Carbs and Dementia

Carbs and Dementia

It’s well documented how much of a pandemic
obesity has become, worldwide. It’s becoming evident that this pandemic of obesity is leading directly into a pandemic of brain damage and dementia. Obesity, after all, leads directly to dementia. Don’t believe me? I’ll show you how and why this disease
acts like it has a mind of it’s own, controlling you to do what it wants.

It’s in the way it influences your hormones, as it uses them to control you, without you even suspecting it.

Dementia is, after all, type 3 diabetes.

If you’re type 2 diabetic now and you don’t change your eating habits, you stand a 100% chance of becoming type 3 diabetic. I can say this confidently because you don’t have to be type 2 diabetic, to get type 3 diabetes, dementia. This is shown in the number of Alzheimer’s patients now in existence. That population is growing exponentially while the diabetic population just multiplies in numbers. Diabetes just has a tendency to hasten the arrival of type 3 diabetes.

If we’re to going stop this epidemic of dementia that’s starting to cripple our population. We need to take drastic measures and the sooner we do so, the better our chance of survival. We have to slow the progression, where it starts, in what we eat. Thus, the reason for this post.

Alzheimer’s Disease

In most cases type 3 diabetes manifests itself in the disorder of Alzheimer’s disease. I know that not everyone who has Alzheimer’s disease has had type 2 diabetes, yet everyone who is type 2 diabetic will lose brain function. That science can’t be changed. The only thing that can stop that runaway train is to stop feeding it.  You must stop feeding carbohydrates into the fat factory that’s responsible for it. Carbs are the only thing that can generate fat inside your body. It’s this body fat, where the visceral fat lies that generates all the hormones and adipokines that dictate what this fat is going to do to your body. And it does plenty, all in the form of damage, damage to every system in your body as well as your brain. The more fat you have, the more damage it does to your body.

Fat creates hormones and adipokines that wreak havoc in your body.

The very first thing fat does, is to generate more fat through the use of the hormones that it produces, mainly leptin, along with Apelin and Chemerin, and it uses 100’s of other adipokines to wreak havoc throughout your entire body, including your brain. These hormones block receptors in the brain that influence behavior. They force us to continue to feed fuel to the cycle unknowingly. I call this our fat factory. This is called also addiction and this is how the addiction of the fat factory works.

By blocking receptor neurons in the brain, the neuropeptides that signal our bodies to stop eating, can’t do their job and tell us to stop eating. This is truly being controlled by your hormones. The pity of this cycle is, the larger you are, the more you experience it. It’s a cycle that feeds itself and it’s science you can’t change, without turning off the spigot.

It seems that this fat has become a self-feeding disease, of its own. I’ve noticed that the worse you have the disease, the harder it is to kick. But it’s also even more crucial to kick at that point because it’s already at the point of no return. Unless drastic measures are taken, a life of forgetfulness and lost memories is right around the corner, if it isn’t happening already? When was the last time you lost your keys or couldn’t remember someone’s name?

Fat, another organ

Even though obesity, excess fat,  is considered to be a disease by many, fat is considered by many professionals to be another internal organ. It’s an organ with its own mind, a mind to keep growing. It’s also one of the few organs that can grow in size, and when it does, it multiplies the hormones’ and adipokines‘ effects on our bodies. And it modifies it exponentially, which isn’t pretty.

Dictionary.com defines an organ as; Biology. a grouping of tissues into a distinct structure, as a heart or kidney in animals or a leaf or stamen in plants, that performs specialized task.”  

By strict definition, fat follows that description. It is a group of tissues in a distinct structure, that performs a specialized task. In this case, it performs many tasks, so many that it’s mind-boggling. This one organ creates more cytokines and hormones than any other organ in the body. That means that fat is one organ in our bodies, that either controls us or that we control it. When I talk about controlling us, I’m talking about control of our hormones which in turn controls our emotions. It also means that this one organ is responsible for more illness and disease than anything else in our entire bodies.

This is exactly why it’s so bad, the worst of these adipokines are cell signaling proteins that trigger hosts of illnesses and diseases. These diseases range from multiple cancers to multiple CVDs, which we’ll talk about later. The fat creates the bad cytokines that muck up your system. They create the adipokines that instruct your cells to turn into amyloid plaque. Amyloids are the foundation of an arm-long list of disorders, many cancers including breast cancer, colorectal cancer, stomach cancer, pancreatic cancer, liver cancer, and on and on. This isn’t even mentioning the mental disorders that come with amyloids. That list is even longer. The devastating effects that these hormones and adipokines have on your body, because of fat in your body, are truly astounding.

Body Fat production depends on Glucose

Now I know that glucose not only creates fat, the fat it creates, creates in turn, hormones and adipokines that trigger the inflammation and cell degradation associated with cancer and CVDs and worse of all brain loss. This fat factory is wasting away your brains and taking with it all of your mental faculties and dignity.

But it’s not only the fat factory that’s destroying our brains. It’s the gliadin that you eat every time you eat gluten. Your body can have this auto-immune response to gliadin, by sending out anti-gliadin antibodies that have the ability to attach themselves to Purkinje cells in your cerebellum as explained by Dr. Davis;. “The antigliadin antibodies triggered by gluten can bind to Purkinje cells of the brain, cells unique to the cerebellum. Brain tissue such as Purkinje cells do not have the capacity to regenerate: Once damaged, cerebellar Purkinje cells are gone . . . forever.” Doesn’t that say brain damage?

Only by taking abrupt action immediately, are you going to interrupt the production of these hormones that the fat factory is producing. And it’s producing these hormones so it can continue to enlarge itself in a vicious cycle. The only  way to stop this cycle at this point is to stop the fuel that feeds it, carbohydrates.

I’m sorry, but there’s no way around it. Not even you can change science. Unless you shut off the spigot of inflammation that you’re pouring into your body, every time you eat carbs, you’re going to feed the the fat that feeds the inflammation that causes all the disorders and disease listed in Carbs, The New Death Sentence, (15 of them, for starters).

A search for Obesity and brain size at NIH’s PMC site brought up over 1200 studies done on obesity and brain size. One in particular that I looked at, showed the influence leptin has on the brain and it’s ability to regulate energy in the body. Leptin is one of the hundreds of hormones and adipokines (cell signaling proteins), that’s manufactured in your body fat.

According to the study on Obesity and Dementia; “Within the brain, leptin regulates energy intake” “Leptin inhibits the expression of orexigenic neuropeptides and stimulates the expression of anorexigenic neuropeptides, which results in inhibition of energy intake (Jequier, 2002).”

That explains why those on a diet high in carbs (which is the only thing that can make people fat), run out of energy so much, and need to refuel every two hours or so. It’s the leptin expressing itself in the brain that inhibits the signals that tell us if we have energy or not and if we need to eat or not. And this is where the problem multiplies. Since leptin is formed in the fat around our body, it tells our brain that our body it needs more (fat) by blocking these signals. So what do we do? We eat more, to feed that need. This is leptin resistance, the leptin blocking those receptors in our brain that tells us that we don’t need to eat and have enough energy. It’s this leptin resistance that gives fat a mind of its own and allows it to work within us without our permission. That to me is an unadulterated robbery of our senses and emotions.

If you don’t have the ability to fight your hormones (leptin in this case) and resist this basic expression of survival, hunger, you’re doomed to everything listed in Carbs, The New Death Sentence. That is what makes carbs so addictive and dangerous and why their continuance must be curbed.

“It is known that adipokines, secretory products of adipose tissue such as leptin, interact directly with specific nuclei in certain areas of the brain such as the hippocampus. This results in regulation of not only feeding behavior but also neurodegeneration, synaptic plasticity, neurogenesis and memory consolidation (Doherty, 2011).” Are you starting to get the picture? Leptin isn’t your friend.

The Dangers of Leptin

Wikipedia says that the first adipokine, leptin was discovered in 1994 and since then 100’s have been discovered. Isn’t that disturbing? The fat that we make from glucose manufacturers hosts of hormones that are wreaking havoc on our bodies.

That means with the carbs we eat, we’re making fat, a fat that grows hormones that have cell signaling proteins that control hunger, energy expenditure and fat oxidation, blood pressure, glucose uptake and insulin resistance just to begin with. I didn’t even make it halfway through all the cell signaling proteins that were listed. The others that I did check all triggered a disorder or inflammation somewhere in the body. Many of them are associated with more than half of the known cancers, a multitude of heart diseases and every form of dementia known to man.

Leptin only plays a small part in the assault that our hormones throw at us. Adiponectin plays just as important role. As does Apelinchemerin, and 6 other hormones that they’ve found so far. And they finding more. All these hormones are adipokines and are manufactured in adipose tissue or fat. The other six adipokines listed on Wikipedia that I didn’t list here are all associated with inflammation and the oxidative stress that’s associated almost all cancers, most heart diseases and all brain damage that’s not caused by concussions and blunt force trauma.

If leptin plays a part in neurodegeneration, synaptic plasticity, neurogenesis and memory consolidation, doesn’t it make sense that it’s the creation of leptin that we need to control, to stem its influence in our bodies. If we’re to control the amount of leptin in our bodies, and leptin is made in adipose tissue (fat), then we need to control the amount of fat in our bodies. The only thing that controls the amount of fat that goes into our bodies is the amount of glucose that we feed it. We know that the glucose is controlled by the number of carbs we put in our bodies, so it’s easy to understand why we need to curb the carbs.

You can’t change the science. Glucose in the body creates fat. Fat creates leptin. The more leptin you have in your body, the more resistant you become to it and the more it needs to feed itself. It’s a cycle that keeps feeding itself again and again and again until you’re hungry 10 minutes right after you finished a big meal. I can remember times after a big spaghetti dinner when I was foraging through the cabinets and refrigerator, looking for something else to eat, on a full stomach. When I think about that now, I think, how sick could I have been to be expressing that kind of behavior? Then I think, I was a kid then, I was only eating what was fed to me. Here’s the scary part, I was eating exactly what the ADA was telling me I should eat. That’s exactly what you’re doing right now, following the dietary guidelines that you grew up with. How could they have gotten it so wrong?

Fortunately. I can only remember those times now, as I don’t get hungry much anymore. (Another advantage of being thin, and on a ketogenic diet.) Leptin doesn’t control anything in my body. I don’t have that much leptin in my body to control my urges and my energy. With a body fat ratio of 16 %, my body isn’t ever going to make enough leptin to create any problems in my body, provided that I don’t feed it what it wants, carbohydrates. This is what makes it so easy now to fast.

The Benefit of Adiponectin

This is where Adiponectin plays its role. “Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation.[3]

It’s adiponectin that not only dictates how glucose is turned into fat, it controls how the fat is burned in the body, and this is where it gets really interesting. Higher levels of adiponectin in the body allow the body to generate more energy from a smaller amount of fat, making adiponectin crucial for maximum energy output with minimal intake of food. That is why Dr. Miller says that people on low carb diets have more energy.

Since adiponectin is made in adipose tissue like all other adipokines, one would think that having a lot of fat would create a lot of adiponectin, when actually, we create just as much of it if not more when we don’t have the fat stores in our bodies. Our bodies use fat in our bones to create adiponectin. Actually, Levels of the hormone are inversely correlated with body fat percentage in adults [5]  “Contrary to expectations, despite being produced in adipose tissue, adiponectin was found to be decreased in obesity.[3][5][15]

“The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes,[5] obesity, atherosclerosis,[3] non-alcoholic fatty liver disease (NAFLD) and an independent risk factor for metabolic syndrome.[9] 

So, how do we increase this hormone? Since levels of the hormone are inversely correlated with body fat percentage, the more fat we have the less adiponectin we have in our systems. This in itself, leads to more obesity, more diabetes and everything that comes along with that.

Again According to Wikipedia;

Weight reduction significantly increases circulating levels.[11]” “A low level of adiponectin is an independent risk factor for developing:

That means to avoid low levels of adiponectin in your body, weight loss is crucial. This places more importance on calorie restriction. But there’s good news for those carboholics who have trouble restricting their calories,   “…omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have shown increased plasma adiponectin.[28] Curcumin, capsaicin, gingerol, and catechins have also been found to increase adiponectin expression.[29]

The most optimum way of reducing calorie intake is fasting. Most every religious practice have some form of fasting within is practice, with the exception of Christianity. When Christians get together, it’s usually in the form of a potluck meal. Christians love to eat. But even Jesus fasted for 40 days and nights. Is it any wonder that Jesus was so smart?

Fasting not only affects your hormones, it has multiple, other effects on the body that are all wondrous. Fasting brings with it, important benefits to the health of your brain.

  • It increases BDNF in your brain. This is what enables your brain to grow.
  • It’s ramps up the expression of Nrf2 in your genes and that can boost your anti-oxidants exponentially. ramping up your immune system and keeping your healthier than any medicine can.

So, it not only boosts brain growth, it boosts anti-oxidant production which keeps you healthier by being better able to fight off illness and disease.

Fasting conjures up images of starvation, though. This may be true is you are one of those unfortunate individuals who is still stuck on a carbohydrate diet. On a carbohydrate diet, fasting is next to impossible. At the least, it’s very difficult and involves a massive amount of discomfort.

The best way to avoid this discomfort
is to convert your diet to a low carb diet,

preferably a diet without any carbs.

This is where a fat tax might be a good idea. Tax carbohydrates by the amount of fat they create, which is influenced directly by their place on the glycemic index. This would force the population to cut back on their intake of this dangerous food. It might also help to pay for all the medical needs that carboholics are going to need if they continue to consume these killing field grains.

We as a population have to do something to correct this aberration to our diet. This food is killing us painfully, expensively and indiscriminately. As a society, we can’t allow this to continue unabated, as it has, for the last 60 years.

It’s Time For A Cure,

Curb Your Carbs

The Power of Being Thin Is Found By Eating Fat

The Power of Being Thin Is Found By Eating Fat

Most everybody wants to be thin simply to
look good,fat-thin-people-13593846 but the advantages of being thin, go a lot further than just looking good. Being thin is not only highly beneficial for your looks but it’s crucial for your health and even more important for your brain’s health. Did you know that the fatter you are, the smaller your brain is? It’s true. That is directly from Dr. Perlmutter’s book Grain Brain. Conversely, the thinner you are, the bigger your brain is. Don’t believe me? Look at the research studies and what Dr. Perlmutter says in Grain Brain: 

“The dots connecting excessive body fat, obesity, and brain dysfunction are not hard to follow given the information you’ve already learned in this book. Excessive body fat increases not only insulin resistance, but also the production of inflammatory chemicals that play directly into brain degeneration. For this very reason, waist circumference is often a measurement of “health,” as it predicts future health challenges and mortality; the higher your waist circumference, the higher your risk for disease and death.”

danger-obesity-grim-reaper-touches-shoulder-happy-overweight-black-woman-big-cupcake-vector-illustration-health-41031554“It’s well documented that visceral fat is uniquely capable of triggering hormonal actions.  This, in turn, keeps the cascade of negative effects from visceral fat going. In addition, visceral fat does more than just generate inflammation down the road through a chain of biological events; visceral fat itself becomes inflamed. This kind of fat houses tribes of inflammatory white blood cells. In fact, the hormonal and inflammatory molecules produced by visceral fat get dumped directly into the liver, which, as you can imagine, responds with another round of ammunition (i.e., inflammatory reactions and hormone-disrupting substances). Long story short: More than merely a predator lurking behind a tree, it is an enemy that is armed and dangerous. The number of health conditions now linked to visceral fat is tremendous, from the obvious ones such as obesity and metabolic syndrome to the not-so-obvious—cancer, autoimmune disorders, and brain disease.”

I copied and pasted the information above from Grain Brain for a reason. Obesity is a danger to more than just your body, by filling it with inflammation, it’s shrinking your brain by using these same process that creates plaque. I will show you exactly how obesity shrinks your brain and on the other hand, I’ll show you exactly how being thin can help your brain to grow in size. It all boils down to consumption of carbohydrates, mostly the high starchy carbs that you find in all pastries and bread, pasta, cereals, snack chips and crackers and some vegetables.

According to  Donald W. Miller, Jr., MD, Carbohydrates are the primary cause of weight gain, not fats. (Animals raised for food are fattened with carbohydrates.)” He goes on to say that eating fat is not only healthier than eating carbohydrates, it makes you thinner. “We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active” (Arch Int Med 1992;152:1271—2). It’s true,  I know from experience that eating fat makes you thin. It’s time for a new news alert;

Eating Fat Makes You Thin

Studies have shown that getting back to what our original metabolism likes for a diet and what our bodies are meant to digest means getting back to a diet high in fats and low in carbohydrates. Low Carb diets date back to 1923 when the ketogenic diet was first created to help control epileptic seizures in infants. Dr. Atkins came out with his low carb diet in 1958,  but it really got its boost when the Paleo diet came out early this century and with Dr. Perlmutter’s recommendation for a ketogenic diet for optimal brain growth.

Wikipedia suggests, “we need to evaluate the low-carbohydrate diets over much longer periods of time, controlled studies as long as two years and survey studies as long as two decades.[7][13][14][15]” 

Dr. Atkins was the first to promote a low carb diet as early as 1958, yet it seems that the carbohydrate addiction complex had already started its devious work in addicting our society to the ravages of the Wheat Belly saga. Too many members of our congress were sold on the notion that it is better to restrict our consumption fats, thinking that’s what was causing all the problem with obesity and diabetes. In all actuality, it is carbs that cause the fat that causes obesity and diabetes, not fat at all. You can find out how that happens in Carbs, The New Death Sentence. (I have to wonder who persuaded them to come to these conclusions, the grain industry?)

It’s all a matter of how they are digested. To digest carbohydrates, your body has to turn them into fat. This is because your body can’t run on glucose. It runs on fat. The studies showing this include,  Iris Shai, R.D., Ph.D. (July 2008), “Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet.” and New England Journal of Medicine 359 (3): 229–41. doi:10.1056/NEJMoa0708681.PMID 18635428, Low-carbohydrate-Diet Score and the Risk of Coronary Heart Disease an Omen, from The New England Journal of Medicineand the two others listed above ([14][15]). What this means is that when you eat carbohydrates, your body can’t use that as food because it burns fat.

When you eat fat, your body doesn’t have to convert that into anything else, so it can use it. Fats are digested in your small intestine, unlike carbs that are digested cellularly with the help of insulin. That means that the glucose that carbs break down to, have to float around in your bloodstream until they can enter a cell to be used as glycogen. This is where the problem begins. Anyone who’s been on a diet of carbohydrates for any amount of time has enough glycogen built up in their systems that they don’t need anymore, so the glucose turns into fat to be stored for future use.

The first place your body stores this fat is around your midsection, hence its name, belly fat or visceral fat. This is a dangerous fat to have in your body as this is where diabetes starts, along with a host of cancers and CVDs or heart diseases and most every kind of dementia, including Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease.

Human biology hasn’t changed evolutionarily enough to allow humans to continue to eat carbohydrates in the massive amounts that everyone everywhere is eating them. The Paleo Diet is a recent addition to the low carb diet choice. The ketogenic diet is the ultimate in a low carb diet and has already shown numerous benefits for better health. It’s the recommended diet for Celiac Disease since Celiac Disease is caused by the gluten that’s found in wheat, barley and rye and a few other grains. It’s also the oldest low carb diet, first designed in 1923, to help control seizures. The diet fell out of use when seizure medicines became more prevalent.

It turns out that a ketogenic diet is the healthiest diet that any human can eat and it brings with it, the most natural form of weight loss, possible. It goes back to the way our bodies have metabolized food for the last 100,000 years. Simply because this diet is based on fat and not carbs, the diet provides much more efficient fuel for our bodies to use. A carbohydrate diet requires refueling every two hours or so and they have a tendency to gum up your body. It does it by creating plaque. That gets into to glycation of proteins and LDL cholesterol, which you can read about in Carbs, How They Cause AGEs

This plaque build-up is the foundation of 75% of the deadliest and costliest diseases, known to man, ranging from breast cancer to Atherosclerosis to 99% of all dementias, making carbohydrates some of the deadliest food that any human can eat. It’s not that this food just makes us fat, it kills us slowly and expensively, with an arm-long list of disorders. For this one reason alone, the power of being thin cannot be overspoken.

Studies have also shown the simple practice of calorie restriction to have multiple beneficial effects for the body, such as extended life. It’s amazing what just going hungry, can do for your body. It not only ramps up your immune system by boosting your anti-oxidants exponentially, it actually helps your brain grow, through a little protein known as BDNF, brain-derived neurotrophic factor. This is what makes your brain grow and it doesn’t happen in obese people. This is part of the power of being thin.

The Power of MCTs and Coconut Oil

Calorie restriction on a carbohydrate diet is next to impossible. Yet I do it every day, quite easily and comfortably, while on my MCT ketogenic diet. MCT ketogenic diet is, in my estimation, the easiest low carbohydrate diet to get adjusted to. MCTs (Medium Chain Triglycerides) work differently in your body than LCTs (Long Chain Triglycerides). MCTs are a good way to actually lower your cholesterol because they build up the HDL cholesterol. Coconut oil and Palm kernel oil are optimal for this, as they contain lauric acid and lauric acid is the foundation of HDL cholesterol, the good cholesterol.

Although curbing your carbs is the best way to lower your LDL cholesterol, adding coconut oil and other saturated fats to your diet will help curb your appetite for carbs, which in turn will cut down your LDL cholesterol and at the same time build up your HDL cholesterol.

Going back to what Dr. Miller had included in his paper, “calorie restriction prolongs life as well as helps to make your brain grow.” This is the true power of being thin. It comes easiest from being on a high-fat low carb diet.

What kind of fats then, do we need to eat, to be thinner? I mentioned before, MCTs. Medium chain triglycerides are the best, along with olive oil and avocado oil, palm kernel oil is also an excellent source of MCTs but coconut oil is by far the best MCT, in my opinion.

Coconut oil and palm Kernel oil have lauric acid in their chains of triglycerides, which is the foundation of HDL cholesterol. This means that a diet high in coconut oil or palm kernel oil MCTs helps build up HDL cholesterol, which in turn can help lower LDL cholesterol. Lauric acid is at the core of apolipoprotein A1, which in turn is at the core of HDL cholesterol. Studies have shown higher levels of HDL particles in the blood to be very beneficial for one’s health.

I can’t recommend staying away from dairy either. As I said before, all milk fats are MCTs. If you truly are lactose intolerant, then it may be best to limit your intake to nothing more than cheese. Cheese loses its lactose as the cheese hardens, so most cheeses have little to no lactose content in them. Just don’t choose the low-fat cheeses.

Butter’s Back

butterFor MCTs, I like milk fats. All milk fats are MCTs. That means that all milk fats can help you lose weight. I’ll bet you didn’t expect that, did you? That means that low-fat milk and skim milk actually help make you fatter by taking away the healthy MCTs in milk fat. That also means butter is back! Wow, how much better can it be? Butter can help you lose weight. What a concept, the more milk fat you eat, the healthier you will be. I love it!!! Cause I love cheese, and cheese is a milk fat.

MCTs are so important, Neuropharmacology just completed a study in June 2013 showing the ability of MCTs to control epileptic seizures. All MCTs are saturated fats. Your body uses saturated fats and would much rather have it fed to it than have to make its own through the ingestion of carbohydrates.

That also means that I can go back to eating bacon. I love bacon. (As a matter of fact, I’ve already gone back to eating bacon. I just enjoyed about 6 slices.) Bacon may not be a medium chain triglyceride, but it’s a saturated fat and I still love it, and I’m not restricted from eating it by my religion, so I eat it and lots of it. I couldn’t do that though if I ate carbs. That would lead to major problems like hypertensive heart disease.

Grass-fed beef is always a good source of fats as well as protein. Lamb is always good also as it’s almost always grass fed. I’m sorry vegans, but a vegetarian diet is too carbohydrate laden to be a fully healthy diet unless you get the bulk of your calories from healthy oils like olive oil, avocado oil, palm kernel oil, and most importantly coconut oil. Simply because carbohydrates are involved in a vegetarian diet, you’re going to be suffering the same consequences as everyone else on a high carbohydrate diet. It may take longer for the disorders to manifest because your vegan diet is a little healthier than most high carbohydrate diets, but they will, simply because carbohydrates are involved. The science of metabolism doesn’t allow any variation on this rule.

Carbs, not fats create body fat, especially visceral fat,  the kind that kills.

The secret is to get more of your calories from fat and fewer from carbohydrates. Fat has more calories per gram of usable food anyway, making it a much more efficient fuel. Like proteins, carbohydrates only give you 4 calories per gram of food, but fat gives you 9 calories per gram of food. That’s over twice as many calories for the same weight of the food you put in your body.

That means that you have to eat more than twice as many carbohydrates to get the same amount of calories. It’s no wonder that a carbohydrate diet is so fattening.

A high fat, low carb diet is like than running high octane gas in your car but it’s even better, for your body. What high octane gas does for your car, fat does more for your body. On the other hand, What sugar does for your car, it also does to your body. Only it does it much slower.If you know of anyone who has put sugar in a gas tank, you know what that did top the engine. The same thing happens in your body. It gums it up. Glucose is to akin too glue, to be healthy.

It does it slower because your body doesn’t burn fuel as fast or as hot as your car engine, so it takes it longer to gum up. But when it does, the results are exactly the same, disastrous. That is the curse of being on a carbohydrate diet.

It’s Time For A Cure

Carbs and High Blood Pressure

Carbs and High Blood Pressure

worried-senior-man-high-blood-pressure-18166563This is something that I don’t even like to talk about because I have high blood pressure. Even though I control it now, because I had high blood pressure in the past, my doctor says that I have high blood pressure now. But she went on to say that I control my high blood pressure, now. I guess that’s true, but I won’t control my  blood pressure with medication. I refuse to. I control mine with diet.

The last three times I saw the doctor, for the first time in my life that I can remember, my blood pressure was as perfect as you could get, 120/60. It was always something around 145/90, 168/95 or what it usually was at rest, 132/86. I can remember a nurse checking my blood pressure after waking up from spending a month in a coma. My blood pressure at that time was 132/86. I thought that was normal. I didn’t learn until recently that it was actually, elevated. Even though it wasn’t considered that elevated at the time, it’s been recently learned that elevation even in this small amount, does enough damage to internal organs that it puts undue strain on the heart, to have to pump harder to get all the blood it needs to, to fuel your entire body.

damage-high-blood-pressure-hypertension-increases-risk-heart-attack-stroke-kidney-failure-52251425 “Wikipedia says about high blood pressure;

Hypertension usually does not cause symptoms initially, but sustained hypertension over time is a major risk factor for hypertensive heart disease, coronary artery disease,[2] strokeaortic aneurysmperipheral artery disease, and chronic kidney disease.”

I can tell you what it’s like to have a stroke. They’re no fun. I still live with the residual effects from the stroke that I had 31 years ago, hemiplegia (right side paralysis). I’m partially paralyzed today from a massive stroke that I had from a severe closed head injury, 31 years ago. I know very well what it’s like to suffer a massive stroke. To say the very least, they are life changing.

“Hypertension is classified as either primary (essential) hypertension or secondary hypertension. About 90–95% of cases are categorized as primary hypertension, defined as high blood pressure with no obvious underlying cause.[3] The remaining 5–10% of cases are categorized as secondary hypertension, defined as hypertension due to an identifiable cause, such as chronic kidney disease, narrowing of the aorta or kidney arteries, or an endocrine disorder such as excess aldosteronecortisol, or catecholamines.

What is defined here, in Wikipedia, as

“no obvious underlying cause” I define as Caused by Carbs.

I define them as caused by carbs because I know the value of restricting carbs in my diet and what that did to control blood my pressure. I attribute my first and continued experience with normal blood pressure to my diet that contains no starchy carbohydrates in it. Glucose, sugar, the food that kills, does so again by causing hypertension.

“Dietary and lifestyle changes can lower blood pressure and decrease the risk of health complications, although treatment with medication is still often necessary in people for whom lifestyle changes are not enough or not effective. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy.[4] The benefits of treatment of blood pressure that is between 140/90 mmHg and 160/100 mmHg are less clear, with some reviews finding absence of a proven benefit[5] and others finding benefit.[6][7]

“Essential hypertension (also called primary hypertension or idiopathic hypertension) is the form of hypertension that by definition has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients,[1][2][3][4] it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebralcardiac, and renal events.[5]

It’s interesting that the most common type of hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. The most important of those genetic factors happens to be diet. The one thing that never changes in a family’s diet that’s passed down from generation to generation, is the number of carbohydrates in the diet. What’s changed over time,  is the carbohydrate itself. It’s become less nutritious. It’s become more dangerous because it creates more LDL particles in the blood, which in turn creates more plaque clogging the arteries, raising the blood pressure.

 “Hypertension is one of the most common complex disorders. The etiology of hypertension differs widely amongst individuals within a large population.[9] And by definition, essential hypertension has no identifiable cause. However, several risk factors have been identified.

The reason there is no “identifiable cause”, apparently is because nobody wants to consider, that the carbs that come in wheat and grains could be the cause, probably because they are just as addicted to them as everyone else is. I know for certain that the major contributing factor for essential hypertension is glucose. Anyone who’s on the diet that I’m on (ketogenic) can tell you the very same thing,

Carbs are the major contributing factor for hypertension.

Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after taking a three-drug regimen.[7] Guidelines for treating resistant hypertension have been published in the UK and US.[8]

“One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries.

This is what interests me. If a reduction in vascular compliance due to stiffening of the arteries is a possible mechanism, we should look at what causes this reduction in vascular compliance. Since it’s due to stiffening of the arteries, we need to look at what stiffens the arteries, Atheroma or atheromatous plaque, a buildup of deposits within the wall of an artery

Veins do not develop atheromata, unless surgically moved to function as an artery, as in bypass surgery. The accumulation (swelling) is always in the tunica intima, between the endothelium lining and the smooth muscle tunica media (middle layer) of the artery wall. While the early stages, based on gross appearance, have traditionally been termed fatty streaks by pathologists, they are not composed of fat cells, i.e. adipose cells, but of accumulations of white blood cells, especially macrophages, that have taken up oxidized low-density lipoprotein (LDL). After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the center to inner surface of each atherosclerotic plaque. Conversely, the outer, older portions of the plaque become more calcified, less metabolically active and more physically stiff over time.”

In short, it’s glycation of the LDL cholesterol that deposits foam cells in the tunica intima of the artery. That is what stiffens the artery and restricts blood flow increasing blood pressure. Understand what creates LDL particles in the body by reading The Value of Balancing Your Cholesterol or The Foundation of LDL Cholesterol. They explain exactly how carbs are the major influence of LDL cholesterol in the body. Reduce the LDL cholesterol and you’ll reduce the amount of plaque that flows through your system, which in turn will guard against stiffening your arteries and raising your blood pressure. Restrict the carbs and you’ll reduce the LDL cholesterol, limiting hypertension.

“Dietary and lifestyle changes can lower blood pressure and decrease the risk of health complications, although treatment with medication is still often necessary in people for whom lifestyle changes are not enough or not effective. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy.[4] The benefits of treatment of blood pressure that is between 140/90 mmHg and 160/100 mmHg are less clear, with some reviews finding absence of a proven benefit[5] and others finding benefit.[6][7]

”Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt-sensitive individuals; lack of exercise, obesity, stress,[9] and depression[25] can play a role in individual cases.”

Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to two-thirds of hypertension cases can be attributed to excess weight.[17] More than 85% of cases occur in those with a Body mass index greater than 25.[17] A definitive link between obesity and hypertension has been found using animal and clinical studies; from these it has been realized that many mechanisms are potential causes of obesity-induced hypertension. These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.[18]

“Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are components of syndrome X, or the metabolic syndromeInsulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin.

Recent studies claims that obesity is a risk factor for hypertension too-high-blood-pressure-14758663because of activation of the renin-angiotensin system (RAS) in adipose tissue,[22][23] and also linked renin-angiotensin system with insulin resistance, and claims that anyone can cause the other.[24]

“Dietary and lifestyle changes can lower blood pressure and decrease the risk of health complications” seems to be the underlying theme in diminishing high blood pressure. When talking about dietary changes, the issue here is weight, and the fact that most of us are carrying too much of it. We all know what influences weight more than anything else, carbs. This is the reasoning behind my conclusion that carbs are the major cause of high blood pressure. Again like the cause of cancer, if you remove any ingredient that it takes to make something, you cannot make that thing anymore and if we remove carbs from the equation of hypertension, it changes the equation completely. If you can curb the carbs, you can cure the disease,

“Much of the disease burden of high blood pressure is experienced by people who are not labeled as hypertensive.[66] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive drug therapy. Lifestyle changes are recommended to lower blood pressure, before starting drug therapy. The 2004 British Hypertension Society guidelines[66] proposed the following lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002[73] for the primary prevention of hypertension:

  • maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2)
  • reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day)
  • engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the week)
  • limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women
  • consume a diet rich in fruit and vegetables (e.g. at least five portions per day);

Effective lifestyle modification may lower blood pressure as much as an individual antihypertensive drug. Combinations of two or more lifestyle modifications can achieve even better results.[66]

The one thing they failed to mention above was carbohydrates. The first thing they mention is to maintain a normal body weight for adults. We all know that limiting carbohydrates is crucial to maintaining a normal body weight, hence, limiting carbohydrates is crucial to limiting hypertension. In my estimation, that means that carbs are a primary cause of hypertension.

“The first line of treatment for hypertension is lifestyle changes, including dietary changes,[82] physical exercise, and weight loss. These have all been shown to significantly reduce blood pressure in people with hypertension.[83] Their potential effectiveness is similar to and at times exceeds a single medication.[64] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication.”

Dietary changes when it comes to obesity, refer to weight loss, but here the recommendations refer only to limiting the use of salt. My contention is that salt isn’t that important if you limit the primary ingredient, and that’s the starchy carbs you get from all grain-based foods, the foundation of LDL cholesterol.

Curb your carbs;
Reduce your LDL cholesterol,
Reduce your plaque,
Reduce your high blood pressure,
It’s Time For A Cure

Banner-improper-nutrition-health-care-concept-diseases-caused-unhealthy-nutrition-diet-

Carbs, The Foundation of LDL Cholesterol

Carbs, The Foundation of Dirty LDL Cholesterol

Hopefully, by now, we’re comfortable with cholesterol and its importance in the body. What we shouldn’t be comfortable with is the presence of LDL cholesterol in the body and where it comes from. If you haven’t read The value of balancing your cholesterol, you might want to read that first.

LDL cholesterolIn my search to find where fat production starts in the body, what I’ve found, when it comes to LDL, tells me to be aware of Apolipoprotein_B. But before we can look at Apolipoprotein B we need to know what these apolipoproteins are.

Apolipoproteins are the foundation of all lipoproteins.

“Apolipoproteins are proteins that bind lipids (oil-soluble substances such as fat and cholesterol) to form lipoproteins. They transport the lipids through the lymphatic and circulatory systems.:

This is the start of cholesterol, these dictate how cholesterol is carried in your bloodstream. They’re the foundation for HDL particles as well as LDL particles and they also dictate how the cholesterol is going to perform in your body. Here is where it gets interesting, because it’s what kind of cholesterol they’re going to make, that dictates how they are classified. Apolipoproteins are protein cells that bind your fats cells into particles, either high density or low density.

“There are two major types of apolipoproteins. Apolipoproteins B form low-density lipoprotein (“bad cholesterol”) particles. These proteins have mostly beta-sheet structure and associate with lipid droplets irreversibly. Most of the other apolipoproteins form high-density lipoprotein (“good cholesterol”) particles. These proteins consist of alpha-helices and associate with lipid droplets reversibly. During binding to the lipid particles these proteins change their three-dimensional structure. There are also intermediate-density lipoproteins formed by Apolipoprotein E.” These are turned into VLDL.

“The lipid components of lipoproteins are insoluble in water. However, because of their detergent-like (amphipathic) properties, apolipoproteins and other amphipathic molecules (such as phospholipids) can surround the lipids, creating the lipoprotein particle that is itself water-soluble, and can thus be carried through water-based circulation (i.e., bloodlymph).”

These amphipathic or amphiphilic properties tell me why we lose weight when we exercise. Fats are water soluble in the body and the body disposes of fats by using them for energy and disposing of them with HDL particles, to be cleaned out in the liver. I think of the HDL particles as cell scrubbers, cleaning out all the used fats and dirt (foreign contents) any LDL particles might carry into the cell.

Since LDL particles are so much larger than the HDL particles and aren’t as tightly bound, so they tend to let other debris in the blood stream drift in and out the particle. This is where these particles get glycated by the excess glucose in the system. Without the glucose, nothing happens to the cholesterol except that it gets to do its job, fuel the body, create hormones, make vitamin D. But then, usually when there’s no glucose in the system, there’s fewer LDL particles and more HDL particles (the ones that are hard to glycate). This lowers the rate of glycation because of the higher concentration of the HDL particles.

This is how the body disposes of used fats, with HDL particles. It’s the LDL particles that feed the fats into the cells, and it appears that this is where the problem with Apolipoprotein B, comes into play. Apolipoprotein B is sometimes a dirty or glycated protein, meaning that it’s bent so that it can’t be used properly. This is when glucose attacks the lipid before it can be used as fuel. It’s the beginning of plaque, and it’s plaque that’s at the base of over one half of all cancers, cardiovascular diseases, and all brain diseases, like Alzheimer’s disease, Parkinson’s disease, and dementia.

“There are six classes of apolipoproteins and several sub-classes:” All are HDL building apolipoproteins except for Apolipoprotein B, E and L. They’re the ones that build LDL, with B being the one that is the genesis for so many ailments and diseases.

Most apolipoproteins are made in the intestine, however, the Apolipoprotein B is formed in the liver.

I have to wonder if this is where its problems begin. This is why Apolipoprotein B is the basis for so many diseases? Knowing that ApoB is responsible for LDL cholesterol particles tell me why ApoB is responsible for all the disease it causes. It’s that they’re more easily invaded by glucose and that is what glycates the cholesterol, and that is where most of the problems with disease begin.

There are six apolipoproteins

“Exchangeable apolipoproteins (apoA, apoC and apoE) have the same genomic structure and are members of a multi-gene family that probably evolved from a common ancestral gene. ApoA1 and ApoA4 are part of the APOA1/C3/A4/A5 gene cluster on chromosome 11.[3]

“Hundreds of genetic polymorphisms of the apolipoproteins have been described, and many of them alter their structure and function.”

“In particular, apoA1 is the major protein component of high-density lipoproteins; apoA4 is thought to act primarily in intestinal lipid absorption.” That tells me that Apolipoprotein A is manufactured in the intestine. This is where fats are digested, the small intestine. That also tells me that the Apolipoprotein B is formed in the liver, the organ that filters the blood.

Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet.
“Apolipoprotein synthesis in the liver is controlled by a host of factors,

including dietary composition, hormones (insulinglucagonthyroxinestrogensandrogens), alcohol intake, and various drugs (statinsniacin, and fibric acids). Apo B is an integral apoprotein whereas the others are peripheral apoproteins.”

It appears that the foundation of HDL type cholesterol particles or Apolipoproteins A, C, D, and H come from the fat you eat, whereas the foundation of LDL type of particles (Apolipoprotein B), comes from many sources, as it’s made in the liver. Maybe it’s polluted Ribosomes that make the protein calls, since they’re made in the liver, rather than in the intestine, like the Apolipoprotein A. Because the liver cleans all the toxins out of the blood, maybe some of the toxins get deposited in some of the Ribosomes the liver manufactures for protein. I don’t know if this is the start of “bad cholesterol” or not, but that’s not the point. The point is that there are too many variables in the manufacture of Apolipoprotein B, from dietary choices to alcohol consumption to hormones and drugs that you take, to make it a steady source of reliable apolipoproteins for consistently healthy cholesterol, thus, “Bad Cholesterol”. This is why, when it comes to LDL, what I have discovered tells me to be aware of Apolipoprotein B and what creates it. So, what does create Apolipoprotein B?

The biggest factor in regulating Apolipoprotein B, it dietary choices, including alcohol consumption. This would entail all consumption of sugars, since we know that fats are responsible for Apolipoprotein A,C, E and H. Since there are only three basic food groups, fats, proteins and carbohydrates, we know that fats are good because they create Apolipoprotein A, proteins are good because they are the basic building blocks or our bodies, leaving sugars or carbohydrates to create Apolipoprotein B….the foundation of most diseases.

Apolipoprotein B and

LDL cholesterol tell me

why it’s so important to 

Stay Away From Sugar

Dietary choices and Alcohol consumption both have to deal with sugar in the diet, because the fats in your diet go to make the foundation of HDL particles. It’s the sugar in the diet or the carbs in the diet that make up the Ribosomes that make the proteins that are the foundation of LDL particles. Put plainly, carbs create LDL particles, fat creates HDL particles. That explains why the LDL is so dangerous, its base proteins are apolipoproteins made in an organ that filters blood for the body. As explained by Wikipedia;

“Apo lipoprotein B (ApoB) is a protein that in humans is encoded by the APOB gene. “Apolipoprotein B is the primary apolipoprotein of chylomicronsVLDLIDL, and LDL particles (LDL – known commonly by the misnomer “bad cholesterol” when in reference to both heart disease and vascular disease in general), which is responsible for carrying fat molecules (lipids), including cholesterol, around the body (within the water outside cells) to all cells within all tissues. While all the functional roles of ApoB within the LDL (and all larger) particles remains somewhat unclear, it is the primary organizing protein (of the entire complex shell enclosing/carrying fat molecules within) component of the particles and is absolutely required for the formation of these particles. What is also clear is that the ApoB on the LDL particle acts as a ligand for LDL receptors in various cells throughout the body (i.e., less formally, ApoB indicates fat carrying particles are ready to enter any cells with ApoB receptors and deliver fats carried within into the cells).”

The National Institute of Health says about Apolipoprotein B;

“Apolipoprotein (apo) B represents most of the protein content in LDL and is also present in intermediate-density lipoproteins (IDL) and VLDL. ApoA-I is the principal apolipoprotein in HDL. Both apolipoproteins, therefore, separately provide information for detecting high-risk individuals. ApoA-I is also believed to be a more reliable parameter for measuring HDL than cholesterol content since it is not subject to variation. Therefore, the apoB/apoA-I ratio is also highly valuable for detecting atherogenic risk, and there is currently sufficient evidence to demonstrate that it is better for estimating vascular risk than the total/HDL cholesterol ratio.1114 The apoB/apoA-I ratio was stronger than the total cholesterol/HDL cholesterol and LDL/HDL cholesterol ratios in predicting risk.11 ” Are you beginning to see the value of balance, in your cholesterol?

“This ratio reflects the balance between two completely opposite processes (Figure 1): transport of cholesterol to peripheral tissues, with its subsequent arterial internalization, and reverse transport to the liver.15 Figure 2shows that the greater the apoB/apoA-I ratio, the larger will be the amount of cholesterol from atherogenic lipoproteins circulating through the plasma compartment and likely to induce endothelial dysfunction and trigger the atherogenic process. On the other hand, a lower apoB/apoA-I ratio will lead to less vascular aggression by plasma cholesterol and increased and more effective reverse transport of cholesterol, as well as other beneficial effects, thereby reducing the risk of cardiovascular disease.”

Wikipedia continues to state;

“Through mechanisms only partially understood, high levels of ApoB, especially associated with the higher LDL particle concentrations, are the primary driver of plaques that cause vascular disease (atherosclerosis), commonly first becoming obviously symptomatic as heart diseasestroke & many other body wide complications after decades of progression. There is considerable evidence that concentrations of ApoB[1][2] and especially the NMR assay[3] (specific for LDL-particle concentrations) are superior indicators of vascular/heart disease driving physiology than either total cholesterol or LDL-cholesterol (as long promoted by the NIH starting in the early 1970s). However, primarily for historic cost/complexity reasons, cholesterol, and estimated LDL-cholesterol by calculation, remains the most commonly promoted lipid test for the risk factor of atherosclerosis. ApoB is routinely measured using immunoassays such as ELISA or nephelometry. Refined and automated NMR methods allow measurement distinctions between the many different ApoB particles.”

“High levels of ApoB are related to heart disease.

Hypobetalipoproteinemia is a genetic disorder that can be caused by a mutation in the ApoB gene, APOB. Abetalipoproteinaemia is usually caused by a mutation in the MTP gene, MTP.
Mutations in gene APOB100 can also cause familial hypercholesterolemia, a hereditary (autosomal dominant) form of metabolic disorder Hypercholesterolemia.”

“Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver.[8]

“Mice overexpressing mApoB have increased levels of LDL “bad cholesterol” and decreased levels of HDL “good cholesterol”.[4] Mice containing only one functional copy of the mApoB gene show the opposite effect, being resistant to hypercholesterolemia. Mice containing no functional copies of the gene are not viable.[5]

It is well established that ApoB100 levels are associated with coronary heart disease, and are even a better predictor of it than is LDL level. A naive way of explaining this observation is to use the idea that ApoB100 reflects lipoprotein particle number (independent of their cholesterol content). In this way, one can infer that the number of ApoB100-containing lipoprotein particles is a determinant of atherosclerosis and heart disease.”

“ApoB100 is found in lipoproteins originating from the liver (VLDLIDLLDL[9]). Importantly, there is one ApoB100 molecule per hepatic-derived lipoprotein. Hence, using that fact, one can quantify the number of lipoprotein particles by noting the total ApoB100 concentration in the circulation. Since there is one and only one ApoB100 per particle, the number of particles is reflected by the ApoB100 concentration. The same technique can be applied to individual lipoprotein classes (e.g. LDL) and thereby enable one to count them as well.”

This tells me that it’s not the amount of cholesterol in your body that’s important. It’s the number of ApoB100 lipoproteins floating around regardless of how much cholesterol is in each individual LDL particle, that’s important. So, what do I need to look out for to keep from building this ApoB100, in my system? What causes ApoB?

“Apolipoproteins are of great physiological importance and are associated with different diseases such as dyslipidemia, cardiovascular and neurodegenerative diseases. Apolipoproteins have therefore emerged as key risk markers and important research targets yet the function of apolipoproteins has not been fully elucidated.” That’s according to Mabtech, they go on to say, “Apolipoproteins are proteins that bind hydrophobic lipids in the blood and help solubilize them. Together with phospholipids, apolipoproteins form lipoprotein particles into which different lipids can be packed. Apolipoproteins have pivotal functions as structural components in lipoprotein particles, ligands to receptors and co-factors to enzymes. Lipoprotein particles are necessary for transportation of lipids used for energy supply and for synthesis of hormones, vitamins and bile acids. ApoB and apoE are important in the transport of dietary and endogenous lipids to peripheral tissues for energy supply, whereas apoA1 is crucial for the returning of excess cholesterol from peripheral tissues back to the liver. Apolipoproteins such as apoE and apoJ are also important for the transportation of lipids in the brain.”

They also added; “There are two major types of apolipoproteins: non-exchangeable and exchangeable. Apolipoprotein B (apoB) is non-exchangeable and anchored in the lipoprotein particle whereas apolipoproteins A, E, D, J and H are exchangeable and can be transferred between different lipoprotein particles. ApoA1 and apoB represent the main protein components of HDL and LDL, respectively.”

With all the different kinds of cholesterol, just lowering it seems to me, to be a little counterproductive. There are just too many good uses for cholesterol to just lower it. In my opinion, that’s like signing your death warrant. One would think that concentrating on the cause of LDL particles would be much more productive than focusing on lowering LDL cholesterol after its arrival.

In conclusion,
  • Apolipoprotein A, C, D, E, H, L – the genesis of HDL, healthy cholesterol, comes from fats
  • Apolipoprotein B – the foundation of LDL cholesterol, comes from primary carbs, and cause too many diseases to list

All cholesterol is so important for fat transportation in our bodies as well as hormone balance, vitamin D production and removing fats from the body, my question is, why would anyone in their right mind, want to lower it when a good balance of cholesterol is so much more important.

Again, I have to thank Wikipedia for their extensive help in putting together this post, Their entries are in quotations marks. I also have an entry directly from the NIH  National Library of Medicine website, PubMed. A lot of what is on Wikipedia has shown to be the same as that on PubMed.

The Value of Balancing Your Cholesterol

The Value of Balancing Your Cholesterol

cholesterol-meter-10069234Too often I hear the phrase I’ve got to get my cholesterol down. People saying this think that high cholesterol is something to fear. High cholesterol isn’t nearly as big of a problem as unbalanced cholesterol.

Cholesterol is a very important part of bodily functions and plays a major impact on your health.

To lower one’s cholesterol is to endanger one’s life.

Low cholesterol has been connected to depression, anxiety, bipolar disorder and statistically higher frequency of violent behavior, suicide, Parkinson’s disease, and cancer mortality. Susceptibilities to tuberculosis and gastrointestinal infections are also associated with lower cholesterol levels. Most significantly, the death rate is doubled in older adults with lower total cholesterol and stroke and cataracts rates are higher. That was according to The Great Plains Laboratory, but you can find the same message from multiple websites, proclaiming the dangers of low cholesterol.

Dr. Mercola says;

The Risks of Low Cholesterol
Impaired memory and dementia are just the tip of the iceberg when it comes to low cholesterol’s impact on your brain. Having too little of this beneficial compound also:


“Unfortunately, in the United States lowering cholesterol levels has become so common that nearly everyone reading this either knows someone struggling to do so or has struggled to do so themselves.”

Cholesterol is not the enemy

cholesterol-check-switch-10079568The Heart Association recognizes that higher HDL cholesterol levels protect against heart disease. I’ll explain how that happens later in this post. But understanding cholesterol and how it works makes it easier to understand why balancing is more important than just lowering cholesterol

“Since cholesterol is essential for all animal life, each cell synthesizes it through a complex process beginning with the mevalonate pathway and ending with a 19 step conversion of lanosterol to cholesterol. Increased dietary intake of industrial trans fats, but not ruminant saturated fats(including cholesterol), is associated with an increased risk in all-cause mortality, cardiovascular diseases or type 2 diabetes.[9]”

“Most ingested cholesterol is esterified, and esterified cholesterol is poorly absorbed. The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis [11]”  “Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the homeostatic mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, whereas lower intake from food has the opposite effect.” Simply stated, the more you eat, the less you make. But because most ingested cholesterol is esterified, it’s important to know where these fats come from.

“In addition to its importance within cells, cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acids, and vitamin D.[5] Cholesterol is crucial in the manufacture of hormones for the body’s function.  As vitamin D is crucial for brain function, cholesterol is crucial in the manufacture of vitamins. This is why statin drugs that are made for lowering cholesterol, are so dangerous.

With a substance as vital as this is, why do people want to lower it? Maybe we should look at how it floats around in your blood as it’s transported to your cells and what role that plays in the cholesterol equation.

“Cholesterol is transported inside lipoproteins.”

Cholesterol comes in many forms of lipoproteins, HDL (High-Density Lipoproteins), LDL (Low-Density Lipoproteins), and VLDL (Very-Low-Density Lipoproteins) just to name a few. It’s the HDL and LDL that we’re interested in for the sake of this post and your health. LDL and HDL are often referred to LDL cholesterol and HDL cholesterol because that’s the type of cholesterol that makes up the respective particles. The difference in the two types is in how the cholesterol is packed in each respective particle. That tells us what kind of particles they are.  That, also, dictates how easy they are to glycate and start reeking havoc in your body. I’ll explain that after we learn the differences between these particles and it has to do with how the HDL and LDL particles are formed.

According to Wikipedia;

Low-density lipoprotein (LDL) is one of the five major groups of lipoproteins. These groups, from least dense to most dense, are: chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein and high-density lipoprotein (HDL), all of them, particles far smaller than human cells. In nutrition, LDL is sometimes referred to as the “bad cholesterol”.”

“Lipoproteins transfer fats around the body in the extracellular fluid, can be sampled from blood and allow fats to be taken up by the cells of the body by receptor-mediated endocytosis.[1][2] Lipoproteins are complex particles composed of multiple proteins which transport all fat molecules (lipids) around the body within the water outside cells. They are typically composed of 80-100 proteins/particle (organized by a single apolipoprotein B for LDL and the larger particles). A single LDL particle is about 260-300 nm in diameter (submicroscopic ) typically transporting 3,000 to 6,000 fat molecules/particle, varying in size according to the number and mix of fat molecules contained within. The fats carried include cholesterol, phospholipids, and triglycerides; amounts of each vary considerably.”

“LDL particles vary in size and density, and studies have shown that a pattern that has more small dense LDL particles, called Pattern B, equates to a higher risk factor for coronary heart disease (CHD) than does a pattern with more of the larger and less-dense LDL particles (Pattern A).”

“LDL particles pose a risk for cardiovascular disease when they invade the endothelium and become oxidized, since the oxidized forms are more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of LDL particles, chiefly stimulated by presence of necrotic cell debris and free radicals in the endothelium.[3] Increasing concentrations of LDL particles are strongly associated with increasing rates of accumulation of atherosclerosis within the walls of arteries over time, eventually resulting in sudden plaque ruptures and triggering clots within the artery opening, or a narrowing or closing of the opening, i.e. cardiovascular disease, stroke, and other vascular disease complications.[4]

It’s easy to see now, the importance of lowering LDL. This is what The National Library of medicine has to say about cholesterol ratios;

“Low-density lipoprotein (LDL) cholesterol concentration has been the prime index of cardiovascular disease risk and the main target for therapy. However, several lipoprotein ratios or “atherogenic indices” have been defined in an attempt to optimize the predictive capacity of the lipid profile. In this review, we summarize their pathophysiological aspects, and highlight the rationale for using these lipoprotein ratios as cardiovascular risk factors in clinical practice, specifying their cut-off risk levels and a target for lipid-lowering therapy. Total/high-density lipoprotein (HDL) cholesterol and LDL/HDL cholesterol ratios are risk indicators with greater predictive value than isolated parameters used independently, particularly LDL. Future recommendations regarding the diagnosis and treatment of dyslipidemia, including instruments for calculating cardiovascular risk or action guidelines, should include the lipoprotein ratios with greater predictive power which, in view of the evidence-based results, are none other than those which include HDL cholesterol.” With the advantages of HDL as opposed to the disadvantages of LDL, it’s become important to know the difference in HDL and LDL because a balance in the ratio seems to be more important than anything else.”

That says to me, what’s important to know is how to create HDL and how to not create LDL. This will go much farther than any medicine to balance HDL/LDL cholesterol.

Wikipedia  goes on to say;

HDL particles remove fats and cholesterol from cells, including within artery wall atheroma, and transport it back to the liver for excretion or re-utilization; thus the cholesterol carried within HDL particles (HDL-C) is sometimes called “good cholesterol” (despite being the same as cholesterol in LDL particles).”

“Increasing concentrations of HDL particles are strongly associated with decreasing accumulation of atherosclerosis within the walls of arteries. This is important because atherosclerosis eventually results in sudden plaque ruptures, cardiovascular disease, stroke and other vascular diseases. HDL particles are sometimes referred to as “good cholesterol” because they can transport fat molecules out of artery walls, reduce macrophage accumulation, and thus help prevent or even regress atherosclerosis.”

“High LDL with low HDL level is an additional risk factor for cardiovascular disease.[24]” “In a large sample of middle-aged adults, low HDL cholesterol was associated with poor memory and decreasing levels over a five-year follow-up period were associated with decline in memory.[27]

With all that said from Wikipedia, it’s easy to see that not all cholesterol is equal. Some are good and some are bad. Thus, the “good cholesterol, bad cholesterol mantra”, which more than anything boasts the value of balancing your cholesterol, rather than lowering it. Knowing how to lower LDL particles while raising HDL particles would be much more beneficial than just lowering total cholesterol.

The paragraph above about HDL cholesterol says it all, increasing HDL cholesterol is a good thing, as it’sassociated with decreasing accumulation of atherosclerosis within the cell walls of the arteries”.

As you can see, HDL, the good cholesterol is something you want in your body, but the LDL, bad cholesterol is something to keep levels low in your body. Wikipedia goes on to say about HDL;

“HDL is the smallest of the lipoprotein particles. It is the densest because it contains the highest proportion of protein to lipids. Its most abundant apolipoproteins are apo A-I and apo A-II.[7] (A rare genetic variant, ApoA-1 Milano, has been documented to be far more effecitive in both protecting against and regressing arterial disease; atherosclerosis). The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free flattened spherical lipoprotein particles; the complexes are capable of picking up cholesterol, carried internally, from cells by interaction with the ATP-binding cassette transporter A1 (ABCA1).[8] A plasma enzyme called lecithin-cholesterol acyltransferase (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into the core of the lipoprotein particle, eventually causing the newly synthesized HDL to assume a spherical shape. HDL particles increase in size as they circulate through the bloodstream and incorporate more cholesterol and phospholipid molecules from cells and other lipoproteins, for example by the interaction with the ABCG1 transporter and the phospholipid transport protein (PLTP).”

“HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by both direct and indirect pathways. HDL is removed by HDL receptors such as scavenger receptor BI (SR-BI), which mediate the selective uptake of cholesterol from HDL. In humans, probably the most relevant pathway is the indirect one, which is mediated by cholesteryl ester transfer protein (CETP). This protein exchanges triglycerides of VLDL against cholesteryl esters of HDL. As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The triglycerides are not stable in HDL, but are degraded by hepatic lipase so that, finally, small HDL particles are left, which restart the uptake of cholesterol from cells.”

“The cholesterol delivered to the liver is excreted into the bile and, hence, intestine either directly or indirectly after conversion into bile acids. Delivery of HDL cholesterol to adrenals, ovaries, and testes is important for the synthesis of steroid hormones.”

This is why it’s important to get your cholesterol into high-density lipoproteins to transfer fats from cells, where they can be used to do the most good. It seems the loose floating fats, the triglycerides, VLDL and LDL cholesterol are more open, for glycation by loose glucose in the system than the tighter more compact fats contained in the HDL packets, making them more likely to become glycated and turned into plaque.

With that said, balancing your cholesterol seems to be much more important than just lowering your cholesterol. You really don’t want to lower your good cholesterol, the HDL because of all the good it does, yet lowering the LDL with all the damage that it does, would be wise.So what is a good way to balance your cholesterol?

There are several ways to balance your cholesterol;

According to Wikipedia;

“Certain changes in diet and exercise may have a positive impact on raising HDL levels:[29]

Most saturated fats increase HDL cholesterol to varying degrees and also raise total and LDL cholesterol.[42] A high-fat, adequate-protein, low-carbohydrate ketogenic diet may have similar response to taking niacin (vitamin B3) as described below (lowered LDL and increased HDL) through beta-hydroxybutyrate coupling the Niacin receptor 1.[43]

MCTs from coconut oil increase HDL cholesterol.

“MCTs passively diffuse from the GI tract to the portal system without requirement for modification like long-chain fatty acids or very-long-chain fatty acids(longer fatty acids are absorbed into the lymphatic system). In addition, MCTs do not require bile salts for digestion. Patients who have malnutrition, malabsorption or particular fatty-acid metabolism disorders are treated with MCTs because MCTs do not require energy for absorption, use, or storage.”

“Some studies have shown that MCTs can help in the process of excess calorie burning, thus weight loss.[4][5][6][7][8] MCTs are also seen as promoting fat oxidation and reduced food intake.[9] look at all the numbers for reference, to take note all the studies done on the weight loss aspect of MCTs, there were 5 of them.

Medium Chain Triglycerides come from Coconut oil, Palm Kernel oil and dairy fats. That means that butter and cheese can actually help you lose weight and balance your cholesterol. How great is that? You can go back to eating butter with healthier consequences than eating margarine.

“Coconut milk is rich in medium-chain fatty acids (MCFAs), which the body processes differently from other saturated fats. If MCFAs are used in a diet to replace long-chain fatty acids (LCFAs) such as animal fats they may help promote weight maintenance without raising cholesterol levels.[14]

“Coconut milk contains a large proportion of lauric acid, a saturated fat that raises blood cholesterol levels by increasing the amount of high-density lipoprotein cholesterol[12]” Like coconut milk, coconut oil is high in Lauric acid.

“Medium-chain triglycerides are generally considered a good biologically inert source of energy that the human body finds reasonably easy to metabolize. They have potentially beneficial attributes in protein metabolism, but may be contraindicated in some situations due to a reported tendency to induce ketogenesis and metabolic acidosis.[12] However, there is other authority reporting no risk of ketoacidosis or ketonemia with MCTs at levels associated with normal consumption. [13]””

“Due to their ability to be absorbed rapidly by the body, medium-chain triglycerides have found use in the treatment of a variety of malabsorption ailments. MCT supplementation with a low-fat diet has been described as the cornerstone of treatment for Waldmann disease.[14] MCTs are an ingredient in some specialised parenteral nutritional emulsions in some countries (not USA).[15][16] Studies have also shown promising results for neurodegenerative disorders (e.g. Alzheimer’s and Parkinson’s diseases)[17] and epilepsy through the use of ketogenic dieting.[18][19]

“MCFA (chain lengths of 10 carbons or less are found in greatest concentrations in coconut oil, approximately 14% by weight but can also be found in butter ( approximately 9.2%) and palm kernel oil (approximately 7.2%)” “MCT oil has been taunted as a potential weight-lowering agent.”

According to the US National Library of Science, The“Weight-loss diet that includes consumption of medium-chain triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil2

“Thirty-one subjects completed the study (body mass index: 29.8 ± 0.4, in kg/m2). MCT oil consumption resulted in lower endpoint body weight than did olive oil (−1.67 ± 0.67 kg, unadjusted P = 0.013). There was a trend toward greater loss of fat mass (P = 0.071) and trunk fat mass (P = 0.10) with MCT consumption than with olive oil. Endpoint trunk fat mass, total fat mass, and intra-abdominal adipose tissue were all lower with MCT consumption than with olive oil consumption (all unadjusted P values < 0.05).”

So the only remaining question, is how do we lower LDL?

In my attempt to find what fats cause LDL, I’ve found nothing to suggest that eating fat causes the formation of LDL. But, on the other hand, I’ve found plenty of data that suggests,  where this kind of fat comes from. That’s is my newest post, about Apolipoprotein B. All that I’ve researched shows wheat-bread-wheat-shock-white-background-34095411that it comes from glucose. Glucose comes from starchy carbohydrates. If you want to read about how that happens, check out Carbs! The Newly Discovered Death Sentence or Diabetes Control. It all has to do with the digestion of carbs. These fats are apportioned to the visceral fat around the belly instead of fats you can use for immediate fuel. and this is where it’s formed into LDL with the help of Ribosomes from your liver. This is also where it becomes so dangerous, but you’ll have to read about it in my next post.
Again, according to Wikipedia, “Lowering the blood lipid concentration of triglycerides helps lower the concentration of small LDL particles because fatty-acid rich VLDL particles convert in the bloodstream into small dense LDL particles.[vague]”

It makes sense then, if you want to stop the productions of LDL, you need to stop the production of triglycerides, the fuel that feeds it, and the best way is to stop that, is to curb the high starchy carbohydrates from the worst offenders, grain-based foods. The guiltiest of the group is wheat, followed closely by corn, then rice and oats. All grain-based foods are at the top of this list, along with starchy vegetables like potatoes, parsnips and carrots, although carrots do have some nutritional value, like beta-carotene. All the others just don’t carry enough nutrition to counterbalance the load of carbs you get, with it.

If you’re not ready to give up your carbs, there are alternatives, to help you lower your LDL, “Niacin (B3), lowers LDL by selectively inhibiting hepatic diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74[35] and HM74A or GPR109A.[36] “A ketogenic diet may have similar response to taking niacin (lowered LDL and increased HDL) through beta-hydroxybutyrate, a ketone body, coupling the niacin receptor (HM74A).[36]

Statin drugs are made to lower LDL also, but I can only recommend steering clear of those, as they cause too many problems in their action of lowering LDL. As a certified caregiver, I’ve seen, too often, the ravages this drug commits to the body. They are nothing short of devastating. In every case of a patient I took care of, the patient died prematurely from the side effects of these drugs. It seems to me that in our attempt to cure ourselves, we’re killing ourselves. Cholesterol is just too important to lower.

“Because LDL particles appear harmless until they are within the blood vessel walls and oxidized by free radicals,[43] it has been postulated that ingesting antioxidants and minimizing free radical exposure may reduce LDL’s contribution to atherosclerosis, though results are not conclusive.[44][45]

I know of something far greater than ingesting antioxidants, to boost them in your system. Boosting them through calorie restriction gives you exponentially more antioxidants than eating or drinking them can ever do for you.

Because MCT ketogenic diets are made for calorie restriction and this next point deals with calorie restriction, I can see the benefits here, as well,  for added  BDNF for brain growth, increased Nrf2 for anti-oxidant production. If you don’t know about the brain growth or anti-oxidant boost of calorie restriction, check it out at the link above. I’m just beginning to understand the benefits of the MCT ketogenic diet and how much healthier it’s kept me. And if it can keep me that healthy, it can keep all those who venture to try it just as healthy.

Don’t you think it’s time for a cure?

I offer these to you, free!

  • MCT ketogenic diet: it can not only help you balance your cholesterol but it can help you lose weight and keep it off forever. With the proper supplements, it will help you grow your brain. Who knew that coconut oil or coconut milk could be so healthy? Who knew that butter could be so healthy? I certainly didn’t. but I do now.
  • Spices like Bay Leaf can help balance out your cholesterol as well, as described on Spices That Heal, “Research on humans showed that after one month, the bay leaf group had up to 26 % reductions in blood sugar! They also showed approximately 35 to 40% reductions in LDL cholesterol and a jump in the good HDL particles by about 25%!”

Just looking halfway through the list, I came across another half dozen spices that can all help balance cholesterol. What an excellent resource. I love free cures since I already have these spices in my cabinet.

I have to thank Wikipedia, from which much of this post comes and is marked by quotations marks and is in italics, where used. Parts are also quoted from the National Library of Medicine and a few other independent websites. It was necessary to copy and paste the information in order to express the argument for balancing one’s cholesterol, as I couldn’t have put the information in better words than it was already expressed. Again, if you find any information you feel is incorrect and have corroboration, to back up your claim, I welcome your correction to help me make this post better.