to be there, and also set off the initiation of inflammation.   Beta-amyloid in your brain, uric acid in your joints, cholesterol in the wall of your arteries can all the set off the same sequence – without a stranger being there to start it all. See the common pathway? The core concept is that seemingly common things, in the wrong place in your body can also inadvertently set off the fire alarm.

For the last decade or so, we thought there was a hopeless maze of signaling that was complex beyond comprehension. Not so. There is a common pathway.   Certain cells called macrophages have the responsibility to eat up “danger” and digest it. They are our body’s garbage trucks.   Here is where it gets interesting. These macrophages respond to broken bits of DNA, or RNA or other DAMPs (Danger associated molecular patterns) with two patterns. One is to initiate the production of danger signals. The other pattern is to assemble a factory to process those signals. That factory is called the inflammasome.

The job of the inflammasome is to process the chemical signals of inflammation and activate them. Finally, it ships them out of the cell to call for help and keep the process going.   IL-18 and IL-1β are the two principle signaling molecules. Those two compounds circulate around, increasing blood flow, making tissue swell and all the other processes of what we call inflammation.

Now, if you want to sound particularly savvy, you can say the phrase, “I’m going to suppress my NLRP3 inflammasome today.” the next time you are offered a brownie and you really didn’t want the carbs.   The modulation of inflammasomes is the future of medicine.   The NLRP3 inflammasome may be one of the most influential because it is the one in Alzheimer’s that responds to amyloid and goes about killing off brain cells. And why is it important?   Because your can shut it down and turn it off by a chemical called beta-hydroxybutyrate. And what is beta-bydroxybutyrate? It’s a ketone body, release by fasting and eating a low carb diet.

WWW.   What will work for me?   Hmmm. I can turn off the inflammatory process by fasting? That’s no fun. But a low carb diet is good for me? Yup, this is how it works.   On a low carb diet, your body turns on fat consumption, and that releases the ketone called beta hydroxybutuerate.  And that turns off your inflammasome.   So, practice this phrase with me. “I’m turning off my NLRP3” as a way of giving yourself the willpower to resist that almond extract flavored chocolate chip triple chocolate chewie gluten free brownie sitting in the fridge.   I need the practice, because I had four of them yesterday.


Pop Quiz

  1. Inflammasomes are the factories our bodies make inside of cells that start the process of inflammation. T or F


  1. Inflammation is when your tissue gets cold, white, quiet and numb. T or F

False. Red, hot, painful and swollen

  1. Your body can respond to “danger” and “stranger” signals in the same way. T or F

Sounds like you are getting it

  1. The particular inflammsome called NRLP3 can be turned off by fasting. T or F

In a nutshell, that’s it. The ketone body called beta-hydroxybuturate is a ketone body you naturally make when you are digesting and releasing fats – and that turns NLRP3 off

  1. Inflammasome explain how many diseases are caused by the same cellular process – just showing up in different cells and tissues. T or F

Yes – this common pathway gives us reason for much more hope at turning those diseases off.

Get a Grip on How Long You Will Live

Get a Grip! Live Longer

Reference:   Lancet April 2015,  Economist May 2015

Want to get an accurate measure of how long you will live?   Give a handshake. Your grip strength will convey your prognosis. This is your most accurate gauge of longevity. How do we know?

Published this week in the Lancet, Darryl Leong from McMaster University in Canada reviewed his data from the PURE (Prospective Urban Rural Epidemiology) study and found the accuracy of this prediction. They measured grip strength in 142,861 people, ages 35-70, in 17 countries who were willing to be followed prospectively for longevity, mortality, cause of death, injuries, falls, fractures, hospitalizations, the works.   They used a very simple and reproducible measurement with the Jamar Dynamometer to measure grip strength.

The study used data from rich, poor and in-between countries.   Canada, Sweden and the Emirates were considered rich.   Bangladesh, India, Pakistan and Zimbabwe were poor and Colombia, South Africa, Poland and 7 others were considered in-between.

They did find cultural differences. Apparently the Swedes take delight in squeezing hard, and Pakistani’s are very gentle but the prognostic value of the strength still pertained.   On average, a person’s grip strength is about 300 newtons.  For every 50 newton drop in grip strength the participants showed a 17% increase in risk of dying, mostly from heart disease.   It also showed an association with stroke and heart attack.   The researchers corrected for age, education, alcohol and tobacco consumption.

Now, grip strength did not predict hospitalization for pneumonia, or mortality from falls.   One would think falls would be correlated, as weakness would seem to be predictive of risk.

Now, this news has raised quite a ruckus on the Economist web site because there are cultural differences between societies. In South Asia, you greet a person respectfully with two hands in front of you – no touching. Shaking hands is a western thing. But the data still holds.

My interpretation is that heart disease is strongly correlated with mitochondrial health. Your heart cells are 33% mitochondria by volume and their health is central to heart health.   As you get fit, the number of mitochondria both increase and get healthier.   Regular muscle cells go from 200 mitochondria to 400 when you get “in shape”. And your fitness overall is transmitted in your handshake.

As research gets down to the nitty-gritty of how fitness benefits us, we will get more details. The topic of taking care of your mitochondria will become the means of coalescing this body of knowledge. For now, you can rest comforted if you supplement yourself with a bit of CoQ10 to help protect your mitochondria, and get fit. This is where statins yield their havoc, they deplete CoQ10 dramatically. I don’t care if you aren’t skinny, I do want you to be fit.

WWW. What will work for me. Because I’m over 50, my CoQ10 is starting to fall. I take 100 mg a day. And I exercise. Mostly walking, but some running, and some gardening, some tree lopping, some mulching.   I need to find a means of getting sweaty more often so that I get a bit more fit. And I’m going to start measuring your hand strength in my office.   Come on down, crush my fingers.


Pop Quiz

  1. Grip strength is the best predictor of how long I will live? T or F

That’s it in a handshake

  1. Fitness all over probably correlates with strength of handshake. T or F


  1. Exercise increases the mitochondria in our cells. T or F

Exactly right. See where I’m leading you?

  1. Number of mitochondria means my cells can produce more energy and do their function better, aka, squeeze harder. T or F


  1. The strength of my hand squeeze isn’t what’s making me live longer, it’s the fact that I’ve gotten fit all over, and that is just plain good for me. T or F


Triglycerides/HDL Ratio – the Best Measure for Heart Disease Risk

The Best Cholesterol Predictor for Artery Disease

Reference: Gaziano Circulation 1997 Lemos de Luz Clinics Wan PLOS April 2015

You want to know how to predict your risk for heart disease, right? Half of us die from it, so having a bit of a warning is a useful thing.   You go to your doctor and get told that you should be on a statin. You don’t know what to say.   Should you, shouldn’t you.   That’s the conundrum.

Want some guidance?   Of course! You want to know the single best predictor for developing heart and vascular disease.   And you want to know how to change it and manage it.   Well, that’s a tall order, and now we know the answer.   And it’s NOT your LDLs and total cholesterol. We focus on LDLs because we have a 30 billion dollar industry of lowering it with statins.

The number you want is your TG(triglycerides)/HDL ratio.   The reference is above. The authors in the Clinics article took 347 high risk patients, most in their later 50s with total cholesterols over 200.   The examined the extent of their coronary artery disease by catheterization and correlated the findings with their lipids.   Because HDLs are known to be protective, and triglycerides known to be risky, the TG/HDL ratio is an attractive summarization to look it.   What the authors found was that this ratio is more accurate than the Total Cholesterol or LDL measures, which we usually use.   This study confirms the landmark first study by Gaziano that identified this ratio as being the best.

Now we have a follow up confirmation about mortality from Wan in PLOS published just last month.   They found the TG/HDL ratio to be the most predictive ratio for subsequent mortality.   After open heart surgery, they grouped their patients into three groups by tertile, (Top third, middle and bottom) and found a 5.32 fold increased mortality for those in the top third over the bottom third.

Now, here is the kicker.   You can get yourself from the top third to the bottom third in about a month with the right diet.   I’ve done it.   You have to stop eating carbohydrates that flood into your body too quickly.

This confirms the hypothesis that your blood fats are completely dominated by the carbohydrates you eat.   When you overwhelm the ability of the body to burn carbs, your insulin goes up, your liver starts to manufacture fats and your blood fats start going up.   Triglycerides reflect that you have so much fat being made that your LDLs can’t even pick it all up, so your blood starts being filled up with triglycerides. There is no drug for that. But you have choice. You can stop eating those carbs.

What food should you eat instead.   Ironically, exactly the foods that look like what is in your blood is what you should be eating to cure your bad blood fats: fat.   If you switch to a diet of 70% fat and less than 20 grams of carbs a day, you can cure your elevated triglycerides in the twinkling of an eye.

There have been some 20 articles published confirming this concept so it’s not new, but it should be considered the main method by which we confirm your risk.   When you get your cholesterol measured, make sure you know those numbers first, not your total cholesterol or your LDLs. Focus on your HDL and your triglyceride.   And then, aim to get your ratio to ONE.   One.   1.   Yes, ONE.   With that, you will be the safest and the healthiest.   Simple.   Just stop eating carbs and remeasure and you can be safe within a month.

WWW. What will work for me.   I’ve done it. I wanted to lose weight so I went on a 70% fat diet. My HDLs went from 29 to 59 in just three months. (I wasn’t measuring monthly).   My triglycerides went from 103 to 49. That makes my ratio 0.83. (Down from 3.55)   Yippeee!   I am now down 30 pounds and don’t need to lose any more weight so my new challenge is to figure out food that doesn’t make me regain weight.   Last night for supper, I started with 4 oz of cream cheese so I kept my fat up. Delicious.   No bread, no potato, no rice.   Short ribs, floating in fat, and avocado salad with olive oil dressing.   Sorry you couldn’t have it with me.


Pop Quiz

  1. Total cholesterol is the best measure for your risk for heart attack and vascular disease. T or F

If you said true, read this column over again. No, false.

  1. HDL is typically considered your “good” cholesterol. T or F


  1. The best risk measure for future cardiac mortality is your Triglyceride/HDL ratio. T or F

That’s it

  1. The means you want your triglycerides to be LESS than your HDLs. T or F

Perfect. With that, your risk of heart attack is less than 20% of the rest of us.

  1. The best way to have low triglycerides is to eat less carbs. T or F

Bingo. Eat fat instead.   And lower your risk for heart disease.

  1. That means the best way to improve your heart disease risk is to do exactly the opposite of what we have been telling your for 40 years. T or F