Monthly Archives: June 2015

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.

Real Women and Real Men Eat FAT

Real Women and Real Men Eat Fat

Reference: Raben Med and Sci in Sports, Wang Jr Clin Endo Metab, Volek, Jr of Applied Phys, Barone PloS One CLA and Testosterone,

June 22, 2015

If I hadn’t seen it a bunch of times, I wouldn’t believe it so avidly. But I’ve seen it.   As men and women switch to higher fat diets, and avoid carbohydrates, their androgens go up.     There isn’t that much literature on just fat because most of it appears to be focused on the protein.   And maybe it’s the protein, but my suspicion is that it is the fat. In fact, the best reviews of ancient, aboriginal diets shows that they had more fat in them, without coronary artery disease.

What we do know is that in the last couple of hundred years we have changed our diet in the Western world massively to much more carbohydrate, particularly of the refined sort. We are eating 5-10 times as much sugar as a century ago, and 50 times 300 hundred years ago.   And for the last 50 years, we have been encouraging ourselves to eat 10-12 servings of carbs and cutting our dietary intake of meat to lower levels, and fat to almost non-existent.   And in that time period we have noticed a decline in testosterone and rise in obesity.

So, what did Volek find in his study? He is one of our premier physiologists who has had a huge impact on our Olympic athletes.   He took 12 men and had them do bench presses and squats to exhaustion with blood testing before and after. What he concludes is that there was a meaningful relationship with exercise and testosterone levels, but an even more remarkable correlation with dietary fat. Yes fat! And in inverse relationship with testosterone to carbohydrates!   Click on his article and see the figures in his posting!

It may be particular fats that matter.   In Barone’s article he shows that CLA seems to be a particular stimulate to making more testosterone.   CLA is found mostly in milk and meat from ruminants.   That study was done in mice fed CLA or not. Mice have an advantage because you can control their diet and activity quite accurately. But they aren’t human. But if I were weight lifting, or exercising regularly, I would add CLA to my supplement list. It’s a pretty compelling study.

What about women?   Well, healthy estrogen levels are clearly of a benefit for brain health, bone health, heart disease health and controversial with breast cancer. So, a meta-analysis by Wu shows that you can lower your estrogen levels dramatically with a low fat, high carb diet. That may be good in breast cancer, but not in normal healthy women. In a recent publication from the American College of Obstetrics, a high protein, low carb diet was shown to dramatically improve fertility.   Dr Russell, in this presentation had noticed that he couldn’t get women pregnant with IVF when they were on high carb, low fat diets.   If they hiked up their protein and fat, their embryos were healthier and they got pregnant more easily.

WWW.   What will work for me.   I’ve seen a dramatic improvement in my own blood fats, my waist line, my energy level and weight with a shift to less carbs and higher fat.   I think this is just another nail in the coffin for the low fat, high carbohydrate diet.   Our distant ancestors sought protein and fat in their diets.   And they were better for it.   If you want to lower your estrogen and testosterone, go ahead, have another donut.

Pop Quiz

  1. Eating a low fat diet with a rich mix of whole grains, vegetables and limited red meat and sugar is our current dietary guidelines. T or F

True.   It may be partially right with the emphasis on less sugar, and ok if it encourages green, low glycemic vegetables, but it is missing the boat on fat.   In fairness, vegetables oils and trans fats are poisons, so a low fat from those sources is critical. Just don’t throw out the baby with the bath water; animal fat is fine (Butter, eggs, bacon, …and coconut and olive oil)

  1. Eating a high carb diet will lower my testosterone.   T or F


  1. Exercise will raise my testosterone. T or F


  1. A low fat, high carb diet will make it easier for a woman to get pregnant. T or F

Diametrically wrong.   Low CARB, high protein and fat will boost her pregnancy chances.

  1. CLA may help me build muscles better than other fats.   T or F

Well, yes. Because it builds your testosterone significantly (if you are a mouse). But probably true in humans too.

The Problem of Lectins

The Problem of Lectins

Reference: Wikipedia, Phytochemistry 2015, PloS One

June 15, 2015

Have your heard of lectins?   Could you give me the one sentence summary of what they do to you? Ok, you will in this column learn what that means.

Lectins are the proteins made by plants to protect themselves from their predators. They are, in effect, poisons that prevent the plant from being eaten.   Plants need to be eaten to propagate – at least their seeds do. That delicate balance leads to lectins needing to be poisonous enough to keep the bugs away long enough so that animals will eat the seeds and spread them around. Animals need to be able to tolerate the poison enough to not be too harmed, but still be benefited by eating some of the plant while spreading the seeds around.   Lectins are sticky.   That results in many useful functions like allowing cells to bind to one another, like Velcro. But it also leads to lectins binding to things and injuring them where they may not be invited, like your gut. As long as we humans ate a wide variety of seasonal foods, each in modest quantity, we weren’t really harmed by them.  Now we are being harmed.

Which foods have the most lectins in them?   Grains.   (Wheat gets the bonus amount.)   And beans.   (Soy wins. Peanuts right behind) Finally, the nightshade family is another occasional bad actor. And finally, dairy products (the cow eats grains and passes them through – remember, you absorb them.)

What’s the problem with lectins? This is where the story gets interesting.   We humans used to eat wheat once a year for a couple of weeks when we came across some ripening wheat while hunting around the Black Sea.   Think grass seed, only bigger.   Now we have changed wheat to be much more calorie containing, grown it in vast fields and stored it year around. Then we added 28 more chromosomes from other grasses and presto, modern wheat, loaded with lectins.   And then Pillsbury made us fine white flour and Dunkin made donuts.   Or bagels, or bread, or cookies.   We now eat wheat year around.   Lectins bind to the cells in our gut and add to their damage, leading to leaky gut. Leaky gut can’t absorb some things, and let other compounds get through without being digested.   With that, even the lectins get absorbed because they are very tough to digest, and may even be the primary cause of leptin resistance.

What’s the problem with leptin resistance?   It ruins your appetite feedback cycle and may be one of the primary underlying causes of obesity.

What’s the problem with leaky gut?   This may be the foundation of autoimmune disease.   We want you to have the means to reverse that foundation. This is a tricky one to prove because the subtle effect takes years to have an impact, and our food supply is to complex you can’t nail down any one source of anything.   But the physiology has been “discovered” and partially worked out and the mechanisms are there, just not proven yet.

The premise of all of this is that we have to start considering the impact of low grade inflammation and irritation as the root cause of much illness. Hmmm.   It’s a hard one to prove, so traditional medicine steers away from it.   We can’t ignore it, it’s happening to all of us.

WWW. What will work for me.  Well, I feel better when I eat less grain and less legumes.   I can feel it. I don’t get much effect from avoiding tomatoes and eggplant. And I love cream cheese and cheese.   I suspect the only real way to prove to yourself is to try a 3-4 week trial of avoiding one food group at a time.   But I have a suspicion this story isn’t over. I wanted you to learn the basics because it’s so interesting.


Pop Quiz

  1. Lectins are poisons? T or F


  1. They are present mostly in plants, with wheat being the champion and tomatoes right behind? T or F

Trick question. True on the wheat, soy right behind.   Tomatoes present but down the list a bit

  1. Lectins are sticky and bind to gut lining cells, damaging them. T or F

That’s it

  1. And thereby cause……what?

Leaky gut

  1. Leptins are hard to digest and get absorbed easily and cause internal damage too.   T or F


  1. Milk can contain leptins if cows are fed corn and beans. T or F

True again

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.