Welcome


My name is Gina and I would like to welcome you to my blog!

On this blog, I not only share the dietary and lifestyle approach which reversed my metabolic disease and achieved my weight loss, but I also debunk many misconceptions surrounding obesity and its treatment.

I am 5'5" and was weighing 300 lbs., at my heaviest. I lost a total of 180 lbs. I went through several phases of low carbohydrate dieting, until I found what worked best and that is what I share on this blog. Once on a carbohydrate restricted diet, along with intermittent fasting, I dropped all of the weight in a little over two years time.

My weight loss was achieved without any kind of surgery, bariatric or cosmetic. I also did not take any weight loss medications or supplements. I did not use any weight loss program. This weight loss was solely the result of a very low carbohydrate, whole foods based diet, along with daily intermittent fasting and exercise.

There are years worth of content on this blog, so I suggest you use Labels to easily find the information you are looking for. If what you are looking for is not under Labels, enter it into the Search Bar.

Showing posts with label Hypercholesterolemia. Show all posts
Showing posts with label Hypercholesterolemia. Show all posts

Six common beliefs addressed, Part 245

1. I eat the same foods daily, but I continue to be overweight. I have chronic and severe irritable bowel syndrome (IBS) so my diet is always the same daily.

Once you are low carb and following your protocol consistently, we don't nitpick it because whatever is going on is not diet related. Changing one little thing in your diet, here and there, is not going to make much of a difference. So, you would have to revisit your diet, which you did not describe, and identify other factors that could be contributing to your overweight.

2. I think that all those who started on that fat-chugging "keto" diet will never stop because it was their ticket out of Type II diabetes. They used the fat as a replacement for medications. Soon it will fail for them, and they will be right back to where they were before. I was also very strict when I started a low carb diet, many years ago, because I lost 60 pounds on it. I followed it religiously and then I gained everything back and I am now diabetic. No matter how strict I followed it, I still ended up here. Is this the case for all diets?

Well, let me break this down a little because there are a few misconceptions here.

First, the fat-chugging "keto" crowd never got a "ticket out of their diabetes". They only got a ticket to continue eating in a disordered way. The vast majority of these people have eating disorders and fad "keto" simply allows them to eat as much as they want as long as it's from the "allowed foods" list and that's basically one food - fat. They won't leave their fad diet because they are using fat as a replacement for carbs, not medications. The most they ever achieved was lower postprandial blood glucose.

Second, they won't "soon fail". They already failed. The most these people have been able to do is lower the dose of their exogenous insulin or get rid of it all together since insulin is basically an end-stage medication for the management of diabetes so any improvement in the condition will do away with insulin injections first. Some have been able to reduce other medications they were on because they were on a slew of them. Again, any improvement in their condition will have to eliminate some of those medications or they will have a deadly drop in blood glucose. Most of those medications were being taken to counteract the dietary glucose they were consuming. Get rid of that dietary glucose and you get rid of those extra medications, but the diabetes remains.

Just because you are off a medicine cabinet full of medications and your blood glucose meter reads 170 mg/dL instead of 300 mg/dL and your doctor tells you your HbA1C is "below what would constitute a diabetes diagnosis", does not mean you aren't diabetic any longer. It just means the high glucose symptom of the condition is not showing up as much as it was before.

Diabetes is not a disease of high blood glucose. It is a condition that tries to keep your blood glucose high so that is only one symptom of it. By the time it gets to that, you're at its end stage. Most of these people don't get that. They are following buffoons that only like throwing out scary words at them like "amputation", "fatty liver disease" and "dialysis". It's a cult where the leader must always espouse dooms day scenarios to keep their flock.

Like I have said many times before - diet is only a palliative treatment for metabolic disorders. It helps reduce symptoms and allows you time to take some control over your lifestyle and try and put the condition under remission, but it doesn't cure anything. The disease continues. So, you can be strict all you want with your diet, the disease is still looming if you aren't addressing other lifestyle factors that contribute and put you at risk for its progression. One of those lifestyle factors is following quackery. Quackery puts you at risk for the condition's progression.

That's what happened to you. You thought that strict diet adherence was all that was needed to cure your "diabetes" and you now had a very rude wake up call. This is precisely what I'm trying to prevent with this blog.

3. I lost enough weight to get to lean in the beginning, but I gained some back and I am now overweight. I have not been able to lose weight again, but I am also not gaining. I just hate that I couldn't remain lean. I have come to the conclusion that I will never be lean again, no matter what I do. Can I remain healthy even while being overweight? I don't want to have the same fate my parents did.

I've addressed this question before, but I will reply to it again since it's so common.

Overweight/obesity are only markers for metabolic problems. Canaries in the coalmine. They are symptoms of an underlying problem as overweight/obesity are not anymore normal than cachexia/anorexia. When you start putting on excessive body fat and sparing it, it means that your metabolism is under some type of stress. This is usually the first symptom of an impending problem. The stress is blood glucose dysregulation.

People can be overweight for a very long time without developing any other metabolic pathology. Once it gets to obesity then things do not stay benign for long. Hence the term "morbid obesity".

But overweight/obesity are not the be all/end all of metabolic dysfunction. If you are doing what you are supposed to do to address your health problems and you have gotten below obesity, but are still overweight, you can remain relatively healthy for a very long time. No one knows just how long but you aren't in any immediate danger.

What we do know is that the metabolic issues causing the overweight/obesity do not halt there. They continue to progress towards pathology. This is especially true with increasing age as metabolic dysfunction is a time dependent disease. It's not so much that your body is failing because you are old but rather the older you are the longer you have lived with this abnormality and so it had plenty of time to progress to its end-stage while you are still alive to witness it.

For this reason, always keep in mind that as long as you're overweight, your metabolism is abnormal, and you aren't 100% healthy. You have to be more vigilante with your diet, exercise and lifestyle choices as it's a very easy hop from overweight to obesity. Don't be like these fools online that try to tell you that you can be healthy while obese. You can't. There is no such thing as a "healthy obese person". There is only an obese person who isn't yet showing clinical symptoms of diabetes, fatty liver disease or cardiovascular disease but these pathologies are well under way.

That's why we don't see healthy obese people in their sixties or a healthy obese eighty-year-old. Obese people start developing a slew of health conditions in their fifties and sixties, if not earlier, and succumb to them way before they hit eighty. Obese people have an average of 14 years less of lifespan. That doesn't even take into consideration the loss of quality of life which begins decades before death.

4. Should I be tested for familial hypercholesterolemia (FH) if I have high LDL?

Your doctor will let you know if this test is required for you so you should have a discussion with them about this.

High LDL is not FH. It is simply hypercholesterolemia. FH is a specific genetic condition that limits the liver's ability to regulate low density lipoprotein (LDL), among other lipid abnormalities related to the body's ability to handle LDL. This condition is serious and will lead to early onset cardiovascular disease (CVD) if not treated properly. Though one of the signs of FH is high LDL cholesterol, this condition presents other signs and symptoms as well such as:

  • Fatty skin deposits called xanthomas over parts of the hands, elbows, knees, ankles and around the cornea of the eye.
  • Cholesterol deposits in the eyelids (xanthelasmas).
  • Chest pain (angina) or other signs of coronary artery disease which may be present at a young age.
  • Cramping of one or both calves when walking.
  • Sores on the toes that do not heal.
  • Sudden stroke-like symptoms such as trouble speaking, drooping on one side of the face, weakness of an arm or leg, and loss of balance.

Because of how serious FH is, do not allow your doctor to diagnose you with this condition simply because you have "high LDL". Many people have high LDL and do not have FH. Like I said above, FH is not simply high LDL. It is a complex condition that can result in early death from CVD. This is not always the case with simple high LDL. High LDL can be a marker of improper lipid management by the body, but this is not true in every case. You can have high LDL and remain completely healthy your entire life. It all boils down to how your body is managing its lipoproteins and that is very difficult to know since lipid function is so complex.

Lipid testing is very expensive, not generally available and the results are up for multiple interpretations depending on what lipidologist/cardiologist views it. This is why these tests are usually confined to the area of research, not general everyday medical practice. Usually, you become aware of your lipid function once you develop CVD, if the CVD is lipid related, and this is why doctors are quick to label high LDL as a risk factor for CVD from the get-go. It makes things easier even if it can result in some people receiving unnecessary treatments. They figure the treatment wouldn't hurt you, even if you don't need it, and it's best to be safe than sorry.

Most people can know immediately if they have FH, with no testing required. They just have to look at their family history. If you have a family history of early onset CVD, and you yourself have high LDL cholesterol, then you might have FH. A way to know you don't have it is if you are already 60 years old, with high LDL cholesterol, but no signs of CVD and neither do any of your family members. But the absolute best way to know is through testing. The testing is not a total cholesterol panel. The testing is genetic.

Genetic testing for FH looks for inherited genetic changes in three different genes (LDLR, APOB, and PCSK9) known to cause FH. This test can also include a study of cells called fibroblasts to see how the body absorbs LDL cholesterol. People who get only one copy of the defective gene, from their parents, may do well with diet changes and medications. People who have a more severe form of the disorder will require more invasive treatments.

This is why you need to talk to your doctor and become informed on which treatment option is appropriate for you. All you need to know is that if you are diagnosed with FH, you will require treatment or you will develop CVD. So, ignore whatever these low carb quacks tell you about statins or other cholesterol managing drugs because the least of your concerns are their possible side effects or how much money the pharmaceuticals are making from them. Your main concern is the impending heart attack or stroke in your near future. There is no way to "prevent" FH. You either have it or you don't. FH is a genetic condition, not a lifestyle result. All you can do is reduce your risk of developing CVD, if you have FH, through proper treatments.

FH is not the only marker of poor management of lipids. It is only one. There is actually a whole class of FH related conditions. These conditions are all as complex as lipid management itself. Some families do not have a history of early onset development of CVD but later onset instead. Some forms of FH do not even develop into any disease at all. This is usually the case for people who have a family history of high LDL with no CVD.

My family for instance has extremely high LDL, on my father's side, but none develop CVD. They all live well into their nineties. This is why you should take family history of CVD so seriously because it affects you. Family history of CVD carries more weight than just the total numbers of any lipoproteins.

5. What's the difference between glycogenolysis and gluconeogenesis? I hear these terms talked about a lot but always get confused as to what they are.

The liver converts glycogen into glucose through a process called glycogenolysis. The liver also can manufacture necessary glucose by converting amino acids, waste products and fat byproducts through gluconeogenesis.

Both of these are interesting, and I am sure you have heard them mentioned many times in low carb spaces, but you don't need to get bogged down remembering what they are as they are both completely out of your control. A lot of people get caught up in things that are neither here nor there. These things can help explain a little about metabolic function, but they aren't practical in any way whatsoever to its treatment. There is also a lot of nuance and context missing in these definitions.

So, keep focused on what you can control yourself and that's lifestyle factors.

6. Does a high fat diet cause fatty liver disease?

The only diet known to reverse fatty liver disease is a ketogenic diet, which is a very low carb diet. The magic seems to come from the elimination of carbs, particularly sugar, rather than the addition of fat as low carb diets alone improve fatty liver disease.

This makes sense as fatty liver disease can be caused by three things:

  • A high sugar diet
  • High alcohol consumption
  • Viral infections

There is no "high fat diet" in that list anywhere. Certain hunter/gatherers who eat extraordinarily high fat diets do not ever develop fatty liver disease and neither do hunter/gatherers who eat a very high carb diet. This is why I made clear that a high sugar diet causes fatty liver, not a high carb diet alone.

Fructose seems to be the culprit for the disease and sugar is half fructose. Fructose is metabolized in the liver the same way as alcohol and this seems to be the catalyst for poor liver function. This is why sugar can be considered a hepatotoxin.

It would not be surprising if certain high fat diets can very well be complicit in the development of fatty liver disease as plant-based oils, particularly vegetable oils, have been implicated in dysregulating the liver's ability of managing fat within itself. Vegetable oils, seem to not be released from the liver as readily as animal-based fats with the exception of coconut oil. These oils also seem to contribute to more subcutaneous fat accumulation which will eventually affect visceral and ectopic fat.

So the make up of the fatty acids in different fats can effect liver function. For this reason, use oils sparingly and stick to saturated fats in moderation.

Six common beliefs addressed, Part 194

1. I lost a lot of weight on "keto" but now I have an iron deficiency.

Iron deficiencies can be caused by numerous things. You need to discuss this with your doctor and get the appropriate testing in order to determine what could be the cause.

2. There are fasting mimicking diets for those who can't tolerate strict extended fasting.

Ketogenic protocols are fasting mimicking diets. This is why they produce ketones. Ketones are a signal to the body that there is some form of starvation occurring.

You should not be doing any extended fasting unless you want to remain fat and become fatter. Extended fasting would be perfect for that as it further down regulates leptin very well.

I have a great way of gaining a lot of fat and keeping it on. You fast for about fourteen days and then eat "keto" bread and ice cream for the next seven. Keep doing that for about six months and you won't fit through the door by the end of it. Guaranteed results.

3. "Insulin is fattening". This is why type I diabetics become thin if they stop dosing exogenous insulin. 

This is part of the dangerous quackery surrounding the low carb community. They just can't shake the nonsense off to save their own life or anyone else's. They are the ones solely responsible of why low carb diets are not taken seriously by anyone. But let's be realistic here. All diet mongers claim to know the "one thing" that's to blame for obesity, which they magically have the easy "cure" for. The problem is that they always get it wrong. There is only one thing to blame for obesity - blood glucose dysregulation which results in insulin dysfunction and causes a chronic under expression of leptin. There is no known "cure" for it.

Insulin is not an obesity hormone. We all know it helps regulate blood glucose but it also stimulates the uptake of amino acids into cells and protein synthesis in muscle tissue. This means that you cannot have proper lean muscle mass without insulin. But aside from these anabolic properties, insulin is also an anticatabolic hormone. In other words, insulin prevents your body from breaking itself down into sugar and ketones through its regulation of glucagon. Leptin also regulates glucagon and leptin is a slave to insulin.

Type I diabetics do not "become thin" when they stop taking their exogenous insulin. They waste away to nothing and then eventually die from "glucagon gone wild". Leanness and wasting are two very different things, just like weight gain and obesity are two very different things. It doesn't matter that they both make the scale go up or down. Insulin surely does not make body builders obese and some inject it exogenously for gains. So it takes very different metabolic profiles to become lean, obese, muscular or emaciated. All of these metabolic profiles use metabolic hormones, like insulin, to acquire the end result but insulin in of itself is not the problem. The problem is the metabolic profile that it's in.

Insulin in a metabolic profile that does nothing but store fat is bad but so is insulin that doesn't build muscle or that breaks you down into sugar. All metabolic hormones are a slave to whatever metabolic profile you put them in. When you deteriorate insulin function from blood glucose dysregulation, then you will get insulin that stores fat and doesn't build muscle.

4. Coconut does not raise LDL cholesterol.

There are two important issues that are not correctly understood in the fad "keto" world - ketosis and lipids

The first one, ketosis, is easy. The type of ketosis that a person with metabolic issues wants to be in, is the ketosis produced from the burning of their own body fat. Not the burning of coconut oil, a dietary fat. Burning coconut oil means nothing. It just means you are alive and can produce heat. Being able to burn your own body fat means a lot. It is an indication that your metabolism is on the road to correcting itself. You need properly working leptin to burn body fat and that's not achieved through the consumption of coconut oil, but through the normalization of insulin expression.

Now comes the hard part, lipids. Coconut oil absolutely raises total cholesterol in some individuals more than others. This rise includes both HDL and LDL (lipoproteins) and the rise between the two depends on genetic variability. Coconut oil is composed of a variety of fatty acids but it's the lauric, myristic and palmitic acids which produce the main effects on LDL. What does that mean? We don't know. The reason we don't know is because rise and fall in lipoproteins do not tell us a thing about whether their function is benign or malignant. We usually discover this when you drop dead of a heart attack, not before.

Unfortunately, lipoprotein function is extremely complicated and science has not caught up with what exactly causes lipoprotein pathology. For this reason, the go-to "treatment" is to lower all lipoproteins (total cholesterol). The premise is that lowering them might cause some good and certainly no harm. That has not panned out for the majority of people but it has for a small segment.

There is a small segment of the population that has an LDL abnormality which puts them at high risk for heart disease and no, it's not simply hypercholesterolemia though it falls under that umbrella. There are actually many forms of hypercholesterolemia, many which are benign. After all, hypercholesterolemia simply means "high cholesterol". Instead, this malignant form of hypercholesterolemia is an actual LDL malfunction which is not fully understood as it is not known if the malfunction is in the LDL itself or in various apolipoproteins or both or what. What is known is that these people benefit significantly from an aggressive reduction of LDL. For this reason, we know that LDL is implicated in the atherosclerotic process but no one knows exactly how it becomes pathological.

To make matters even more complicated, many people have LDL malfunction with absolutely no rise in its levels. In fact, that is the most common form of LDL malfunction. This is why the vast majority of people suffer from heart disease or die of heart attacks with low to normal total cholesterol. I am no even taking into account all of the cardiovascular disease that is not lipid related at all.

I tried to keep the above explanation as simple as possible because it's an extremely complex topic and goes way beyond the scope of this blog. It is so complex than even lipidologists, who have dedicated their entire lives researching this, have differing opinions on what has been found so far. Worse, this is not only complex, it is not helpful to you. It's interesting. It's fascinating. But it's not helpful, particularly for those trying to resolve their metabolic syndrome. This is what irks me about "low carb doctors". They are trying to act as if they know about a subject matter that is so incredibly difficult, and goes way beyond the scope of their practice and knowledge, that they shouldn't be advising on it at all. All they want to do is find an excuse for you to continue taking their snake oil, even if it's at your detriment. Well, I don't sacrifice people in order to push an agenda.

For this reason, the best approach that someone should take with their cholesterol is that of caution. That's how we deal with this subject matter on this blog – very cautiously, because unlike "low carb doctors", I do not claim to know everything and I am certainly not a lipidologist.

Use common sense and stay away from coconut oil if it's raising your LDL cholesterol. In fact, you should stay away from coconut oil even if it's not, particularly if you have a family history of heart disease. This is because you can be one of those people that simply cannot metabolize these fatty acids well and end up with early onset heart disease. No one will be able to tell you in advance if you are that person or not until you have heart disease, unless you are able to perform extremely expensive genetic lipid testing that has to be interpreted by a lipidologist. If your doctor has issues prescribing you an insulin test, you can only imagine how they will feel about a rare genetic test, that they might not have even heard of before. Don't wait for your doctor and don't wait for a heart attack to get answers. You also don't want your answers coming from a low carb bozo. You have to advocate for yourself. Stop putting your health in someone else's hands.

The vast majority of us are of ancestry that did not evolve consuming coconut oil. Particularly not out of a hunter/gatherer environment. Coconuts are quite rare. They are only available in very specific regions. This means you can easily swap out coconut oil for ghee and not eat gallons of it. If your lipids are particularly sensitive, you can swap out all saturated fats for monounsaturated fats and still be in ketosis. Like I said before, ketosis is only beneficial if it's coming from the burning of your own body fat and that is achieved through very low carbohydrate intake.

5. I want to follow this diet but I get tired of eating the same foods.

I am assuming that "this diet" is referring to low carb diets as you never specified. 

Every time someone comes with this type of complaint, I know they are full of BS. On planet earth, food only comes in two forms - meat and vegetables. This means that there isn't much variety on what to eat except by preparing and combining these items in different ways with varying spices and herbs. What you are truly tired of eating is food. You want junk and I can't help with that.

I have said before, that on this blog, we do not coddle obesity by giving credence to excuses. You either follow the diet properly, or you don't. You always have a choice. You can choose to remain obese.

6. I am struggling with staying carnivore. I just think my “addiction” is very strong.

This is a blog for advice on metabolic health. We are not a sobriety group so we do not recognize “addiction”, in the context of food, as a legitimate condition. Here, we only recognize habits, excuses and negligence.

Changing your diet is a very difficult thing to do as all living things are creatures of habit and seek to continue with familiar norms. But if you are truly concerned with your health and lifespan, then you would do whatever it takes to correct it. This should take precedence over the desire to keep old habits.