Your gallbladder and why it’s important

Yesterday I had a video coaching session with one of my patrons, and the last thing we talked about was the gall bladder. They recently had an ultrasound done to check out the insides of the abdomen—obviously to make sure everything looks good. The kidneys looked good, the liver had a small benign lump of 1–2 mm  in size (angioma sounds so much more serious), and the gall bladder had a bunch of little stones. I asked what the doctor recommended.

“There’s nothing to worry about. Let’s check again in half a year.” That was it. Nothing more. So, they asked me if there was anything that could be done to help in some way.

What do you think? Is there not always something that can be done to help—to help the body cleanse itself, repair itself, heal itself, improve its physiological and metabolic functions?

We’ll take the time to study and explore the liver and its functions in greater detail later—the liver is a lot more complex. The gall bladder is quite simple, and so, I just wanted to share with you what I explained yesterday, and at the same time, take the opportunity to expand a little on that.

First the Anatomy

Looking at the abdomen from the bottom of the sternum (the bone between the pectorals) to below the hips, after having removed the skin and layers of muscle, cut out the front part of the ribs, and changed the appearance to make it cartoon-like, without any blood, veins, arteries, or nerves, and thus not so shocking to look at, we would see something like this:

abdomen-front-labels

Digestive system: front view with labels

The large, dark red organ that is the liver sits at the very top of the abdomen with its largest lobe located on the right side of the body. On the left, below the liver’s smaller left lobe, is the stomach that curves back towards the middle where it connects to the small intestine (duodenum). The gallbladder—the small dark green pouch—is nestled between the bottom of the liver’s right lobe and the first part of the duodenum. Below the stomach, sweeping across the abdomen from one side of the body to the other is the transverse part of the large intestine (colon). The entire lower portion of the abdomen is filled with the longest segment of the intestines.

If we zoom in on the upper abdomen,

upper-abdomen-front-nolabels

Upper digestive system: close up front view

and then hide the liver,

upper-abdomen-front-noLiver-nolabels

Upper digestive system: close up front view without liver to show bile ducts

we see all of the little green ducts embedded into the liver whose function it is carry the bile from the different parts of the organ to the main bile duct and gallbladder.

Taking a look at the same part of the abdomen from the back,

upper-abdomen-back-top-labels

Upper digestive system: close up back view with labels

we see how the gallbladder sits between the liver and duodenum, and how the main bile duct sweeps down behind the pancreas to connect to the main pancreatic duct such that the bile from the liver and gallbladder can be injected into the small intestine together with the enzymes, insulin, glucagon, and bicarbonate from the pancreas. We also see from this side the dark red, bean shaped, right and left kidneys, and the yellow adrenal glands sitting on top of them.

And then the physiology

Why do we need bile and what does it do? Why is there a gallbladder? And what is bile anyway?

Bile is 97% water, 0.7% bile salts (sodium and potassium), 0.5% cholesterol, fatty acids, and lecithin, 0.2% bilirubin, and a tiny bit of inorganic salts. In human adults the liver produces 400–800 ml of bile per day (Wikipedia).

The liver produces bile continuously but slowly. When we eat, depending on how much fat there is in the meal, the digestive system may need quite a bit of bile to handle the fat that was just ingested. Hence the need for storage and thus the function of the gallbladder.

The purpose of bile is to emulsify fat. Emulsifying means making into tiny droplets that can mix into another liquid to form a smooth homogeneous solution. For example, a bit of mustard works very well to emulsify the oil and vinegar that would otherwise not mix into a smooth creamy vinaigrette. After emulsification, fat droplets are typically 15–30 microns in size.

We need bile to emulsify the fats that we eat so that the pancreatic enzyme lipase can then break these triglycerides down into monoglycerides and free fatty acids. This is done in the small intestine where the bile and enzymes are secreted from the pancreas with the bicarbonate solution. This in turn allows the fat to be transported through the intestinal wall before being reassembled into triglycerides and absorbed into the lymphatic system. Without bile, fat could not be absorbed. It would go straight through the gut and be excreted undigested.

Why would stones form in the gallbladder? Is there a way to prevent the formation of gallstones? And what actually are these gallstones?

Gallstones are basically little hard lumps of cholesterol. One of the functions of the gallbladder is to concentrate the bile which comes in quite diluted, as we saw earlier, being 97% water. But when the concentration grows too high, then cholesterol precipitates out and forms little lumps. These are what we call gallstones.

Given that we know that stones form out of precipitated cholesterol when the concentration of the bile is too high in the gallbladder, it is simply logical that if the concentration can be kept low enough, below the threshold at which cholesterol will precipitate, then no stones would form. But why does the concentration of bile grow to the point of precipitation?

Let’s ask another question: what happens if we don’t eat much fat? The liver produces bile continuously, between 400 and 800 ml per day. This bile is stored into the gallbladder until it is needed after a meal in which fat was ingested. If we don’t eat much fat in a meal, then, naturally, not much bile will be needed, and most of the available bile will therefore remain in the gallbladder. Because the liver continues to produce it, the gallbladder needs to make room for it, and thus concentrate its contents further.

So, what happens if we never eat very much fat, and if actually, every meal is a relatively low fat meal? Well, what happens in a pool of water if the water does not flow out, and is by this not renewed by fresh water? Stagnation. In the case of the pool of water, we all know what happens: it grows dirty, then thick, then greenish, then totally filled with lumpy green gelatinous stuff. In the case of the gallbladder, we can imagine that something analogous takes place, and that the lumps of cholesterol are like the lumps of green gelatinous stuff in the water.

The solution is simple: eat plenty of fat on a regular basis. This way, the gallbladder can empty itself out regularly, and the bile does not stagnate, grow more concentrated, and eventually lumpy with gallstones.

Your gallbladder and why it’s important

Here’s what we learned:

The gallbladder sits between the right lobe of the liver and the first part of the small intestine. It stores and concentrates bile which is mostly water with small amounts of salts, bilirubin, lecithin, and cholesterol. The liver produces bile continuously in the amount of 400 to 800 ml per day.

The function of bile is to emulsify the fat we eat to make it absorbable. Without bile, fat just go through and gets excreted undigested. The same is therefore true for all fat-soluble minerals and vitamins, including some of the most important of them all, the crucial vitamins A, D, E, and K2.

If we don’t eat fat, there’s no need for bile. If we don’t eat much fat for a long time, the bile will get more and more concentrated. Eventually, the concentration will be high enough for cholesterol to precipitate out of the bile and form little lumps. These lumps of cholesterol are called gallstones.

Imagine that this continues for years and even decades, following a good “heart-healthy” low-fat diet. What do you think will eventually happen based on what we’ve just discussed? More stagnation, more highly concentrated bile, more gallstones, and then at one point, this whole thing explodes into acute infection, acute inflammation, excruciating pain, and emergency surgery to remove the infected gallbladder.

And then what? I’ll you finish this exercise in deductive reasoning which you now have all the necessary background to complete.

 

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Eat your salt, and eat your fat

A couple of months ago, I had just gotten to the locker room at the gym, when a buddy of mine came in. Changing into his workout clothes, looking at himself in the mirror with his shirt off, he said he was tired of this layer of fat over his abs, that he just couldn’t get rid of it no matter how much he tried. He’s a handsome Columbian guy in his mid thirties, super nice, friendly, and easy going, big open smile with nice white teeth. He’s well built, strong, with balanced musculature but … there’s not much definition.

Everyone wants to be cut, of course, and when you’re working out 5 or 6 times a week, like he does, and you can’t get cut, you get frustrated by that. Quite understandable. Meanwhile, I work out typically three times, and I’m “rallado” as he says to me. In english, the term is shredded: so lean that under tension, we see the muscles fibres. In my case, we can see them in every muscle, including the abs. He knew that, obviously, since I’ve been like this ever since we first met a year and a half ago. The only thing that’s changed is that I’ve put on some muscle and use heavier weights in my workouts.

And so, naturally, that was my queue:

– You just need to cut the carbs. The fat is going to melt off on its own in no time. Especially if you are working out the way you do. Just stick to meat and vegetables. Make it simple for yourself. Have eggs and avocados for breakfast, and meat and veggies the rest of the time. If you can skip breakfast, that’s even better: you’ll give your body a longer time to burn fat.

– Alright! I’ll try it!

After our workout, we said goodbye, and he told me he was going to Columbia for a while for his work (he’s part of a several-generation, several-family-member meat business based there, but lives here in Madrid with his wife and young child). He said that even though they always serve so rice, pasta, and potatoes with every meal, he would do his best to stick to the plan of having only meat and veggies. I gave him a good handshake, told him he could do it, and that it was important to be strict for the first month to allow for a good transition to fat-burning.

A few weeks later, he came back. We bumped into each other at the gym again. I was doing chest and back, he had come to do shoulders. He looked noticeably different: his face was smaller, his features more defined, his neck was thinner and more visible, his eyes were whiter and his skin was smoother. He looked 5 years younger! As soon as I saw him, I told him he looked very good, thinner in the face and neck, younger, and clearly healthier. He was happy to hear me say it, of course. He said that many people had told him that he looked younger, and obviously, he could also see it himself when he looked in the mirror. But it’s always nice when someone tells us we look good; it doesn’t happen very often. He had already lost 4 kg.

We saw each other a few more times at the gym like that, working out, but it took a while before he told me that he was feeling weak, that he couldn’t push as much weight as before, that he was often tired, and strangely, often in an angry mood. Naturally, he thought it was because he wasn’t eating carbs. That somehow he was carb-deficient.

– Do you add plenty of salt and fat with your meals meat and veggies?

– No! I don’t! I haven’t added salt to food in years. And I don’t add fat either.

– That’s the problem. You need to start right away. Lots of salt, and lots of fat with your food, whenever you eat.

– What kind of salt, and what kind of fat?

– Unrefined sea salt, organic butter and coconut oil, and olive oil with salads. With every meal. When you go low carb, you not only get rid of accumulated water in your tissues due to the chronic inflammation triggered by carbohydrate exposure (that’s why your face and neck thin out in the first week or two), but you also excrete more salt in the urine. It’s crucial to eat plenty of unrefined salt every day.

butterAndSalt

Organic butter and unrefined salt

 

Two days later, when I got to the gym, he was already into his workout, and he was pushing heavy weights on the benchpress, he was walking around with a spring in his step, and he was smiling. I didn’t even need to ask, but I did anyway:

– So, how are things going? Lots of salt and fat?

– Yes! And I feel great! I feel strong, I feel powerful, I’m not tired, and I’m not angry anymore.

– Fantastic! Glad to hear that. And from now on, you’ll always feel like this. No ups and downs, no weakness or lack of energy, no hunger pangs, no mood swings.

Each time we saw each other at the gym in the next weeks, I could tell he was getting more defined. The last time we met, he was again walking around feeling strong and working heavy weights with a smile on his face, and he looked ripped, a lot more defined. And he knew it too. I could tell by the self-confidence.

When we parted, I told him he looked good, that he looked more defined, and more energetic. He was happy: “Thanks a lot for all your advice. It’s really made a huge difference. I feel great, and my abs are starting to show!”

Not eating enough salt and not eating enough fat is a classic mistake that too many people do. We have been brainwashed into thinking we should avoid fats and we should avoid salt. So, when we cut the carbs, we continue to avoid fat and avoid salt. Then, we get tired and weak, and we think it’s because we don’t eat carbs. Totally not! We’re just not getting enough salt and fat.

And so, we have to repeat this, and repeat it over and over again. Eventually, it sinks in. Especially when we feel the difference it makes. Just like it happened in this case with my Columbian buddy at the gym. So, what’s the moral of the story?

You want to feel strong, and energetic? You want to look healthy and young? You want to get ripped with tight 6-pack abs? The formula is simple:

Cut the carbs. Fast intermittently. Drink alkaline water on an empty stomach. Work heavy weights 3 times a week. Eat enough protein. Eat your salt. And eat your fat. Try it. You’ll see. It works like a charm.

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Cure diabetes in a matter of weeks

Both the incidence and growth rate of insulin-resistant diabetes have reached epidemic proportions in many countries. It is most remarkable in the US with probably close to 30 million by now, and thus about 10% of the population (1, 2). Globally, the numbers are even more impressive: 370 million with diabetes predicted to grow to 550 by 2030 (3). This entails that as a disease, type-II diabetes (90% of diabetics) is one of the fastest growing causes of death, now in close competition with the well-established leaders, cardio-vascular disease and cancer, that each account for 25% of deaths in more or less all industrialised countries.

Insulin-resistant diabetes is very similar to both vascular disease (cardio and cerebro) and cancer, as well as intestinal, kidney, pancreatic and liver disease, arthritis, Parkinson’s and Alzheimer’s, in the sense that it is also a degenerative disease that develops over a lifetime, or at least over several decades. It is, however, quite different from all other chronic degenerative diseases because it is, in a way, the ultimate degenerative disease, in which the occurrence of all others increases markedly, and in some cases two to four times (4).  That’s not 10 or 15%, this is 200 to 400% more!

For this reason alone, it seems clear that all these degenerative conditions are intimitely related, and that furthermore, understanding insulin-resistant diabetes will most definitely give us keen insights into the genesis of degenerative diseases in general.

What boggles the mind is that, in a very real sense, we understand precisely and in exquisite detail how and why insulin-resitant diabetes develops, how and why it is related to all other degenerative diseases, and consequently, both how to prevent diabetes and all disease conditions for which it is a proxy, and why what is needed to achieve this actually works (5, 6).

In fact, type-II diabetes can be cured; not just controlled or managed, but cured; not just partially or temporarily, but completely and permanently. And this, in a matter of weeks.

This may seem simply impossible to the millions of suffering diabetics that live with their disease for years and more often decades, but it is the plain and simple truth, which has been demonstrated by more than one, but unfortunately rather few exceptional health care practitioners, already several decades ago by Robert Atkins (7), and more recently by Ron Rosedale and Joseph Mercola, for example (89), in a remarkably repeatable, predictable and immensely successful manner on most probably tens of thousands of people by now.

About insulin and glucose (or should it be glucose and insulin)

Insulin is a master hormone one of whose important roles is to regulate uptake of macronutrients (carbs, proteins and fats) by facilitating their crossing the cellular membrane through channels guarded by insulin receptors, from the bloodstream into the cell, either for usage or storage. It is for this role that insulin is mostly known.

However, arguably insulin’s most important and critical role is the regulation of cellular reproduction and lifespan, a role which is, as amazing as it may seem, common to all animals that have been studied from this perspective, from microscopic worms to the largest animals.

As such, insulin is a master and commander for regulating reproduction and growth in immature and therefore growing individuals, and regulating lifespan and ageing in mature and therefore full-grown adults (10).

Insulin is absolutely essential to life because in its absence cells can neither use glucose—a most basic cellular fuel, nor reproduce correctly—making growth impossible. It is, however, needed in only very small amounts. Why? Because insulin is very damaging to tissues and especially blood vessels, something that has been well known for a long time (look at this short review on the role of insulin in atherosclerosis from Nov 1981—that’s 32 years ago!, and you’ll see what I mean.)

Insulin is secreted by the beta cells of the pancreas in response to glucose concentration inside of these. As blood passes through the pancreas, these special cells that produce and store insulin, sense how much glucose there is by taking it in, and release insulin into circulation proportionally. This release is pulsed (while eating, for example) with a period of between 5 and 10 minutes, but only in response to blood sugar concentration, meaning that insulin is released only if blood sugar rises above the individual’s threshold, which depends on the metabolic and hormonal state of that individual.

However, it is important to note that pretty much no matter what the metabolic or hormonal states may be, eating fat and having fatty acids circulating in the bloodstream does not stimulate the release of insulin, while eating protein, in particular the animo acids arginine and leucine, does, albeit a lot less than glucose. This is because insulin is generally needed for cells to take in and use amino acids.

An insulin molecule that has delivered a nutrient to a cell can be degraded by the cell, or it can be released back into the bloodstream. A circulating insulin molecule will be cleared by either the liver or the kidneys within about one hour from the time of release by the pancreas.

Exposure to most substances, including lethal poisons such as arsenic and cyanide, naturally and systematically decreases sensitivity, or from the reverse perspective, increases resistance to it (as demonstrated by generations of Roman emperors and their relatives). This applies to cells, tissues and organs, and happens in the same way for biochemical molecule like messenger hormones, for the one that concerns us here, insulin. Thus, as cells are more  frequently and repeatedly exposed to insulin, they lose sensitivity and grow resistant to it.

Insulin primarily acts on muscle and liver cells where glucose is stored as glycogen, and on fat cells where both glucose and fats are stored as … fat, of course. Muscle cells grow resistant first, then liver cells and in the end, fat cells. Fortunately or unfortunately, endothelial cells (those that line the blood vessels), do not become resistant to insulin, and this is why they continue to store glucose as fat, suffer severely from glycation, and proliferate until the arteries are completely occluded and blocked by atherosclerotic plaques.

What happens when a large portion of the muscle and liver cells, and enough of the fat cells have become insulin-resistant? Glucose cannot be cleared from the bloodstream: it thus grows in concentration which then stays dangerously high. This is type-II, adult onset, or most appropriately called, insulin-resistant diabetes.

Unnaturally high glucose concentrations lead to, among other things, increased blood pressure, extremely high rates of glycation (typically permanent and fatal damage) of protein and fat molecules on cells throughout the body, heightened stimulation of hundreds of inflammatory pathways, and strongly exaggerated formation of highly damaging free radicals, which, all in all, is not so good. This is why insulin is secreted from the pancreas so quickly when glucose is high in the first place: to avoid all this damage and furiously accelerated ageing of all tissues throughout the body.

The five points to remember

  1. Insulin is a master hormone that regulates nutrient storage, as well as cellular reproduction, ageing and therefore lifespan.
  2. Insulin is vital to life, but in excess concentrations it is highly damaging to all tissues, especially blood vessels.
  3. If blood sugar is high, insulin is secreted to facilitate the uptake of the glucose into cells, but at the same time, because it is present, also promotes the storage of amino and fatty acids (protein and fat); if blood sugar is low, insulin is not secreted.
  4. Chronically high blood glucose is remarkably damaging to the organism through several mechanisms that are all strongly associated with degenerative disease conditions in general.
  5. Chronically high blood glucose concentration leads to chronically high insulin concentration; chronic exposure to insulin leads to desensitisation of muscle, liver and fat cells, and, in the end, to type-II or insulin-resistant diabetes.

And in this succinct summary, in these five points to remember, we have the keys to understanding not only how diabetes develops and manifests, to understand not only the relationship between diabetes and other degenerative diseases, but also to understand how to prevent and cure diabetes as well as degenerative conditions in general.

And I’m suppose to say …

But you already know what I’m going to say:

Because the basic, the underlying, the fundamental cause of insulin-resistant diabetes is chronic over-exposure to insulin, it means that to prevent—but also reverse and cure it—what we need is to not have chronic over-exposure to insulin. And this means to have the very least, the minimal exposure to insulin, at all times, day after day.

The good news, which is indeed very good news, is, on the one hand, that it is utterly simple to do and accomplish, and on the other, that almost independently of how prone we are to insulin resistance (genetically and/or hormonally) or how insulin-resistant we actually are right now, insulin sensitivity can be recovered quite quickly. And here, “quite quickly” means in a matter of days, which is truly remarkable in light of the fact that our state of insulin resistance grows over decades, day after day, and year after year. It is rather amazing, miraculous even, that the body can respond in this way so incredibly quickly.

Now, type-II diabetes is nothing other than extreme insulin-resistance. Naturally, the longer we are diabetic, the more insulin-resistant we become. But unbeknownst to most (almost all MDs the world over included), if your fasting blood glucose is higher than 75-80 mg/dl or your insulin higher than 5 (mU/L or microU/ml), then the muscle and liver cells are insulin resistant. And the higher the insulin, the more resistant they are. In fact, if you have any amount of excess body fat, your cells are insulin resistant. And the more body fat, especially abdominal but also everywhere else, the more insulin resistant they are.

Because insulin sensitivity is lost gradually over our lifetime through daily exposure, some consider that everyone is becoming diabetic more or less quickly, and that eventually, if we live long enough, we all become diabetic. But this is only true in a world where virtually everyone suffers from chronic over-exposure to glucose and insulin. It is not true in a world in which we eat and drink to promote optimal health.

In practice, because basically everyone is more or less (but more than less) insulin-resistant, concentrations around 10 mU/L are considered normal. But when I wrote earlier that insulin is vital but needed in very small amounts, I really meant very small amounts: like optimally between 1 and 3, and definitely less than 5 mU/L (or microU/mL; and the conversion from traditional to SI units is 1 mU/L = 7 pmol/L).

So how do we do it?

You already know what I’m going to say:

Because insulin is secreted in response and in proportion to glucose concentration, when it is low, insulin is not secreted. Therefore, insulin sensitivity is regained by completely eliminating insulin-stimulating carbohydrates. This means zero simple sugars without distinction between white sugar, honey or fruit; zero starchy carbs without distinction between refined or whole grains, wheat or rice, bread or pasta, potatoes or sweet potatoes; and zero dairy, which triggers insulin secretion even when sugar content is low. It also means minimal protein, just enough to cover the basic metabolic needs (0.5-0.75 g/kg of lean mass per day). Consequently, it means that almost all calories come from fat—coconut oil, coconut cream, animal fats from organic fish and meats, olive oil and avocados, as well as nuts and seeds—and that the bulk of what we eat in volume comes from fibrous and leafy vegetables.

And what happens? In 24 hours, blood glucose and insulin have dropped significantly, and the metabolism begins to shift from sugar-burning to fat-burning. In 48 hours, the shift has taken place, and the body begins to burn off body fat stores, while it starts the journey towards regaining insulin sensitivity. In a matter of days during the first couple of weeks, the body has released a couple to a few kilos of water and has burnt a couple to a few kilos of fat. We feel much lighter, much thinner, much more flexible and agile, and naturally, much better. In four weeks, blood sugar and insulin levels are now stable in the lower normal range. All of the consequences and side effects brought on by the condition of insulin-resisitant diabetes decrease in severity and amplitude with each passing day, and eventually disappear completely. In eight weeks, the metabolism has fully adapted to fat-burning as the primary source of energy, and we feel great. (See 11 for more technical details.)

The result is that within a matter of weeks, we are diabetic no longer: we have regained insulin sensitivity, and have thus cured our insulin-resistant diabetes. Over time, a few months or maybe a few years, feeling better with each passing day, there remain very few if any traces of our diabetes, and we live as if we never were diabetic. Amazing, isn’t it? So simple. So easy. So straight-forward. And yet, still so rare.

And what about the relationship between diabetes and heart disease, diabetes and stroke, diabetes and cancer, diabetes and Alzheimer’s? Why do diabetics suffer the various health problems that they do, like high blood pressure, water retention, blindness, kidney disease, and how do those come about? What of the lifespan-regulating functions of insulin, how does that work? All these interesting and important questions and issues will have to wait for another day. This article is already long enough.

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